Ingrid Pinzon, MD, FACP, was working as a medical assistant to a physician a decade ago when she heard the doctor prescribe ibuprofen to a woman who was in the latter stages of pregnancy. Dr. Pinzon was a doctor, having received her education and training in Colombia, but because she had emigrated to the United States and hadn’t yet completed her certification and training here, she was not recognized yet as an American physician.

But she knew that ibuprofen was not recommended during late-term pregnancy, and she was alarmed. She informed the physician of the mistake. The doctor headed to Google, Dr. Pinzon said, and called the patient to rescind the ibuprofen prescription. But she soon fired Dr. Pinzon, seemingly for having had the courage to speak up.

Dr. Pinzon, now medical director of care coordination at Emory Johns Creek Hospital in Atlanta, will describe her experience as an immigrant physician in the Society of Hospital Medicine Converge session: “A Walk in Our Shoes: Immigrant Physicians Sharing Their Stories.” She will be joined by Patricia O’Brien, MD, PhD, FAAP, a pediatric hospitalist in Tampa; Manpreet Malik, MD, a hospitalist at Emory University; and Benji Mathews, MD, SFHM, FACP, chief of hospital medicine at HealthPartners and associate professor at the University of Minnesota.

They will describe their struggles to find their way in the United States, along with the satisfaction of having hard work pay off with better lives for themselves and their families. And together, they’ll provide a variety of narratives that will show, contrary to how many Americans view immigrants, how the experiences of immigrants don’t follow the same path, but each one carves out a path of his or her own.

“The thrust of this is really storytelling, along with putting into context what we can do to help our hospitalist brothers and sisters who are immigrants, and shining the light on it,” Dr. O’Brien said.

Dr. Pinzon was working as a doctor for the Colombian government when she began receiving threats from soldiers in a guerrilla army, which didn’t agree with her alignment with the government. One day, a guerrilla soldier threatened her and her two daughters – aged 5 and 11 at the time – and accurately described her daughters’ whereabouts.

Less than a week later, she and her daughters flew from Bogota to the United States, never to return to Colombia.

“I dropped everything I had when I came here,” she said. An immigration attorney initially recommended that she marry an American man in order to stay in the United States. When Dr. Pinzon declined, they pursued political asylum, and she received it less than a year later.

For 3 years, she worked jobs as assistants in medical offices and in other jobs, well below her education level, as she guided her daughters through school and went through the U.S. medical certification process. She was besieged by doubt constantly, she said.

“I cried for 3 years in a row,” she said. “I wanted to go back to my country. I didn’t want to stay here.”

Finally, she did her medical residency between 2011 and 2014, and got a job with Emory. Her daughters are grown, and one is a doctor in general surgery residency. Dr. Pinzon said she is happy to care for patients, particularly those who are Spanish-speaking and struggle as she did. But she often encounters patients who don’t hide that they dislike her accent.

“I will mute the TV and I will say: ‘I have a strong accent and so I want to make sure communication is clear,’ ” she said. “We have to prove ourselves all of the time. I feel like I have to prove myself to my patients that I’m a good doctor all of the time.” American-born doctors, she added, “shouldn’t take for granted what they already have.”

Dr. O’Brien grew up in Ireland, but in the late 1980s, the country was in a serious recession, with unemployment close to 20%, and her father applied for residency in Canada and the United States. They were accepted in Canada first, and moved there in 1988. A few years later, her parents moved them to Florida.

“They knew in order for us to do well, we had to go abroad,” she said. Dr. O’Brien went to college, medical school and graduate school in Florida, and completed residency in Cincinnati. Feeling the tug of her birthplace, she moved back to Ireland and worked there for a couple years.

“I never really wanted to leave because it was my home,” she said. While there, she came to a new-found appreciation for the U.S. health care system. It’s true that, in Ireland, everyone is insured, but there long wait times – for example, up to 2 years for a sedated nonurgent MRI for a child. She once had to send a patient to Dublin in a taxi with a nurse because an ambulance was unavailable.

“After going back to Ireland, where – I honestly thought I was going to go back and settle there – I realized how visionary my parents were in moving us,” Dr. O’Brien said. “This system in the U.S., there are lot of things broken about it, but we have all the resources.”

She moved back to the United States in August 2016, during a period of anti-immigrant rhetoric.

Nonetheless, Dr. O’Brien said she is happy to be here despite the lack of tolerance she sees in a minority of the U.S. population.

“Have a bit of sensitivity toward your provider. Maybe they speak with an accent. Maybe they don’t speak English perfectly. Maybe they have a different skin color. But their intention is good and it’s to help you and improve your health,” she said.

Ingrid Pinzon, MD, FACP, was working as a medical assistant to a physician a decade ago when she heard the doctor prescribe ibuprofen to a woman who was in the latter stages of pregnancy. Dr. Pinzon was a doctor, having received her education and training in Colombia, but because she had emigrated to the United States and hadn’t yet completed her certification and training here, she was not recognized yet as an American physician.

But she knew that ibuprofen was not recommended during late-term pregnancy, and she was alarmed. She informed the physician of the mistake. The doctor headed to Google, Dr. Pinzon said, and called the patient to rescind the ibuprofen prescription. But she soon fired Dr. Pinzon, seemingly for having had the courage to speak up.

Dr. Pinzon, now medical director of care coordination at Emory Johns Creek Hospital in Atlanta, will describe her experience as an immigrant physician in the Society of Hospital Medicine Converge session: “A Walk in Our Shoes: Immigrant Physicians Sharing Their Stories.” She will be joined by Patricia O’Brien, MD, PhD, FAAP, a pediatric hospitalist in Tampa; Manpreet Malik, MD, a hospitalist at Emory University; and Benji Mathews, MD, SFHM, FACP, chief of hospital medicine at HealthPartners and associate professor at the University of Minnesota.

They will describe their struggles to find their way in the United States, along with the satisfaction of having hard work pay off with better lives for themselves and their families. And together, they’ll provide a variety of narratives that will show, contrary to how many Americans view immigrants, how the experiences of immigrants don’t follow the same path, but each one carves out a path of his or her own.

“The thrust of this is really storytelling, along with putting into context what we can do to help our hospitalist brothers and sisters who are immigrants, and shining the light on it,” Dr. O’Brien said.

Dr. Pinzon was working as a doctor for the Colombian government when she began receiving threats from soldiers in a guerrilla army, which didn’t agree with her alignment with the government. One day, a guerrilla soldier threatened her and her two daughters – aged 5 and 11 at the time – and accurately described her daughters’ whereabouts.

Less than a week later, she and her daughters flew from Bogota to the United States, never to return to Colombia.

“I dropped everything I had when I came here,” she said. An immigration attorney initially recommended that she marry an American man in order to stay in the United States. When Dr. Pinzon declined, they pursued political asylum, and she received it less than a year later.

For 3 years, she worked jobs as assistants in medical offices and in other jobs, well below her education level, as she guided her daughters through school and went through the U.S. medical certification process. She was besieged by doubt constantly, she said.

“I cried for 3 years in a row,” she said. “I wanted to go back to my country. I didn’t want to stay here.”

Finally, she did her medical residency between 2011 and 2014, and got a job with Emory. Her daughters are grown, and one is a doctor in general surgery residency. Dr. Pinzon said she is happy to care for patients, particularly those who are Spanish-speaking and struggle as she did. But she often encounters patients who don’t hide that they dislike her accent.

“I will mute the TV and I will say: ‘I have a strong accent and so I want to make sure communication is clear,’ ” she said. “We have to prove ourselves all of the time. I feel like I have to prove myself to my patients that I’m a good doctor all of the time.” American-born doctors, she added, “shouldn’t take for granted what they already have.”

Dr. O’Brien grew up in Ireland, but in the late 1980s, the country was in a serious recession, with unemployment close to 20%, and her father applied for residency in Canada and the United States. They were accepted in Canada first, and moved there in 1988. A few years later, her parents moved them to Florida.

“They knew in order for us to do well, we had to go abroad,” she said. Dr. O’Brien went to college, medical school and graduate school in Florida, and completed residency in Cincinnati. Feeling the tug of her birthplace, she moved back to Ireland and worked there for a couple years.

“I never really wanted to leave because it was my home,” she said. While there, she came to a new-found appreciation for the U.S. health care system. It’s true that, in Ireland, everyone is insured, but there long wait times – for example, up to 2 years for a sedated nonurgent MRI for a child. She once had to send a patient to Dublin in a taxi with a nurse because an ambulance was unavailable.

“After going back to Ireland, where – I honestly thought I was going to go back and settle there – I realized how visionary my parents were in moving us,” Dr. O’Brien said. “This system in the U.S., there are lot of things broken about it, but we have all the resources.”

She moved back to the United States in August 2016, during a period of anti-immigrant rhetoric.

Nonetheless, Dr. O’Brien said she is happy to be here despite the lack of tolerance she sees in a minority of the U.S. population.

“Have a bit of sensitivity toward your provider. Maybe they speak with an accent. Maybe they don’t speak English perfectly. Maybe they have a different skin color. But their intention is good and it’s to help you and improve your health,” she said.

Ingrid Pinzon, MD, FACP, was working as a medical assistant to a physician a decade ago when she heard the doctor prescribe ibuprofen to a woman who was in the latter stages of pregnancy. Dr. Pinzon was a doctor, having received her education and training in Colombia, but because she had emigrated to the United States and hadn’t yet completed her certification and training here, she was not recognized yet as an American physician.

But she knew that ibuprofen was not recommended during late-term pregnancy, and she was alarmed. She informed the physician of the mistake. The doctor headed to Google, Dr. Pinzon said, and called the patient to rescind the ibuprofen prescription. But she soon fired Dr. Pinzon, seemingly for having had the courage to speak up.

Dr. Pinzon, now medical director of care coordination at Emory Johns Creek Hospital in Atlanta, will describe her experience as an immigrant physician in the Society of Hospital Medicine Converge session: “A Walk in Our Shoes: Immigrant Physicians Sharing Their Stories.” She will be joined by Patricia O’Brien, MD, PhD, FAAP, a pediatric hospitalist in Tampa; Manpreet Malik, MD, a hospitalist at Emory University; and Benji Mathews, MD, SFHM, FACP, chief of hospital medicine at HealthPartners and associate professor at the University of Minnesota.

They will describe their struggles to find their way in the United States, along with the satisfaction of having hard work pay off with better lives for themselves and their families. And together, they’ll provide a variety of narratives that will show, contrary to how many Americans view immigrants, how the experiences of immigrants don’t follow the same path, but each one carves out a path of his or her own.

“The thrust of this is really storytelling, along with putting into context what we can do to help our hospitalist brothers and sisters who are immigrants, and shining the light on it,” Dr. O’Brien said.

Dr. Pinzon was working as a doctor for the Colombian government when she began receiving threats from soldiers in a guerrilla army, which didn’t agree with her alignment with the government. One day, a guerrilla soldier threatened her and her two daughters – aged 5 and 11 at the time – and accurately described her daughters’ whereabouts.

Less than a week later, she and her daughters flew from Bogota to the United States, never to return to Colombia.

“I dropped everything I had when I came here,” she said. An immigration attorney initially recommended that she marry an American man in order to stay in the United States. When Dr. Pinzon declined, they pursued political asylum, and she received it less than a year later.

For 3 years, she worked jobs as assistants in medical offices and in other jobs, well below her education level, as she guided her daughters through school and went through the U.S. medical certification process. She was besieged by doubt constantly, she said.

“I cried for 3 years in a row,” she said. “I wanted to go back to my country. I didn’t want to stay here.”

Finally, she did her medical residency between 2011 and 2014, and got a job with Emory. Her daughters are grown, and one is a doctor in general surgery residency. Dr. Pinzon said she is happy to care for patients, particularly those who are Spanish-speaking and struggle as she did. But she often encounters patients who don’t hide that they dislike her accent.

“I will mute the TV and I will say: ‘I have a strong accent and so I want to make sure communication is clear,’ ” she said. “We have to prove ourselves all of the time. I feel like I have to prove myself to my patients that I’m a good doctor all of the time.” American-born doctors, she added, “shouldn’t take for granted what they already have.”

Dr. O’Brien grew up in Ireland, but in the late 1980s, the country was in a serious recession, with unemployment close to 20%, and her father applied for residency in Canada and the United States. They were accepted in Canada first, and moved there in 1988. A few years later, her parents moved them to Florida.

“They knew in order for us to do well, we had to go abroad,” she said. Dr. O’Brien went to college, medical school and graduate school in Florida, and completed residency in Cincinnati. Feeling the tug of her birthplace, she moved back to Ireland and worked there for a couple years.

“I never really wanted to leave because it was my home,” she said. While there, she came to a new-found appreciation for the U.S. health care system. It’s true that, in Ireland, everyone is insured, but there long wait times – for example, up to 2 years for a sedated nonurgent MRI for a child. She once had to send a patient to Dublin in a taxi with a nurse because an ambulance was unavailable.

“After going back to Ireland, where – I honestly thought I was going to go back and settle there – I realized how visionary my parents were in moving us,” Dr. O’Brien said. “This system in the U.S., there are lot of things broken about it, but we have all the resources.”

She moved back to the United States in August 2016, during a period of anti-immigrant rhetoric.

Nonetheless, Dr. O’Brien said she is happy to be here despite the lack of tolerance she sees in a minority of the U.S. population.

“Have a bit of sensitivity toward your provider. Maybe they speak with an accent. Maybe they don’t speak English perfectly. Maybe they have a different skin color. But their intention is good and it’s to help you and improve your health,” she said.

An overview of five important advances in pulmonary and critical care medicine are on the agenda for the “Update in Pulmonary and Critical Care” session on Tuesday, May 4, at the virtual 2021 SHM Converge conference.

“I hope this session gives attendees a nice, broad look at advances both in the intensive care unit and in general pulmonary medicine,” said James Walter, MD, of Northwestern Medicine in Chicago, who serves as director of the session.

On the critical care medicine side, Dr. Walter will review the latest research on the efficacy of ascorbic acid in treating patients with severe sepsis and septic shock. “There was a lot of excitement and some skepticism about early results promising a really large treatment effect in giving critically ill patients with sepsis large doses of vitamin C,” Dr. Walter said. The last year has produced some high-quality randomized trials that have contributed to a better understanding of the potential effects ascorbic acid in sepsis can have, he noted.

Dr. Walter, who is also medical director of the Northwestern Lung Rescue Program, intends to discuss what he believes is a definitive trial regarding the benefit of preemptively starting critically ill patients with acute kidney injury on renal replacement therapy instead of waiting until there are specific clinical signs. “This has been another area of uncertainty in critical care and I think we finally have a very definitive answer with this high quality, randomized, controlled trial that I plan to review,” he said.

Though he said there have been a number of important advances in pulmonary medicine over the past year, Dr. Walter will highlight just two.

Up until recently, the antifibrotics nintedanib and pirfenidone have mostly been used in patients with idiopathic pulmonary fibrosis. However, recent research suggests there may be a potential benefit to using these drugs in patients with fibrotic lung disease outside of idiopathic pulmonary fibrosis. “I think this is an important advance for hospital medicine providers to be aware of,” said Dr. Walter.

He will also go over some large randomized controlled trials of the use of triple therapy – a combination of a long-acting beta agonist (LABA), a long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid in one inhaler – in chronic obstructive pulmonary disease. The trials looked at whether triple inhaler therapy was beneficial compared to the typical therapies used for COPD.

The session wouldn’t be complete without a nod to COVID-19, which Dr. Walter said has significantly changed the landscape for hospital medicine providers. He plans to discuss what he considers the most impactful study – the RECOVERY trial. This study looked at the role of dexamethasone in patients with more severe manifestations of SARS-CoV-2.

“From the incredible amount of data that’s come out in the last year about COVID, I think this is probably the trial that’s changed practice the most and shown the largest therapeutic benefit of all the pharmacotherapies,” Dr. Walter said. “It’s an important one for providers to be aware of in terms of what the trial shows and how it informs which patients are most likely to benefit from dexamethasone therapy.”

Dr. Walter hopes clinicians who participate in the session will leave with these takeaways:

• Be able to summarize recent trials of ascorbic acid in sepsis and think about how to incorporate – or not – the use of vitamin C in critically ill sepsis patients.
• A thorough understanding of when renal replacement therapy should be offered to critically ill patients with acute kidney dysfunction.
• Be able to discuss the impact of antifibrotic therapy in interstitial lung diseases outside of idiopathic pulmonary fibrosis.
• An understanding of the role of triple inhaler combinations in COPD.
• Be able to explain when dexamethasone is most likely to benefit hypoxemic patients with COVID-19.

An overview of five important advances in pulmonary and critical care medicine are on the agenda for the “Update in Pulmonary and Critical Care” session on Tuesday, May 4, at the virtual 2021 SHM Converge conference.

“I hope this session gives attendees a nice, broad look at advances both in the intensive care unit and in general pulmonary medicine,” said James Walter, MD, of Northwestern Medicine in Chicago, who serves as director of the session.

On the critical care medicine side, Dr. Walter will review the latest research on the efficacy of ascorbic acid in treating patients with severe sepsis and septic shock. “There was a lot of excitement and some skepticism about early results promising a really large treatment effect in giving critically ill patients with sepsis large doses of vitamin C,” Dr. Walter said. The last year has produced some high-quality randomized trials that have contributed to a better understanding of the potential effects ascorbic acid in sepsis can have, he noted.

Dr. Walter, who is also medical director of the Northwestern Lung Rescue Program, intends to discuss what he believes is a definitive trial regarding the benefit of preemptively starting critically ill patients with acute kidney injury on renal replacement therapy instead of waiting until there are specific clinical signs. “This has been another area of uncertainty in critical care and I think we finally have a very definitive answer with this high quality, randomized, controlled trial that I plan to review,” he said.

Though he said there have been a number of important advances in pulmonary medicine over the past year, Dr. Walter will highlight just two.

Up until recently, the antifibrotics nintedanib and pirfenidone have mostly been used in patients with idiopathic pulmonary fibrosis. However, recent research suggests there may be a potential benefit to using these drugs in patients with fibrotic lung disease outside of idiopathic pulmonary fibrosis. “I think this is an important advance for hospital medicine providers to be aware of,” said Dr. Walter.

He will also go over some large randomized controlled trials of the use of triple therapy – a combination of a long-acting beta agonist (LABA), a long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid in one inhaler – in chronic obstructive pulmonary disease. The trials looked at whether triple inhaler therapy was beneficial compared to the typical therapies used for COPD.

The session wouldn’t be complete without a nod to COVID-19, which Dr. Walter said has significantly changed the landscape for hospital medicine providers. He plans to discuss what he considers the most impactful study – the RECOVERY trial. This study looked at the role of dexamethasone in patients with more severe manifestations of SARS-CoV-2.

“From the incredible amount of data that’s come out in the last year about COVID, I think this is probably the trial that’s changed practice the most and shown the largest therapeutic benefit of all the pharmacotherapies,” Dr. Walter said. “It’s an important one for providers to be aware of in terms of what the trial shows and how it informs which patients are most likely to benefit from dexamethasone therapy.”

Dr. Walter hopes clinicians who participate in the session will leave with these takeaways:

• Be able to summarize recent trials of ascorbic acid in sepsis and think about how to incorporate – or not – the use of vitamin C in critically ill sepsis patients.
• A thorough understanding of when renal replacement therapy should be offered to critically ill patients with acute kidney dysfunction.
• Be able to discuss the impact of antifibrotic therapy in interstitial lung diseases outside of idiopathic pulmonary fibrosis.
• An understanding of the role of triple inhaler combinations in COPD.
• Be able to explain when dexamethasone is most likely to benefit hypoxemic patients with COVID-19.

An overview of five important advances in pulmonary and critical care medicine are on the agenda for the “Update in Pulmonary and Critical Care” session on Tuesday, May 4, at the virtual 2021 SHM Converge conference.

“I hope this session gives attendees a nice, broad look at advances both in the intensive care unit and in general pulmonary medicine,” said James Walter, MD, of Northwestern Medicine in Chicago, who serves as director of the session.

On the critical care medicine side, Dr. Walter will review the latest research on the efficacy of ascorbic acid in treating patients with severe sepsis and septic shock. “There was a lot of excitement and some skepticism about early results promising a really large treatment effect in giving critically ill patients with sepsis large doses of vitamin C,” Dr. Walter said. The last year has produced some high-quality randomized trials that have contributed to a better understanding of the potential effects ascorbic acid in sepsis can have, he noted.

Dr. Walter, who is also medical director of the Northwestern Lung Rescue Program, intends to discuss what he believes is a definitive trial regarding the benefit of preemptively starting critically ill patients with acute kidney injury on renal replacement therapy instead of waiting until there are specific clinical signs. “This has been another area of uncertainty in critical care and I think we finally have a very definitive answer with this high quality, randomized, controlled trial that I plan to review,” he said.

Though he said there have been a number of important advances in pulmonary medicine over the past year, Dr. Walter will highlight just two.

Up until recently, the antifibrotics nintedanib and pirfenidone have mostly been used in patients with idiopathic pulmonary fibrosis. However, recent research suggests there may be a potential benefit to using these drugs in patients with fibrotic lung disease outside of idiopathic pulmonary fibrosis. “I think this is an important advance for hospital medicine providers to be aware of,” said Dr. Walter.

He will also go over some large randomized controlled trials of the use of triple therapy – a combination of a long-acting beta agonist (LABA), a long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid in one inhaler – in chronic obstructive pulmonary disease. The trials looked at whether triple inhaler therapy was beneficial compared to the typical therapies used for COPD.

The session wouldn’t be complete without a nod to COVID-19, which Dr. Walter said has significantly changed the landscape for hospital medicine providers. He plans to discuss what he considers the most impactful study – the RECOVERY trial. This study looked at the role of dexamethasone in patients with more severe manifestations of SARS-CoV-2.

“From the incredible amount of data that’s come out in the last year about COVID, I think this is probably the trial that’s changed practice the most and shown the largest therapeutic benefit of all the pharmacotherapies,” Dr. Walter said. “It’s an important one for providers to be aware of in terms of what the trial shows and how it informs which patients are most likely to benefit from dexamethasone therapy.”

Dr. Walter hopes clinicians who participate in the session will leave with these takeaways:

• Be able to summarize recent trials of ascorbic acid in sepsis and think about how to incorporate – or not – the use of vitamin C in critically ill sepsis patients.
• A thorough understanding of when renal replacement therapy should be offered to critically ill patients with acute kidney dysfunction.
• Be able to discuss the impact of antifibrotic therapy in interstitial lung diseases outside of idiopathic pulmonary fibrosis.
• An understanding of the role of triple inhaler combinations in COPD.
• Be able to explain when dexamethasone is most likely to benefit hypoxemic patients with COVID-19.

The weeks leading up to our Annual Conference always trigger certain rituals for me.

Deciding which sessions to attend feels like planning an intellectual feast mixed with an exercise in compromise, as I realize there is just no way to attend every session that I want to. Scheduling all my plans to connect over dinner and drinks with current and former colleagues is a logistical challenge I undertake with anticipation and some stress, especially when I’m the one tasked with making restaurant reservations. Thinking about how to pay for it all means digging out the rules around my CME faculty allowance, after first figuring out if I still even have a CME allowance, of course.

In the years that I am presenting, there are the last-minute emails with my co-presenters to arrange a time to run through our slides together on site. The prospect of seeing cherished colleagues and friends from SHM mixes with the fact that I know I will miss my wife and young son while I am away. Overall though, I am filled with a tremendous sense of excitement, a feeling that I enjoy in a sustained way for weeks before the meeting.

My excitement for SHM Converge is just as strong, but different in some great and important ways. The availability of on-demand content means I won’t have to choose one session over another this year – I can have my cake and eat it, too. Without the need to travel, expenses will be considerably less, and I won’t need to be away from my family.

But what I am most thrilled about when I think about SHM Converge is the content. A year of planning by our outstanding SHM staff, leadership, and Annual Conference Committee has produced a lineup of world-class speakers. Our virtual platform will offer a rich interactive and networking experience. Perennial favorite sessions, such as the Great Debate, Rapid Fire, and Update sessions will provide attendees the chance to update their core clinical knowledge across the breadth of hospital medicine.

Many aspects of health equity will be explored. Over 15 sessions and four special-interest forums covering topics such as racial and gender inequities, implicit bias, vulnerable populations, and ethics will help attendees not only understand the issues but also will show them how they can take action to make a difference.

Clinical and operational aspects of COVID-19 will also be covered at SHM Converge as speakers share the tremendous innovation, triumphs, and challenges that have taken place over the past year. Wellness and resilience are, of course, as relevant as ever, and sessions on balancing parenthood and work, learning from personal failures, and how to handle uncertainty and be resilient are among the topics that will be covered.

The essence of what we will do at SHM Converge in May is captured in our new meeting logo, an animation of nodes connecting with each other through lines that travel short and long, and intersect along the way. It’s a great representation of the togetherness, community, and mutual support that is at the core of who we are as SHM – now, more than ever. Thank you for joining us!

Dr. Steinberg is chief patient safety officer at Mount Sinai Downtown, and associate dean for quality/patient safety in GME, Mount Sinai Health System, New York. He is professor of medicine and medical education at the Icahn School of Medicine at Mount Sinai, and course director of SHM Converge.

The weeks leading up to our Annual Conference always trigger certain rituals for me.

Deciding which sessions to attend feels like planning an intellectual feast mixed with an exercise in compromise, as I realize there is just no way to attend every session that I want to. Scheduling all my plans to connect over dinner and drinks with current and former colleagues is a logistical challenge I undertake with anticipation and some stress, especially when I’m the one tasked with making restaurant reservations. Thinking about how to pay for it all means digging out the rules around my CME faculty allowance, after first figuring out if I still even have a CME allowance, of course.

In the years that I am presenting, there are the last-minute emails with my co-presenters to arrange a time to run through our slides together on site. The prospect of seeing cherished colleagues and friends from SHM mixes with the fact that I know I will miss my wife and young son while I am away. Overall though, I am filled with a tremendous sense of excitement, a feeling that I enjoy in a sustained way for weeks before the meeting.

My excitement for SHM Converge is just as strong, but different in some great and important ways. The availability of on-demand content means I won’t have to choose one session over another this year – I can have my cake and eat it, too. Without the need to travel, expenses will be considerably less, and I won’t need to be away from my family.

But what I am most thrilled about when I think about SHM Converge is the content. A year of planning by our outstanding SHM staff, leadership, and Annual Conference Committee has produced a lineup of world-class speakers. Our virtual platform will offer a rich interactive and networking experience. Perennial favorite sessions, such as the Great Debate, Rapid Fire, and Update sessions will provide attendees the chance to update their core clinical knowledge across the breadth of hospital medicine.

Many aspects of health equity will be explored. Over 15 sessions and four special-interest forums covering topics such as racial and gender inequities, implicit bias, vulnerable populations, and ethics will help attendees not only understand the issues but also will show them how they can take action to make a difference.

Clinical and operational aspects of COVID-19 will also be covered at SHM Converge as speakers share the tremendous innovation, triumphs, and challenges that have taken place over the past year. Wellness and resilience are, of course, as relevant as ever, and sessions on balancing parenthood and work, learning from personal failures, and how to handle uncertainty and be resilient are among the topics that will be covered.

The essence of what we will do at SHM Converge in May is captured in our new meeting logo, an animation of nodes connecting with each other through lines that travel short and long, and intersect along the way. It’s a great representation of the togetherness, community, and mutual support that is at the core of who we are as SHM – now, more than ever. Thank you for joining us!

Dr. Steinberg is chief patient safety officer at Mount Sinai Downtown, and associate dean for quality/patient safety in GME, Mount Sinai Health System, New York. He is professor of medicine and medical education at the Icahn School of Medicine at Mount Sinai, and course director of SHM Converge.

The weeks leading up to our Annual Conference always trigger certain rituals for me.

Deciding which sessions to attend feels like planning an intellectual feast mixed with an exercise in compromise, as I realize there is just no way to attend every session that I want to. Scheduling all my plans to connect over dinner and drinks with current and former colleagues is a logistical challenge I undertake with anticipation and some stress, especially when I’m the one tasked with making restaurant reservations. Thinking about how to pay for it all means digging out the rules around my CME faculty allowance, after first figuring out if I still even have a CME allowance, of course.

In the years that I am presenting, there are the last-minute emails with my co-presenters to arrange a time to run through our slides together on site. The prospect of seeing cherished colleagues and friends from SHM mixes with the fact that I know I will miss my wife and young son while I am away. Overall though, I am filled with a tremendous sense of excitement, a feeling that I enjoy in a sustained way for weeks before the meeting.

My excitement for SHM Converge is just as strong, but different in some great and important ways. The availability of on-demand content means I won’t have to choose one session over another this year – I can have my cake and eat it, too. Without the need to travel, expenses will be considerably less, and I won’t need to be away from my family.

But what I am most thrilled about when I think about SHM Converge is the content. A year of planning by our outstanding SHM staff, leadership, and Annual Conference Committee has produced a lineup of world-class speakers. Our virtual platform will offer a rich interactive and networking experience. Perennial favorite sessions, such as the Great Debate, Rapid Fire, and Update sessions will provide attendees the chance to update their core clinical knowledge across the breadth of hospital medicine.

Many aspects of health equity will be explored. Over 15 sessions and four special-interest forums covering topics such as racial and gender inequities, implicit bias, vulnerable populations, and ethics will help attendees not only understand the issues but also will show them how they can take action to make a difference.

Clinical and operational aspects of COVID-19 will also be covered at SHM Converge as speakers share the tremendous innovation, triumphs, and challenges that have taken place over the past year. Wellness and resilience are, of course, as relevant as ever, and sessions on balancing parenthood and work, learning from personal failures, and how to handle uncertainty and be resilient are among the topics that will be covered.

The essence of what we will do at SHM Converge in May is captured in our new meeting logo, an animation of nodes connecting with each other through lines that travel short and long, and intersect along the way. It’s a great representation of the togetherness, community, and mutual support that is at the core of who we are as SHM – now, more than ever. Thank you for joining us!

Dr. Steinberg is chief patient safety officer at Mount Sinai Downtown, and associate dean for quality/patient safety in GME, Mount Sinai Health System, New York. He is professor of medicine and medical education at the Icahn School of Medicine at Mount Sinai, and course director of SHM Converge.

The antibody-drug conjugate enfortumab vedotin is superior to chemotherapy in patients with previously treated advanced urothelial carcinoma, primary results of the EV-301 trial show.

Findings were reported at the 2021 Genitourinary Cancers Symposium (Abstract 393).

“Treatment after platinum-based chemotherapy and immune checkpoint inhibitors is challenging. Overall survival is short, and therapeutic options are also limited,” noted first author Thomas Powles, MD, a professor of genitourinary oncology and director of the Barts Cancer Centre, Queen Mary University of London. “Chemotherapy is being used as the global standard of care, but randomized trials supporting these treatment choices are actually lacking. In this setting, new therapeutic agents supported by randomized trials are needed.”

Patients enrolled in EV-301 (NCT03474107), an international open-label, phase 3 trial, had locally advanced or metastatic urothelial carcinoma, had received platinum-based chemotherapy, and had experienced progression during or after immune checkpoint inhibitor therapy (anti–PD1/PD-L1 therapy).

The trial met its primary endpoint, showing that, relative to chemotherapy, enfortumab vedotin reduced the risk of death by 30%, giving patients nearly 4 additional months of life. The toxicity profile was similar to that seen in earlier trials and was manageable.

“Enfortumab vedotin is the first drug, beyond chemotherapy and immunotherapy, to show a significant survival advantage in previously treated urothelial cancer. This is a big step in the right direction for patients with advanced urothelial cancer, where treatment options remain quite limited,” Dr. Powles maintained.

The drug is also showing promising activity when used in the immunotherapy-treated but cisplatin-ineligible patients in the second cohort of the predecessor EV-201 trial, reported at the symposium as well (Abstract 394), he noted. “I hope that, as we move it earlier, we will show better efficacy.”

The Food and Drug Administration granted enfortumab vedotin accelerated approval as third-line therapy in 2019 on the basis of data from the EV-201 trial’s first cohort. With these new data from both trials, the manufacturers have submitted applications to convert the accelerated approval to regular approval, and to expand the current label to include cisplatin-ineligible patients.
 

Trial details

In EV-301, a total of 608 patients were randomized evenly to enfortumab vedotin (an antibody-drug conjugate that targets nectin-4, a cell-adhesion molecule highly expressed in urothelial carcinoma) or the physician’s choice among three standard chemotherapy options having similar efficacy (docetaxel, paclitaxel, or vinflunine).

“None of these chemotherapy drugs have spectacular response rates, and the overall survival is best described as modest,” Dr. Powles said.

He reported results of the trial’s planned interim analysis, which became the primary analysis because the primary endpoint was positive. Specifically, median overall survival was 12.9 months with enfortumab vedotin and 9.0 months with chemotherapy (hazard ratio, 0.70; P = .00142). Benefit was similar across most patient subgroups.

The enfortumab vedotin group also had a better median progression-free survival (5.6 vs. 3.7 months; HR, 0.62; P < .00001) and investigator-assessed overall response rate (40.6% vs. 17.9%; P < .001).

The rate of grade 3 or worse treatment-related adverse events was 51% with enfortumab vedotin and 50% with chemotherapy. The former was associated with a higher rate of grade 3 or worse maculopapular rash (7% vs. 0%), whereas the latter was associated with higher rates of grade 3 or worse decreased neutrophil count (13% vs. 6%), decreased white blood cell count (7% vs. 1%), and febrile neutropenia (6% vs. 1%).

Regarding events of special interest, enfortumab vedotin led to more grade 3 or worse skin reactions of any type (15% vs. 1%), peripheral neuropathy (5% vs. 2%), and hyperglycemia (4% vs. 0%). However, the majority of all treatment-related adverse events of special interest were mild to moderate in severity and consistent with those previously reported.

“There is a skill associated with the management of toxicity, and there is going to be a learning curve for people who haven’t used the drug before,” Dr. Powles acknowledged. “But my experience is, it’s a manageable drug, and delays and dose interruptions actually make it a relatively straightforward drug to give in the context of the profile that we’ve seen today.”
 

Level 1 evidence

“We now know that enfortumab vedotin is here to stay in the armamentarium for the treatment of urothelial cancer, adding its name to the ranks of others which have shown level 1 evidence, proof of a survival benefit in metastatic urothelial carcinoma,” commented invited discussant Arlene O. Siefker-Radtke, MD, a professor in the department of genitourinary medical oncology, University of Texas MD Anderson Cancer Center, Houston.

“I’ve been impressed not only by the activity of enfortumab vedotin in visceral and liver metastases, but also by the impact in patients with bone metastases as this appears very helpful in controlling bone pain in many patients,” she noted.

Preventing and managing toxicity requires appropriate patient selection, careful monitoring, and dose modifications, with knowledge of the agent’s adverse event profile and of factors conferring elevated risk for events, Dr. Siefker-Radtke said.

“The early evidence for enfortumab vedotin in the postimmunotherapy, platinum-ineligible group suggests that this can help treat patients with an unmet need due to their inability to receive platinum-based therapy,” she concluded. “And while it’s currently approved in the third-line setting, we are all eagerly awaiting the outcomes of the frontline studies of enfortumab vedotin combined with pembrolizumab, which showed such a promising objective response rate, as has been presented at earlier meetings.”

The trial was sponsored by Astellas Pharma and Seagen. Dr. Powles disclosed relationships with Astellas Pharma, AstraZeneca, Bristol-Myers Squibb, and numerous other pharmaceutical and biotechnology companies. Dr. Siefker-Radtke disclosed relationships with AstraZeneca, Bavarian Nordic, Bristol-Myers Squibb, and a variety of other pharmaceutical and biotechnology companies, as well as patents, royalties, and/or other intellectual property pertaining to methods of characterizing and treating molecular subsets of muscle-invasive bladder cancer.

The antibody-drug conjugate enfortumab vedotin is superior to chemotherapy in patients with previously treated advanced urothelial carcinoma, primary results of the EV-301 trial show.

Findings were reported at the 2021 Genitourinary Cancers Symposium (Abstract 393).

“Treatment after platinum-based chemotherapy and immune checkpoint inhibitors is challenging. Overall survival is short, and therapeutic options are also limited,” noted first author Thomas Powles, MD, a professor of genitourinary oncology and director of the Barts Cancer Centre, Queen Mary University of London. “Chemotherapy is being used as the global standard of care, but randomized trials supporting these treatment choices are actually lacking. In this setting, new therapeutic agents supported by randomized trials are needed.”

Patients enrolled in EV-301 (NCT03474107), an international open-label, phase 3 trial, had locally advanced or metastatic urothelial carcinoma, had received platinum-based chemotherapy, and had experienced progression during or after immune checkpoint inhibitor therapy (anti–PD1/PD-L1 therapy).

The trial met its primary endpoint, showing that, relative to chemotherapy, enfortumab vedotin reduced the risk of death by 30%, giving patients nearly 4 additional months of life. The toxicity profile was similar to that seen in earlier trials and was manageable.

“Enfortumab vedotin is the first drug, beyond chemotherapy and immunotherapy, to show a significant survival advantage in previously treated urothelial cancer. This is a big step in the right direction for patients with advanced urothelial cancer, where treatment options remain quite limited,” Dr. Powles maintained.

The drug is also showing promising activity when used in the immunotherapy-treated but cisplatin-ineligible patients in the second cohort of the predecessor EV-201 trial, reported at the symposium as well (Abstract 394), he noted. “I hope that, as we move it earlier, we will show better efficacy.”

The Food and Drug Administration granted enfortumab vedotin accelerated approval as third-line therapy in 2019 on the basis of data from the EV-201 trial’s first cohort. With these new data from both trials, the manufacturers have submitted applications to convert the accelerated approval to regular approval, and to expand the current label to include cisplatin-ineligible patients.
 

Trial details

In EV-301, a total of 608 patients were randomized evenly to enfortumab vedotin (an antibody-drug conjugate that targets nectin-4, a cell-adhesion molecule highly expressed in urothelial carcinoma) or the physician’s choice among three standard chemotherapy options having similar efficacy (docetaxel, paclitaxel, or vinflunine).

“None of these chemotherapy drugs have spectacular response rates, and the overall survival is best described as modest,” Dr. Powles said.

He reported results of the trial’s planned interim analysis, which became the primary analysis because the primary endpoint was positive. Specifically, median overall survival was 12.9 months with enfortumab vedotin and 9.0 months with chemotherapy (hazard ratio, 0.70; P = .00142). Benefit was similar across most patient subgroups.

The enfortumab vedotin group also had a better median progression-free survival (5.6 vs. 3.7 months; HR, 0.62; P < .00001) and investigator-assessed overall response rate (40.6% vs. 17.9%; P < .001).

The rate of grade 3 or worse treatment-related adverse events was 51% with enfortumab vedotin and 50% with chemotherapy. The former was associated with a higher rate of grade 3 or worse maculopapular rash (7% vs. 0%), whereas the latter was associated with higher rates of grade 3 or worse decreased neutrophil count (13% vs. 6%), decreased white blood cell count (7% vs. 1%), and febrile neutropenia (6% vs. 1%).

Regarding events of special interest, enfortumab vedotin led to more grade 3 or worse skin reactions of any type (15% vs. 1%), peripheral neuropathy (5% vs. 2%), and hyperglycemia (4% vs. 0%). However, the majority of all treatment-related adverse events of special interest were mild to moderate in severity and consistent with those previously reported.

“There is a skill associated with the management of toxicity, and there is going to be a learning curve for people who haven’t used the drug before,” Dr. Powles acknowledged. “But my experience is, it’s a manageable drug, and delays and dose interruptions actually make it a relatively straightforward drug to give in the context of the profile that we’ve seen today.”
 

Level 1 evidence

“We now know that enfortumab vedotin is here to stay in the armamentarium for the treatment of urothelial cancer, adding its name to the ranks of others which have shown level 1 evidence, proof of a survival benefit in metastatic urothelial carcinoma,” commented invited discussant Arlene O. Siefker-Radtke, MD, a professor in the department of genitourinary medical oncology, University of Texas MD Anderson Cancer Center, Houston.

“I’ve been impressed not only by the activity of enfortumab vedotin in visceral and liver metastases, but also by the impact in patients with bone metastases as this appears very helpful in controlling bone pain in many patients,” she noted.

Preventing and managing toxicity requires appropriate patient selection, careful monitoring, and dose modifications, with knowledge of the agent’s adverse event profile and of factors conferring elevated risk for events, Dr. Siefker-Radtke said.

“The early evidence for enfortumab vedotin in the postimmunotherapy, platinum-ineligible group suggests that this can help treat patients with an unmet need due to their inability to receive platinum-based therapy,” she concluded. “And while it’s currently approved in the third-line setting, we are all eagerly awaiting the outcomes of the frontline studies of enfortumab vedotin combined with pembrolizumab, which showed such a promising objective response rate, as has been presented at earlier meetings.”

The trial was sponsored by Astellas Pharma and Seagen. Dr. Powles disclosed relationships with Astellas Pharma, AstraZeneca, Bristol-Myers Squibb, and numerous other pharmaceutical and biotechnology companies. Dr. Siefker-Radtke disclosed relationships with AstraZeneca, Bavarian Nordic, Bristol-Myers Squibb, and a variety of other pharmaceutical and biotechnology companies, as well as patents, royalties, and/or other intellectual property pertaining to methods of characterizing and treating molecular subsets of muscle-invasive bladder cancer.

The antibody-drug conjugate enfortumab vedotin is superior to chemotherapy in patients with previously treated advanced urothelial carcinoma, primary results of the EV-301 trial show.

Findings were reported at the 2021 Genitourinary Cancers Symposium (Abstract 393).

“Treatment after platinum-based chemotherapy and immune checkpoint inhibitors is challenging. Overall survival is short, and therapeutic options are also limited,” noted first author Thomas Powles, MD, a professor of genitourinary oncology and director of the Barts Cancer Centre, Queen Mary University of London. “Chemotherapy is being used as the global standard of care, but randomized trials supporting these treatment choices are actually lacking. In this setting, new therapeutic agents supported by randomized trials are needed.”

Patients enrolled in EV-301 (NCT03474107), an international open-label, phase 3 trial, had locally advanced or metastatic urothelial carcinoma, had received platinum-based chemotherapy, and had experienced progression during or after immune checkpoint inhibitor therapy (anti–PD1/PD-L1 therapy).

The trial met its primary endpoint, showing that, relative to chemotherapy, enfortumab vedotin reduced the risk of death by 30%, giving patients nearly 4 additional months of life. The toxicity profile was similar to that seen in earlier trials and was manageable.

“Enfortumab vedotin is the first drug, beyond chemotherapy and immunotherapy, to show a significant survival advantage in previously treated urothelial cancer. This is a big step in the right direction for patients with advanced urothelial cancer, where treatment options remain quite limited,” Dr. Powles maintained.

The drug is also showing promising activity when used in the immunotherapy-treated but cisplatin-ineligible patients in the second cohort of the predecessor EV-201 trial, reported at the symposium as well (Abstract 394), he noted. “I hope that, as we move it earlier, we will show better efficacy.”

The Food and Drug Administration granted enfortumab vedotin accelerated approval as third-line therapy in 2019 on the basis of data from the EV-201 trial’s first cohort. With these new data from both trials, the manufacturers have submitted applications to convert the accelerated approval to regular approval, and to expand the current label to include cisplatin-ineligible patients.
 

Trial details

In EV-301, a total of 608 patients were randomized evenly to enfortumab vedotin (an antibody-drug conjugate that targets nectin-4, a cell-adhesion molecule highly expressed in urothelial carcinoma) or the physician’s choice among three standard chemotherapy options having similar efficacy (docetaxel, paclitaxel, or vinflunine).

“None of these chemotherapy drugs have spectacular response rates, and the overall survival is best described as modest,” Dr. Powles said.

He reported results of the trial’s planned interim analysis, which became the primary analysis because the primary endpoint was positive. Specifically, median overall survival was 12.9 months with enfortumab vedotin and 9.0 months with chemotherapy (hazard ratio, 0.70; P = .00142). Benefit was similar across most patient subgroups.

The enfortumab vedotin group also had a better median progression-free survival (5.6 vs. 3.7 months; HR, 0.62; P < .00001) and investigator-assessed overall response rate (40.6% vs. 17.9%; P < .001).

The rate of grade 3 or worse treatment-related adverse events was 51% with enfortumab vedotin and 50% with chemotherapy. The former was associated with a higher rate of grade 3 or worse maculopapular rash (7% vs. 0%), whereas the latter was associated with higher rates of grade 3 or worse decreased neutrophil count (13% vs. 6%), decreased white blood cell count (7% vs. 1%), and febrile neutropenia (6% vs. 1%).

Regarding events of special interest, enfortumab vedotin led to more grade 3 or worse skin reactions of any type (15% vs. 1%), peripheral neuropathy (5% vs. 2%), and hyperglycemia (4% vs. 0%). However, the majority of all treatment-related adverse events of special interest were mild to moderate in severity and consistent with those previously reported.

“There is a skill associated with the management of toxicity, and there is going to be a learning curve for people who haven’t used the drug before,” Dr. Powles acknowledged. “But my experience is, it’s a manageable drug, and delays and dose interruptions actually make it a relatively straightforward drug to give in the context of the profile that we’ve seen today.”
 

Level 1 evidence

“We now know that enfortumab vedotin is here to stay in the armamentarium for the treatment of urothelial cancer, adding its name to the ranks of others which have shown level 1 evidence, proof of a survival benefit in metastatic urothelial carcinoma,” commented invited discussant Arlene O. Siefker-Radtke, MD, a professor in the department of genitourinary medical oncology, University of Texas MD Anderson Cancer Center, Houston.

“I’ve been impressed not only by the activity of enfortumab vedotin in visceral and liver metastases, but also by the impact in patients with bone metastases as this appears very helpful in controlling bone pain in many patients,” she noted.

Preventing and managing toxicity requires appropriate patient selection, careful monitoring, and dose modifications, with knowledge of the agent’s adverse event profile and of factors conferring elevated risk for events, Dr. Siefker-Radtke said.

“The early evidence for enfortumab vedotin in the postimmunotherapy, platinum-ineligible group suggests that this can help treat patients with an unmet need due to their inability to receive platinum-based therapy,” she concluded. “And while it’s currently approved in the third-line setting, we are all eagerly awaiting the outcomes of the frontline studies of enfortumab vedotin combined with pembrolizumab, which showed such a promising objective response rate, as has been presented at earlier meetings.”

The trial was sponsored by Astellas Pharma and Seagen. Dr. Powles disclosed relationships with Astellas Pharma, AstraZeneca, Bristol-Myers Squibb, and numerous other pharmaceutical and biotechnology companies. Dr. Siefker-Radtke disclosed relationships with AstraZeneca, Bavarian Nordic, Bristol-Myers Squibb, and a variety of other pharmaceutical and biotechnology companies, as well as patents, royalties, and/or other intellectual property pertaining to methods of characterizing and treating molecular subsets of muscle-invasive bladder cancer.

Girls with more body fat experienced earlier menarche and hormone changes, but later full breast development, compared with those with normal weight, according to longitudinal data from 90 girls aged 8-15 years.

A link between obesity and early puberty has been observed among U.S. girls for decades, but more recent studies suggest that “girls with greater childhood adiposity have earlier thelarche and progress through puberty at a faster rate than normal weight girls,” wrote Madison T. Ortega, MD, of the National Institute of Environmental Health Sciences, Durham, N.C., and colleagues. However, studies involving hormone levels have yielded mixed results, they said.

In a study published in the Journal of Clinical Endocrinology & Metabolism , the researchers followed 36 girls with overweight or obesity and 54 girls with normal weight for 4 years; normal weight was defined as body mass index in the 5th to 85th percentile, overweight was defined as BMI in the 85th to 95th percentile, and obese was defined as greater than 95th percentile. Overweight and obese were combined into one category for comparison with normal weight girls.

Participants had an average of 2.8 study visits during this period and provided additional information by phone and online. Visits included measurement of total body fat using dual-energy x-ray absorptiometry (DXA), Tanner staging, breast ultrasound for morphological staging (BMORPH; A-E), pelvic ultrasound, hormone tests, and menarchal status assessment.

Overall, girls with overweight/obesity (OW/OB) had significantly more advanced breast development at baseline than did those with normal weight (NW), but these girls progressed through BMORPH stage D later than did NW girls. Early-stage breast development was not affected by total body fat. However, “an increase of 5 percentage points in mean total body fat, for example, was associated with a 26% decrease in the transition rate out of stage D,” the researchers noted.

Hormone levels were similar at baseline for follicle-stimulating hormone, inhibin B, estrone (E1), total and free testosterone, and androstenedione. However, these levels increased more quickly after 1 year for girls with OW/OB, while they plateaued in girls with NW and dropped among girls with lower total body fat. Total body fat had no apparent effect on other reproductive hormones including luteinizing hormone, modified vaginal maturation index, and estradiol 2.

The average age of menarche was 12.4 years across all participants, but girls with higher total body fat at baseline were more likely to reach menarche at a younger age. “For every 1-unit increase in visit one total body fat, the chance of achieving menarche at any given time point was 3% higher,” the researchers said. No interaction appeared between race and total body fat with regard to menarche.


 

Several surprising findings

The study is important because “there have been no longitudinal studies in U.S. girls to examine how total body fat affects serum reproductive hormones or the development of the breast and ovaries using ultrasound imaging,” corresponding author Natalie Shaw, MD, of the National Institute of Environmental Health Sciences, said in an interview.

Dr. Shaw said she was surprised by several of the study findings. “Others have reported increased male-like hormones (androgens) in overweight/obese girls in cross-sectional studies; however, we were surprised to find that FSH and inhibin B were also elevated in girls with excess body fat,” she said. “We also found, unexpectedly, that even though the breast bud appears earlier in overweight/obese girls (thelarche), which signals the onset of puberty, the breast matured more slowly during the course of puberty in overweight/obese girls compared with normal weight girls,” she noted.

“The main take-home message is that puberty looks different in girls with excess body fat; they develop breast tissue earlier, yet take longer to achieve a fully mature breast, and they undergo menarche earlier,” Dr. Shaw said. Clinicians should be aware of the hormonal differences based on body fat, Dr. Shaw emphasized. “Girls with greater body fat had higher levels of FSH (a pituitary hormone), inhibin B (an ovarian hormone), and male-like reproductive hormones (e.g., testosterone) that are made by the adrenal glands and the ovaries in the late stages of puberty,” she said.
 

Potential implications for adulthood

“The findings in this study contribute to better understanding how total body fat impacts hormonal findings of puberty,” M. Susan Jay, MD, of the Medical College of Wisconsin and Children’s Hospital of Wisconsin, Milwaukee, said in an interview. “Prior studies have linked weight gain as a factor that contributes to pubertal development, but this study is attempting to longitudinally investigate how body weight may affect clinical and biochemical pubertal markers in girls,” she noted.

“The take-home message is that this study and other earlier studies have illustrated that puberty is not a fixed pattern in all individual girls,” Dr. Jay emphasized. “Rather, there are environmental factors which can impact pubertal course,” she said. “In effect, there are pathways through puberty in individual adolescents that require greater ongoing studies to further identify the arc of puberty and the impact of how the length in various stages may affect exposure to estrogen and other neurohormonal factors,” she explained. These factors impact not only adolescence but also future health in adulthood, she said.

“Ongoing prospective studies are needed to identify how factors such as body weight can affect adolescent pubertal development and the possible impact long after adolescence for health issues such as breast cancer,” Dr. Jay added.

The study findings were limited by several factors including the available data from only two completed study visits for most participants, as well as the racial differences among body weight groups and lack of standardized timing for blood draws, the researchers noted.

The study was supported in part by the National Institute of Environmental Health Sciences, and corresponding author Dr. Shaw disclosed support as a Lasker Clinical Research Scholar. The other researchers, as well as Dr. Jay, had no disclosures.

Girls with more body fat experienced earlier menarche and hormone changes, but later full breast development, compared with those with normal weight, according to longitudinal data from 90 girls aged 8-15 years.

A link between obesity and early puberty has been observed among U.S. girls for decades, but more recent studies suggest that “girls with greater childhood adiposity have earlier thelarche and progress through puberty at a faster rate than normal weight girls,” wrote Madison T. Ortega, MD, of the National Institute of Environmental Health Sciences, Durham, N.C., and colleagues. However, studies involving hormone levels have yielded mixed results, they said.

In a study published in the Journal of Clinical Endocrinology & Metabolism , the researchers followed 36 girls with overweight or obesity and 54 girls with normal weight for 4 years; normal weight was defined as body mass index in the 5th to 85th percentile, overweight was defined as BMI in the 85th to 95th percentile, and obese was defined as greater than 95th percentile. Overweight and obese were combined into one category for comparison with normal weight girls.

Participants had an average of 2.8 study visits during this period and provided additional information by phone and online. Visits included measurement of total body fat using dual-energy x-ray absorptiometry (DXA), Tanner staging, breast ultrasound for morphological staging (BMORPH; A-E), pelvic ultrasound, hormone tests, and menarchal status assessment.

Overall, girls with overweight/obesity (OW/OB) had significantly more advanced breast development at baseline than did those with normal weight (NW), but these girls progressed through BMORPH stage D later than did NW girls. Early-stage breast development was not affected by total body fat. However, “an increase of 5 percentage points in mean total body fat, for example, was associated with a 26% decrease in the transition rate out of stage D,” the researchers noted.

Hormone levels were similar at baseline for follicle-stimulating hormone, inhibin B, estrone (E1), total and free testosterone, and androstenedione. However, these levels increased more quickly after 1 year for girls with OW/OB, while they plateaued in girls with NW and dropped among girls with lower total body fat. Total body fat had no apparent effect on other reproductive hormones including luteinizing hormone, modified vaginal maturation index, and estradiol 2.

The average age of menarche was 12.4 years across all participants, but girls with higher total body fat at baseline were more likely to reach menarche at a younger age. “For every 1-unit increase in visit one total body fat, the chance of achieving menarche at any given time point was 3% higher,” the researchers said. No interaction appeared between race and total body fat with regard to menarche.


 

Several surprising findings

The study is important because “there have been no longitudinal studies in U.S. girls to examine how total body fat affects serum reproductive hormones or the development of the breast and ovaries using ultrasound imaging,” corresponding author Natalie Shaw, MD, of the National Institute of Environmental Health Sciences, said in an interview.

Dr. Shaw said she was surprised by several of the study findings. “Others have reported increased male-like hormones (androgens) in overweight/obese girls in cross-sectional studies; however, we were surprised to find that FSH and inhibin B were also elevated in girls with excess body fat,” she said. “We also found, unexpectedly, that even though the breast bud appears earlier in overweight/obese girls (thelarche), which signals the onset of puberty, the breast matured more slowly during the course of puberty in overweight/obese girls compared with normal weight girls,” she noted.

“The main take-home message is that puberty looks different in girls with excess body fat; they develop breast tissue earlier, yet take longer to achieve a fully mature breast, and they undergo menarche earlier,” Dr. Shaw said. Clinicians should be aware of the hormonal differences based on body fat, Dr. Shaw emphasized. “Girls with greater body fat had higher levels of FSH (a pituitary hormone), inhibin B (an ovarian hormone), and male-like reproductive hormones (e.g., testosterone) that are made by the adrenal glands and the ovaries in the late stages of puberty,” she said.
 

Potential implications for adulthood

“The findings in this study contribute to better understanding how total body fat impacts hormonal findings of puberty,” M. Susan Jay, MD, of the Medical College of Wisconsin and Children’s Hospital of Wisconsin, Milwaukee, said in an interview. “Prior studies have linked weight gain as a factor that contributes to pubertal development, but this study is attempting to longitudinally investigate how body weight may affect clinical and biochemical pubertal markers in girls,” she noted.

“The take-home message is that this study and other earlier studies have illustrated that puberty is not a fixed pattern in all individual girls,” Dr. Jay emphasized. “Rather, there are environmental factors which can impact pubertal course,” she said. “In effect, there are pathways through puberty in individual adolescents that require greater ongoing studies to further identify the arc of puberty and the impact of how the length in various stages may affect exposure to estrogen and other neurohormonal factors,” she explained. These factors impact not only adolescence but also future health in adulthood, she said.

“Ongoing prospective studies are needed to identify how factors such as body weight can affect adolescent pubertal development and the possible impact long after adolescence for health issues such as breast cancer,” Dr. Jay added.

The study findings were limited by several factors including the available data from only two completed study visits for most participants, as well as the racial differences among body weight groups and lack of standardized timing for blood draws, the researchers noted.

The study was supported in part by the National Institute of Environmental Health Sciences, and corresponding author Dr. Shaw disclosed support as a Lasker Clinical Research Scholar. The other researchers, as well as Dr. Jay, had no disclosures.

Girls with more body fat experienced earlier menarche and hormone changes, but later full breast development, compared with those with normal weight, according to longitudinal data from 90 girls aged 8-15 years.

A link between obesity and early puberty has been observed among U.S. girls for decades, but more recent studies suggest that “girls with greater childhood adiposity have earlier thelarche and progress through puberty at a faster rate than normal weight girls,” wrote Madison T. Ortega, MD, of the National Institute of Environmental Health Sciences, Durham, N.C., and colleagues. However, studies involving hormone levels have yielded mixed results, they said.

In a study published in the Journal of Clinical Endocrinology & Metabolism , the researchers followed 36 girls with overweight or obesity and 54 girls with normal weight for 4 years; normal weight was defined as body mass index in the 5th to 85th percentile, overweight was defined as BMI in the 85th to 95th percentile, and obese was defined as greater than 95th percentile. Overweight and obese were combined into one category for comparison with normal weight girls.

Participants had an average of 2.8 study visits during this period and provided additional information by phone and online. Visits included measurement of total body fat using dual-energy x-ray absorptiometry (DXA), Tanner staging, breast ultrasound for morphological staging (BMORPH; A-E), pelvic ultrasound, hormone tests, and menarchal status assessment.

Overall, girls with overweight/obesity (OW/OB) had significantly more advanced breast development at baseline than did those with normal weight (NW), but these girls progressed through BMORPH stage D later than did NW girls. Early-stage breast development was not affected by total body fat. However, “an increase of 5 percentage points in mean total body fat, for example, was associated with a 26% decrease in the transition rate out of stage D,” the researchers noted.

Hormone levels were similar at baseline for follicle-stimulating hormone, inhibin B, estrone (E1), total and free testosterone, and androstenedione. However, these levels increased more quickly after 1 year for girls with OW/OB, while they plateaued in girls with NW and dropped among girls with lower total body fat. Total body fat had no apparent effect on other reproductive hormones including luteinizing hormone, modified vaginal maturation index, and estradiol 2.

The average age of menarche was 12.4 years across all participants, but girls with higher total body fat at baseline were more likely to reach menarche at a younger age. “For every 1-unit increase in visit one total body fat, the chance of achieving menarche at any given time point was 3% higher,” the researchers said. No interaction appeared between race and total body fat with regard to menarche.


 

Several surprising findings

The study is important because “there have been no longitudinal studies in U.S. girls to examine how total body fat affects serum reproductive hormones or the development of the breast and ovaries using ultrasound imaging,” corresponding author Natalie Shaw, MD, of the National Institute of Environmental Health Sciences, said in an interview.

Dr. Shaw said she was surprised by several of the study findings. “Others have reported increased male-like hormones (androgens) in overweight/obese girls in cross-sectional studies; however, we were surprised to find that FSH and inhibin B were also elevated in girls with excess body fat,” she said. “We also found, unexpectedly, that even though the breast bud appears earlier in overweight/obese girls (thelarche), which signals the onset of puberty, the breast matured more slowly during the course of puberty in overweight/obese girls compared with normal weight girls,” she noted.

“The main take-home message is that puberty looks different in girls with excess body fat; they develop breast tissue earlier, yet take longer to achieve a fully mature breast, and they undergo menarche earlier,” Dr. Shaw said. Clinicians should be aware of the hormonal differences based on body fat, Dr. Shaw emphasized. “Girls with greater body fat had higher levels of FSH (a pituitary hormone), inhibin B (an ovarian hormone), and male-like reproductive hormones (e.g., testosterone) that are made by the adrenal glands and the ovaries in the late stages of puberty,” she said.
 

Potential implications for adulthood

“The findings in this study contribute to better understanding how total body fat impacts hormonal findings of puberty,” M. Susan Jay, MD, of the Medical College of Wisconsin and Children’s Hospital of Wisconsin, Milwaukee, said in an interview. “Prior studies have linked weight gain as a factor that contributes to pubertal development, but this study is attempting to longitudinally investigate how body weight may affect clinical and biochemical pubertal markers in girls,” she noted.

“The take-home message is that this study and other earlier studies have illustrated that puberty is not a fixed pattern in all individual girls,” Dr. Jay emphasized. “Rather, there are environmental factors which can impact pubertal course,” she said. “In effect, there are pathways through puberty in individual adolescents that require greater ongoing studies to further identify the arc of puberty and the impact of how the length in various stages may affect exposure to estrogen and other neurohormonal factors,” she explained. These factors impact not only adolescence but also future health in adulthood, she said.

“Ongoing prospective studies are needed to identify how factors such as body weight can affect adolescent pubertal development and the possible impact long after adolescence for health issues such as breast cancer,” Dr. Jay added.

The study findings were limited by several factors including the available data from only two completed study visits for most participants, as well as the racial differences among body weight groups and lack of standardized timing for blood draws, the researchers noted.

The study was supported in part by the National Institute of Environmental Health Sciences, and corresponding author Dr. Shaw disclosed support as a Lasker Clinical Research Scholar. The other researchers, as well as Dr. Jay, had no disclosures.

The American Society for Dermatologic Surgery (ASDS) addresses a worrying knowledge gap with the publication of its first evidence-based clinical practice guidelines for the prevention and treatment of adverse events from injectable fillers.

The recommendations, published in the February issue of Dermatologic Surgery, are from a multidisciplinary task force convened by the ASDS, comprising 11 physicians – 8 board-certified in dermatology, 2 board-certified in plastic and reconstructive surgery, and 1 board-certified in oculoplastic surgery (all ASDS members) – and 2 patient representatives.

While redness, swelling, and other injection site reactions associated with injectable fillers are common, and usually resolve within 1-2 weeks, “rare but more serious adverse events from injectable fillers include vascular occlusion leading to skin necrosis or blindness, inflammatory events, and nodule formation, among others,” the authors wrote. They are “likely underreported” and cases are increasing as injectable fillers become more popular.

He described the two most important cornerstones for preventing vascular occlusion. The first, he said, is “having impeccable knowledge and understanding of vascular anatomy and the cutaneous landmarks for blood vessels that are at risk.” The second pertains to injection techniques, he said, noting that “it’s becoming clearer – although it’s somewhat controversial – that cannulas are safer than needles.”

While anatomical knowledge might seem like the most basic requirement for practitioners who inject fillers, Dr. Jones said it is not. “It is true that we study anatomy in great detail in medical school, but injection anatomy is a completely different bird. Of course someone can study the facial arteries and have a basic understanding, but understanding it in a way that it relates to safe filler injections is a completely different thing. Our understanding of this has evolved over the last couple of decades ... and there are new papers that come out all the time that refine our knowledge.”

In terms of treating an IRVC resulting from hyaluronic acid (HA) filler, “the take-home point is the hyaluronidase is the mainstay of treatment, and not a little bit of hyaluronidase, but a lot of hyaluronidase – hundreds of units injected into the area of ischemia,” he said. However, while the new guidelines emphasize that time is of the essence – “the most cited window of time for reperfusion is 90 minutes” – the authors also strongly advise practitioners to evaluate immediate post-event visual status first, before attempting any intervention.

Dr. Jones said the goal is to untangle some confusion about whether it is the filler or the rescue that does more damage. “There is a lot of controversy with ophthalmology, ophthalmologic surgeons, plastic surgeons, and dermatologists,” he said, and “there has been finger-pointing between specialists when people make an intervention … that the actual rescue procedure created the problem,” which is why “it is imperative to document the visual status prior to doing anything.”

Beyond IRVC, and nonvisual skin ischemia due to vascular occlusion, the document addresses prevention and treatment of nodules, both inflammatory and noninflammatory, that occur either early or more than a month after treatment with HA fillers, as well with semi-permanent and permanent fillers.

For HA-related nodules, “the mainstay of treatment is steroids – either oral or intralesional – antibiotics, and hyaluronidase, which erases the substance,” said Dr. Jones. As for nodules related to permanent fillers, he said that they are difficult to treat, and “tend to respond best to repetitive monthly injections of 5-fluououracil combined with small amounts of triamcinolone.”

Dr. Jones is an investigator or consultant for Allergan, Galderma, Merz, and Revance; other authors had disclosures that included serving as a consultant, investigator, and/or trainer for these and/or other companies; one author received partial funding from ASDS to do this work; and one author had no disclosures.

The American Society for Dermatologic Surgery (ASDS) addresses a worrying knowledge gap with the publication of its first evidence-based clinical practice guidelines for the prevention and treatment of adverse events from injectable fillers.

The recommendations, published in the February issue of Dermatologic Surgery, are from a multidisciplinary task force convened by the ASDS, comprising 11 physicians – 8 board-certified in dermatology, 2 board-certified in plastic and reconstructive surgery, and 1 board-certified in oculoplastic surgery (all ASDS members) – and 2 patient representatives.

While redness, swelling, and other injection site reactions associated with injectable fillers are common, and usually resolve within 1-2 weeks, “rare but more serious adverse events from injectable fillers include vascular occlusion leading to skin necrosis or blindness, inflammatory events, and nodule formation, among others,” the authors wrote. They are “likely underreported” and cases are increasing as injectable fillers become more popular.

He described the two most important cornerstones for preventing vascular occlusion. The first, he said, is “having impeccable knowledge and understanding of vascular anatomy and the cutaneous landmarks for blood vessels that are at risk.” The second pertains to injection techniques, he said, noting that “it’s becoming clearer – although it’s somewhat controversial – that cannulas are safer than needles.”

While anatomical knowledge might seem like the most basic requirement for practitioners who inject fillers, Dr. Jones said it is not. “It is true that we study anatomy in great detail in medical school, but injection anatomy is a completely different bird. Of course someone can study the facial arteries and have a basic understanding, but understanding it in a way that it relates to safe filler injections is a completely different thing. Our understanding of this has evolved over the last couple of decades ... and there are new papers that come out all the time that refine our knowledge.”

In terms of treating an IRVC resulting from hyaluronic acid (HA) filler, “the take-home point is the hyaluronidase is the mainstay of treatment, and not a little bit of hyaluronidase, but a lot of hyaluronidase – hundreds of units injected into the area of ischemia,” he said. However, while the new guidelines emphasize that time is of the essence – “the most cited window of time for reperfusion is 90 minutes” – the authors also strongly advise practitioners to evaluate immediate post-event visual status first, before attempting any intervention.

Dr. Jones said the goal is to untangle some confusion about whether it is the filler or the rescue that does more damage. “There is a lot of controversy with ophthalmology, ophthalmologic surgeons, plastic surgeons, and dermatologists,” he said, and “there has been finger-pointing between specialists when people make an intervention … that the actual rescue procedure created the problem,” which is why “it is imperative to document the visual status prior to doing anything.”

Beyond IRVC, and nonvisual skin ischemia due to vascular occlusion, the document addresses prevention and treatment of nodules, both inflammatory and noninflammatory, that occur either early or more than a month after treatment with HA fillers, as well with semi-permanent and permanent fillers.

For HA-related nodules, “the mainstay of treatment is steroids – either oral or intralesional – antibiotics, and hyaluronidase, which erases the substance,” said Dr. Jones. As for nodules related to permanent fillers, he said that they are difficult to treat, and “tend to respond best to repetitive monthly injections of 5-fluououracil combined with small amounts of triamcinolone.”

Dr. Jones is an investigator or consultant for Allergan, Galderma, Merz, and Revance; other authors had disclosures that included serving as a consultant, investigator, and/or trainer for these and/or other companies; one author received partial funding from ASDS to do this work; and one author had no disclosures.

The American Society for Dermatologic Surgery (ASDS) addresses a worrying knowledge gap with the publication of its first evidence-based clinical practice guidelines for the prevention and treatment of adverse events from injectable fillers.

The recommendations, published in the February issue of Dermatologic Surgery, are from a multidisciplinary task force convened by the ASDS, comprising 11 physicians – 8 board-certified in dermatology, 2 board-certified in plastic and reconstructive surgery, and 1 board-certified in oculoplastic surgery (all ASDS members) – and 2 patient representatives.

While redness, swelling, and other injection site reactions associated with injectable fillers are common, and usually resolve within 1-2 weeks, “rare but more serious adverse events from injectable fillers include vascular occlusion leading to skin necrosis or blindness, inflammatory events, and nodule formation, among others,” the authors wrote. They are “likely underreported” and cases are increasing as injectable fillers become more popular.

He described the two most important cornerstones for preventing vascular occlusion. The first, he said, is “having impeccable knowledge and understanding of vascular anatomy and the cutaneous landmarks for blood vessels that are at risk.” The second pertains to injection techniques, he said, noting that “it’s becoming clearer – although it’s somewhat controversial – that cannulas are safer than needles.”

While anatomical knowledge might seem like the most basic requirement for practitioners who inject fillers, Dr. Jones said it is not. “It is true that we study anatomy in great detail in medical school, but injection anatomy is a completely different bird. Of course someone can study the facial arteries and have a basic understanding, but understanding it in a way that it relates to safe filler injections is a completely different thing. Our understanding of this has evolved over the last couple of decades ... and there are new papers that come out all the time that refine our knowledge.”

In terms of treating an IRVC resulting from hyaluronic acid (HA) filler, “the take-home point is the hyaluronidase is the mainstay of treatment, and not a little bit of hyaluronidase, but a lot of hyaluronidase – hundreds of units injected into the area of ischemia,” he said. However, while the new guidelines emphasize that time is of the essence – “the most cited window of time for reperfusion is 90 minutes” – the authors also strongly advise practitioners to evaluate immediate post-event visual status first, before attempting any intervention.

Dr. Jones said the goal is to untangle some confusion about whether it is the filler or the rescue that does more damage. “There is a lot of controversy with ophthalmology, ophthalmologic surgeons, plastic surgeons, and dermatologists,” he said, and “there has been finger-pointing between specialists when people make an intervention … that the actual rescue procedure created the problem,” which is why “it is imperative to document the visual status prior to doing anything.”

Beyond IRVC, and nonvisual skin ischemia due to vascular occlusion, the document addresses prevention and treatment of nodules, both inflammatory and noninflammatory, that occur either early or more than a month after treatment with HA fillers, as well with semi-permanent and permanent fillers.

For HA-related nodules, “the mainstay of treatment is steroids – either oral or intralesional – antibiotics, and hyaluronidase, which erases the substance,” said Dr. Jones. As for nodules related to permanent fillers, he said that they are difficult to treat, and “tend to respond best to repetitive monthly injections of 5-fluououracil combined with small amounts of triamcinolone.”

Dr. Jones is an investigator or consultant for Allergan, Galderma, Merz, and Revance; other authors had disclosures that included serving as a consultant, investigator, and/or trainer for these and/or other companies; one author received partial funding from ASDS to do this work; and one author had no disclosures.

Childhood trauma, which is also called adverse childhood experiences (ACEs), can have lasting detrimental effects on individuals as they grow and mature into adulthood. ACEs may occur in children age ≤18 years if they experience abuse or neglect, violence, or other traumatic losses. More than 60% of people experience at least 1 ACE, and 1 in 6 individuals reported that they had experienced ≥4 ACEs.¹ Subsequent additional ACEs have a cumulative deteriorating impact on the brain. This predisposes individuals to mental health disorders, substance use disorders, and other psychosocial problems. The efficacy of current therapeutic approaches provides only partial symptom resolution. For such individuals, the illness load and health care costs typically remain high across the lifespan.^1,2 

In this article, we discuss types of ACEs, protective factors and risk factors that influence the development of posttraumatic stress disorder (PTSD) in individuals who experience ACEs, how ACEs can negatively impact mental health in adulthood, and approaches to prevent or treat PTSD and other symptoms.

Types of trauma and correlation with PTSD

ACEs can be indexed as neglect or emotional, physical, or sexual abuse. Physical and sexual abuse strongly correlate with an increased risk of PTSD.³ Although neglect and emotional abuse do not directly predict the development of PTSD, these experiences foretell high rates of lifelong trauma exposure and are indirectly related to late PTSD symptoms.^4,5 ACEs can impede an individual’s cognitive, social, and emotional development, diminish quality of life, and lead to an early death.⁶ The lifetime prevalence of PTSD is 6.1% to 9.2%.⁷ Compared with men, women are 4 times more likely to develop PTSD following a traumatic event.⁷

The development of PTSD is influenced by the nature, duration, and degree of trauma, and age at the time of exposure to trauma. Children who survive complex trauma (≥2 types of trauma) have a higher likelihood of developing PTSD.⁸ Prolonged trauma exposure has a more substantial negative impact than a one-time occurrence. However, it is an erroneous oversimplification to assume that each type of ACE has an equally traumatic effect.⁶

Factors that protect against PTSD

Factors that can protect against developing PTSD are listed in Table 1.⁷ Two of these are resilience and hope.

Resilience is defined as an individual’s strength to cope with difficulties in life.⁹ Resilience has internal psychological characteristics and external factors that aid in protecting against childhood adversities.^10,11 The Brief Resilience Scale is a self-assessment that measures innate abilities to cope, including optimism, self-efficacy, patience, faith, and humor.^12,13 External factors associated with resilience are family, friends, and community support.^11,13

Hope can help in surmounting ACEs. The Adult Hope Scale has been used in many studies to assess this construct in individuals who have survived trauma.¹³ Some studies have found decreased hope in individuals who sustained early trauma and were diagnosed with PTSD in adulthood.¹⁴ A study examining children exposed to domestic violence found that children who showed high hope, endurance, and curiosity were better able to cope with adversities.¹⁵

Continue to: PTSD risk factors

PTSD risk factors

Many individual and societal risk factors can influence the likelihood of developing PTSD. Some of these factors are outlined in Table 1.⁷

Pathophysiology of PTSD

Multiple brain regions, pathways, and neurotransmitters are involved in the development of PTSD. Neuroimaging has identified volume and activity changes of the hippocampus, prefrontal cortex, and amygdala in patients with early trauma and PTSD. Some researchers have suggested a gross reduction in locus coeruleus neuronal volume in war veterans with a likely diagnosis of PTSD compared with controls.^16,17 In other studies, chronic stress exposure has been found to cause neuronal cell death and affect neuronal plasticity in the limbic area of the brain.¹⁸

Diagnosing PTSD

More than 30% of individuals who experience ACEs develop PTSD.¹⁹ The DSM-5 diagnostic criteria for PTSD are outlined in Table 2.²⁰ Several instruments are used to determine the diagnosis and assess the severity of PTSD. These include the Clinician-Administered PTSD Scale for DSM-5,²¹ which is a 30-item structured interview that can be administered in 45 to 60 minutes; the PTSD Symptom Scale Self-Report Version, which is a 17-item, Likert scale, self-report questionnaire; and the Structured Clinical Interview: PTSD Module, which is a semi-structured interview that can take up to several hours to administer.²¹

Other disorders. In addition to PTSD, individuals with ACEs are at high risk for other mental health issues throughout their lifetime. Individuals with ACE often experience depressive symptoms (approximately 40%); anxiety (approximately 30%); anger; guilt or shame; negative self-cognition; interpersonal difficulties; rumination; and thoughts of self-harm and suicide.²² Epidemiological studies suggest that patients who experience childhood sexual abuse are more likely to develop mood, anxiety, and substance use disorders in adulthood.^23,24

Psychotherapeutic treatments for PTSD

Cognitive-behavioral therapy (CBT) addresses the relationship between an individual’s thoughts, emotions, and behaviors. CBT can be used to treat adults and children with PTSD. Before starting CBT, assess the patient’s current safety to ensure that they have the coping skills to manage distress related to their ACEs, and address any coexisting substance use.²⁵

Continue to: According to the American Psychological Association...

According to the American Psychological Association, several CBT-based psychotherapies are recommended for treating PTSD²⁶:

Trauma-focused–CBT includes psychoeducation, trauma narrative, processing, exposure, and relaxation skills training. It consists of approximately 12 to 16 sessions and incorporates elements of family therapy.

Cognitive processing therapy (CPT) focuses on helping patients develop adaptive cognitive domains about the self, the people around them, and the world. CPT therapists assist in information processing by accessing the traumatic memory and trying to eliminate emotions tied to it.^25,27 CPT consists of 12 to 16 structured individual, group, or combined sessions.

Prolonged exposure (PE) targets fear-related emotions and works on the principles of habituation to extinguish trauma and fear response to the trigger. This increases self-reliance and competence and decreases the generalization of anxiety to innocuous triggers. PE typically consists of 9 to 12 sessions. PE alone or in combination with cognitive restructuring is successful in treating patients with PTSD, but cognitive restructuring has limited utility in young children.^25,27

Cognitive exposure can be individual or group therapy delivered over 3 months, where negative self-evaluation and traumatic memories are challenged with the goal of interrupting maladaptive behaviors and thoughts.²⁷ 

Continue to: Stress inoculation training

Stress inoculation training (SIT) provides psychoeducation, skills training, role-playing, deep muscle relaxation, paced breathing, and thought stopping. Emphasis is on coaching skills to alleviate anxiety, fear, and symptoms of depression associated with trauma. In SIT, exposures to traumatic memories are indirect (eg, role play), compared with PE, where the exposures are direct.²⁵

The American Psychological Association conditionally recommended several other forms for psychotherapy for treating patients with PTSD²⁶:

Brief eclectic psychotherapy uses CBT and psychodynamic approaches to target feelings of guilt and shame in 16 sessions.²⁷

Narrative exposure therapy consists of 4 to 10 group sessions in which individuals provide detailed narration of the events; the focus is on self-respect and personal rights.²⁷

Eye movement desensitization and reprocessing (EMDR) is a 6- to 12-session, 8-phase treatment that uses principles of accelerated information processing to target nonverbal expression of trauma and dissociative experiences. Patients with PTSD are suggested to have disrupted rapid eye movements. In EMDR, patients follow rhythmic movements of the therapist’s hands or flashed light. This is designed to decrease stress associated with accessing trauma memories, the emotional/physiologic response from the memories, and negative cognitive distortions about self, and to replace negative cognition distortions with positive thoughts about self.^25,27

Continue to: Accelerated resolution therapy

Accelerated resolution therapy is a derivative of EMDR. It helps to reconsolidate the emotional and physical experiences associated with distressing memories by replacing them with positive ones or decreasing physiological arousal and anxiety related to the recall of traumatic memories.²⁸

Pharmacologic treatments

Selective serotonin reuptake inhibitors (SSRIs). Multiple studies using different scales have found that paroxetine, sertraline, and fluoxetine can decrease PTSD symptoms. Approximately 60% of patients treated with SSRIs experience partial remission of symptoms, and 20% to 30% experience complete symptom resolution.²⁹ Davidson et al³⁰ found that 22% of patients with PTSD who received fluoxetine had a relapse of symptoms, compared with 50% of patients who received placebo.

Serotonin-norepinephrine reuptake inhibitors (SNRIs) and other antidepressants. The SNRIs venlafaxine and duloxetine can help reduce hyperarousal symptoms and improve mood, anxiety, and sleep.²⁶ Mirtazapine, an alpha 2A/2C adrenoceptor antagonist/5-HT 2A/2C/3 antagonist, can address PTSD symptoms from both serotonergic pathways and increase norepinephrine release by blocking autoreceptors and enhancing alpha-1 receptor activity. This alleviates hyperarousal symptoms and promotes sleep.²⁹ In addition to having monoaminergic effects, antidepressant medications also regulate the hypothalamic–pituitary–adrenal (HPA) axis response to stress and promote neurogenesis in the hippocampal region.²⁹

Adrenergic agents

Adrenergic receptor antagonists. Prazosin, an alpha-1 adrenoceptor antagonist, decreases hyperarousal symptoms, improves sleep, and decreases nightmares related to PTSD by decreasing noradrenergic hyperactivity.²⁹

Beta-blockers such as propranolol can decrease physiological response to trauma but have mixed results in the prevention or improvement of PTSD symptoms.^29,31

Continue to: Glucocorticoid receptor agonists

Glucocorticoid receptor agonists. In a very small study, low-dose cortisol decreased the severity of traumatic memory (consolidation phase).³² Glucocorticoid receptor agonists can also diminish memory retrieval (reconsolidation phase) through intrusive thoughts and flashbacks.²⁹ 

Anticonvulsants, benzodiazepines, and antipsychotics

These medications have had a limited role in the treatment of PTSD.^26,29

Future directions: Preventive treatments

Because PTSD has a profound impact on an individual’s quality of life and the development of other illnesses, there is strong interest in finding treatments that can prevent PTSD. Based on limited evidence primarily from animal studies, some researchers have suggested that certain agents may someday be helpful for PTSD prevention²⁹:

Glucocorticoid antagonists such as corticotropin-releasing factor 1 (CRF1) antagonists or cholecystokinin 2 (CCK2) receptor antagonists might promote resilience to stress by inhibiting the HPA axis and influencing the amygdala by decreasing fear conditioning, as observed in animal models. Similarly, in animal models, CRF1 and CCK2 are predicted to decrease memory consolidation in response to exposure to stress. 

Adrenoceptor antagonists and agonists also might have a role in preventive treatment, but the evidence is scarce. Prazosin, an alpha-1 adrenoceptor antagonist, was ineffective in animal models.^29,31 Propranolol, a beta-adrenoceptor blocker, has had mixed results but can decrease trauma-induced physiological arousal when administered soon after exposure.²⁹ 

Continue to: N-methyl-d-aspartate (NMDA) receptor antagonists

N-methyl-d-aspartate (NMDA) receptor antagonists. NMDA receptor function decline has also been hypothesized to decrease the reconsolidation symptoms of PTSD.²⁹ One study examined the prevalence of PTSD in service members who were treated for burns in a military treatment center.³³ The use of the NMDA receptor antagonist ketamine lowered the prevalence of PTSD among service members who were treated for burns.The suggested mechanism is preventing memory consolidation after trauma exposure.³³

Bottom Line

Adverse childhood experiences (ACEs) are strong predictors for the development of posttraumatic stress disorder (PTSD) and other mental health or medical issues in late adolescence and adulthood. Experiencing a higher number of ACEs increases the risk of developing PTSD as an adult. Timely psychotherapeutic and pharmacologic interventions can help limit symptoms and reduce the severity of PTSD.

Related Resources

• Smith P, Dalglesih T, Meiser-Stedman R. Practitioner review: posttraumatic stress disorder and its treatment in children and adolescents. J Child Psychol Psychiatry. 2019;60(5):500-515.
• North CS, Hong BA, Downs DL. PTSD: a systematic approach to diagnosis and treatment. Current Psychiatry 2018;17(4):35-43.

Drug Brand Names

Duloxetine • Cymbalta
Fluoxetine • Prozac
Mirtazapine • Remeron
Paroxetine • Paxil
Prazosin • Minipress
Propranolol • Inderal, Pronol
Sertraline • Zoloft
Venlafaxine • Effexor

Childhood trauma, which is also called adverse childhood experiences (ACEs), can have lasting detrimental effects on individuals as they grow and mature into adulthood. ACEs may occur in children age ≤18 years if they experience abuse or neglect, violence, or other traumatic losses. More than 60% of people experience at least 1 ACE, and 1 in 6 individuals reported that they had experienced ≥4 ACEs.¹ Subsequent additional ACEs have a cumulative deteriorating impact on the brain. This predisposes individuals to mental health disorders, substance use disorders, and other psychosocial problems. The efficacy of current therapeutic approaches provides only partial symptom resolution. For such individuals, the illness load and health care costs typically remain high across the lifespan.^1,2 

In this article, we discuss types of ACEs, protective factors and risk factors that influence the development of posttraumatic stress disorder (PTSD) in individuals who experience ACEs, how ACEs can negatively impact mental health in adulthood, and approaches to prevent or treat PTSD and other symptoms.

Types of trauma and correlation with PTSD

ACEs can be indexed as neglect or emotional, physical, or sexual abuse. Physical and sexual abuse strongly correlate with an increased risk of PTSD.³ Although neglect and emotional abuse do not directly predict the development of PTSD, these experiences foretell high rates of lifelong trauma exposure and are indirectly related to late PTSD symptoms.^4,5 ACEs can impede an individual’s cognitive, social, and emotional development, diminish quality of life, and lead to an early death.⁶ The lifetime prevalence of PTSD is 6.1% to 9.2%.⁷ Compared with men, women are 4 times more likely to develop PTSD following a traumatic event.⁷

The development of PTSD is influenced by the nature, duration, and degree of trauma, and age at the time of exposure to trauma. Children who survive complex trauma (≥2 types of trauma) have a higher likelihood of developing PTSD.⁸ Prolonged trauma exposure has a more substantial negative impact than a one-time occurrence. However, it is an erroneous oversimplification to assume that each type of ACE has an equally traumatic effect.⁶

Factors that protect against PTSD

Factors that can protect against developing PTSD are listed in Table 1.⁷ Two of these are resilience and hope.

Resilience is defined as an individual’s strength to cope with difficulties in life.⁹ Resilience has internal psychological characteristics and external factors that aid in protecting against childhood adversities.^10,11 The Brief Resilience Scale is a self-assessment that measures innate abilities to cope, including optimism, self-efficacy, patience, faith, and humor.^12,13 External factors associated with resilience are family, friends, and community support.^11,13

Hope can help in surmounting ACEs. The Adult Hope Scale has been used in many studies to assess this construct in individuals who have survived trauma.¹³ Some studies have found decreased hope in individuals who sustained early trauma and were diagnosed with PTSD in adulthood.¹⁴ A study examining children exposed to domestic violence found that children who showed high hope, endurance, and curiosity were better able to cope with adversities.¹⁵

Continue to: PTSD risk factors

PTSD risk factors

Many individual and societal risk factors can influence the likelihood of developing PTSD. Some of these factors are outlined in Table 1.⁷

Pathophysiology of PTSD

Multiple brain regions, pathways, and neurotransmitters are involved in the development of PTSD. Neuroimaging has identified volume and activity changes of the hippocampus, prefrontal cortex, and amygdala in patients with early trauma and PTSD. Some researchers have suggested a gross reduction in locus coeruleus neuronal volume in war veterans with a likely diagnosis of PTSD compared with controls.^16,17 In other studies, chronic stress exposure has been found to cause neuronal cell death and affect neuronal plasticity in the limbic area of the brain.¹⁸

Diagnosing PTSD

More than 30% of individuals who experience ACEs develop PTSD.¹⁹ The DSM-5 diagnostic criteria for PTSD are outlined in Table 2.²⁰ Several instruments are used to determine the diagnosis and assess the severity of PTSD. These include the Clinician-Administered PTSD Scale for DSM-5,²¹ which is a 30-item structured interview that can be administered in 45 to 60 minutes; the PTSD Symptom Scale Self-Report Version, which is a 17-item, Likert scale, self-report questionnaire; and the Structured Clinical Interview: PTSD Module, which is a semi-structured interview that can take up to several hours to administer.²¹

Other disorders. In addition to PTSD, individuals with ACEs are at high risk for other mental health issues throughout their lifetime. Individuals with ACE often experience depressive symptoms (approximately 40%); anxiety (approximately 30%); anger; guilt or shame; negative self-cognition; interpersonal difficulties; rumination; and thoughts of self-harm and suicide.²² Epidemiological studies suggest that patients who experience childhood sexual abuse are more likely to develop mood, anxiety, and substance use disorders in adulthood.^23,24

Psychotherapeutic treatments for PTSD

Cognitive-behavioral therapy (CBT) addresses the relationship between an individual’s thoughts, emotions, and behaviors. CBT can be used to treat adults and children with PTSD. Before starting CBT, assess the patient’s current safety to ensure that they have the coping skills to manage distress related to their ACEs, and address any coexisting substance use.²⁵

Continue to: According to the American Psychological Association...

According to the American Psychological Association, several CBT-based psychotherapies are recommended for treating PTSD²⁶:

Trauma-focused–CBT includes psychoeducation, trauma narrative, processing, exposure, and relaxation skills training. It consists of approximately 12 to 16 sessions and incorporates elements of family therapy.

Cognitive processing therapy (CPT) focuses on helping patients develop adaptive cognitive domains about the self, the people around them, and the world. CPT therapists assist in information processing by accessing the traumatic memory and trying to eliminate emotions tied to it.^25,27 CPT consists of 12 to 16 structured individual, group, or combined sessions.

Prolonged exposure (PE) targets fear-related emotions and works on the principles of habituation to extinguish trauma and fear response to the trigger. This increases self-reliance and competence and decreases the generalization of anxiety to innocuous triggers. PE typically consists of 9 to 12 sessions. PE alone or in combination with cognitive restructuring is successful in treating patients with PTSD, but cognitive restructuring has limited utility in young children.^25,27

Cognitive exposure can be individual or group therapy delivered over 3 months, where negative self-evaluation and traumatic memories are challenged with the goal of interrupting maladaptive behaviors and thoughts.²⁷ 

Continue to: Stress inoculation training

Stress inoculation training (SIT) provides psychoeducation, skills training, role-playing, deep muscle relaxation, paced breathing, and thought stopping. Emphasis is on coaching skills to alleviate anxiety, fear, and symptoms of depression associated with trauma. In SIT, exposures to traumatic memories are indirect (eg, role play), compared with PE, where the exposures are direct.²⁵

The American Psychological Association conditionally recommended several other forms for psychotherapy for treating patients with PTSD²⁶:

Brief eclectic psychotherapy uses CBT and psychodynamic approaches to target feelings of guilt and shame in 16 sessions.²⁷

Narrative exposure therapy consists of 4 to 10 group sessions in which individuals provide detailed narration of the events; the focus is on self-respect and personal rights.²⁷

Eye movement desensitization and reprocessing (EMDR) is a 6- to 12-session, 8-phase treatment that uses principles of accelerated information processing to target nonverbal expression of trauma and dissociative experiences. Patients with PTSD are suggested to have disrupted rapid eye movements. In EMDR, patients follow rhythmic movements of the therapist’s hands or flashed light. This is designed to decrease stress associated with accessing trauma memories, the emotional/physiologic response from the memories, and negative cognitive distortions about self, and to replace negative cognition distortions with positive thoughts about self.^25,27

Continue to: Accelerated resolution therapy

Accelerated resolution therapy is a derivative of EMDR. It helps to reconsolidate the emotional and physical experiences associated with distressing memories by replacing them with positive ones or decreasing physiological arousal and anxiety related to the recall of traumatic memories.²⁸

Pharmacologic treatments

Selective serotonin reuptake inhibitors (SSRIs). Multiple studies using different scales have found that paroxetine, sertraline, and fluoxetine can decrease PTSD symptoms. Approximately 60% of patients treated with SSRIs experience partial remission of symptoms, and 20% to 30% experience complete symptom resolution.²⁹ Davidson et al³⁰ found that 22% of patients with PTSD who received fluoxetine had a relapse of symptoms, compared with 50% of patients who received placebo.

Serotonin-norepinephrine reuptake inhibitors (SNRIs) and other antidepressants. The SNRIs venlafaxine and duloxetine can help reduce hyperarousal symptoms and improve mood, anxiety, and sleep.²⁶ Mirtazapine, an alpha 2A/2C adrenoceptor antagonist/5-HT 2A/2C/3 antagonist, can address PTSD symptoms from both serotonergic pathways and increase norepinephrine release by blocking autoreceptors and enhancing alpha-1 receptor activity. This alleviates hyperarousal symptoms and promotes sleep.²⁹ In addition to having monoaminergic effects, antidepressant medications also regulate the hypothalamic–pituitary–adrenal (HPA) axis response to stress and promote neurogenesis in the hippocampal region.²⁹

Adrenergic agents

Adrenergic receptor antagonists. Prazosin, an alpha-1 adrenoceptor antagonist, decreases hyperarousal symptoms, improves sleep, and decreases nightmares related to PTSD by decreasing noradrenergic hyperactivity.²⁹

Beta-blockers such as propranolol can decrease physiological response to trauma but have mixed results in the prevention or improvement of PTSD symptoms.^29,31

Continue to: Glucocorticoid receptor agonists

Glucocorticoid receptor agonists. In a very small study, low-dose cortisol decreased the severity of traumatic memory (consolidation phase).³² Glucocorticoid receptor agonists can also diminish memory retrieval (reconsolidation phase) through intrusive thoughts and flashbacks.²⁹ 

Anticonvulsants, benzodiazepines, and antipsychotics

These medications have had a limited role in the treatment of PTSD.^26,29

Future directions: Preventive treatments

Because PTSD has a profound impact on an individual’s quality of life and the development of other illnesses, there is strong interest in finding treatments that can prevent PTSD. Based on limited evidence primarily from animal studies, some researchers have suggested that certain agents may someday be helpful for PTSD prevention²⁹:

Glucocorticoid antagonists such as corticotropin-releasing factor 1 (CRF1) antagonists or cholecystokinin 2 (CCK2) receptor antagonists might promote resilience to stress by inhibiting the HPA axis and influencing the amygdala by decreasing fear conditioning, as observed in animal models. Similarly, in animal models, CRF1 and CCK2 are predicted to decrease memory consolidation in response to exposure to stress. 

Adrenoceptor antagonists and agonists also might have a role in preventive treatment, but the evidence is scarce. Prazosin, an alpha-1 adrenoceptor antagonist, was ineffective in animal models.^29,31 Propranolol, a beta-adrenoceptor blocker, has had mixed results but can decrease trauma-induced physiological arousal when administered soon after exposure.²⁹ 

Continue to: N-methyl-d-aspartate (NMDA) receptor antagonists

N-methyl-d-aspartate (NMDA) receptor antagonists. NMDA receptor function decline has also been hypothesized to decrease the reconsolidation symptoms of PTSD.²⁹ One study examined the prevalence of PTSD in service members who were treated for burns in a military treatment center.³³ The use of the NMDA receptor antagonist ketamine lowered the prevalence of PTSD among service members who were treated for burns.The suggested mechanism is preventing memory consolidation after trauma exposure.³³

Bottom Line

Adverse childhood experiences (ACEs) are strong predictors for the development of posttraumatic stress disorder (PTSD) and other mental health or medical issues in late adolescence and adulthood. Experiencing a higher number of ACEs increases the risk of developing PTSD as an adult. Timely psychotherapeutic and pharmacologic interventions can help limit symptoms and reduce the severity of PTSD.

Related Resources

• Smith P, Dalglesih T, Meiser-Stedman R. Practitioner review: posttraumatic stress disorder and its treatment in children and adolescents. J Child Psychol Psychiatry. 2019;60(5):500-515.
• North CS, Hong BA, Downs DL. PTSD: a systematic approach to diagnosis and treatment. Current Psychiatry 2018;17(4):35-43.

Drug Brand Names

Duloxetine • Cymbalta
Fluoxetine • Prozac
Mirtazapine • Remeron
Paroxetine • Paxil
Prazosin • Minipress
Propranolol • Inderal, Pronol
Sertraline • Zoloft
Venlafaxine • Effexor

Childhood trauma, which is also called adverse childhood experiences (ACEs), can have lasting detrimental effects on individuals as they grow and mature into adulthood. ACEs may occur in children age ≤18 years if they experience abuse or neglect, violence, or other traumatic losses. More than 60% of people experience at least 1 ACE, and 1 in 6 individuals reported that they had experienced ≥4 ACEs.¹ Subsequent additional ACEs have a cumulative deteriorating impact on the brain. This predisposes individuals to mental health disorders, substance use disorders, and other psychosocial problems. The efficacy of current therapeutic approaches provides only partial symptom resolution. For such individuals, the illness load and health care costs typically remain high across the lifespan.^1,2 

In this article, we discuss types of ACEs, protective factors and risk factors that influence the development of posttraumatic stress disorder (PTSD) in individuals who experience ACEs, how ACEs can negatively impact mental health in adulthood, and approaches to prevent or treat PTSD and other symptoms.

Types of trauma and correlation with PTSD

ACEs can be indexed as neglect or emotional, physical, or sexual abuse. Physical and sexual abuse strongly correlate with an increased risk of PTSD.³ Although neglect and emotional abuse do not directly predict the development of PTSD, these experiences foretell high rates of lifelong trauma exposure and are indirectly related to late PTSD symptoms.^4,5 ACEs can impede an individual’s cognitive, social, and emotional development, diminish quality of life, and lead to an early death.⁶ The lifetime prevalence of PTSD is 6.1% to 9.2%.⁷ Compared with men, women are 4 times more likely to develop PTSD following a traumatic event.⁷

The development of PTSD is influenced by the nature, duration, and degree of trauma, and age at the time of exposure to trauma. Children who survive complex trauma (≥2 types of trauma) have a higher likelihood of developing PTSD.⁸ Prolonged trauma exposure has a more substantial negative impact than a one-time occurrence. However, it is an erroneous oversimplification to assume that each type of ACE has an equally traumatic effect.⁶

Factors that protect against PTSD

Factors that can protect against developing PTSD are listed in Table 1.⁷ Two of these are resilience and hope.

Resilience is defined as an individual’s strength to cope with difficulties in life.⁹ Resilience has internal psychological characteristics and external factors that aid in protecting against childhood adversities.^10,11 The Brief Resilience Scale is a self-assessment that measures innate abilities to cope, including optimism, self-efficacy, patience, faith, and humor.^12,13 External factors associated with resilience are family, friends, and community support.^11,13

Hope can help in surmounting ACEs. The Adult Hope Scale has been used in many studies to assess this construct in individuals who have survived trauma.¹³ Some studies have found decreased hope in individuals who sustained early trauma and were diagnosed with PTSD in adulthood.¹⁴ A study examining children exposed to domestic violence found that children who showed high hope, endurance, and curiosity were better able to cope with adversities.¹⁵

Continue to: PTSD risk factors

PTSD risk factors

Many individual and societal risk factors can influence the likelihood of developing PTSD. Some of these factors are outlined in Table 1.⁷

Pathophysiology of PTSD

Multiple brain regions, pathways, and neurotransmitters are involved in the development of PTSD. Neuroimaging has identified volume and activity changes of the hippocampus, prefrontal cortex, and amygdala in patients with early trauma and PTSD. Some researchers have suggested a gross reduction in locus coeruleus neuronal volume in war veterans with a likely diagnosis of PTSD compared with controls.^16,17 In other studies, chronic stress exposure has been found to cause neuronal cell death and affect neuronal plasticity in the limbic area of the brain.¹⁸

Diagnosing PTSD

More than 30% of individuals who experience ACEs develop PTSD.¹⁹ The DSM-5 diagnostic criteria for PTSD are outlined in Table 2.²⁰ Several instruments are used to determine the diagnosis and assess the severity of PTSD. These include the Clinician-Administered PTSD Scale for DSM-5,²¹ which is a 30-item structured interview that can be administered in 45 to 60 minutes; the PTSD Symptom Scale Self-Report Version, which is a 17-item, Likert scale, self-report questionnaire; and the Structured Clinical Interview: PTSD Module, which is a semi-structured interview that can take up to several hours to administer.²¹

Other disorders. In addition to PTSD, individuals with ACEs are at high risk for other mental health issues throughout their lifetime. Individuals with ACE often experience depressive symptoms (approximately 40%); anxiety (approximately 30%); anger; guilt or shame; negative self-cognition; interpersonal difficulties; rumination; and thoughts of self-harm and suicide.²² Epidemiological studies suggest that patients who experience childhood sexual abuse are more likely to develop mood, anxiety, and substance use disorders in adulthood.^23,24

Psychotherapeutic treatments for PTSD

Cognitive-behavioral therapy (CBT) addresses the relationship between an individual’s thoughts, emotions, and behaviors. CBT can be used to treat adults and children with PTSD. Before starting CBT, assess the patient’s current safety to ensure that they have the coping skills to manage distress related to their ACEs, and address any coexisting substance use.²⁵

Continue to: According to the American Psychological Association...

According to the American Psychological Association, several CBT-based psychotherapies are recommended for treating PTSD²⁶:

Trauma-focused–CBT includes psychoeducation, trauma narrative, processing, exposure, and relaxation skills training. It consists of approximately 12 to 16 sessions and incorporates elements of family therapy.

Cognitive processing therapy (CPT) focuses on helping patients develop adaptive cognitive domains about the self, the people around them, and the world. CPT therapists assist in information processing by accessing the traumatic memory and trying to eliminate emotions tied to it.^25,27 CPT consists of 12 to 16 structured individual, group, or combined sessions.

Prolonged exposure (PE) targets fear-related emotions and works on the principles of habituation to extinguish trauma and fear response to the trigger. This increases self-reliance and competence and decreases the generalization of anxiety to innocuous triggers. PE typically consists of 9 to 12 sessions. PE alone or in combination with cognitive restructuring is successful in treating patients with PTSD, but cognitive restructuring has limited utility in young children.^25,27

Cognitive exposure can be individual or group therapy delivered over 3 months, where negative self-evaluation and traumatic memories are challenged with the goal of interrupting maladaptive behaviors and thoughts.²⁷ 

Continue to: Stress inoculation training

Stress inoculation training (SIT) provides psychoeducation, skills training, role-playing, deep muscle relaxation, paced breathing, and thought stopping. Emphasis is on coaching skills to alleviate anxiety, fear, and symptoms of depression associated with trauma. In SIT, exposures to traumatic memories are indirect (eg, role play), compared with PE, where the exposures are direct.²⁵

The American Psychological Association conditionally recommended several other forms for psychotherapy for treating patients with PTSD²⁶:

Brief eclectic psychotherapy uses CBT and psychodynamic approaches to target feelings of guilt and shame in 16 sessions.²⁷

Narrative exposure therapy consists of 4 to 10 group sessions in which individuals provide detailed narration of the events; the focus is on self-respect and personal rights.²⁷

Eye movement desensitization and reprocessing (EMDR) is a 6- to 12-session, 8-phase treatment that uses principles of accelerated information processing to target nonverbal expression of trauma and dissociative experiences. Patients with PTSD are suggested to have disrupted rapid eye movements. In EMDR, patients follow rhythmic movements of the therapist’s hands or flashed light. This is designed to decrease stress associated with accessing trauma memories, the emotional/physiologic response from the memories, and negative cognitive distortions about self, and to replace negative cognition distortions with positive thoughts about self.^25,27

Continue to: Accelerated resolution therapy

Accelerated resolution therapy is a derivative of EMDR. It helps to reconsolidate the emotional and physical experiences associated with distressing memories by replacing them with positive ones or decreasing physiological arousal and anxiety related to the recall of traumatic memories.²⁸

Pharmacologic treatments

Selective serotonin reuptake inhibitors (SSRIs). Multiple studies using different scales have found that paroxetine, sertraline, and fluoxetine can decrease PTSD symptoms. Approximately 60% of patients treated with SSRIs experience partial remission of symptoms, and 20% to 30% experience complete symptom resolution.²⁹ Davidson et al³⁰ found that 22% of patients with PTSD who received fluoxetine had a relapse of symptoms, compared with 50% of patients who received placebo.

Serotonin-norepinephrine reuptake inhibitors (SNRIs) and other antidepressants. The SNRIs venlafaxine and duloxetine can help reduce hyperarousal symptoms and improve mood, anxiety, and sleep.²⁶ Mirtazapine, an alpha 2A/2C adrenoceptor antagonist/5-HT 2A/2C/3 antagonist, can address PTSD symptoms from both serotonergic pathways and increase norepinephrine release by blocking autoreceptors and enhancing alpha-1 receptor activity. This alleviates hyperarousal symptoms and promotes sleep.²⁹ In addition to having monoaminergic effects, antidepressant medications also regulate the hypothalamic–pituitary–adrenal (HPA) axis response to stress and promote neurogenesis in the hippocampal region.²⁹

Adrenergic agents

Adrenergic receptor antagonists. Prazosin, an alpha-1 adrenoceptor antagonist, decreases hyperarousal symptoms, improves sleep, and decreases nightmares related to PTSD by decreasing noradrenergic hyperactivity.²⁹

Beta-blockers such as propranolol can decrease physiological response to trauma but have mixed results in the prevention or improvement of PTSD symptoms.^29,31

Continue to: Glucocorticoid receptor agonists

Glucocorticoid receptor agonists. In a very small study, low-dose cortisol decreased the severity of traumatic memory (consolidation phase).³² Glucocorticoid receptor agonists can also diminish memory retrieval (reconsolidation phase) through intrusive thoughts and flashbacks.²⁹ 

Anticonvulsants, benzodiazepines, and antipsychotics

These medications have had a limited role in the treatment of PTSD.^26,29

Future directions: Preventive treatments

Because PTSD has a profound impact on an individual’s quality of life and the development of other illnesses, there is strong interest in finding treatments that can prevent PTSD. Based on limited evidence primarily from animal studies, some researchers have suggested that certain agents may someday be helpful for PTSD prevention²⁹:

Glucocorticoid antagonists such as corticotropin-releasing factor 1 (CRF1) antagonists or cholecystokinin 2 (CCK2) receptor antagonists might promote resilience to stress by inhibiting the HPA axis and influencing the amygdala by decreasing fear conditioning, as observed in animal models. Similarly, in animal models, CRF1 and CCK2 are predicted to decrease memory consolidation in response to exposure to stress. 

Adrenoceptor antagonists and agonists also might have a role in preventive treatment, but the evidence is scarce. Prazosin, an alpha-1 adrenoceptor antagonist, was ineffective in animal models.^29,31 Propranolol, a beta-adrenoceptor blocker, has had mixed results but can decrease trauma-induced physiological arousal when administered soon after exposure.²⁹ 

Continue to: N-methyl-d-aspartate (NMDA) receptor antagonists

N-methyl-d-aspartate (NMDA) receptor antagonists. NMDA receptor function decline has also been hypothesized to decrease the reconsolidation symptoms of PTSD.²⁹ One study examined the prevalence of PTSD in service members who were treated for burns in a military treatment center.³³ The use of the NMDA receptor antagonist ketamine lowered the prevalence of PTSD among service members who were treated for burns.The suggested mechanism is preventing memory consolidation after trauma exposure.³³

Bottom Line

Adverse childhood experiences (ACEs) are strong predictors for the development of posttraumatic stress disorder (PTSD) and other mental health or medical issues in late adolescence and adulthood. Experiencing a higher number of ACEs increases the risk of developing PTSD as an adult. Timely psychotherapeutic and pharmacologic interventions can help limit symptoms and reduce the severity of PTSD.

Related Resources

• Smith P, Dalglesih T, Meiser-Stedman R. Practitioner review: posttraumatic stress disorder and its treatment in children and adolescents. J Child Psychol Psychiatry. 2019;60(5):500-515.
• North CS, Hong BA, Downs DL. PTSD: a systematic approach to diagnosis and treatment. Current Psychiatry 2018;17(4):35-43.

Drug Brand Names

Duloxetine • Cymbalta
Fluoxetine • Prozac
Mirtazapine • Remeron
Paroxetine • Paxil
Prazosin • Minipress
Propranolol • Inderal, Pronol
Sertraline • Zoloft
Venlafaxine • Effexor

As humans live longer, a renewed focus on quality of life has made the prompt diagnosis and treatment of sleep-related disorders in older adults increasingly necessary.¹ Normative aging results in multiple changes in sleep architecture, including decreased total sleep time, decreased sleep efficiency, decreased slow-wave sleep (SWS), and increased awakenings after sleep onset.² Sleep disturbances in older adults are increasingly recognized as multifactorial health conditions requiring comprehensive modification of risk factors, diagnosis, and treatment.³

In this article, we discuss the effects of aging on sleep architecture and provide an overview of primary sleep disorders in older adults. We also summarize strategies for diagnosing and treating sleep disorders in these patients.

Elements of the sleep cycle

The human sleep cycle begins with light sleep (sleep stages 1 and 2), progresses into SWS (sleep stage 3), and culminates in rapid eye movement (REM) sleep. The first 3 stages are referred to as non-rapid eye movement sleep (NREM). Throughout the night, this coupling of NREM and REM cycles occurs 4 to 6 times, with each successive cycle decreasing in length until awakening.⁴

Two complex neurologic pathways intersect to regulate the timing of sleep and wakefulness on arousal. The first pathway, the circadian system, is located within the suprachiasmatic nucleus of the hypothalamus and is highly dependent on external stimuli (light, food, etc.) to synchronize sleep/wake cycles. The suprachiasmatic nucleus regulates melatonin secretion by the pineal gland, which signals day-night transitions. The other pathway, the homeostatic system, modifies the amount of sleep needed daily. When multiple days of poor sleep occur, homeostatic sleep pressure (colloquially described as sleep debt) compensates by increasing the amount of sleep required in the following days. Together, the circadian and homeostatic systems work in conjunction to regulate sleep quantity to approximately one-third of the total sleep-wake cycle.^2,5

Age-related dysfunction of the regulatory sleep pathways leads to blunting of the ability to initiate and sustain high-quality sleep.⁶ Dysregulation of homeostatic sleep pressure decreases time spent in SWS, and failure of the circadian signaling apparatus results in delays in sleep/wake timing.² While research into the underlying neurobiology of sleep reveals that some of these changes are inherent to aging (Box^7-14), significant underdiagnosed pathologies may adversely affect sleep architecture, including polypharmacy, comorbid neuropathology (eg, synucleinopathies, tauopathies, etc.), and primary sleep disorders (insomnias, hypersomnias, and parasomnias).¹⁵

Box

Primary sleep disorders

Obstructive sleep apnea (OSA) is one of the most common, yet frequently underdiagnosed reversible causes of sleep disturbances. It is characterized by partial or complete airway obstruction culminating in periods of involuntary cessation of respirations during sleep. The resultant fragmentation in sleep leads to significant downstream effects over time, including excessive daytime sleepiness and fatigue, poor occupational and social performance, and substantial cognitive impairment.³ While it is well known that OSA increases in prevalence throughout middle age, this relationship plateaus after age 60.¹⁶ An estimated 40% to 60% of Americans age >60 are affected by OSA.¹⁷ The hypoxemia and fragmented sleep caused by unrecognized OSA are associated with a significant decline in activities of daily living (ADL).¹⁸ Untreated OSA is strongly linked to the development and progression of several major health conditions, including cardiovascular disease, diabetes mellitus, hypertension, stroke, and depression.¹⁹ In studies of long-term care facility residents—many of whom may have comorbid cognitive decline—researchers found that unrecognized OSA often mimics the progressive cognitive decline seen in major neurocognitive disorders.²⁰ However, classic symptoms of OSA may not always be present in these patients, and their daytime sleepiness is often attributed to old age rather than to a pathological etiology.¹⁶ Screening for OSA and prompt initiation of the appropriate treatment may reverse OSA-induced cognitive changes in these patients.²¹

The primary presenting symptom of OSA is snoring, which is correlated with pauses in breathing. Risk factors include increased body mass index (BMI), thick neck circumference, male sex, and advanced age. In older adults, BMI has a lower impact on the Apnea-Hypopnea Index, an indicator of the number of pauses in breathing per hour, when compared with young and middle-age adults.¹⁶ Validated screening questionnaires for OSA include the STOP-Bang Questionnaire (Table 1²²), OSA50, Berlin Questionnaire, and Epworth Sleepiness Scale, each of which is used in different subpopulations. The current diagnostic standard for OSA is nocturnal polysomnography in a sleep laboratory, but recent advances in home sleep apnea testing have made it a viable, low-cost alternative for patients who do not have significant medical comorbidities.²³ Standard utilized cutoffs for diagnosis are ≥5 events/hour (hypopneas associated with at least 4% oxygen desaturations) in conjunction with clinical symptoms of OSA.²⁴

Continue to: Treatment

Treatment. First-line treatment for OSA is continuous positive airway pressure therapy, but adherence rates vary widely with patient education and regular follow-up.²⁵ Adjunctive therapy includes weight loss, oral appliances, and uvulopalatopharyngoplasty, a procedure in which tissue in the throat is remodeled or removed.

Central sleep apnea (CSA) is a pause in breathing without evidence of associated respiratory effort. In adults, the development of CSA is indicative of underlying lower brainstem dysfunction, due to intermittent failures in the pontomedullary centers responsible for regulation of rhythmic breathing.²⁶ This can occur as a consequence of multiple diseases, including congestive heart failure, stroke, renal failure, chronic medication use (opioids), and brain tumors.

The Sleep Heart Health Study—the largest community-based cohort study to date examining CSA—estimated that the prevalence of CSA among adults age >65 was 1.1% (compared with 0.4% in those age <65).²⁷ Subgroup analysis revealed that men had significantly higher rates of CSA compared with women (2.7% vs 0.2%, respectively).

CSA may present similarly to OSA (excessive daytime somnolence, insomnia, poor sleep quality, difficulties with attention and concentration). Symptoms may also mimic those of coexisting medical conditions in older adults, such as nocturnal angina or paroxysmal nocturnal dyspnea.²⁷ Any older patient with daytime sleepiness and risk factors for CSA should be referred for in-laboratory nocturnal polysomnography, the gold standard diagnostic test. Unlike in OSA, ambulatory diagnostic measures (home sleep apnea testing) have not been validated for this disorder.²⁷

Treatment. The primary treatment for CSA is to address the underlying medical problem. Positive pressure ventilation has been attempted with mixed results. Supplemental oxygen and medical management (acetazolamide or theophylline) can help stimulate breathing. Newer studies have shown favorable outcomes with transvenous neurostimulation or adaptive servoventilation.^28-30

Continue to: Insomnia

Insomnia. For a primary diagnosis of insomnia, DSM-5 requires at least 3 nights per week of sleep disturbances that induce distress or functional impairment for at least 3 months.³¹ The International Classification of Disease, 10th Edition requires at least 1 month of symptoms (lying awake for a long time before falling asleep, sleeping for short periods, being awake for most of the night, feeling lack of sleep, waking up early) after ruling out other sleep disorders, substance use, or other medical conditions.⁴ Clinically, insomnia tends to present in older adults as a subjective complaint of dissatisfaction with the quality and/or quantity of their sleep. Insomnia has been consistently shown to be a significant risk factor for both the development or exacerbation of depression in older adults.^32-34

While the diagnosis of insomnia is mainly clinical via a thorough sleep and medication history, assistive ancillary testing can include wrist actigraphy and screening questionnaires (the Insomnia Severity Index and the Pittsburgh Sleep Quality Index).⁴ Because population studies of older adults have found discrepancies between objective and subjective methods of assessing sleep quality, relying on the accuracy of self-reported symptoms alone is questionable.³⁵

Treatment. Given that drug elimination half-life increases with age, and the risks of adverse effects are increased in older adults, the preferred treatment modalities for insomnia are nonpharmacologic.⁴ Sleep hygiene education (Table 2) and cognitive-behavioral therapy (CBT) for insomnia are often the first-line therapies.^4,36,37 It is crucial to manage comorbidities such as heart disease and obesity, as well as sources of discomfort from conditions such as arthritic pain.^38,39 If nonpharmacologic therapies are not effective, pharmacologic options can be considered.⁴ Before prescribing sleep medications, it may be more fruitful to treat underlying psychiatric disorders such as depression and anxiety with antidepressants.⁴ Although benzodiazepines are helpful for their sedative effects, they are not recommended for older adults because of an increased risk of falls, rebound insomnia, potential tolerance, and associated cognitive impairment.⁴⁰ Benzodiazepine receptor agonists (eg, zolpidem, eszopiclone, zaleplon) were initially developed as a first-line treatment for insomnia to replace the reliance on benzodiazepines, but these medications have a “black-box” warning of a serious risk of complex sleep behaviors, including life-threatening parasomnias.⁴¹ As a result, guidelines suggest a shorter duration of treatment with a benzodiazepine receptor agonist may still provide benefit while limiting the risk of adverse effects.⁴²

Doxepin is the only antidepressant FDA-approved for insomnia; it improves sleep latency (time taken to initiate sleep after lying down), duration, and quality in adults age >65.⁴³ Melatonin receptor agonists such as ramelteon and melatonin have shown positive results in older patients with insomnia. In clinical trials of patients age ≥65, ramelteon, which is FDA-approved for insomnia, produced no rebound insomnia, withdrawal effects, memory impairment, or gait instability.^44-46 Suvorexant, an orexin receptor antagonist, decreases sleep latency and increases total sleep time equally in both young and older adults.^47-49Table 3^40-51 provides a list of medications used to treat insomnia (including off-label agents) and their common adverse effects in older adults.

Parasomnias are undesirable behaviors that occur during sleep, commonly associated with the sleep-wake transition period. These behaviors can occur during REM sleep (nightmare disorder, sleep paralysis, REM sleep behavior disorder) or NREM sleep (somnambulism [sleepwalking], confusional arousals, sleep terrors). According to a cross-sectional Norwegian study of parasomnias, the estimated lifetime prevalence of sleep walking is 22.4%; sleep talking, 66.8%; confusional arousal, 18.5%; and sleep terror, 10.4%.⁵²

Continue to: When evaluating a patient...

When evaluating a patient with parasomnias, it is important to review their drug and substance use as well as coexisting medical conditions. Drugs and substances that can affect sleep include prescription medications (second-generation antidepressants, stimulants, dopamine agonists), excessive caffeine, alcohol, certain foods (coffee, chocolate milk, black tea, caffeinated soft drinks), environmental exposures (smoking, pesticides), and recreational drugs (amphetamines).^53-56 Certain medical conditions are correlated with specific parasomnias (eg, sleep paralysis and narcolepsy, REM sleep behavior disorder and Parkinson’s disease [PD], etc.).⁵⁴ Diagnosis of parasomnias is mainly clinical but supporting evidence can be obtained through in-lab polysomnography.

Treatment. For parasomnias, treatment is primarily supportive and includes creating a safe sleeping environment to reduce the risk of self-harm. Recommendations include sleeping in a room on the ground floor, minimizing furniture in the bedroom, padding any bedside furniture, child-proofing doorknobs, and locking up weapons and other dangerous household items.⁵⁴

REM sleep behavior disorder (RBD). This disorder is characterized by a loss of the typical REM sleep-associated atonia and the presence of motor activity during dreaming (dream-enacted behaviors). While the estimated incidence of RBD in the general adult population is approximately 0.5%, it increases to 7.7% among those age >60.⁵⁷ RBD occurs most commonly in the setting of the alpha-synucleinopathies (PD, Lewy body dementia, multisystem atrophy), but can also be found in patients with cerebral ischemia, demyelinating disorders, or alcohol misuse, or can be medication-induced (primarily antidepressants and antipsychotics).⁵⁸ In patients with PD, the presence of RBD is associated with a more impaired cognitive profile, suggestive of widespread neurodegeneration.⁵⁹ Recent studies revealed that RBD may also be a prodromal state of neurodegenerative diseases such as PD, which should prompt close monitoring and long-term follow up.⁶⁰ Similar to other parasomnias, the diagnosis of RBD is primarily clinical, but polysomnography plays an important role in demonstrating loss of REM-related atonia.⁵⁴

Treatment. Clonazepam and melatonin have been shown to be effective in treating the symptoms of RBD.⁵⁴

Depression, anxiety, and sleep disturbances

Major depressive disorder (MDD) and generalized anxiety disorder (GAD) affect sleep in patients of all ages, but are underreported in older adults. According to national epidemiologic surveys, the estimated prevalence of MDD and GAD among older adults is 13% and 11.4%, respectively.^61,62 Rates as high as 42% and 39% have been reported in meta-regression analyses among patients with Alzheimer’s dementia.⁶³

Continue to: Depression and anxiety

Depression and anxiety may have additive effects and manifest as poor sleep satisfaction, increased sleep latency, insomnia, and daytime sleepiness.⁶⁴ However, they may also have independent effects. Studies showed that patients with depression alone reported overall poor sleep satisfaction, whereas patients with anxiety alone reported problems with sleep latency, daytime drowsiness, and waking up at night in addition to their overall poor sleep satisfaction.^65-67 Both depression and anxiety are risk factors for developing cognitive decline, and may be an early sign/prodrome of neurodegenerative diseases (dementias).⁶⁸ The bidirectional relationship between depression/anxiety and sleep is complex and needs further investigation.

Treatment. Pharmacologic treatments for patients with depression/anxiety and sleep disturbances include selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, and other serotonin receptor agonists.^69-72 Nonpharmacologic treatments include CBT for both depression and anxiety, and problem-solving therapy for patients with mild cognitive impairment and depression.^73,74 For severe depression and/or anxiety, electroconvulsive therapy is effective.⁷⁵

Bottom Line

Sleep disorders in older adults are common but often underdiagnosed. Timely recognition of obstructive sleep apnea, central sleep apnea, insomnia, parasomnias, and other sleep disturbances can facilitate effective treatment and greatly improve older adults’ quality of life.

Related Resources

• American Academy of Sleep Medicine. International Classification of Sleep Disorders—Third Edition. https://aasm.org
• SleepFoundation.org. Sleep hygiene. https://www.sleepfoundation.org/articles/sleep-hygiene

Drug Brand Names

Acetazolamide • Diamox
Clonazepam • Klonopin
Doxepin • Silenor
Eszopiclone • Lunesta
Gabapentin • Neurontin
Mirtazapine • Remeron
Pramipexole • Mirapex
Quetiapine • Seroquel
Ramelteon • Rozerem
Suvorexant • Belsomra
Temazepam • Restoril
Theophylline • Elixophyllin
Tiagabine • Gabitril
Trazadone • Desyrel
Triazolam • Halcion
Zaleplon • Sonata
Zolpidem • Ambien

As humans live longer, a renewed focus on quality of life has made the prompt diagnosis and treatment of sleep-related disorders in older adults increasingly necessary.¹ Normative aging results in multiple changes in sleep architecture, including decreased total sleep time, decreased sleep efficiency, decreased slow-wave sleep (SWS), and increased awakenings after sleep onset.² Sleep disturbances in older adults are increasingly recognized as multifactorial health conditions requiring comprehensive modification of risk factors, diagnosis, and treatment.³

In this article, we discuss the effects of aging on sleep architecture and provide an overview of primary sleep disorders in older adults. We also summarize strategies for diagnosing and treating sleep disorders in these patients.

Elements of the sleep cycle

The human sleep cycle begins with light sleep (sleep stages 1 and 2), progresses into SWS (sleep stage 3), and culminates in rapid eye movement (REM) sleep. The first 3 stages are referred to as non-rapid eye movement sleep (NREM). Throughout the night, this coupling of NREM and REM cycles occurs 4 to 6 times, with each successive cycle decreasing in length until awakening.⁴

Two complex neurologic pathways intersect to regulate the timing of sleep and wakefulness on arousal. The first pathway, the circadian system, is located within the suprachiasmatic nucleus of the hypothalamus and is highly dependent on external stimuli (light, food, etc.) to synchronize sleep/wake cycles. The suprachiasmatic nucleus regulates melatonin secretion by the pineal gland, which signals day-night transitions. The other pathway, the homeostatic system, modifies the amount of sleep needed daily. When multiple days of poor sleep occur, homeostatic sleep pressure (colloquially described as sleep debt) compensates by increasing the amount of sleep required in the following days. Together, the circadian and homeostatic systems work in conjunction to regulate sleep quantity to approximately one-third of the total sleep-wake cycle.^2,5

Age-related dysfunction of the regulatory sleep pathways leads to blunting of the ability to initiate and sustain high-quality sleep.⁶ Dysregulation of homeostatic sleep pressure decreases time spent in SWS, and failure of the circadian signaling apparatus results in delays in sleep/wake timing.² While research into the underlying neurobiology of sleep reveals that some of these changes are inherent to aging (Box^7-14), significant underdiagnosed pathologies may adversely affect sleep architecture, including polypharmacy, comorbid neuropathology (eg, synucleinopathies, tauopathies, etc.), and primary sleep disorders (insomnias, hypersomnias, and parasomnias).¹⁵

Box

Primary sleep disorders

Obstructive sleep apnea (OSA) is one of the most common, yet frequently underdiagnosed reversible causes of sleep disturbances. It is characterized by partial or complete airway obstruction culminating in periods of involuntary cessation of respirations during sleep. The resultant fragmentation in sleep leads to significant downstream effects over time, including excessive daytime sleepiness and fatigue, poor occupational and social performance, and substantial cognitive impairment.³ While it is well known that OSA increases in prevalence throughout middle age, this relationship plateaus after age 60.¹⁶ An estimated 40% to 60% of Americans age >60 are affected by OSA.¹⁷ The hypoxemia and fragmented sleep caused by unrecognized OSA are associated with a significant decline in activities of daily living (ADL).¹⁸ Untreated OSA is strongly linked to the development and progression of several major health conditions, including cardiovascular disease, diabetes mellitus, hypertension, stroke, and depression.¹⁹ In studies of long-term care facility residents—many of whom may have comorbid cognitive decline—researchers found that unrecognized OSA often mimics the progressive cognitive decline seen in major neurocognitive disorders.²⁰ However, classic symptoms of OSA may not always be present in these patients, and their daytime sleepiness is often attributed to old age rather than to a pathological etiology.¹⁶ Screening for OSA and prompt initiation of the appropriate treatment may reverse OSA-induced cognitive changes in these patients.²¹

The primary presenting symptom of OSA is snoring, which is correlated with pauses in breathing. Risk factors include increased body mass index (BMI), thick neck circumference, male sex, and advanced age. In older adults, BMI has a lower impact on the Apnea-Hypopnea Index, an indicator of the number of pauses in breathing per hour, when compared with young and middle-age adults.¹⁶ Validated screening questionnaires for OSA include the STOP-Bang Questionnaire (Table 1²²), OSA50, Berlin Questionnaire, and Epworth Sleepiness Scale, each of which is used in different subpopulations. The current diagnostic standard for OSA is nocturnal polysomnography in a sleep laboratory, but recent advances in home sleep apnea testing have made it a viable, low-cost alternative for patients who do not have significant medical comorbidities.²³ Standard utilized cutoffs for diagnosis are ≥5 events/hour (hypopneas associated with at least 4% oxygen desaturations) in conjunction with clinical symptoms of OSA.²⁴

Continue to: Treatment

Treatment. First-line treatment for OSA is continuous positive airway pressure therapy, but adherence rates vary widely with patient education and regular follow-up.²⁵ Adjunctive therapy includes weight loss, oral appliances, and uvulopalatopharyngoplasty, a procedure in which tissue in the throat is remodeled or removed.

Central sleep apnea (CSA) is a pause in breathing without evidence of associated respiratory effort. In adults, the development of CSA is indicative of underlying lower brainstem dysfunction, due to intermittent failures in the pontomedullary centers responsible for regulation of rhythmic breathing.²⁶ This can occur as a consequence of multiple diseases, including congestive heart failure, stroke, renal failure, chronic medication use (opioids), and brain tumors.

The Sleep Heart Health Study—the largest community-based cohort study to date examining CSA—estimated that the prevalence of CSA among adults age >65 was 1.1% (compared with 0.4% in those age <65).²⁷ Subgroup analysis revealed that men had significantly higher rates of CSA compared with women (2.7% vs 0.2%, respectively).

CSA may present similarly to OSA (excessive daytime somnolence, insomnia, poor sleep quality, difficulties with attention and concentration). Symptoms may also mimic those of coexisting medical conditions in older adults, such as nocturnal angina or paroxysmal nocturnal dyspnea.²⁷ Any older patient with daytime sleepiness and risk factors for CSA should be referred for in-laboratory nocturnal polysomnography, the gold standard diagnostic test. Unlike in OSA, ambulatory diagnostic measures (home sleep apnea testing) have not been validated for this disorder.²⁷

Treatment. The primary treatment for CSA is to address the underlying medical problem. Positive pressure ventilation has been attempted with mixed results. Supplemental oxygen and medical management (acetazolamide or theophylline) can help stimulate breathing. Newer studies have shown favorable outcomes with transvenous neurostimulation or adaptive servoventilation.^28-30

Continue to: Insomnia

Insomnia. For a primary diagnosis of insomnia, DSM-5 requires at least 3 nights per week of sleep disturbances that induce distress or functional impairment for at least 3 months.³¹ The International Classification of Disease, 10th Edition requires at least 1 month of symptoms (lying awake for a long time before falling asleep, sleeping for short periods, being awake for most of the night, feeling lack of sleep, waking up early) after ruling out other sleep disorders, substance use, or other medical conditions.⁴ Clinically, insomnia tends to present in older adults as a subjective complaint of dissatisfaction with the quality and/or quantity of their sleep. Insomnia has been consistently shown to be a significant risk factor for both the development or exacerbation of depression in older adults.^32-34

While the diagnosis of insomnia is mainly clinical via a thorough sleep and medication history, assistive ancillary testing can include wrist actigraphy and screening questionnaires (the Insomnia Severity Index and the Pittsburgh Sleep Quality Index).⁴ Because population studies of older adults have found discrepancies between objective and subjective methods of assessing sleep quality, relying on the accuracy of self-reported symptoms alone is questionable.³⁵

Treatment. Given that drug elimination half-life increases with age, and the risks of adverse effects are increased in older adults, the preferred treatment modalities for insomnia are nonpharmacologic.⁴ Sleep hygiene education (Table 2) and cognitive-behavioral therapy (CBT) for insomnia are often the first-line therapies.^4,36,37 It is crucial to manage comorbidities such as heart disease and obesity, as well as sources of discomfort from conditions such as arthritic pain.^38,39 If nonpharmacologic therapies are not effective, pharmacologic options can be considered.⁴ Before prescribing sleep medications, it may be more fruitful to treat underlying psychiatric disorders such as depression and anxiety with antidepressants.⁴ Although benzodiazepines are helpful for their sedative effects, they are not recommended for older adults because of an increased risk of falls, rebound insomnia, potential tolerance, and associated cognitive impairment.⁴⁰ Benzodiazepine receptor agonists (eg, zolpidem, eszopiclone, zaleplon) were initially developed as a first-line treatment for insomnia to replace the reliance on benzodiazepines, but these medications have a “black-box” warning of a serious risk of complex sleep behaviors, including life-threatening parasomnias.⁴¹ As a result, guidelines suggest a shorter duration of treatment with a benzodiazepine receptor agonist may still provide benefit while limiting the risk of adverse effects.⁴²

Doxepin is the only antidepressant FDA-approved for insomnia; it improves sleep latency (time taken to initiate sleep after lying down), duration, and quality in adults age >65.⁴³ Melatonin receptor agonists such as ramelteon and melatonin have shown positive results in older patients with insomnia. In clinical trials of patients age ≥65, ramelteon, which is FDA-approved for insomnia, produced no rebound insomnia, withdrawal effects, memory impairment, or gait instability.^44-46 Suvorexant, an orexin receptor antagonist, decreases sleep latency and increases total sleep time equally in both young and older adults.^47-49Table 3^40-51 provides a list of medications used to treat insomnia (including off-label agents) and their common adverse effects in older adults.

Parasomnias are undesirable behaviors that occur during sleep, commonly associated with the sleep-wake transition period. These behaviors can occur during REM sleep (nightmare disorder, sleep paralysis, REM sleep behavior disorder) or NREM sleep (somnambulism [sleepwalking], confusional arousals, sleep terrors). According to a cross-sectional Norwegian study of parasomnias, the estimated lifetime prevalence of sleep walking is 22.4%; sleep talking, 66.8%; confusional arousal, 18.5%; and sleep terror, 10.4%.⁵²

Continue to: When evaluating a patient...

When evaluating a patient with parasomnias, it is important to review their drug and substance use as well as coexisting medical conditions. Drugs and substances that can affect sleep include prescription medications (second-generation antidepressants, stimulants, dopamine agonists), excessive caffeine, alcohol, certain foods (coffee, chocolate milk, black tea, caffeinated soft drinks), environmental exposures (smoking, pesticides), and recreational drugs (amphetamines).^53-56 Certain medical conditions are correlated with specific parasomnias (eg, sleep paralysis and narcolepsy, REM sleep behavior disorder and Parkinson’s disease [PD], etc.).⁵⁴ Diagnosis of parasomnias is mainly clinical but supporting evidence can be obtained through in-lab polysomnography.

Treatment. For parasomnias, treatment is primarily supportive and includes creating a safe sleeping environment to reduce the risk of self-harm. Recommendations include sleeping in a room on the ground floor, minimizing furniture in the bedroom, padding any bedside furniture, child-proofing doorknobs, and locking up weapons and other dangerous household items.⁵⁴

REM sleep behavior disorder (RBD). This disorder is characterized by a loss of the typical REM sleep-associated atonia and the presence of motor activity during dreaming (dream-enacted behaviors). While the estimated incidence of RBD in the general adult population is approximately 0.5%, it increases to 7.7% among those age >60.⁵⁷ RBD occurs most commonly in the setting of the alpha-synucleinopathies (PD, Lewy body dementia, multisystem atrophy), but can also be found in patients with cerebral ischemia, demyelinating disorders, or alcohol misuse, or can be medication-induced (primarily antidepressants and antipsychotics).⁵⁸ In patients with PD, the presence of RBD is associated with a more impaired cognitive profile, suggestive of widespread neurodegeneration.⁵⁹ Recent studies revealed that RBD may also be a prodromal state of neurodegenerative diseases such as PD, which should prompt close monitoring and long-term follow up.⁶⁰ Similar to other parasomnias, the diagnosis of RBD is primarily clinical, but polysomnography plays an important role in demonstrating loss of REM-related atonia.⁵⁴

Treatment. Clonazepam and melatonin have been shown to be effective in treating the symptoms of RBD.⁵⁴

Depression, anxiety, and sleep disturbances

Major depressive disorder (MDD) and generalized anxiety disorder (GAD) affect sleep in patients of all ages, but are underreported in older adults. According to national epidemiologic surveys, the estimated prevalence of MDD and GAD among older adults is 13% and 11.4%, respectively.^61,62 Rates as high as 42% and 39% have been reported in meta-regression analyses among patients with Alzheimer’s dementia.⁶³

Continue to: Depression and anxiety

Depression and anxiety may have additive effects and manifest as poor sleep satisfaction, increased sleep latency, insomnia, and daytime sleepiness.⁶⁴ However, they may also have independent effects. Studies showed that patients with depression alone reported overall poor sleep satisfaction, whereas patients with anxiety alone reported problems with sleep latency, daytime drowsiness, and waking up at night in addition to their overall poor sleep satisfaction.^65-67 Both depression and anxiety are risk factors for developing cognitive decline, and may be an early sign/prodrome of neurodegenerative diseases (dementias).⁶⁸ The bidirectional relationship between depression/anxiety and sleep is complex and needs further investigation.

Treatment. Pharmacologic treatments for patients with depression/anxiety and sleep disturbances include selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, and other serotonin receptor agonists.^69-72 Nonpharmacologic treatments include CBT for both depression and anxiety, and problem-solving therapy for patients with mild cognitive impairment and depression.^73,74 For severe depression and/or anxiety, electroconvulsive therapy is effective.⁷⁵

Bottom Line

Sleep disorders in older adults are common but often underdiagnosed. Timely recognition of obstructive sleep apnea, central sleep apnea, insomnia, parasomnias, and other sleep disturbances can facilitate effective treatment and greatly improve older adults’ quality of life.

Related Resources

• American Academy of Sleep Medicine. International Classification of Sleep Disorders—Third Edition. https://aasm.org
• SleepFoundation.org. Sleep hygiene. https://www.sleepfoundation.org/articles/sleep-hygiene

Drug Brand Names

Acetazolamide • Diamox
Clonazepam • Klonopin
Doxepin • Silenor
Eszopiclone • Lunesta
Gabapentin • Neurontin
Mirtazapine • Remeron
Pramipexole • Mirapex
Quetiapine • Seroquel
Ramelteon • Rozerem
Suvorexant • Belsomra
Temazepam • Restoril
Theophylline • Elixophyllin
Tiagabine • Gabitril
Trazadone • Desyrel
Triazolam • Halcion
Zaleplon • Sonata
Zolpidem • Ambien

As humans live longer, a renewed focus on quality of life has made the prompt diagnosis and treatment of sleep-related disorders in older adults increasingly necessary.¹ Normative aging results in multiple changes in sleep architecture, including decreased total sleep time, decreased sleep efficiency, decreased slow-wave sleep (SWS), and increased awakenings after sleep onset.² Sleep disturbances in older adults are increasingly recognized as multifactorial health conditions requiring comprehensive modification of risk factors, diagnosis, and treatment.³

In this article, we discuss the effects of aging on sleep architecture and provide an overview of primary sleep disorders in older adults. We also summarize strategies for diagnosing and treating sleep disorders in these patients.

Elements of the sleep cycle

The human sleep cycle begins with light sleep (sleep stages 1 and 2), progresses into SWS (sleep stage 3), and culminates in rapid eye movement (REM) sleep. The first 3 stages are referred to as non-rapid eye movement sleep (NREM). Throughout the night, this coupling of NREM and REM cycles occurs 4 to 6 times, with each successive cycle decreasing in length until awakening.⁴

Two complex neurologic pathways intersect to regulate the timing of sleep and wakefulness on arousal. The first pathway, the circadian system, is located within the suprachiasmatic nucleus of the hypothalamus and is highly dependent on external stimuli (light, food, etc.) to synchronize sleep/wake cycles. The suprachiasmatic nucleus regulates melatonin secretion by the pineal gland, which signals day-night transitions. The other pathway, the homeostatic system, modifies the amount of sleep needed daily. When multiple days of poor sleep occur, homeostatic sleep pressure (colloquially described as sleep debt) compensates by increasing the amount of sleep required in the following days. Together, the circadian and homeostatic systems work in conjunction to regulate sleep quantity to approximately one-third of the total sleep-wake cycle.^2,5

Age-related dysfunction of the regulatory sleep pathways leads to blunting of the ability to initiate and sustain high-quality sleep.⁶ Dysregulation of homeostatic sleep pressure decreases time spent in SWS, and failure of the circadian signaling apparatus results in delays in sleep/wake timing.² While research into the underlying neurobiology of sleep reveals that some of these changes are inherent to aging (Box^7-14), significant underdiagnosed pathologies may adversely affect sleep architecture, including polypharmacy, comorbid neuropathology (eg, synucleinopathies, tauopathies, etc.), and primary sleep disorders (insomnias, hypersomnias, and parasomnias).¹⁵

Box

Primary sleep disorders

Obstructive sleep apnea (OSA) is one of the most common, yet frequently underdiagnosed reversible causes of sleep disturbances. It is characterized by partial or complete airway obstruction culminating in periods of involuntary cessation of respirations during sleep. The resultant fragmentation in sleep leads to significant downstream effects over time, including excessive daytime sleepiness and fatigue, poor occupational and social performance, and substantial cognitive impairment.³ While it is well known that OSA increases in prevalence throughout middle age, this relationship plateaus after age 60.¹⁶ An estimated 40% to 60% of Americans age >60 are affected by OSA.¹⁷ The hypoxemia and fragmented sleep caused by unrecognized OSA are associated with a significant decline in activities of daily living (ADL).¹⁸ Untreated OSA is strongly linked to the development and progression of several major health conditions, including cardiovascular disease, diabetes mellitus, hypertension, stroke, and depression.¹⁹ In studies of long-term care facility residents—many of whom may have comorbid cognitive decline—researchers found that unrecognized OSA often mimics the progressive cognitive decline seen in major neurocognitive disorders.²⁰ However, classic symptoms of OSA may not always be present in these patients, and their daytime sleepiness is often attributed to old age rather than to a pathological etiology.¹⁶ Screening for OSA and prompt initiation of the appropriate treatment may reverse OSA-induced cognitive changes in these patients.²¹

The primary presenting symptom of OSA is snoring, which is correlated with pauses in breathing. Risk factors include increased body mass index (BMI), thick neck circumference, male sex, and advanced age. In older adults, BMI has a lower impact on the Apnea-Hypopnea Index, an indicator of the number of pauses in breathing per hour, when compared with young and middle-age adults.¹⁶ Validated screening questionnaires for OSA include the STOP-Bang Questionnaire (Table 1²²), OSA50, Berlin Questionnaire, and Epworth Sleepiness Scale, each of which is used in different subpopulations. The current diagnostic standard for OSA is nocturnal polysomnography in a sleep laboratory, but recent advances in home sleep apnea testing have made it a viable, low-cost alternative for patients who do not have significant medical comorbidities.²³ Standard utilized cutoffs for diagnosis are ≥5 events/hour (hypopneas associated with at least 4% oxygen desaturations) in conjunction with clinical symptoms of OSA.²⁴

Continue to: Treatment

Treatment. First-line treatment for OSA is continuous positive airway pressure therapy, but adherence rates vary widely with patient education and regular follow-up.²⁵ Adjunctive therapy includes weight loss, oral appliances, and uvulopalatopharyngoplasty, a procedure in which tissue in the throat is remodeled or removed.

Central sleep apnea (CSA) is a pause in breathing without evidence of associated respiratory effort. In adults, the development of CSA is indicative of underlying lower brainstem dysfunction, due to intermittent failures in the pontomedullary centers responsible for regulation of rhythmic breathing.²⁶ This can occur as a consequence of multiple diseases, including congestive heart failure, stroke, renal failure, chronic medication use (opioids), and brain tumors.

The Sleep Heart Health Study—the largest community-based cohort study to date examining CSA—estimated that the prevalence of CSA among adults age >65 was 1.1% (compared with 0.4% in those age <65).²⁷ Subgroup analysis revealed that men had significantly higher rates of CSA compared with women (2.7% vs 0.2%, respectively).

CSA may present similarly to OSA (excessive daytime somnolence, insomnia, poor sleep quality, difficulties with attention and concentration). Symptoms may also mimic those of coexisting medical conditions in older adults, such as nocturnal angina or paroxysmal nocturnal dyspnea.²⁷ Any older patient with daytime sleepiness and risk factors for CSA should be referred for in-laboratory nocturnal polysomnography, the gold standard diagnostic test. Unlike in OSA, ambulatory diagnostic measures (home sleep apnea testing) have not been validated for this disorder.²⁷

Treatment. The primary treatment for CSA is to address the underlying medical problem. Positive pressure ventilation has been attempted with mixed results. Supplemental oxygen and medical management (acetazolamide or theophylline) can help stimulate breathing. Newer studies have shown favorable outcomes with transvenous neurostimulation or adaptive servoventilation.^28-30

Continue to: Insomnia

Insomnia. For a primary diagnosis of insomnia, DSM-5 requires at least 3 nights per week of sleep disturbances that induce distress or functional impairment for at least 3 months.³¹ The International Classification of Disease, 10th Edition requires at least 1 month of symptoms (lying awake for a long time before falling asleep, sleeping for short periods, being awake for most of the night, feeling lack of sleep, waking up early) after ruling out other sleep disorders, substance use, or other medical conditions.⁴ Clinically, insomnia tends to present in older adults as a subjective complaint of dissatisfaction with the quality and/or quantity of their sleep. Insomnia has been consistently shown to be a significant risk factor for both the development or exacerbation of depression in older adults.^32-34

While the diagnosis of insomnia is mainly clinical via a thorough sleep and medication history, assistive ancillary testing can include wrist actigraphy and screening questionnaires (the Insomnia Severity Index and the Pittsburgh Sleep Quality Index).⁴ Because population studies of older adults have found discrepancies between objective and subjective methods of assessing sleep quality, relying on the accuracy of self-reported symptoms alone is questionable.³⁵

Treatment. Given that drug elimination half-life increases with age, and the risks of adverse effects are increased in older adults, the preferred treatment modalities for insomnia are nonpharmacologic.⁴ Sleep hygiene education (Table 2) and cognitive-behavioral therapy (CBT) for insomnia are often the first-line therapies.^4,36,37 It is crucial to manage comorbidities such as heart disease and obesity, as well as sources of discomfort from conditions such as arthritic pain.^38,39 If nonpharmacologic therapies are not effective, pharmacologic options can be considered.⁴ Before prescribing sleep medications, it may be more fruitful to treat underlying psychiatric disorders such as depression and anxiety with antidepressants.⁴ Although benzodiazepines are helpful for their sedative effects, they are not recommended for older adults because of an increased risk of falls, rebound insomnia, potential tolerance, and associated cognitive impairment.⁴⁰ Benzodiazepine receptor agonists (eg, zolpidem, eszopiclone, zaleplon) were initially developed as a first-line treatment for insomnia to replace the reliance on benzodiazepines, but these medications have a “black-box” warning of a serious risk of complex sleep behaviors, including life-threatening parasomnias.⁴¹ As a result, guidelines suggest a shorter duration of treatment with a benzodiazepine receptor agonist may still provide benefit while limiting the risk of adverse effects.⁴²

Doxepin is the only antidepressant FDA-approved for insomnia; it improves sleep latency (time taken to initiate sleep after lying down), duration, and quality in adults age >65.⁴³ Melatonin receptor agonists such as ramelteon and melatonin have shown positive results in older patients with insomnia. In clinical trials of patients age ≥65, ramelteon, which is FDA-approved for insomnia, produced no rebound insomnia, withdrawal effects, memory impairment, or gait instability.^44-46 Suvorexant, an orexin receptor antagonist, decreases sleep latency and increases total sleep time equally in both young and older adults.^47-49Table 3^40-51 provides a list of medications used to treat insomnia (including off-label agents) and their common adverse effects in older adults.

Parasomnias are undesirable behaviors that occur during sleep, commonly associated with the sleep-wake transition period. These behaviors can occur during REM sleep (nightmare disorder, sleep paralysis, REM sleep behavior disorder) or NREM sleep (somnambulism [sleepwalking], confusional arousals, sleep terrors). According to a cross-sectional Norwegian study of parasomnias, the estimated lifetime prevalence of sleep walking is 22.4%; sleep talking, 66.8%; confusional arousal, 18.5%; and sleep terror, 10.4%.⁵²

Continue to: When evaluating a patient...

When evaluating a patient with parasomnias, it is important to review their drug and substance use as well as coexisting medical conditions. Drugs and substances that can affect sleep include prescription medications (second-generation antidepressants, stimulants, dopamine agonists), excessive caffeine, alcohol, certain foods (coffee, chocolate milk, black tea, caffeinated soft drinks), environmental exposures (smoking, pesticides), and recreational drugs (amphetamines).^53-56 Certain medical conditions are correlated with specific parasomnias (eg, sleep paralysis and narcolepsy, REM sleep behavior disorder and Parkinson’s disease [PD], etc.).⁵⁴ Diagnosis of parasomnias is mainly clinical but supporting evidence can be obtained through in-lab polysomnography.

Treatment. For parasomnias, treatment is primarily supportive and includes creating a safe sleeping environment to reduce the risk of self-harm. Recommendations include sleeping in a room on the ground floor, minimizing furniture in the bedroom, padding any bedside furniture, child-proofing doorknobs, and locking up weapons and other dangerous household items.⁵⁴

REM sleep behavior disorder (RBD). This disorder is characterized by a loss of the typical REM sleep-associated atonia and the presence of motor activity during dreaming (dream-enacted behaviors). While the estimated incidence of RBD in the general adult population is approximately 0.5%, it increases to 7.7% among those age >60.⁵⁷ RBD occurs most commonly in the setting of the alpha-synucleinopathies (PD, Lewy body dementia, multisystem atrophy), but can also be found in patients with cerebral ischemia, demyelinating disorders, or alcohol misuse, or can be medication-induced (primarily antidepressants and antipsychotics).⁵⁸ In patients with PD, the presence of RBD is associated with a more impaired cognitive profile, suggestive of widespread neurodegeneration.⁵⁹ Recent studies revealed that RBD may also be a prodromal state of neurodegenerative diseases such as PD, which should prompt close monitoring and long-term follow up.⁶⁰ Similar to other parasomnias, the diagnosis of RBD is primarily clinical, but polysomnography plays an important role in demonstrating loss of REM-related atonia.⁵⁴

Treatment. Clonazepam and melatonin have been shown to be effective in treating the symptoms of RBD.⁵⁴

Depression, anxiety, and sleep disturbances

Major depressive disorder (MDD) and generalized anxiety disorder (GAD) affect sleep in patients of all ages, but are underreported in older adults. According to national epidemiologic surveys, the estimated prevalence of MDD and GAD among older adults is 13% and 11.4%, respectively.^61,62 Rates as high as 42% and 39% have been reported in meta-regression analyses among patients with Alzheimer’s dementia.⁶³

Continue to: Depression and anxiety

Depression and anxiety may have additive effects and manifest as poor sleep satisfaction, increased sleep latency, insomnia, and daytime sleepiness.⁶⁴ However, they may also have independent effects. Studies showed that patients with depression alone reported overall poor sleep satisfaction, whereas patients with anxiety alone reported problems with sleep latency, daytime drowsiness, and waking up at night in addition to their overall poor sleep satisfaction.^65-67 Both depression and anxiety are risk factors for developing cognitive decline, and may be an early sign/prodrome of neurodegenerative diseases (dementias).⁶⁸ The bidirectional relationship between depression/anxiety and sleep is complex and needs further investigation.

Treatment. Pharmacologic treatments for patients with depression/anxiety and sleep disturbances include selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, and other serotonin receptor agonists.^69-72 Nonpharmacologic treatments include CBT for both depression and anxiety, and problem-solving therapy for patients with mild cognitive impairment and depression.^73,74 For severe depression and/or anxiety, electroconvulsive therapy is effective.⁷⁵

Bottom Line

Sleep disorders in older adults are common but often underdiagnosed. Timely recognition of obstructive sleep apnea, central sleep apnea, insomnia, parasomnias, and other sleep disturbances can facilitate effective treatment and greatly improve older adults’ quality of life.

Related Resources

• American Academy of Sleep Medicine. International Classification of Sleep Disorders—Third Edition. https://aasm.org
• SleepFoundation.org. Sleep hygiene. https://www.sleepfoundation.org/articles/sleep-hygiene

Drug Brand Names

Acetazolamide • Diamox
Clonazepam • Klonopin
Doxepin • Silenor
Eszopiclone • Lunesta
Gabapentin • Neurontin
Mirtazapine • Remeron
Pramipexole • Mirapex
Quetiapine • Seroquel
Ramelteon • Rozerem
Suvorexant • Belsomra
Temazepam • Restoril
Theophylline • Elixophyllin
Tiagabine • Gabitril
Trazadone • Desyrel
Triazolam • Halcion
Zaleplon • Sonata
Zolpidem • Ambien

Editor’s note: Readers’ Forum is a new department for correspondence from readers that is not in response to articles published in Current Psychiatry . All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.

Since the completion of the human genome project, the role of pharmacogenomics in treating mental health disorders has become more prevalent. Recently discovered genetic polymorphisms and mutations in the methylenetetrahydrofolate reductase (MTHFR) gene have led clinicians to seek out new therapeutic approaches to personalize mental health care. MTHFR is a key enzyme of folate metabolism, and changes in its gene can result in reduced enzyme activity, which has been associated with psychiatric illnesses such as schizophrenia, major depressive disorder (MDD), attention-deficit/hyperactivity disorder (ADHD), and autism.¹ Supplementation with L-methylfolate, the active form of folate, has been found to improve clinical and social recovery in patients with psychiatric illnesses such as schizophrenia and MDD.² While L-methylfolate is classified as an FDA-approved medicinal food for patients with depression and schizophrenia, its role in ADHD remains controversial.³ L-methylfolate modulates the synthesis of monoamines such as dopamine and norepinephrine, which are pivotal in reducing inattentiveness and hyperactivity in patients with ADHD.^4,5 As a result, it could play an important role in the management of ADHD in patients with MTHFR deficiency.

Despite its high prevalence in many children, ADHD can persist into adulthood with impairing symptoms that have long-term social and economic impacts. Conventional methods of treating ADHD include stimulant medications such as methylphenidate, which can increase the levels of dopamine and norepinephrine in the brain. Unfortunately, stimulants’ cost, adverse effect profile, and high potential for abuse can hinder their use and contribute to treatment resistance.⁶ Because L-methylfolate can cross the blood-brain barrier and lacks the adverse effect profile of stimulants, it represents an alternative that could improve the quality of life for ADHD patients, particularly those with MTHFR polymorphisms or mutations.

Conflicting evidence

Several researchers have investigated the role of L-methylfolate as a supplement or alternative to stimulant therapy for patients with ADHD. While some preliminary studies have found some benefit, others have not. Here we describe 2 studies with differing results.

Quilliin⁷ (2013). In an open-label study at a children’s hospital in Texas, Quillin⁷ investi­gated L-methylfolate for alleviating attention-deficit disorder/ADHD symptoms in 59 patients age 5 to 18. Twenty-seven patients received stimulant therapy. All patients were treated with L-methylfolate, 0.2 mg/kg/d in a chewable tablet form, for 6 weeks. The primary endpoint was change on the average Vanderbilt Assessment Scale Total Symptom Score (TSS), which was 30 at baseline. At the study’s conclusion, the average TSS score was 22, a 27% reduction. Patients who were taking only L-methylfolate had an average score of 21 at the end of the study, which was a 34% improvement, compared with an average TSS score of 23 in those who were taking stimulants.

Surman et al³ (2019). In this 12-week, double-blind, placebo-controlled clinical trial, researchers assessed the efficacy and tolerability of L-methylfolate when added to osmotic-release oral system methylphenidate (OROS-MPH).³ Surman et al³ randomized 44 adult patients (age 18 to 55) who met the DSM-5 criteria for ADHD to a placebo group or an active group. The placebo group was treated with placebo plus OROS-MPH, while the active group received L-methylfolate, 15 mg/d, plus OROS-MPH. OROS-MPH was started at 36 mg/d and titrated to optimal response. The primary endpoint was change in score from baseline on the Adult ADHD Investigator Symptom Report scale. Although it was well tolerated, L-methylfolate was not associated with a significant change in measures of ADHD or mental health function.³ However, researchers noticed that patients who received L-methylfolate needed to receive higher doses of methylphenidate over time. This suggests that supplementation with L-methylfolate could reduce the effectiveness of methylphenidate in adult patients with ADHD.³

While more research is needed, the contradictory results of these studies suggests that the relationship between L-methylfolate and ADHD could be impacted by dosing, as well as by differences in adult and childhood ADHD that are not yet fully understood.

Continue to: An area warranting future research

An area warranting future research

The growth of pharmacogenomics represents an important opportunity to bridge the gap between our understanding of psychiatric illnesses and new ways to treat them. Using L-methylfolate to treat ADHD might help bridge this gap. For this to occur, psychiatrists need to use evidence-based pharmacogenetic research to inform their decision-making. The differing results in studies evaluating the use of L-methylfolate in adult and pediatric patients pose interesting questions that will require more robust research to answer. Clinicians should be cautious in the use of L-methylfolate and recognize the importance of evaluating every patient with ADHD for MTHFR deficiency. This could help personalize care in ways that may improve the quality of life for patients and their families.

Editor’s note: Readers’ Forum is a new department for correspondence from readers that is not in response to articles published in Current Psychiatry . All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.

Since the completion of the human genome project, the role of pharmacogenomics in treating mental health disorders has become more prevalent. Recently discovered genetic polymorphisms and mutations in the methylenetetrahydrofolate reductase (MTHFR) gene have led clinicians to seek out new therapeutic approaches to personalize mental health care. MTHFR is a key enzyme of folate metabolism, and changes in its gene can result in reduced enzyme activity, which has been associated with psychiatric illnesses such as schizophrenia, major depressive disorder (MDD), attention-deficit/hyperactivity disorder (ADHD), and autism.¹ Supplementation with L-methylfolate, the active form of folate, has been found to improve clinical and social recovery in patients with psychiatric illnesses such as schizophrenia and MDD.² While L-methylfolate is classified as an FDA-approved medicinal food for patients with depression and schizophrenia, its role in ADHD remains controversial.³ L-methylfolate modulates the synthesis of monoamines such as dopamine and norepinephrine, which are pivotal in reducing inattentiveness and hyperactivity in patients with ADHD.^4,5 As a result, it could play an important role in the management of ADHD in patients with MTHFR deficiency.

Despite its high prevalence in many children, ADHD can persist into adulthood with impairing symptoms that have long-term social and economic impacts. Conventional methods of treating ADHD include stimulant medications such as methylphenidate, which can increase the levels of dopamine and norepinephrine in the brain. Unfortunately, stimulants’ cost, adverse effect profile, and high potential for abuse can hinder their use and contribute to treatment resistance.⁶ Because L-methylfolate can cross the blood-brain barrier and lacks the adverse effect profile of stimulants, it represents an alternative that could improve the quality of life for ADHD patients, particularly those with MTHFR polymorphisms or mutations.

Conflicting evidence

Several researchers have investigated the role of L-methylfolate as a supplement or alternative to stimulant therapy for patients with ADHD. While some preliminary studies have found some benefit, others have not. Here we describe 2 studies with differing results.

Quilliin⁷ (2013). In an open-label study at a children’s hospital in Texas, Quillin⁷ investi­gated L-methylfolate for alleviating attention-deficit disorder/ADHD symptoms in 59 patients age 5 to 18. Twenty-seven patients received stimulant therapy. All patients were treated with L-methylfolate, 0.2 mg/kg/d in a chewable tablet form, for 6 weeks. The primary endpoint was change on the average Vanderbilt Assessment Scale Total Symptom Score (TSS), which was 30 at baseline. At the study’s conclusion, the average TSS score was 22, a 27% reduction. Patients who were taking only L-methylfolate had an average score of 21 at the end of the study, which was a 34% improvement, compared with an average TSS score of 23 in those who were taking stimulants.

Surman et al³ (2019). In this 12-week, double-blind, placebo-controlled clinical trial, researchers assessed the efficacy and tolerability of L-methylfolate when added to osmotic-release oral system methylphenidate (OROS-MPH).³ Surman et al³ randomized 44 adult patients (age 18 to 55) who met the DSM-5 criteria for ADHD to a placebo group or an active group. The placebo group was treated with placebo plus OROS-MPH, while the active group received L-methylfolate, 15 mg/d, plus OROS-MPH. OROS-MPH was started at 36 mg/d and titrated to optimal response. The primary endpoint was change in score from baseline on the Adult ADHD Investigator Symptom Report scale. Although it was well tolerated, L-methylfolate was not associated with a significant change in measures of ADHD or mental health function.³ However, researchers noticed that patients who received L-methylfolate needed to receive higher doses of methylphenidate over time. This suggests that supplementation with L-methylfolate could reduce the effectiveness of methylphenidate in adult patients with ADHD.³

While more research is needed, the contradictory results of these studies suggests that the relationship between L-methylfolate and ADHD could be impacted by dosing, as well as by differences in adult and childhood ADHD that are not yet fully understood.

Continue to: An area warranting future research

An area warranting future research

The growth of pharmacogenomics represents an important opportunity to bridge the gap between our understanding of psychiatric illnesses and new ways to treat them. Using L-methylfolate to treat ADHD might help bridge this gap. For this to occur, psychiatrists need to use evidence-based pharmacogenetic research to inform their decision-making. The differing results in studies evaluating the use of L-methylfolate in adult and pediatric patients pose interesting questions that will require more robust research to answer. Clinicians should be cautious in the use of L-methylfolate and recognize the importance of evaluating every patient with ADHD for MTHFR deficiency. This could help personalize care in ways that may improve the quality of life for patients and their families.

Editor’s note: Readers’ Forum is a new department for correspondence from readers that is not in response to articles published in Current Psychiatry . All submissions to Readers’ Forum undergo peer review and are subject to editing for length and style. For more information, contact letters@currentpsychiatry.

Since the completion of the human genome project, the role of pharmacogenomics in treating mental health disorders has become more prevalent. Recently discovered genetic polymorphisms and mutations in the methylenetetrahydrofolate reductase (MTHFR) gene have led clinicians to seek out new therapeutic approaches to personalize mental health care. MTHFR is a key enzyme of folate metabolism, and changes in its gene can result in reduced enzyme activity, which has been associated with psychiatric illnesses such as schizophrenia, major depressive disorder (MDD), attention-deficit/hyperactivity disorder (ADHD), and autism.¹ Supplementation with L-methylfolate, the active form of folate, has been found to improve clinical and social recovery in patients with psychiatric illnesses such as schizophrenia and MDD.² While L-methylfolate is classified as an FDA-approved medicinal food for patients with depression and schizophrenia, its role in ADHD remains controversial.³ L-methylfolate modulates the synthesis of monoamines such as dopamine and norepinephrine, which are pivotal in reducing inattentiveness and hyperactivity in patients with ADHD.^4,5 As a result, it could play an important role in the management of ADHD in patients with MTHFR deficiency.

Despite its high prevalence in many children, ADHD can persist into adulthood with impairing symptoms that have long-term social and economic impacts. Conventional methods of treating ADHD include stimulant medications such as methylphenidate, which can increase the levels of dopamine and norepinephrine in the brain. Unfortunately, stimulants’ cost, adverse effect profile, and high potential for abuse can hinder their use and contribute to treatment resistance.⁶ Because L-methylfolate can cross the blood-brain barrier and lacks the adverse effect profile of stimulants, it represents an alternative that could improve the quality of life for ADHD patients, particularly those with MTHFR polymorphisms or mutations.

Conflicting evidence

Several researchers have investigated the role of L-methylfolate as a supplement or alternative to stimulant therapy for patients with ADHD. While some preliminary studies have found some benefit, others have not. Here we describe 2 studies with differing results.

Quilliin⁷ (2013). In an open-label study at a children’s hospital in Texas, Quillin⁷ investi­gated L-methylfolate for alleviating attention-deficit disorder/ADHD symptoms in 59 patients age 5 to 18. Twenty-seven patients received stimulant therapy. All patients were treated with L-methylfolate, 0.2 mg/kg/d in a chewable tablet form, for 6 weeks. The primary endpoint was change on the average Vanderbilt Assessment Scale Total Symptom Score (TSS), which was 30 at baseline. At the study’s conclusion, the average TSS score was 22, a 27% reduction. Patients who were taking only L-methylfolate had an average score of 21 at the end of the study, which was a 34% improvement, compared with an average TSS score of 23 in those who were taking stimulants.

Surman et al³ (2019). In this 12-week, double-blind, placebo-controlled clinical trial, researchers assessed the efficacy and tolerability of L-methylfolate when added to osmotic-release oral system methylphenidate (OROS-MPH).³ Surman et al³ randomized 44 adult patients (age 18 to 55) who met the DSM-5 criteria for ADHD to a placebo group or an active group. The placebo group was treated with placebo plus OROS-MPH, while the active group received L-methylfolate, 15 mg/d, plus OROS-MPH. OROS-MPH was started at 36 mg/d and titrated to optimal response. The primary endpoint was change in score from baseline on the Adult ADHD Investigator Symptom Report scale. Although it was well tolerated, L-methylfolate was not associated with a significant change in measures of ADHD or mental health function.³ However, researchers noticed that patients who received L-methylfolate needed to receive higher doses of methylphenidate over time. This suggests that supplementation with L-methylfolate could reduce the effectiveness of methylphenidate in adult patients with ADHD.³

While more research is needed, the contradictory results of these studies suggests that the relationship between L-methylfolate and ADHD could be impacted by dosing, as well as by differences in adult and childhood ADHD that are not yet fully understood.

Continue to: An area warranting future research

An area warranting future research

The growth of pharmacogenomics represents an important opportunity to bridge the gap between our understanding of psychiatric illnesses and new ways to treat them. Using L-methylfolate to treat ADHD might help bridge this gap. For this to occur, psychiatrists need to use evidence-based pharmacogenetic research to inform their decision-making. The differing results in studies evaluating the use of L-methylfolate in adult and pediatric patients pose interesting questions that will require more robust research to answer. Clinicians should be cautious in the use of L-methylfolate and recognize the importance of evaluating every patient with ADHD for MTHFR deficiency. This could help personalize care in ways that may improve the quality of life for patients and their families.

In 2009, the Health Information Technology for Economic and Clinical Health Act (HITECH Act), which is part of the American Recovery and Reinvestment Act, provided several billion dollars of grants and incentives to stimulate the implementation of electronic health records (EHRs) and supporting technology in the United States.¹ Since then, almost all health care organizations have employed EHRs and supporting technologies. Unfortunately, this has created new liability risks. One potential risk is that in malpractice claims, there is more discoverable evidence, including metadata, with which to prove the claims.² In this article, I explain what metadata is and how it can be used in medical malpractice cases. In addition, because we cannot change metadata, I provide guidance on making corrections in your EHR documentation to minimize liability in medical malpractice cases.

What is metadata?

Metadata—commonly described as data about data—lurk behind the words and images we can see on our computer screens. Metadata can be conceptualized as data that provides details about the information we enter into a computer system, creating a permanent electronic footprint that can be used to track our activity.^2,3 Examples of metadata include (but are not limited to) the user’s name, date and time of a record entry, changes or deletions made to the record, the date an entry was created or modified, annotations that the user added over a period of time, and any other data that the software captures without the user manually entering the information.³ Metadata is typically stored on a server or file that users cannot access, which ensures data integrity because a user cannot alter a patient’s medical record without those changes being captured.³

How metadata is used in malpractice claims

When a psychiatrist is sued for medical negligence, the integrity of the EHR is an important aspect of defending against the lawsuit. A plaintiff’s (patient’s) attorney can more readily discover changes to the patient’s medical record by requesting the metadata and having it analyzed by an information technology specialist. Because the computer system captures everything a user does, it is difficult to alter a patient’s record without being detected. Consequently, plaintiff attorneys frequently request metadata during discovery in the hopes of learning whether the defendant psychiatrist altered or attempted to hide information that was contained or missing from the original version of the medical record.³ If the medical record was revised at a time unrelated to the treatment, metadata can raise suspicion of deception, even in the absence of wrongdoing.² Alternatively, metadata can be used to validate that the EHR was changed when treatment occurred, which can bolster a defendant psychiatrist’s ability to rely on the EHR against a claim of medical negligence.²

Depending on the jurisdiction, metadata may or may not be discoverable. The Federal Rules of Civil Procedure emphasize producing documents in their original format.⁴ For federal cases, these rules suggest that the parties discuss discovery of this material when they are initially conferring; however, the rules do not specify whether a party must produce metadata, which leaves the courts to refine these rules through case law.^4,5 In one case, a federal court ruled that a party had to produce documents with metadata intact.⁵ Without an agreement between both parties to exclude metadata from produced documents, the parties must produce the metadata.⁵ State laws differ in regards to the discoverability of metadata.

Corrections vs alterations

A patient’s medical record is the best evidence of the care we provided, should that care ever be challenged in court. We can preserve the medical record’s effectiveness through appropriate changes to it. Appropriately executed corrections are a normal part of documentation, whereas alterations to the medical record can cast doubt on our credibility and lead an otherwise defensible case to require a settlement.⁶

Corrections are changes to a patient’s medical record during the normal course of treatment.⁶ These are acceptable, provided the changes are made appropriately. Health care facilities and practices have their own policies for making appropriate corrections and addendums to the medical record. Once a correction and/or addendum is made, do not remove or delete the erroneous entry, because health care colleagues may have relied on it, and deleting an erroneous entry also would alter the integrity of the medical record.⁶ When done appropriately, corrections will not be misconstrued as alterations.

Alterations are changes to a patient’s medical record after a psychiatrist receives notice of a lawsuit and “clarifies” certain points in the medical record to aid the defense against the claim.⁶ Alterations are considered deliberate misrepresentations of facts and, if discovered during litigation, can significantly impact the ability to defend against a claim.⁶ In addition, many medical liability policies exclude coverage for claims in which the medical record was altered, which might result in a psychiatrist having to pay for the judgment and defense costs out of pocket.⁶ Psychiatrists facing litigation who have a legitimate need to change an EHR entry after a claim is filed should consult with legal counsel or a risk management professional for guidance before making any changes.³ If they concur with updating the patient’s record to correct an error (including an addendum or a late entry; see below), the original entry, date, and time stamp must be accessible.³ This should also include the current date/time of the amended entry, the name of the person making the change, and the reasons for the change.³

Continue to: How to handle corrections and late entries

Sometimes situations occur that require us to make late entries, enter addendums, or add clarification notes to patient information in the EHRs. Regardless of your work environment (ie, hospital, your own practice), there should be clear procedures in place for correcting patients’ EHRs that are in accordance with applicable federal and state laws. Correcting an error in the EHR should follow the same basic principles of correcting paper records: do not obscure the original entry, make timely corrections, sign all entries, ensure the person making the change is identified, and document the reason(s) for the correction.⁷ The EHR must be able to track corrections or changes to an entry once they are entered or authenticated. Any physical copies of documentation must also have the same corrections or changes if they have been previously printed from the EHR.

You may need to make an entry that is late (out of sequence) or provides additional documentation to supplement previously written entries.⁷ A late entry should be used to record information when a pertinent entry was missed or not written in a timely manner.⁷ Label the new entry as a “late entry,” enter the current date and time (do not give the appearance that the entry was made on a previous date or at an earlier time), and identify or refer to the date and incident for which the late entry is written.⁷ If the late entry is used to document an omission, validate the source of additional information as best you can (ie, details of where you obtained the information to write the late entry).⁷ Make late entries as soon as possible after the original entry; although there is no time limit on writing a late entry, delays in corrections might diminish the credibility of the changes.

Addendums are used to provide additional information in conjunction with a previous entry.⁷ They also provide additional information to address a specific situation or incident referenced in a previous note. Addendums should not be used to document information that was forgotten or written in error.⁷ A clarification note is used to avoid incorrect interpretation of previously documented information.⁷ When writing an addendum or a clarification note, you should label it as an “addendum” or a “clarification note”; document the current date and time; state the reason for the addendum (referring back to the original entry) or clarification note (referring back to the entry being clarified); and identify any sources of information used to support an addendum or a clarification note.⁷

In 2009, the Health Information Technology for Economic and Clinical Health Act (HITECH Act), which is part of the American Recovery and Reinvestment Act, provided several billion dollars of grants and incentives to stimulate the implementation of electronic health records (EHRs) and supporting technology in the United States.¹ Since then, almost all health care organizations have employed EHRs and supporting technologies. Unfortunately, this has created new liability risks. One potential risk is that in malpractice claims, there is more discoverable evidence, including metadata, with which to prove the claims.² In this article, I explain what metadata is and how it can be used in medical malpractice cases. In addition, because we cannot change metadata, I provide guidance on making corrections in your EHR documentation to minimize liability in medical malpractice cases.

What is metadata?

Metadata—commonly described as data about data—lurk behind the words and images we can see on our computer screens. Metadata can be conceptualized as data that provides details about the information we enter into a computer system, creating a permanent electronic footprint that can be used to track our activity.^2,3 Examples of metadata include (but are not limited to) the user’s name, date and time of a record entry, changes or deletions made to the record, the date an entry was created or modified, annotations that the user added over a period of time, and any other data that the software captures without the user manually entering the information.³ Metadata is typically stored on a server or file that users cannot access, which ensures data integrity because a user cannot alter a patient’s medical record without those changes being captured.³

How metadata is used in malpractice claims

When a psychiatrist is sued for medical negligence, the integrity of the EHR is an important aspect of defending against the lawsuit. A plaintiff’s (patient’s) attorney can more readily discover changes to the patient’s medical record by requesting the metadata and having it analyzed by an information technology specialist. Because the computer system captures everything a user does, it is difficult to alter a patient’s record without being detected. Consequently, plaintiff attorneys frequently request metadata during discovery in the hopes of learning whether the defendant psychiatrist altered or attempted to hide information that was contained or missing from the original version of the medical record.³ If the medical record was revised at a time unrelated to the treatment, metadata can raise suspicion of deception, even in the absence of wrongdoing.² Alternatively, metadata can be used to validate that the EHR was changed when treatment occurred, which can bolster a defendant psychiatrist’s ability to rely on the EHR against a claim of medical negligence.²

Depending on the jurisdiction, metadata may or may not be discoverable. The Federal Rules of Civil Procedure emphasize producing documents in their original format.⁴ For federal cases, these rules suggest that the parties discuss discovery of this material when they are initially conferring; however, the rules do not specify whether a party must produce metadata, which leaves the courts to refine these rules through case law.^4,5 In one case, a federal court ruled that a party had to produce documents with metadata intact.⁵ Without an agreement between both parties to exclude metadata from produced documents, the parties must produce the metadata.⁵ State laws differ in regards to the discoverability of metadata.

Corrections vs alterations

A patient’s medical record is the best evidence of the care we provided, should that care ever be challenged in court. We can preserve the medical record’s effectiveness through appropriate changes to it. Appropriately executed corrections are a normal part of documentation, whereas alterations to the medical record can cast doubt on our credibility and lead an otherwise defensible case to require a settlement.⁶

Corrections are changes to a patient’s medical record during the normal course of treatment.⁶ These are acceptable, provided the changes are made appropriately. Health care facilities and practices have their own policies for making appropriate corrections and addendums to the medical record. Once a correction and/or addendum is made, do not remove or delete the erroneous entry, because health care colleagues may have relied on it, and deleting an erroneous entry also would alter the integrity of the medical record.⁶ When done appropriately, corrections will not be misconstrued as alterations.

Alterations are changes to a patient’s medical record after a psychiatrist receives notice of a lawsuit and “clarifies” certain points in the medical record to aid the defense against the claim.⁶ Alterations are considered deliberate misrepresentations of facts and, if discovered during litigation, can significantly impact the ability to defend against a claim.⁶ In addition, many medical liability policies exclude coverage for claims in which the medical record was altered, which might result in a psychiatrist having to pay for the judgment and defense costs out of pocket.⁶ Psychiatrists facing litigation who have a legitimate need to change an EHR entry after a claim is filed should consult with legal counsel or a risk management professional for guidance before making any changes.³ If they concur with updating the patient’s record to correct an error (including an addendum or a late entry; see below), the original entry, date, and time stamp must be accessible.³ This should also include the current date/time of the amended entry, the name of the person making the change, and the reasons for the change.³

Continue to: How to handle corrections and late entries

Sometimes situations occur that require us to make late entries, enter addendums, or add clarification notes to patient information in the EHRs. Regardless of your work environment (ie, hospital, your own practice), there should be clear procedures in place for correcting patients’ EHRs that are in accordance with applicable federal and state laws. Correcting an error in the EHR should follow the same basic principles of correcting paper records: do not obscure the original entry, make timely corrections, sign all entries, ensure the person making the change is identified, and document the reason(s) for the correction.⁷ The EHR must be able to track corrections or changes to an entry once they are entered or authenticated. Any physical copies of documentation must also have the same corrections or changes if they have been previously printed from the EHR.

You may need to make an entry that is late (out of sequence) or provides additional documentation to supplement previously written entries.⁷ A late entry should be used to record information when a pertinent entry was missed or not written in a timely manner.⁷ Label the new entry as a “late entry,” enter the current date and time (do not give the appearance that the entry was made on a previous date or at an earlier time), and identify or refer to the date and incident for which the late entry is written.⁷ If the late entry is used to document an omission, validate the source of additional information as best you can (ie, details of where you obtained the information to write the late entry).⁷ Make late entries as soon as possible after the original entry; although there is no time limit on writing a late entry, delays in corrections might diminish the credibility of the changes.

Addendums are used to provide additional information in conjunction with a previous entry.⁷ They also provide additional information to address a specific situation or incident referenced in a previous note. Addendums should not be used to document information that was forgotten or written in error.⁷ A clarification note is used to avoid incorrect interpretation of previously documented information.⁷ When writing an addendum or a clarification note, you should label it as an “addendum” or a “clarification note”; document the current date and time; state the reason for the addendum (referring back to the original entry) or clarification note (referring back to the entry being clarified); and identify any sources of information used to support an addendum or a clarification note.⁷

In 2009, the Health Information Technology for Economic and Clinical Health Act (HITECH Act), which is part of the American Recovery and Reinvestment Act, provided several billion dollars of grants and incentives to stimulate the implementation of electronic health records (EHRs) and supporting technology in the United States.¹ Since then, almost all health care organizations have employed EHRs and supporting technologies. Unfortunately, this has created new liability risks. One potential risk is that in malpractice claims, there is more discoverable evidence, including metadata, with which to prove the claims.² In this article, I explain what metadata is and how it can be used in medical malpractice cases. In addition, because we cannot change metadata, I provide guidance on making corrections in your EHR documentation to minimize liability in medical malpractice cases.

What is metadata?

Metadata—commonly described as data about data—lurk behind the words and images we can see on our computer screens. Metadata can be conceptualized as data that provides details about the information we enter into a computer system, creating a permanent electronic footprint that can be used to track our activity.^2,3 Examples of metadata include (but are not limited to) the user’s name, date and time of a record entry, changes or deletions made to the record, the date an entry was created or modified, annotations that the user added over a period of time, and any other data that the software captures without the user manually entering the information.³ Metadata is typically stored on a server or file that users cannot access, which ensures data integrity because a user cannot alter a patient’s medical record without those changes being captured.³

How metadata is used in malpractice claims

When a psychiatrist is sued for medical negligence, the integrity of the EHR is an important aspect of defending against the lawsuit. A plaintiff’s (patient’s) attorney can more readily discover changes to the patient’s medical record by requesting the metadata and having it analyzed by an information technology specialist. Because the computer system captures everything a user does, it is difficult to alter a patient’s record without being detected. Consequently, plaintiff attorneys frequently request metadata during discovery in the hopes of learning whether the defendant psychiatrist altered or attempted to hide information that was contained or missing from the original version of the medical record.³ If the medical record was revised at a time unrelated to the treatment, metadata can raise suspicion of deception, even in the absence of wrongdoing.² Alternatively, metadata can be used to validate that the EHR was changed when treatment occurred, which can bolster a defendant psychiatrist’s ability to rely on the EHR against a claim of medical negligence.²

Depending on the jurisdiction, metadata may or may not be discoverable. The Federal Rules of Civil Procedure emphasize producing documents in their original format.⁴ For federal cases, these rules suggest that the parties discuss discovery of this material when they are initially conferring; however, the rules do not specify whether a party must produce metadata, which leaves the courts to refine these rules through case law.^4,5 In one case, a federal court ruled that a party had to produce documents with metadata intact.⁵ Without an agreement between both parties to exclude metadata from produced documents, the parties must produce the metadata.⁵ State laws differ in regards to the discoverability of metadata.

Corrections vs alterations

A patient’s medical record is the best evidence of the care we provided, should that care ever be challenged in court. We can preserve the medical record’s effectiveness through appropriate changes to it. Appropriately executed corrections are a normal part of documentation, whereas alterations to the medical record can cast doubt on our credibility and lead an otherwise defensible case to require a settlement.⁶

Corrections are changes to a patient’s medical record during the normal course of treatment.⁶ These are acceptable, provided the changes are made appropriately. Health care facilities and practices have their own policies for making appropriate corrections and addendums to the medical record. Once a correction and/or addendum is made, do not remove or delete the erroneous entry, because health care colleagues may have relied on it, and deleting an erroneous entry also would alter the integrity of the medical record.⁶ When done appropriately, corrections will not be misconstrued as alterations.

Alterations are changes to a patient’s medical record after a psychiatrist receives notice of a lawsuit and “clarifies” certain points in the medical record to aid the defense against the claim.⁶ Alterations are considered deliberate misrepresentations of facts and, if discovered during litigation, can significantly impact the ability to defend against a claim.⁶ In addition, many medical liability policies exclude coverage for claims in which the medical record was altered, which might result in a psychiatrist having to pay for the judgment and defense costs out of pocket.⁶ Psychiatrists facing litigation who have a legitimate need to change an EHR entry after a claim is filed should consult with legal counsel or a risk management professional for guidance before making any changes.³ If they concur with updating the patient’s record to correct an error (including an addendum or a late entry; see below), the original entry, date, and time stamp must be accessible.³ This should also include the current date/time of the amended entry, the name of the person making the change, and the reasons for the change.³

Continue to: How to handle corrections and late entries

Sometimes situations occur that require us to make late entries, enter addendums, or add clarification notes to patient information in the EHRs. Regardless of your work environment (ie, hospital, your own practice), there should be clear procedures in place for correcting patients’ EHRs that are in accordance with applicable federal and state laws. Correcting an error in the EHR should follow the same basic principles of correcting paper records: do not obscure the original entry, make timely corrections, sign all entries, ensure the person making the change is identified, and document the reason(s) for the correction.⁷ The EHR must be able to track corrections or changes to an entry once they are entered or authenticated. Any physical copies of documentation must also have the same corrections or changes if they have been previously printed from the EHR.

You may need to make an entry that is late (out of sequence) or provides additional documentation to supplement previously written entries.⁷ A late entry should be used to record information when a pertinent entry was missed or not written in a timely manner.⁷ Label the new entry as a “late entry,” enter the current date and time (do not give the appearance that the entry was made on a previous date or at an earlier time), and identify or refer to the date and incident for which the late entry is written.⁷ If the late entry is used to document an omission, validate the source of additional information as best you can (ie, details of where you obtained the information to write the late entry).⁷ Make late entries as soon as possible after the original entry; although there is no time limit on writing a late entry, delays in corrections might diminish the credibility of the changes.

Addendums are used to provide additional information in conjunction with a previous entry.⁷ They also provide additional information to address a specific situation or incident referenced in a previous note. Addendums should not be used to document information that was forgotten or written in error.⁷ A clarification note is used to avoid incorrect interpretation of previously documented information.⁷ When writing an addendum or a clarification note, you should label it as an “addendum” or a “clarification note”; document the current date and time; state the reason for the addendum (referring back to the original entry) or clarification note (referring back to the entry being clarified); and identify any sources of information used to support an addendum or a clarification note.⁷