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Are oncologists any better at facing their own mortality?
Douglas Flora, MD, an oncologist with St. Elizabeth Healthcare, in Edgewood, Ky., considers himself a deep empath. It’s one reason he became an oncologist.
But when he was diagnosed with kidney cancer in 2017, he was shocked at the places his brain took him. His mind fast-forwarded through treatment options, statistical probabilities, and anguish over his wife and children.
“It’s a very surreal experience,” Dr. Flora said. “In 20 seconds, you go from diagnostics to, ‘What videos will I have to film for my babies?’ “
He could be having a wonderful evening surrounded by friends, music, and beer. Then he would go to the restroom and the realization of what was lurking inside his would body hit him like a brick.
“It’s like the scene in the Harry Potter movies where the Dementors fly over,” he explained. “Everything feels dark. There’s no hope. Everything you thought was good is gone.”
Oncologists counsel patients through life-threatening diagnoses and frightening decisions every day, so one might think they’d be ready to confront their own diagnosis, treatment, and mortality better than anyone. But that’s not always the case.
Does their expertise equip them to navigate their diagnosis and treatment better than their patients? How does the emotional toll of their personal cancer journey change the way they interact with their patients?
Navigating the diagnosis and treatment
In January 2017, Karen Hendershott, MD, a breast surgical oncologist, felt a lump in her armpit while taking a shower. The blunt force of her fate came into view in an instant: It was almost certainly a locally advanced breast cancer that had spread to her lymph nodes and would require surgery, radiotherapy, and chemotherapy.
She said a few unprintable words and headed to work at St. Mary’s Hospital, in Tucson, Ariz., where her assumptions were confirmed.
Taylor Riall, MD, PhD, also suspected cancer.
Last December, Dr. Riall, a general surgeon and surgical oncologist at the University of Arizona Cancer Center, in Tucson, developed a persistent cough. An x-ray revealed a mass in her lung. Initially, she was misdiagnosed with a fungal infection and was given medication that made her skin peel off.
Doctors advised Dr. Riall to monitor her condition for another 6 months. But her knowledge of oncology made her think cancer, so she insisted on more tests. In June 2021, a biopsy confirmed she had lung cancer.
Having oncology expertise helped Dr. Riall and Dr. Hendershott recognize the signs of cancer and push for a diagnosis. But there are also downsides to being hyper-informed, Dr. Hendershott, said.
“I think sometimes knowing everything at once is harder vs. giving yourself time to wrap your mind around this and do it in baby steps,” she explained. “There weren’t any baby steps here.”
Still, oncology practitioners who are diagnosed with cancer are navigating a familiar landscape and are often buoyed by a support network of expert colleagues. That makes a huge difference psychologically, explained Shenitha Edwards, a pharmacy technician at Cancer Specialists of North Florida, in Jacksonville, who was diagnosed with breast cancer in July.
“I felt stronger and a little more ready to fight because I had resources, whereas my patients sometimes do not,” Ms. Edwards said. “I was connected with a lot of people who could help me make informed decisions, so I didn’t have to walk so much in fear.”
It can also prepare practitioners to make bold treatment choices. In Dr. Riall’s case, surgeons were reluctant to excise her tumor because they would have to remove the entire upper lobe of her lung, and she is a marathoner and triathlete. Still, because of her surgical oncology experience, Dr. Riall didn’t flinch at the prospect of a major operation.
“I was, like, ‘Look, just take it out.’ I’m less afraid to have cancer than I am to not know and let it grow,” said Dr. Riall, whose Peloton name is WhoNeeds2Lungs.
Similarly, Dr. Hendershott’s experience gave her the assurance to pursue a more intense strategy. “Because I had a really candid understanding of the risks and what the odds looked like, it helped me be more comfortable with a more aggressive approach,” she said. “There wasn’t a doubt in my mind, particularly [having] a 10-year-old child, that I wanted to do everything I could, and even do a couple of things that were still in clinical trials.”
Almost paradoxically, Mark Lewis’ oncology training gave him the courage to risk watching and waiting after finding benign growths in his parathyroid and malignant tumors in his pancreas. Dr. Lewis monitored the tumors amassing in his pancreas for 8 years. When some grew so large they threatened to metastasize to his liver, he underwent the Whipple procedure to remove the head of the pancreas, part of the small intestine, and the gallbladder.
“It was a bit of a gamble, but one that paid off and allowed me to get my career off the ground and have another child,” said Dr. Lewis, a gastrointestinal oncologist at Intermountain Healthcare, in Salt Lake City. Treating patients for nearly a decade also showed him how fortunate he was to have a slow-growing, operable cancer. That gratitude, he said, gave him mental strength to endure the ordeal.
Whether taking a more aggressive or minimalist approach to their own care, each practitioner’s decision was deeply personal and deeply informed by their oncology expertise.
Although research on this question is scarce, studies show that differences in end-of-life care may occur. According to a 2016 study published in JAMA, physicians choose significantly less intensive end-stage care in three of five categories — undergoing surgery, being admitted to the intensive care unit (ICU), and dying in the hospital — than the general U.S. population. The reason, the researchers posited, is because doctors know these eleventh-hour interventions are typically brutal and futile.
But these differences were fairly small, and a 2019 study published in JAMA Open Network found the opposite: Physicians with cancer were more likely to die in an ICU and receive chemotherapy in the last 6 months of life, suggesting a more aggressive approach to end-of-life care.
When it comes to their own long-term or curative cancer care, oncologists generally don’t seem to approach treatment differently than their patients. In a 2015 study, researchers compared two groups of people with early breast cancer — 46 physicians and 230 well-educated, nonmedically qualified patients — and found no differences in the choices the groups made about whether to undergo mastectomy, chemotherapy, radiotherapy, or breast reconstruction.
Still, no amount of oncology expertise can fully prepare a person for the emotional crucible of cancer.
“A very surreal experience”
Although the fear can become less intense and more manageable over time, it may never truly go away.
At first, despair dragged Flora into an abyss for 6 hours a night, then overcame him 10 times a day, then gripped him briefly at random moments. Four years later and cancer-free, the dread still returns.
Hendershott cried every time she got into her car and contemplated her prognosis. Now 47, she has about a 60% chance of being alive in 15 years, and the fear still hits her.
“I think it’s hard to understand the moments of sheer terror that you have at 2 AM when you’re confronting your own mortality,” she said. “The implications that has not just for you but more importantly for the people that you love and want to protect. That just kind of washes over you in waves that you don’t have much control over.”
Cancer, Riall felt, had smashed her life, but she figured out a way to help herself cope. Severe blood loss, chest tubes, and tests and needles ad nauseum left Riall feeling excruciatingly exhausted after her surgery and delayed her return to work. At the same time, she was passed over for a promotion. Frustrated and dejected, she took comfort in the memory of doing Kintsugi with her surgery residents. The Japanese art form involves shattering pottery with a hammer, fitting the fragments back together, and painting the cracks gold.
“My instinct as a surgeon is to pick up those pieces and put them back together so nobody sees it’s broken,” she reflected. But as a patient, she learned that an important part of recovery is to allow yourself to sit in a broken state and feel angry, miserable, and betrayed by your body. And then examine your shattered priorities and consider how you want to reassemble them.
For Barbara Buttin, MD, a gynecologic oncologist at Cancer Treatment Centers of America, in Chicago, Illinois, it wasn’t cancer that almost took her life. Rather, a near-death experience and life-threatening diagnosis made her a better, more empathetic cancer doctor — a refrain echoed by many oncologist-patients. Confronting her own mortality crystallized what matters in life. She uses that understanding to make sure she understands what matters to her patients ― what they care about most, what their greatest fear is, what is going to keep them up at night.
“We’re part of the same club”
Ultimately, when oncology practitioners become patients, it balances the in-control and vulnerable, the rational and emotional. And their patients respond positively.
In fall 2020, oncology nurse Jenn Adams, RN, turned 40 and underwent her first mammogram. Unexpectedly, it revealed invasive stage I cancer that would require a double mastectomy, chemotherapy, and a year of immunotherapy. A week after her diagnosis, she was scheduled to start a new job at Cancer Clinic, in Bryan, Tex. So, she asked her manager if she could become a patient and an employee.
Ms. Adams worked 5 days a week, but every Thursday at 2 PM, she sat next to her patients while her coworkers became her nurses. Her chemo port was implanted, she lost her hair, and she felt terrible along with her patients. “It just created this incredible bond,” said the mother of three.
Having cancer, Dr. Flora said, “was completely different than I had imagined. When I thought I was walking with [my patients] in the depths of their caves, I wasn’t even visiting their caves.” But, he added, it has also “let me connect with [patients] on a deeper level because we’re part of the same club. You can see their body language change when I share that. They almost relax, like, ‘Oh, this guy gets it. He does understand how terrified I am.’ And I do.”
When Dr. Flora’s patients are scanned, he gives them their results immediately, because he knows what it’s like to wait on tenterhooks. He tells his patients to text him anytime they’re afraid or depressed, which he admits isn’t great for his own mental health but believes is worth it.
Likewise, Dr. Hendershott can hold out her shoulder-length locks to reassure a crying patient that hair does grow back after chemo. She can describe her experience with hormone-blocking pills to allay the fears of a pharmaceutical skeptic.
This role equalizer fosters so much empathy that doctors sometimes find themselves being helped by their patients. When one of Dr. Flora’s patients heard he had cancer, she sent him an email that began. “A wise doctor once told me....” and repeated the advice he’d given her years before.
Dr. Lewis has a special bond with his patients because people who have pancreatic neuroendocrine tumors seek him out for treatment. “I’m getting to take care of people who, on some level, are like my kindred spirits,” he said. “So, I get to see their coping mechanisms and how they do.”
Ms. Edwards told some of her patients about her breast cancer diagnosis, and now they give each other high-fives and share words of encouragement. “I made it a big thing of mine to associate my patients as my family,” she said. “If you’ve learned to embrace love and love people, there’s nothing you wouldn’t do for people. I’ve chosen that to be my practice when I’m dealing with all of my patients.”
Ms. Adams is on a similar mission. She joined a group of moms with cancer so she can receive guidance and then become a guide for others. “I feel like that’s what I want to be at my cancer practice,” she said, “so [my patients] have someone to say, ‘I’m gonna walk alongside you because I’ve been there.’ “
That transformation has made all the heartbreaking moments worth it, Ms. Adams said. “I love the oncology nurse that I get to be now because of my diagnosis. I don’t love the diagnosis. But I love the way it’s changed what I do.”
A version of this article first appeared on Medscape.com.
Douglas Flora, MD, an oncologist with St. Elizabeth Healthcare, in Edgewood, Ky., considers himself a deep empath. It’s one reason he became an oncologist.
But when he was diagnosed with kidney cancer in 2017, he was shocked at the places his brain took him. His mind fast-forwarded through treatment options, statistical probabilities, and anguish over his wife and children.
“It’s a very surreal experience,” Dr. Flora said. “In 20 seconds, you go from diagnostics to, ‘What videos will I have to film for my babies?’ “
He could be having a wonderful evening surrounded by friends, music, and beer. Then he would go to the restroom and the realization of what was lurking inside his would body hit him like a brick.
“It’s like the scene in the Harry Potter movies where the Dementors fly over,” he explained. “Everything feels dark. There’s no hope. Everything you thought was good is gone.”
Oncologists counsel patients through life-threatening diagnoses and frightening decisions every day, so one might think they’d be ready to confront their own diagnosis, treatment, and mortality better than anyone. But that’s not always the case.
Does their expertise equip them to navigate their diagnosis and treatment better than their patients? How does the emotional toll of their personal cancer journey change the way they interact with their patients?
Navigating the diagnosis and treatment
In January 2017, Karen Hendershott, MD, a breast surgical oncologist, felt a lump in her armpit while taking a shower. The blunt force of her fate came into view in an instant: It was almost certainly a locally advanced breast cancer that had spread to her lymph nodes and would require surgery, radiotherapy, and chemotherapy.
She said a few unprintable words and headed to work at St. Mary’s Hospital, in Tucson, Ariz., where her assumptions were confirmed.
Taylor Riall, MD, PhD, also suspected cancer.
Last December, Dr. Riall, a general surgeon and surgical oncologist at the University of Arizona Cancer Center, in Tucson, developed a persistent cough. An x-ray revealed a mass in her lung. Initially, she was misdiagnosed with a fungal infection and was given medication that made her skin peel off.
Doctors advised Dr. Riall to monitor her condition for another 6 months. But her knowledge of oncology made her think cancer, so she insisted on more tests. In June 2021, a biopsy confirmed she had lung cancer.
Having oncology expertise helped Dr. Riall and Dr. Hendershott recognize the signs of cancer and push for a diagnosis. But there are also downsides to being hyper-informed, Dr. Hendershott, said.
“I think sometimes knowing everything at once is harder vs. giving yourself time to wrap your mind around this and do it in baby steps,” she explained. “There weren’t any baby steps here.”
Still, oncology practitioners who are diagnosed with cancer are navigating a familiar landscape and are often buoyed by a support network of expert colleagues. That makes a huge difference psychologically, explained Shenitha Edwards, a pharmacy technician at Cancer Specialists of North Florida, in Jacksonville, who was diagnosed with breast cancer in July.
“I felt stronger and a little more ready to fight because I had resources, whereas my patients sometimes do not,” Ms. Edwards said. “I was connected with a lot of people who could help me make informed decisions, so I didn’t have to walk so much in fear.”
It can also prepare practitioners to make bold treatment choices. In Dr. Riall’s case, surgeons were reluctant to excise her tumor because they would have to remove the entire upper lobe of her lung, and she is a marathoner and triathlete. Still, because of her surgical oncology experience, Dr. Riall didn’t flinch at the prospect of a major operation.
“I was, like, ‘Look, just take it out.’ I’m less afraid to have cancer than I am to not know and let it grow,” said Dr. Riall, whose Peloton name is WhoNeeds2Lungs.
Similarly, Dr. Hendershott’s experience gave her the assurance to pursue a more intense strategy. “Because I had a really candid understanding of the risks and what the odds looked like, it helped me be more comfortable with a more aggressive approach,” she said. “There wasn’t a doubt in my mind, particularly [having] a 10-year-old child, that I wanted to do everything I could, and even do a couple of things that were still in clinical trials.”
Almost paradoxically, Mark Lewis’ oncology training gave him the courage to risk watching and waiting after finding benign growths in his parathyroid and malignant tumors in his pancreas. Dr. Lewis monitored the tumors amassing in his pancreas for 8 years. When some grew so large they threatened to metastasize to his liver, he underwent the Whipple procedure to remove the head of the pancreas, part of the small intestine, and the gallbladder.
“It was a bit of a gamble, but one that paid off and allowed me to get my career off the ground and have another child,” said Dr. Lewis, a gastrointestinal oncologist at Intermountain Healthcare, in Salt Lake City. Treating patients for nearly a decade also showed him how fortunate he was to have a slow-growing, operable cancer. That gratitude, he said, gave him mental strength to endure the ordeal.
Whether taking a more aggressive or minimalist approach to their own care, each practitioner’s decision was deeply personal and deeply informed by their oncology expertise.
Although research on this question is scarce, studies show that differences in end-of-life care may occur. According to a 2016 study published in JAMA, physicians choose significantly less intensive end-stage care in three of five categories — undergoing surgery, being admitted to the intensive care unit (ICU), and dying in the hospital — than the general U.S. population. The reason, the researchers posited, is because doctors know these eleventh-hour interventions are typically brutal and futile.
But these differences were fairly small, and a 2019 study published in JAMA Open Network found the opposite: Physicians with cancer were more likely to die in an ICU and receive chemotherapy in the last 6 months of life, suggesting a more aggressive approach to end-of-life care.
When it comes to their own long-term or curative cancer care, oncologists generally don’t seem to approach treatment differently than their patients. In a 2015 study, researchers compared two groups of people with early breast cancer — 46 physicians and 230 well-educated, nonmedically qualified patients — and found no differences in the choices the groups made about whether to undergo mastectomy, chemotherapy, radiotherapy, or breast reconstruction.
Still, no amount of oncology expertise can fully prepare a person for the emotional crucible of cancer.
“A very surreal experience”
Although the fear can become less intense and more manageable over time, it may never truly go away.
At first, despair dragged Flora into an abyss for 6 hours a night, then overcame him 10 times a day, then gripped him briefly at random moments. Four years later and cancer-free, the dread still returns.
Hendershott cried every time she got into her car and contemplated her prognosis. Now 47, she has about a 60% chance of being alive in 15 years, and the fear still hits her.
“I think it’s hard to understand the moments of sheer terror that you have at 2 AM when you’re confronting your own mortality,” she said. “The implications that has not just for you but more importantly for the people that you love and want to protect. That just kind of washes over you in waves that you don’t have much control over.”
Cancer, Riall felt, had smashed her life, but she figured out a way to help herself cope. Severe blood loss, chest tubes, and tests and needles ad nauseum left Riall feeling excruciatingly exhausted after her surgery and delayed her return to work. At the same time, she was passed over for a promotion. Frustrated and dejected, she took comfort in the memory of doing Kintsugi with her surgery residents. The Japanese art form involves shattering pottery with a hammer, fitting the fragments back together, and painting the cracks gold.
“My instinct as a surgeon is to pick up those pieces and put them back together so nobody sees it’s broken,” she reflected. But as a patient, she learned that an important part of recovery is to allow yourself to sit in a broken state and feel angry, miserable, and betrayed by your body. And then examine your shattered priorities and consider how you want to reassemble them.
For Barbara Buttin, MD, a gynecologic oncologist at Cancer Treatment Centers of America, in Chicago, Illinois, it wasn’t cancer that almost took her life. Rather, a near-death experience and life-threatening diagnosis made her a better, more empathetic cancer doctor — a refrain echoed by many oncologist-patients. Confronting her own mortality crystallized what matters in life. She uses that understanding to make sure she understands what matters to her patients ― what they care about most, what their greatest fear is, what is going to keep them up at night.
“We’re part of the same club”
Ultimately, when oncology practitioners become patients, it balances the in-control and vulnerable, the rational and emotional. And their patients respond positively.
In fall 2020, oncology nurse Jenn Adams, RN, turned 40 and underwent her first mammogram. Unexpectedly, it revealed invasive stage I cancer that would require a double mastectomy, chemotherapy, and a year of immunotherapy. A week after her diagnosis, she was scheduled to start a new job at Cancer Clinic, in Bryan, Tex. So, she asked her manager if she could become a patient and an employee.
Ms. Adams worked 5 days a week, but every Thursday at 2 PM, she sat next to her patients while her coworkers became her nurses. Her chemo port was implanted, she lost her hair, and she felt terrible along with her patients. “It just created this incredible bond,” said the mother of three.
Having cancer, Dr. Flora said, “was completely different than I had imagined. When I thought I was walking with [my patients] in the depths of their caves, I wasn’t even visiting their caves.” But, he added, it has also “let me connect with [patients] on a deeper level because we’re part of the same club. You can see their body language change when I share that. They almost relax, like, ‘Oh, this guy gets it. He does understand how terrified I am.’ And I do.”
When Dr. Flora’s patients are scanned, he gives them their results immediately, because he knows what it’s like to wait on tenterhooks. He tells his patients to text him anytime they’re afraid or depressed, which he admits isn’t great for his own mental health but believes is worth it.
Likewise, Dr. Hendershott can hold out her shoulder-length locks to reassure a crying patient that hair does grow back after chemo. She can describe her experience with hormone-blocking pills to allay the fears of a pharmaceutical skeptic.
This role equalizer fosters so much empathy that doctors sometimes find themselves being helped by their patients. When one of Dr. Flora’s patients heard he had cancer, she sent him an email that began. “A wise doctor once told me....” and repeated the advice he’d given her years before.
Dr. Lewis has a special bond with his patients because people who have pancreatic neuroendocrine tumors seek him out for treatment. “I’m getting to take care of people who, on some level, are like my kindred spirits,” he said. “So, I get to see their coping mechanisms and how they do.”
Ms. Edwards told some of her patients about her breast cancer diagnosis, and now they give each other high-fives and share words of encouragement. “I made it a big thing of mine to associate my patients as my family,” she said. “If you’ve learned to embrace love and love people, there’s nothing you wouldn’t do for people. I’ve chosen that to be my practice when I’m dealing with all of my patients.”
Ms. Adams is on a similar mission. She joined a group of moms with cancer so she can receive guidance and then become a guide for others. “I feel like that’s what I want to be at my cancer practice,” she said, “so [my patients] have someone to say, ‘I’m gonna walk alongside you because I’ve been there.’ “
That transformation has made all the heartbreaking moments worth it, Ms. Adams said. “I love the oncology nurse that I get to be now because of my diagnosis. I don’t love the diagnosis. But I love the way it’s changed what I do.”
A version of this article first appeared on Medscape.com.
Douglas Flora, MD, an oncologist with St. Elizabeth Healthcare, in Edgewood, Ky., considers himself a deep empath. It’s one reason he became an oncologist.
But when he was diagnosed with kidney cancer in 2017, he was shocked at the places his brain took him. His mind fast-forwarded through treatment options, statistical probabilities, and anguish over his wife and children.
“It’s a very surreal experience,” Dr. Flora said. “In 20 seconds, you go from diagnostics to, ‘What videos will I have to film for my babies?’ “
He could be having a wonderful evening surrounded by friends, music, and beer. Then he would go to the restroom and the realization of what was lurking inside his would body hit him like a brick.
“It’s like the scene in the Harry Potter movies where the Dementors fly over,” he explained. “Everything feels dark. There’s no hope. Everything you thought was good is gone.”
Oncologists counsel patients through life-threatening diagnoses and frightening decisions every day, so one might think they’d be ready to confront their own diagnosis, treatment, and mortality better than anyone. But that’s not always the case.
Does their expertise equip them to navigate their diagnosis and treatment better than their patients? How does the emotional toll of their personal cancer journey change the way they interact with their patients?
Navigating the diagnosis and treatment
In January 2017, Karen Hendershott, MD, a breast surgical oncologist, felt a lump in her armpit while taking a shower. The blunt force of her fate came into view in an instant: It was almost certainly a locally advanced breast cancer that had spread to her lymph nodes and would require surgery, radiotherapy, and chemotherapy.
She said a few unprintable words and headed to work at St. Mary’s Hospital, in Tucson, Ariz., where her assumptions were confirmed.
Taylor Riall, MD, PhD, also suspected cancer.
Last December, Dr. Riall, a general surgeon and surgical oncologist at the University of Arizona Cancer Center, in Tucson, developed a persistent cough. An x-ray revealed a mass in her lung. Initially, she was misdiagnosed with a fungal infection and was given medication that made her skin peel off.
Doctors advised Dr. Riall to monitor her condition for another 6 months. But her knowledge of oncology made her think cancer, so she insisted on more tests. In June 2021, a biopsy confirmed she had lung cancer.
Having oncology expertise helped Dr. Riall and Dr. Hendershott recognize the signs of cancer and push for a diagnosis. But there are also downsides to being hyper-informed, Dr. Hendershott, said.
“I think sometimes knowing everything at once is harder vs. giving yourself time to wrap your mind around this and do it in baby steps,” she explained. “There weren’t any baby steps here.”
Still, oncology practitioners who are diagnosed with cancer are navigating a familiar landscape and are often buoyed by a support network of expert colleagues. That makes a huge difference psychologically, explained Shenitha Edwards, a pharmacy technician at Cancer Specialists of North Florida, in Jacksonville, who was diagnosed with breast cancer in July.
“I felt stronger and a little more ready to fight because I had resources, whereas my patients sometimes do not,” Ms. Edwards said. “I was connected with a lot of people who could help me make informed decisions, so I didn’t have to walk so much in fear.”
It can also prepare practitioners to make bold treatment choices. In Dr. Riall’s case, surgeons were reluctant to excise her tumor because they would have to remove the entire upper lobe of her lung, and she is a marathoner and triathlete. Still, because of her surgical oncology experience, Dr. Riall didn’t flinch at the prospect of a major operation.
“I was, like, ‘Look, just take it out.’ I’m less afraid to have cancer than I am to not know and let it grow,” said Dr. Riall, whose Peloton name is WhoNeeds2Lungs.
Similarly, Dr. Hendershott’s experience gave her the assurance to pursue a more intense strategy. “Because I had a really candid understanding of the risks and what the odds looked like, it helped me be more comfortable with a more aggressive approach,” she said. “There wasn’t a doubt in my mind, particularly [having] a 10-year-old child, that I wanted to do everything I could, and even do a couple of things that were still in clinical trials.”
Almost paradoxically, Mark Lewis’ oncology training gave him the courage to risk watching and waiting after finding benign growths in his parathyroid and malignant tumors in his pancreas. Dr. Lewis monitored the tumors amassing in his pancreas for 8 years. When some grew so large they threatened to metastasize to his liver, he underwent the Whipple procedure to remove the head of the pancreas, part of the small intestine, and the gallbladder.
“It was a bit of a gamble, but one that paid off and allowed me to get my career off the ground and have another child,” said Dr. Lewis, a gastrointestinal oncologist at Intermountain Healthcare, in Salt Lake City. Treating patients for nearly a decade also showed him how fortunate he was to have a slow-growing, operable cancer. That gratitude, he said, gave him mental strength to endure the ordeal.
Whether taking a more aggressive or minimalist approach to their own care, each practitioner’s decision was deeply personal and deeply informed by their oncology expertise.
Although research on this question is scarce, studies show that differences in end-of-life care may occur. According to a 2016 study published in JAMA, physicians choose significantly less intensive end-stage care in three of five categories — undergoing surgery, being admitted to the intensive care unit (ICU), and dying in the hospital — than the general U.S. population. The reason, the researchers posited, is because doctors know these eleventh-hour interventions are typically brutal and futile.
But these differences were fairly small, and a 2019 study published in JAMA Open Network found the opposite: Physicians with cancer were more likely to die in an ICU and receive chemotherapy in the last 6 months of life, suggesting a more aggressive approach to end-of-life care.
When it comes to their own long-term or curative cancer care, oncologists generally don’t seem to approach treatment differently than their patients. In a 2015 study, researchers compared two groups of people with early breast cancer — 46 physicians and 230 well-educated, nonmedically qualified patients — and found no differences in the choices the groups made about whether to undergo mastectomy, chemotherapy, radiotherapy, or breast reconstruction.
Still, no amount of oncology expertise can fully prepare a person for the emotional crucible of cancer.
“A very surreal experience”
Although the fear can become less intense and more manageable over time, it may never truly go away.
At first, despair dragged Flora into an abyss for 6 hours a night, then overcame him 10 times a day, then gripped him briefly at random moments. Four years later and cancer-free, the dread still returns.
Hendershott cried every time she got into her car and contemplated her prognosis. Now 47, she has about a 60% chance of being alive in 15 years, and the fear still hits her.
“I think it’s hard to understand the moments of sheer terror that you have at 2 AM when you’re confronting your own mortality,” she said. “The implications that has not just for you but more importantly for the people that you love and want to protect. That just kind of washes over you in waves that you don’t have much control over.”
Cancer, Riall felt, had smashed her life, but she figured out a way to help herself cope. Severe blood loss, chest tubes, and tests and needles ad nauseum left Riall feeling excruciatingly exhausted after her surgery and delayed her return to work. At the same time, she was passed over for a promotion. Frustrated and dejected, she took comfort in the memory of doing Kintsugi with her surgery residents. The Japanese art form involves shattering pottery with a hammer, fitting the fragments back together, and painting the cracks gold.
“My instinct as a surgeon is to pick up those pieces and put them back together so nobody sees it’s broken,” she reflected. But as a patient, she learned that an important part of recovery is to allow yourself to sit in a broken state and feel angry, miserable, and betrayed by your body. And then examine your shattered priorities and consider how you want to reassemble them.
For Barbara Buttin, MD, a gynecologic oncologist at Cancer Treatment Centers of America, in Chicago, Illinois, it wasn’t cancer that almost took her life. Rather, a near-death experience and life-threatening diagnosis made her a better, more empathetic cancer doctor — a refrain echoed by many oncologist-patients. Confronting her own mortality crystallized what matters in life. She uses that understanding to make sure she understands what matters to her patients ― what they care about most, what their greatest fear is, what is going to keep them up at night.
“We’re part of the same club”
Ultimately, when oncology practitioners become patients, it balances the in-control and vulnerable, the rational and emotional. And their patients respond positively.
In fall 2020, oncology nurse Jenn Adams, RN, turned 40 and underwent her first mammogram. Unexpectedly, it revealed invasive stage I cancer that would require a double mastectomy, chemotherapy, and a year of immunotherapy. A week after her diagnosis, she was scheduled to start a new job at Cancer Clinic, in Bryan, Tex. So, she asked her manager if she could become a patient and an employee.
Ms. Adams worked 5 days a week, but every Thursday at 2 PM, she sat next to her patients while her coworkers became her nurses. Her chemo port was implanted, she lost her hair, and she felt terrible along with her patients. “It just created this incredible bond,” said the mother of three.
Having cancer, Dr. Flora said, “was completely different than I had imagined. When I thought I was walking with [my patients] in the depths of their caves, I wasn’t even visiting their caves.” But, he added, it has also “let me connect with [patients] on a deeper level because we’re part of the same club. You can see their body language change when I share that. They almost relax, like, ‘Oh, this guy gets it. He does understand how terrified I am.’ And I do.”
When Dr. Flora’s patients are scanned, he gives them their results immediately, because he knows what it’s like to wait on tenterhooks. He tells his patients to text him anytime they’re afraid or depressed, which he admits isn’t great for his own mental health but believes is worth it.
Likewise, Dr. Hendershott can hold out her shoulder-length locks to reassure a crying patient that hair does grow back after chemo. She can describe her experience with hormone-blocking pills to allay the fears of a pharmaceutical skeptic.
This role equalizer fosters so much empathy that doctors sometimes find themselves being helped by their patients. When one of Dr. Flora’s patients heard he had cancer, she sent him an email that began. “A wise doctor once told me....” and repeated the advice he’d given her years before.
Dr. Lewis has a special bond with his patients because people who have pancreatic neuroendocrine tumors seek him out for treatment. “I’m getting to take care of people who, on some level, are like my kindred spirits,” he said. “So, I get to see their coping mechanisms and how they do.”
Ms. Edwards told some of her patients about her breast cancer diagnosis, and now they give each other high-fives and share words of encouragement. “I made it a big thing of mine to associate my patients as my family,” she said. “If you’ve learned to embrace love and love people, there’s nothing you wouldn’t do for people. I’ve chosen that to be my practice when I’m dealing with all of my patients.”
Ms. Adams is on a similar mission. She joined a group of moms with cancer so she can receive guidance and then become a guide for others. “I feel like that’s what I want to be at my cancer practice,” she said, “so [my patients] have someone to say, ‘I’m gonna walk alongside you because I’ve been there.’ “
That transformation has made all the heartbreaking moments worth it, Ms. Adams said. “I love the oncology nurse that I get to be now because of my diagnosis. I don’t love the diagnosis. But I love the way it’s changed what I do.”
A version of this article first appeared on Medscape.com.
Tiny insects reveal some big secrets in cancer
Uncontrolled growth isn’t the only way cancers wreak havoc on the human body. These aggregations of freely dividing cells also release chemicals that can cause damage from a distance. But pinning down how they harm faraway healthy tissues isn’t straightforward.
Fortunately, biologists can turn to the tiny fruit fly to address some of these questions: This insect’s body is not as complex as ours in many ways, but we share important genes and organ functions.
Fruit flies already are a crucial and inexpensive animal for genetics research. Because their life span is about 7 weeks, investigators can track the effects of mutations across several generations in a short period. The animals also are proving useful for learning how chemicals released by malignant tumors can harm tissues in the body that are not near the cancer.
One recent lesson from the fruit flies involves the blood-brain barrier, which determines which molecules gain access to the brain. Researchers at the University of California, Berkeley, have found that malignant tumors in the tiny insects release interleukin 6 (IL-6), an inflammatory chemical that disrupts this important barrier. The investigators showed that the tumors act similarly in mice.
Even if cancer cells persisted, damage related to IL-6 could be diminished.
Fruit flies and mice are only distant relatives of each other and of humans, and the relevance of this discovery to human cancers has not been established. One hurdle is that IL-6 has many important, normal functions related to health. Researchers need to learn how to target only its unwanted blood-brain barrier effects.
A version of this article first appeared on Medscape.com.
Uncontrolled growth isn’t the only way cancers wreak havoc on the human body. These aggregations of freely dividing cells also release chemicals that can cause damage from a distance. But pinning down how they harm faraway healthy tissues isn’t straightforward.
Fortunately, biologists can turn to the tiny fruit fly to address some of these questions: This insect’s body is not as complex as ours in many ways, but we share important genes and organ functions.
Fruit flies already are a crucial and inexpensive animal for genetics research. Because their life span is about 7 weeks, investigators can track the effects of mutations across several generations in a short period. The animals also are proving useful for learning how chemicals released by malignant tumors can harm tissues in the body that are not near the cancer.
One recent lesson from the fruit flies involves the blood-brain barrier, which determines which molecules gain access to the brain. Researchers at the University of California, Berkeley, have found that malignant tumors in the tiny insects release interleukin 6 (IL-6), an inflammatory chemical that disrupts this important barrier. The investigators showed that the tumors act similarly in mice.
Even if cancer cells persisted, damage related to IL-6 could be diminished.
Fruit flies and mice are only distant relatives of each other and of humans, and the relevance of this discovery to human cancers has not been established. One hurdle is that IL-6 has many important, normal functions related to health. Researchers need to learn how to target only its unwanted blood-brain barrier effects.
A version of this article first appeared on Medscape.com.
Uncontrolled growth isn’t the only way cancers wreak havoc on the human body. These aggregations of freely dividing cells also release chemicals that can cause damage from a distance. But pinning down how they harm faraway healthy tissues isn’t straightforward.
Fortunately, biologists can turn to the tiny fruit fly to address some of these questions: This insect’s body is not as complex as ours in many ways, but we share important genes and organ functions.
Fruit flies already are a crucial and inexpensive animal for genetics research. Because their life span is about 7 weeks, investigators can track the effects of mutations across several generations in a short period. The animals also are proving useful for learning how chemicals released by malignant tumors can harm tissues in the body that are not near the cancer.
One recent lesson from the fruit flies involves the blood-brain barrier, which determines which molecules gain access to the brain. Researchers at the University of California, Berkeley, have found that malignant tumors in the tiny insects release interleukin 6 (IL-6), an inflammatory chemical that disrupts this important barrier. The investigators showed that the tumors act similarly in mice.
Even if cancer cells persisted, damage related to IL-6 could be diminished.
Fruit flies and mice are only distant relatives of each other and of humans, and the relevance of this discovery to human cancers has not been established. One hurdle is that IL-6 has many important, normal functions related to health. Researchers need to learn how to target only its unwanted blood-brain barrier effects.
A version of this article first appeared on Medscape.com.
Ulcer on the Leg
The Diagnosis: Calcinosis Cutis Due to Systemic Sclerosis Sine Scleroderma
Laboratory evaluation was notable for high titers of antinuclear antibodies (>1/320; reference range, 0–1/80) and positive anticentromere antibodies. There were no other relevant laboratory findings; phosphocalcic metabolism was within normal limits, and urinary sediment was normal. Biopsy of the edge of the ulcer revealed basophilic material compatible with calcium deposits. In a 3D volume rendering reconstruction from the lower limb scanner, grouped calcifications were observed in subcutaneous cellular tissue near the ulcer (Figure). The patient had a restrictive ventilatory pattern observed in a pulmonary function test. An esophageal motility study was normal.
The patient was diagnosed with systemic sclerosis sine scleroderma (ssSSc) type II because she met the 4 criteria established by Poormoghim et al1 : (1) Raynaud phenomenon or a peripheral vascular equivalent (ie, digital pitting scars, digital-tip ulcers, digital-tip gangrene, abnormal nail fold capillaries); (2) positive antinuclear antibodies; (3) distal esophageal hypomotility, small bowel hypomotility, pulmonary interstitial fibrosis, primary pulmonary arterial hypertension (without fibrosis), cardiac involvement typical of scleroderma, or renal failure; and (4) no other defined connective tissue or other disease as a cause of the prior conditions.
Systemic sclerosis is a chronic disease characterized by progressive fibrosis of the skin and other internal organs—especially the lungs, kidneys, digestive tract, and heart—as well as generalized vascular dysfunction. Cutaneous induration is its hallmark; however, up to 10% of affected patients have ssSSc.2 This entity is characterized by the total or partial absence of cutaneous manifestations of systemic sclerosis with the occurrence of internal organ involvement and serologic abnormalities. There are 3 types of ssSSc depending on the grade of skin involvement. Type I is characterized by the lack of any typical cutaneous stigmata of the disease. Type II is without sclerodactyly but can coexist with other cutaneous findings such as calcifications, telangiectases, or pitting scars. Type III is characterized clinically by internal organ involvement, typical of systemic sclerosis, that has appeared before skin changes.2
An abnormal deposit of calcium in the cutaneous and subcutaneous tissue is called calcinosis cutis. There are 5 subtypes of calcinosis cutis: dystrophic, metastatic, idiopathic, iatrogenic, and calciphylaxis. Dystrophic skin calcifications may appear in patients with connective tissue diseases such as dermatomyositis or systemic sclerosis.3 Up to 25% of patients with systemic sclerosis can develop calcinosis cutis due to local tissue damage, with normal phosphocalcic metabolism.3
Calcinosis cutis is more common in patients with systemic sclerosis and positive anticentromere antibodies.4 The calcifications usually are located in areas that are subject to repeated trauma, such as the fingers or arms, though other locations have been described such as cervical, paraspinal, or on the hips.5,6 Our patient developed calcifications on both legs, which represent atypical areas for this process.
Dermatomyositis also can present with calcinosis cutis. There are 4 patterns of calcification: superficial nodulelike calcified masses; deep calcified masses; deep sheetlike calcifications within the fascial planes; and a rare, diffuse, superficial lacy and reticular calcification that involves almost the entire body surface area.7 Patients with calcinosis cutis secondary to dermatomyositis usually develop proximal muscle weakness, high titers of creatine kinase, heliotrope rash, or interstitial lung disease with specific antibodies.
Calciphylaxis is a serious disorder involving the calcification of dermal and subcutaneous arterioles and capillaries. It presents with painful cutaneous areas of necrosis.
Venous ulcers also can present with secondary dystrophic calcification due to local tissue damage. These patients usually have cutaneous signs of chronic venous insufficiency. Our patient denied prior trauma to the area; therefore, a traumatic ulcer with secondary calcification was ruled out.
The most concerning complication of calcinosis cutis is the development of ulcers, which occurred in 154 of 316 calcinoses (48.7%) in patients with systemic sclerosis and secondary calcifications.8 These ulcers can cause disabling pain or become superinfected, as in our patient.
There currently is no drug capable of removing dystrophic calcifications, but diltiazem, minocycline, or colchicine can reduce their size and prevent their progression. In the event of neurologic compromise or intractable pain, the treatment of choice is surgical removal of the calcification.9 Curettage, intralesional sodium thiosulfate, and intravenous sodium thiosulfate also have been suggested as therapeutic options.10 Antibiotic treatment was carried out in our patient, which controlled the superinfection of the ulcers. Diltiazem also was started, with stabilization of the calcium deposits without a reduction in their size.
There are few studies evaluating the presence of nondigital ulcers in patients with systemic sclerosis. Shanmugam et al11 calculated a 4% (N=249) prevalence of ulcers in the lower limbs of systemic sclerosis patients. In a study by Bohelay et al12 of 45 patients, the estimated prevalence of lower limb ulcers was 12.8%, and the etiologies consisted of 22 cases of venous insufficiency (49%), 21 cases of ischemic causes (47%), and 2 cases of other causes (4%).
We present the case of a woman with ssSSc who developed dystrophic calcinosis cutis in atypical areas with secondary ulceration and superinfection. The skin usually plays a key role in the diagnosis of systemic sclerosis, as sclerodactyly and the characteristic generalized skin induration stand out in affected individuals. Although our patient was diagnosed with ssSSc, her skin manifestations also were crucial for the diagnosis, as she had ulcers on the lower limbs.
- Poormoghim H, Lucas M, Fertig N, et al. Systemic sclerosis sine scleroderma: demographic, clinical, and serologic features and survival in forty-eight patients. Arthritis Rheum. 2000;43:444-451.
- Kucharz EJ, Kopec´-Me˛ drek M. Systemic sclerosis sine scleroderma. Adv Clin Exp Med. 2017;26:875-880.
- Valenzuela A, Baron M, Herrick AL, et al. Calcinosis is associated with digital ulcers and osteoporosis in patients with systemic sclerosis: a scleroderma clinical trials consortium study. Semin Arthritis Rheum. 2016;46:344-349.
- D’Aoust J, Hudson M, Tatibouet S, et al. Clinical and serologic correlates of antiPM/Scl antibodies in systemic sclerosis: a multicenter study of 763 patients. Arthritis Rheum. 2014;66:1608-1615.
- Contreras I, Sallés M, Mínguez S, et al. Hard paracervical tumor in a patient with limited systemic sclerosis. Rheumatol Clin. 2014; 10:336-337.
- Meriglier E, Lafourcade F, Gombert B, et al. Giant calcinosis revealing systemic sclerosis. Int J Rheum Dis. 2019;22:1787-1788.
- Chung CH. Calcinosis universalis in juvenile dermatomyositis [published online September 24, 2020]. Chonnam Med J. 2020;56:212-213.
- Bartoli F, Fiori G, Braschi F, et al. Calcinosis in systemic sclerosis: subsets, distribution and complications [published online May 30, 2016]. Rheumatology (Oxford). 2016;55:1610-1614.
- Jung H, Lee D, Cho J, et al. Surgical treatment of extensive tumoral calcinosis associated with systemic sclerosis. Korean J Thorac Cardiovasc Surg. 2015;48:151-154.
- Badawi AH, Patel V, Warner AE, et al. Dystrophic calcinosis cutis: treatment with intravenous sodium thiosulfate. Cutis. 2020;106:E15-E17.
- Shanmugam V, Price P, Attinger C, et al. Lower extremity ulcers in systemic sclerosis: features and response to therapy [published online August 18, 2010]. Int J Rheumatol. doi:10.1155/2010/747946
- Bohelay G, Blaise S, Levy P, et al. Lower-limb ulcers in systemic sclerosis: a multicentre retrospective case-control study. Acta Derm Venereol. 2018;98:677-682.
The Diagnosis: Calcinosis Cutis Due to Systemic Sclerosis Sine Scleroderma
Laboratory evaluation was notable for high titers of antinuclear antibodies (>1/320; reference range, 0–1/80) and positive anticentromere antibodies. There were no other relevant laboratory findings; phosphocalcic metabolism was within normal limits, and urinary sediment was normal. Biopsy of the edge of the ulcer revealed basophilic material compatible with calcium deposits. In a 3D volume rendering reconstruction from the lower limb scanner, grouped calcifications were observed in subcutaneous cellular tissue near the ulcer (Figure). The patient had a restrictive ventilatory pattern observed in a pulmonary function test. An esophageal motility study was normal.
The patient was diagnosed with systemic sclerosis sine scleroderma (ssSSc) type II because she met the 4 criteria established by Poormoghim et al1 : (1) Raynaud phenomenon or a peripheral vascular equivalent (ie, digital pitting scars, digital-tip ulcers, digital-tip gangrene, abnormal nail fold capillaries); (2) positive antinuclear antibodies; (3) distal esophageal hypomotility, small bowel hypomotility, pulmonary interstitial fibrosis, primary pulmonary arterial hypertension (without fibrosis), cardiac involvement typical of scleroderma, or renal failure; and (4) no other defined connective tissue or other disease as a cause of the prior conditions.
Systemic sclerosis is a chronic disease characterized by progressive fibrosis of the skin and other internal organs—especially the lungs, kidneys, digestive tract, and heart—as well as generalized vascular dysfunction. Cutaneous induration is its hallmark; however, up to 10% of affected patients have ssSSc.2 This entity is characterized by the total or partial absence of cutaneous manifestations of systemic sclerosis with the occurrence of internal organ involvement and serologic abnormalities. There are 3 types of ssSSc depending on the grade of skin involvement. Type I is characterized by the lack of any typical cutaneous stigmata of the disease. Type II is without sclerodactyly but can coexist with other cutaneous findings such as calcifications, telangiectases, or pitting scars. Type III is characterized clinically by internal organ involvement, typical of systemic sclerosis, that has appeared before skin changes.2
An abnormal deposit of calcium in the cutaneous and subcutaneous tissue is called calcinosis cutis. There are 5 subtypes of calcinosis cutis: dystrophic, metastatic, idiopathic, iatrogenic, and calciphylaxis. Dystrophic skin calcifications may appear in patients with connective tissue diseases such as dermatomyositis or systemic sclerosis.3 Up to 25% of patients with systemic sclerosis can develop calcinosis cutis due to local tissue damage, with normal phosphocalcic metabolism.3
Calcinosis cutis is more common in patients with systemic sclerosis and positive anticentromere antibodies.4 The calcifications usually are located in areas that are subject to repeated trauma, such as the fingers or arms, though other locations have been described such as cervical, paraspinal, or on the hips.5,6 Our patient developed calcifications on both legs, which represent atypical areas for this process.
Dermatomyositis also can present with calcinosis cutis. There are 4 patterns of calcification: superficial nodulelike calcified masses; deep calcified masses; deep sheetlike calcifications within the fascial planes; and a rare, diffuse, superficial lacy and reticular calcification that involves almost the entire body surface area.7 Patients with calcinosis cutis secondary to dermatomyositis usually develop proximal muscle weakness, high titers of creatine kinase, heliotrope rash, or interstitial lung disease with specific antibodies.
Calciphylaxis is a serious disorder involving the calcification of dermal and subcutaneous arterioles and capillaries. It presents with painful cutaneous areas of necrosis.
Venous ulcers also can present with secondary dystrophic calcification due to local tissue damage. These patients usually have cutaneous signs of chronic venous insufficiency. Our patient denied prior trauma to the area; therefore, a traumatic ulcer with secondary calcification was ruled out.
The most concerning complication of calcinosis cutis is the development of ulcers, which occurred in 154 of 316 calcinoses (48.7%) in patients with systemic sclerosis and secondary calcifications.8 These ulcers can cause disabling pain or become superinfected, as in our patient.
There currently is no drug capable of removing dystrophic calcifications, but diltiazem, minocycline, or colchicine can reduce their size and prevent their progression. In the event of neurologic compromise or intractable pain, the treatment of choice is surgical removal of the calcification.9 Curettage, intralesional sodium thiosulfate, and intravenous sodium thiosulfate also have been suggested as therapeutic options.10 Antibiotic treatment was carried out in our patient, which controlled the superinfection of the ulcers. Diltiazem also was started, with stabilization of the calcium deposits without a reduction in their size.
There are few studies evaluating the presence of nondigital ulcers in patients with systemic sclerosis. Shanmugam et al11 calculated a 4% (N=249) prevalence of ulcers in the lower limbs of systemic sclerosis patients. In a study by Bohelay et al12 of 45 patients, the estimated prevalence of lower limb ulcers was 12.8%, and the etiologies consisted of 22 cases of venous insufficiency (49%), 21 cases of ischemic causes (47%), and 2 cases of other causes (4%).
We present the case of a woman with ssSSc who developed dystrophic calcinosis cutis in atypical areas with secondary ulceration and superinfection. The skin usually plays a key role in the diagnosis of systemic sclerosis, as sclerodactyly and the characteristic generalized skin induration stand out in affected individuals. Although our patient was diagnosed with ssSSc, her skin manifestations also were crucial for the diagnosis, as she had ulcers on the lower limbs.
The Diagnosis: Calcinosis Cutis Due to Systemic Sclerosis Sine Scleroderma
Laboratory evaluation was notable for high titers of antinuclear antibodies (>1/320; reference range, 0–1/80) and positive anticentromere antibodies. There were no other relevant laboratory findings; phosphocalcic metabolism was within normal limits, and urinary sediment was normal. Biopsy of the edge of the ulcer revealed basophilic material compatible with calcium deposits. In a 3D volume rendering reconstruction from the lower limb scanner, grouped calcifications were observed in subcutaneous cellular tissue near the ulcer (Figure). The patient had a restrictive ventilatory pattern observed in a pulmonary function test. An esophageal motility study was normal.
The patient was diagnosed with systemic sclerosis sine scleroderma (ssSSc) type II because she met the 4 criteria established by Poormoghim et al1 : (1) Raynaud phenomenon or a peripheral vascular equivalent (ie, digital pitting scars, digital-tip ulcers, digital-tip gangrene, abnormal nail fold capillaries); (2) positive antinuclear antibodies; (3) distal esophageal hypomotility, small bowel hypomotility, pulmonary interstitial fibrosis, primary pulmonary arterial hypertension (without fibrosis), cardiac involvement typical of scleroderma, or renal failure; and (4) no other defined connective tissue or other disease as a cause of the prior conditions.
Systemic sclerosis is a chronic disease characterized by progressive fibrosis of the skin and other internal organs—especially the lungs, kidneys, digestive tract, and heart—as well as generalized vascular dysfunction. Cutaneous induration is its hallmark; however, up to 10% of affected patients have ssSSc.2 This entity is characterized by the total or partial absence of cutaneous manifestations of systemic sclerosis with the occurrence of internal organ involvement and serologic abnormalities. There are 3 types of ssSSc depending on the grade of skin involvement. Type I is characterized by the lack of any typical cutaneous stigmata of the disease. Type II is without sclerodactyly but can coexist with other cutaneous findings such as calcifications, telangiectases, or pitting scars. Type III is characterized clinically by internal organ involvement, typical of systemic sclerosis, that has appeared before skin changes.2
An abnormal deposit of calcium in the cutaneous and subcutaneous tissue is called calcinosis cutis. There are 5 subtypes of calcinosis cutis: dystrophic, metastatic, idiopathic, iatrogenic, and calciphylaxis. Dystrophic skin calcifications may appear in patients with connective tissue diseases such as dermatomyositis or systemic sclerosis.3 Up to 25% of patients with systemic sclerosis can develop calcinosis cutis due to local tissue damage, with normal phosphocalcic metabolism.3
Calcinosis cutis is more common in patients with systemic sclerosis and positive anticentromere antibodies.4 The calcifications usually are located in areas that are subject to repeated trauma, such as the fingers or arms, though other locations have been described such as cervical, paraspinal, or on the hips.5,6 Our patient developed calcifications on both legs, which represent atypical areas for this process.
Dermatomyositis also can present with calcinosis cutis. There are 4 patterns of calcification: superficial nodulelike calcified masses; deep calcified masses; deep sheetlike calcifications within the fascial planes; and a rare, diffuse, superficial lacy and reticular calcification that involves almost the entire body surface area.7 Patients with calcinosis cutis secondary to dermatomyositis usually develop proximal muscle weakness, high titers of creatine kinase, heliotrope rash, or interstitial lung disease with specific antibodies.
Calciphylaxis is a serious disorder involving the calcification of dermal and subcutaneous arterioles and capillaries. It presents with painful cutaneous areas of necrosis.
Venous ulcers also can present with secondary dystrophic calcification due to local tissue damage. These patients usually have cutaneous signs of chronic venous insufficiency. Our patient denied prior trauma to the area; therefore, a traumatic ulcer with secondary calcification was ruled out.
The most concerning complication of calcinosis cutis is the development of ulcers, which occurred in 154 of 316 calcinoses (48.7%) in patients with systemic sclerosis and secondary calcifications.8 These ulcers can cause disabling pain or become superinfected, as in our patient.
There currently is no drug capable of removing dystrophic calcifications, but diltiazem, minocycline, or colchicine can reduce their size and prevent their progression. In the event of neurologic compromise or intractable pain, the treatment of choice is surgical removal of the calcification.9 Curettage, intralesional sodium thiosulfate, and intravenous sodium thiosulfate also have been suggested as therapeutic options.10 Antibiotic treatment was carried out in our patient, which controlled the superinfection of the ulcers. Diltiazem also was started, with stabilization of the calcium deposits without a reduction in their size.
There are few studies evaluating the presence of nondigital ulcers in patients with systemic sclerosis. Shanmugam et al11 calculated a 4% (N=249) prevalence of ulcers in the lower limbs of systemic sclerosis patients. In a study by Bohelay et al12 of 45 patients, the estimated prevalence of lower limb ulcers was 12.8%, and the etiologies consisted of 22 cases of venous insufficiency (49%), 21 cases of ischemic causes (47%), and 2 cases of other causes (4%).
We present the case of a woman with ssSSc who developed dystrophic calcinosis cutis in atypical areas with secondary ulceration and superinfection. The skin usually plays a key role in the diagnosis of systemic sclerosis, as sclerodactyly and the characteristic generalized skin induration stand out in affected individuals. Although our patient was diagnosed with ssSSc, her skin manifestations also were crucial for the diagnosis, as she had ulcers on the lower limbs.
- Poormoghim H, Lucas M, Fertig N, et al. Systemic sclerosis sine scleroderma: demographic, clinical, and serologic features and survival in forty-eight patients. Arthritis Rheum. 2000;43:444-451.
- Kucharz EJ, Kopec´-Me˛ drek M. Systemic sclerosis sine scleroderma. Adv Clin Exp Med. 2017;26:875-880.
- Valenzuela A, Baron M, Herrick AL, et al. Calcinosis is associated with digital ulcers and osteoporosis in patients with systemic sclerosis: a scleroderma clinical trials consortium study. Semin Arthritis Rheum. 2016;46:344-349.
- D’Aoust J, Hudson M, Tatibouet S, et al. Clinical and serologic correlates of antiPM/Scl antibodies in systemic sclerosis: a multicenter study of 763 patients. Arthritis Rheum. 2014;66:1608-1615.
- Contreras I, Sallés M, Mínguez S, et al. Hard paracervical tumor in a patient with limited systemic sclerosis. Rheumatol Clin. 2014; 10:336-337.
- Meriglier E, Lafourcade F, Gombert B, et al. Giant calcinosis revealing systemic sclerosis. Int J Rheum Dis. 2019;22:1787-1788.
- Chung CH. Calcinosis universalis in juvenile dermatomyositis [published online September 24, 2020]. Chonnam Med J. 2020;56:212-213.
- Bartoli F, Fiori G, Braschi F, et al. Calcinosis in systemic sclerosis: subsets, distribution and complications [published online May 30, 2016]. Rheumatology (Oxford). 2016;55:1610-1614.
- Jung H, Lee D, Cho J, et al. Surgical treatment of extensive tumoral calcinosis associated with systemic sclerosis. Korean J Thorac Cardiovasc Surg. 2015;48:151-154.
- Badawi AH, Patel V, Warner AE, et al. Dystrophic calcinosis cutis: treatment with intravenous sodium thiosulfate. Cutis. 2020;106:E15-E17.
- Shanmugam V, Price P, Attinger C, et al. Lower extremity ulcers in systemic sclerosis: features and response to therapy [published online August 18, 2010]. Int J Rheumatol. doi:10.1155/2010/747946
- Bohelay G, Blaise S, Levy P, et al. Lower-limb ulcers in systemic sclerosis: a multicentre retrospective case-control study. Acta Derm Venereol. 2018;98:677-682.
- Poormoghim H, Lucas M, Fertig N, et al. Systemic sclerosis sine scleroderma: demographic, clinical, and serologic features and survival in forty-eight patients. Arthritis Rheum. 2000;43:444-451.
- Kucharz EJ, Kopec´-Me˛ drek M. Systemic sclerosis sine scleroderma. Adv Clin Exp Med. 2017;26:875-880.
- Valenzuela A, Baron M, Herrick AL, et al. Calcinosis is associated with digital ulcers and osteoporosis in patients with systemic sclerosis: a scleroderma clinical trials consortium study. Semin Arthritis Rheum. 2016;46:344-349.
- D’Aoust J, Hudson M, Tatibouet S, et al. Clinical and serologic correlates of antiPM/Scl antibodies in systemic sclerosis: a multicenter study of 763 patients. Arthritis Rheum. 2014;66:1608-1615.
- Contreras I, Sallés M, Mínguez S, et al. Hard paracervical tumor in a patient with limited systemic sclerosis. Rheumatol Clin. 2014; 10:336-337.
- Meriglier E, Lafourcade F, Gombert B, et al. Giant calcinosis revealing systemic sclerosis. Int J Rheum Dis. 2019;22:1787-1788.
- Chung CH. Calcinosis universalis in juvenile dermatomyositis [published online September 24, 2020]. Chonnam Med J. 2020;56:212-213.
- Bartoli F, Fiori G, Braschi F, et al. Calcinosis in systemic sclerosis: subsets, distribution and complications [published online May 30, 2016]. Rheumatology (Oxford). 2016;55:1610-1614.
- Jung H, Lee D, Cho J, et al. Surgical treatment of extensive tumoral calcinosis associated with systemic sclerosis. Korean J Thorac Cardiovasc Surg. 2015;48:151-154.
- Badawi AH, Patel V, Warner AE, et al. Dystrophic calcinosis cutis: treatment with intravenous sodium thiosulfate. Cutis. 2020;106:E15-E17.
- Shanmugam V, Price P, Attinger C, et al. Lower extremity ulcers in systemic sclerosis: features and response to therapy [published online August 18, 2010]. Int J Rheumatol. doi:10.1155/2010/747946
- Bohelay G, Blaise S, Levy P, et al. Lower-limb ulcers in systemic sclerosis: a multicentre retrospective case-control study. Acta Derm Venereol. 2018;98:677-682.
A 49-year-old woman with type 2 diabetes mellitus, morbid obesity, pulmonary fibrosis, and pulmonary arterial hypertension presented to our hospital with an ulcer on the left leg of unknown etiology that was superinfected by multidrug-resistant Klebsiella according to bacterial culture. She had an axillary temperature of 38.6 °C. She underwent amputation of the second and third toes on the left foot 5 years prior to presentation due to distal necrotic ulcers of ischemic origin. Physical examination revealed an 8×2-cm deep ulcer with abrupt edges on the left leg with fibrin and a purulent exudate. Deep palpation of the perilesional skin revealed indurated subcutaneous nodules. She also had scars on the fingertips of both hands with no induration on the rest of the skin surface. Capillaroscopy showed no pathologic findings. Blood cultures were performed, and she was admitted to the hospital for intravenous antibiotic therapy. During ulcer debridement, some solid whitish material was released.
Rural hospitalists confront COVID-19
Unique demands of patient care in small hospitals
In 2018, Atashi Mandal, MD, a hospitalist residing in Orange County, Calif., was recruited along with several other doctors to fill hospitalist positions in rural Bishop, Calif. She has since driven 600 miles round trip every month for a week of hospital medicine shifts at Northern Inyo Hospital.
Dr. Mandal said she has really enjoyed her time at the small rural hospital and found it professionally fulfilling to participate so fully in the health of its local community. She was building personal bonds and calling the experience the pinnacle of her career when the COVID-19 pandemic swept across America and the world, even reaching up into Bishop, population 3,760, in the isolated Owens Valley.
The 25-bed hospital has seen at least 100 COVID patients in the past year and some months. Responsibility for taking care of these patients has been both humbling and gratifying, Dr. Mandal said. The facility’s hospitalists made a commitment to keep working through the pandemic. “We were able to come together (around COVID) as a team and our teamwork really made a difference,” she said.
“One of the advantages in a smaller hospital is you can have greater cohesiveness and your communication can be tighter. That played a big role in how we were able to accomplish so much with fewer resources as a rural hospital.” But staffing shortages, recruitment, and retention remain a perennial challenge for rural hospitals. “And COVID only exacerbated the problems,” she said. “I’ve had my challenges trying to make proper treatment plans without access to specialists.”
It was also difficult to witness so many patients severely ill or dying from COVID, Dr. Mandal said, especially since patients were not allowed family visitors – even though that was for a good reason, to minimize the virus’s spread.
HM in rural communities
Hospital medicine continues to extend into rural communities and small rural hospitals. In 2018, 35.7% of all rural counties in America had hospitals staffed with hospitalists, and 63.3% of rural hospitals had hospitalist programs (compared with 79.2% of urban hospitals). These numbers come from Medicare resources files from the Department of Health & Human Services, analyzed by Peiyin Hung, PhD, assistant professor of health services management and policy at the University of South Carolina, Columbia.1 Hospitalist penetration rates rose steadily from 2011 to 2017, with a slight dip in 2018, Dr. Hung said in an interview.
A total of 138 rural hospitals have closed since 2010, according to the Cecil G. Sheps Center for Health Services Research in Chapel Hill, N.C. Nineteen rural hospitals closed in 2020 alone, although many of those were caused by factors predating the pandemic. Only one has closed so far in 2021. But financial pressures, including low patient volumes and loss of revenue from canceled routine services like elective surgeries during the pandemic, have added to hospitals’ difficulties. Pandemic relief funding may have helped some hospitals stay open, but that support eventually will go away.
Experts emphasize the diversity of rural America and its health care systems. Rural economies are volatile and more diverse than is often appreciated. The hospital may be a cornerstone of the local economy; when one closes, it can devastate the community. Workforce is one of the chief components of a hospital’s ability to meet its strategic vision, and hospitalists are a big part in that. But while hospitalists are valued and appreciated, if the hospital is suffering severe financial problems, that will impact its doctors’ jobs and livelihoods.
“Bandwidth” varies widely for rural hospitalists and their hospitalist groups, said Ken Simone, DO, SFHM, executive chair of SHM’s Rural Special Interest Group and founder and principal of KGS Consultants, a Hospital Medicine and Primary Care Practice Management Consulting company. They may face scarce resources, scarce clinical staffing, lack of support staff to help operations run smoothly, lack of access to specialists locally, and lack of technology. While practicing in a rural setting presents various challenges, it can be rewarding for those clinicians who embrace its autonomy and broad scope of services, Dr. Simone said.
SHM’s Rural SIG focuses on the unique needs of rural hospitalists, providing them with an opportunity to share their concerns, challenges and solutions through roundtable discussions every other month and a special interest forum held in conjunction with the SHM Converge annual conference, Dr. Simone said. (The next SHM Converge will be April 7-10, 2022, in Nashville, Tenn.) The Rural SIG also collaborates with other hospital medicine SIGs and committees and is working on a white paper, “Key Principles and Characteristics of an Effective Rural Hospital Medicine Group.” It is also looking to develop a rural mentorship exchange program.
COVID reaches rural America
Early COVID caseloads tended to be in urban areas, but subsequent surges of infections have spread to many rural areas. Some rural settings became epicenters for the pandemic in November and December 2020. More recent troubling rises in COVID cases, particularly in areas with lower vaccination rates – suggest that the challenges of the pandemic are still not behind us.
“By no means is the crisis done in rural America,” said Alan Morgan, CEO of the National Rural Health Association, in a Virtual Rural Health Journalism workshop on rural health care sponsored by the Association of Health Care Journalists.2
Mr. Morgan’s colleague, Brock Slabach, NRHA’s chief operations officer, said in an interview that, while 453 of the 1,800 hospitals in rural areas fit NRHA’s criteria as being vulnerable to closure, the rest are not, and are fulfilling their missions for their communities. Hospitalists are becoming more common in these hospitals, he said, and rural hospitalists can be an important asset in attracting primary care physicians – who might not appreciate being perpetually on call for their hospitalized patients – to rural communities.
In many cases, traveling doctors like Dr. Mandal or telemedicine backup, particularly for after-hours coverage or ICU beds, are important pieces of the puzzle for smaller hospitals. There are different ways to use the spectrum of telemedicine services to interact with a hospital’s daytime and night routines. In some isolated locations, nurse practitioners or physician assistants provide on-the-ground coverage with virtual backup. Rural hospitals often affiliate with telemedicine networks within health systems – or else contract with independent specialized providers of telemedicine consultation.
Mr. Slabach said another alternative for staffing hospitals with smaller ED and inpatient volumes is to have one doctor on duty who can cover both departments simultaneously. Meanwhile, the new federal Rural Emergency Hospital Program proposes to allow rural hospitals to become essentially freestanding EDs – starting Jan. 1, 2023 – that can manage patients for a maximum of 24 hours.3
Community connections and proactive staffing
Lisa Kaufmann, MD, works as a hospitalist for a two-hospital system in North Carolina, Appalachian Regional Health Care. She practices at Watauga Medical Center, with 100 licensed beds in Boone, and at Cannon Memorial Hospital, a critical access hospital in unincorporated Linville. “We are proud of what we have been able to accomplish during the pandemic,” she said.
A former critical care unit at Watauga had been shut down, but its wiring remained intact. “We turned it into a COVID unit in three days. Then we opened another COVID unit with 18 beds, but that still wasn’t enough. We converted half of our med/surg capacity into a COVID unit. At one point almost half of all of our acute beds were for COVID patients. We made plans for what we would do if it got worse, since we had almost run out of beds,” she said. Demand peaked at the end of January 2021.
“The biggest barrier for us was if someone needed to be transferred, for example, if they needed ECMO [extracorporeal membrane oxygenation], and we couldn’t find another hospital to provide that technology.” In ARHC’s mountainous region – known as the “High Country” – weather can also make it difficult to transport patients. “Sometimes the ambulance can’t make it off the mountain, and half of the time the medical helicopter can’t fly. So we have to be prepared to keep people who we might think ought to be transferred,” she said.
Like many rural communities, the High Country is tightly knit, and its hospitals are really connected to their communities, Dr. Kaufmann said. The health system already had a lot of community connections beyond acute care, and that meant the pandemic wasn’t experienced as severely as it was in some other rural communities. “But without hospitalists in our hospitals, it would have been much more difficult.”
Proactive supply fulfillment meant that her hospitals never ran out of personal protective equipment. “Staffing was a challenge, but we were proactive in getting traveling doctors to come here. We also utilized extra doctors from the local community,” she said. Another key was well-established disaster planning, with regular drills, and a robust incident command structure, which just needed to be activated in the crisis. “Small hospitals need to be prepared for disaster,” Dr. Kaufmann said.
For Dale Wiersma, MD, a hospitalist with Spectrum Health, a 14-hospital system in western Michigan, telemedicine services are coordinated across 8 rural regional hospitals. “We don’t tend to use it for direct hospitalist work during daytime hours, unless a facility is swamped, in which case we can cross-cover. We do more telemedicine at night. But during daytime hours we have access to stroke neurology, cardiology, psychiatry, critical care and infectious disease specialists who are able to offer virtual consults,” Dr. Wiersma said. A virtual critical care team of doctor and nurse is often the only intensivist service covering Spectrum’s rural hospitals.
“In our system, the pandemic accelerated the adoption of telemedicine,” Dr. Wiersma said. “We had been working on the tele-ICU program, trying to get it rolled out. When the pandemic hit, we launched it in just 6 weeks.”
There have been several COVID surges in Michigan, he said. “We were stretched pretty close to our limit several times, but never to the breaking point. For our physicians, it was the protracted nature of the pandemic that was fatiguing for everyone involved. Our system worked hard to staff up as well as it could, to make sure our people didn’t go over the edge.” It was also hard for hospitals that typically might see one or two deaths in a month to suddenly have five in a week.
Another Spectrum hospitalist, Christopher Skinner, MD, works at two rural Michigan hospitals 15 minutes apart in Big Rapids and Reed City. “I prefer working in rural areas. I’ve never had an ambition to be a top dog. I like the style of practice where you don’t have all of the medical subspecialties on site. It frees you up to use all your skills,” Dr. Skinner said.
But that approach was put to the test by the pandemic, since it was harder to transfer those patients who normally would not have stayed at these rural hospitals. “We had to make do,” he said, although virtual backup and second opinions from Spectrum’s virtual critical care team helped.
“It was a great collaboration, which helped us to handle critical care cases that we hadn’t had to manage pre-COVID. We’ve gotten used to it, with the backup, so I expect we’ll still be taking care of these kind of sick ventilator patients even after the pandemic ends,” Dr. Skinner said. “We’ve gotten pretty good at it.”
Sukhbir Pannu, MD, a hospitalist in Denver and CEO and founder of Rural Physicians Group, said the pandemic was highly impactful, operationally and logistically, for his firm, which contracts with 54 hospitals to provide their hospitalist staffing. “There was no preparation. Everything had to be done on the fly. Initially, it was felt that rural areas weren’t at as great a risk for COVID, but that proved not to be true. Many experienced a sudden increase in very sick patients. We set up a task force to manage daily census in all of our contracted facilities.”
How did Rural Physicians Group manage through the crisis? “The short answer is telemedicine,” he said. “We had physicians on the ground in these hospitals. But we needed intensivists at the other end of the line to support them.” A lot of conversations about telemedicine were already going on in the company, but the pandemic provided the impetus to launch its network, which has grown to include rheumatologists, pulmonologists, cardiologists, infection medicine, neurology, and psychiatry, all reachable through a central command structure.
Telemedicine is not a cure-all, Dr. Pannu said. It doesn’t work in a vacuum. It requires both a provider on the ground and specialists available remotely. “But it can be a massive multiplier.”
Critical medicine
Other hospitals, including small and rural ones, have reported taking on the challenge of covering critical care with nonintensivist physicians because the pandemic demanded it. David Aymond, MD, a hospitalist at 60-bed Byrd Regional Hospital in Leesville, La., population 6,612, has advocated for years for expanded training and credentialing opportunities in intensive care medicine beyond the traditional path of becoming a board-certified intensivist. Some rural hospitalists were already experienced in providing critical care for ICU patients even before the pandemic hit.
“What COVID did was to highlight the problem that there aren’t enough intensivists in this country, particular for smaller hospitals,” Dr. Aymond said. Some hospitalists who stepped into crisis roles in ICUs during COVID surges showed that they could take care of COVID patients very well.
Dr. Aymond, who is a fellowship-trained hospitalist with primary training in family medicine, has used his ICU experience in both fellowship and practice to make a thorough study of critical care medicine, which he put to good use when the seven-bed ICU at Byrd Memorial filled with COVID patients. “Early on, we were managing multiple ventilators throughout the hospital,” he said. “But we were having good outcomes. Our COVID patients were surviving.” That led to Dr. Aymond being interviewed by local news media, which led to other patients across the state asking to be transferred to “the COVID specialist who practices at Byrd.”
Dr. Aymond would like to see opportunities for abbreviated 1-year critical care fellowships for hospitalists who have amassed enough ICU experience in practice or in residency, and to make room for family medicine physicians in such programs. He is also working through SHM with the Society of Critical Care Medicine to generate educational ICU content. SHM now has a critical care lecture series at: www.hospitalmedicine.org/clinical-topics/critical-care/.
Dr. Mandal, who also works as a pediatric hospitalist, said that experience gave her more familiarity with using noninvasive methods for delivering respiratory therapies like high-flow oxygen. “When I saw a COVID patient who had hypoxia but was still able to talk, I didn’t hesitate to deliver oxygen through noninvasive means.” Eventually hospital practice generally for COVID caught up with this approach.
But she ran into personal difficulties because N95 face masks didn’t fit her face. Instead, she had to wear a portable respirator, which made it hard to hear what her patients were saying. “I formulated a lot of workarounds, such as interviewing the patient over the phone before going into the room for the physical exam.”
Throughout the pandemic, she never wavered in her commitment to rural hospital medicine and its opportunities for working in a small and wonderful community, where she could practice at the top of her license, with a degree of autonomy not granted in other settings. For doctors who want that kind of practice, she said, “the rewards will be paid back in spades. That’s been my experience.”
For more information on SHM’s Rural SIG and its supports for rural hospitalists, contact its executive chair, Kenneth Simone, DO, at ksimone911@gmail.com.
References
1. Personal communication from Peiyin Hung, June 2021.
2. Association of Health Care Journalists. Rural Health Journalism Workshop 2021. June 21, 2021. https://healthjournalism.org/calendar-details.php?id=2369.
3. Congress Establishes New Medicare Provider Category and Reimbursement for Rural Emergency Hospitals. National Law Review. Jan. 5, 2021. https://www.natlawreview.com/article/congress-establishes-new-medicare-provider-category-and-reimbursement-rural.
Unique demands of patient care in small hospitals
Unique demands of patient care in small hospitals
In 2018, Atashi Mandal, MD, a hospitalist residing in Orange County, Calif., was recruited along with several other doctors to fill hospitalist positions in rural Bishop, Calif. She has since driven 600 miles round trip every month for a week of hospital medicine shifts at Northern Inyo Hospital.
Dr. Mandal said she has really enjoyed her time at the small rural hospital and found it professionally fulfilling to participate so fully in the health of its local community. She was building personal bonds and calling the experience the pinnacle of her career when the COVID-19 pandemic swept across America and the world, even reaching up into Bishop, population 3,760, in the isolated Owens Valley.
The 25-bed hospital has seen at least 100 COVID patients in the past year and some months. Responsibility for taking care of these patients has been both humbling and gratifying, Dr. Mandal said. The facility’s hospitalists made a commitment to keep working through the pandemic. “We were able to come together (around COVID) as a team and our teamwork really made a difference,” she said.
“One of the advantages in a smaller hospital is you can have greater cohesiveness and your communication can be tighter. That played a big role in how we were able to accomplish so much with fewer resources as a rural hospital.” But staffing shortages, recruitment, and retention remain a perennial challenge for rural hospitals. “And COVID only exacerbated the problems,” she said. “I’ve had my challenges trying to make proper treatment plans without access to specialists.”
It was also difficult to witness so many patients severely ill or dying from COVID, Dr. Mandal said, especially since patients were not allowed family visitors – even though that was for a good reason, to minimize the virus’s spread.
HM in rural communities
Hospital medicine continues to extend into rural communities and small rural hospitals. In 2018, 35.7% of all rural counties in America had hospitals staffed with hospitalists, and 63.3% of rural hospitals had hospitalist programs (compared with 79.2% of urban hospitals). These numbers come from Medicare resources files from the Department of Health & Human Services, analyzed by Peiyin Hung, PhD, assistant professor of health services management and policy at the University of South Carolina, Columbia.1 Hospitalist penetration rates rose steadily from 2011 to 2017, with a slight dip in 2018, Dr. Hung said in an interview.
A total of 138 rural hospitals have closed since 2010, according to the Cecil G. Sheps Center for Health Services Research in Chapel Hill, N.C. Nineteen rural hospitals closed in 2020 alone, although many of those were caused by factors predating the pandemic. Only one has closed so far in 2021. But financial pressures, including low patient volumes and loss of revenue from canceled routine services like elective surgeries during the pandemic, have added to hospitals’ difficulties. Pandemic relief funding may have helped some hospitals stay open, but that support eventually will go away.
Experts emphasize the diversity of rural America and its health care systems. Rural economies are volatile and more diverse than is often appreciated. The hospital may be a cornerstone of the local economy; when one closes, it can devastate the community. Workforce is one of the chief components of a hospital’s ability to meet its strategic vision, and hospitalists are a big part in that. But while hospitalists are valued and appreciated, if the hospital is suffering severe financial problems, that will impact its doctors’ jobs and livelihoods.
“Bandwidth” varies widely for rural hospitalists and their hospitalist groups, said Ken Simone, DO, SFHM, executive chair of SHM’s Rural Special Interest Group and founder and principal of KGS Consultants, a Hospital Medicine and Primary Care Practice Management Consulting company. They may face scarce resources, scarce clinical staffing, lack of support staff to help operations run smoothly, lack of access to specialists locally, and lack of technology. While practicing in a rural setting presents various challenges, it can be rewarding for those clinicians who embrace its autonomy and broad scope of services, Dr. Simone said.
SHM’s Rural SIG focuses on the unique needs of rural hospitalists, providing them with an opportunity to share their concerns, challenges and solutions through roundtable discussions every other month and a special interest forum held in conjunction with the SHM Converge annual conference, Dr. Simone said. (The next SHM Converge will be April 7-10, 2022, in Nashville, Tenn.) The Rural SIG also collaborates with other hospital medicine SIGs and committees and is working on a white paper, “Key Principles and Characteristics of an Effective Rural Hospital Medicine Group.” It is also looking to develop a rural mentorship exchange program.
COVID reaches rural America
Early COVID caseloads tended to be in urban areas, but subsequent surges of infections have spread to many rural areas. Some rural settings became epicenters for the pandemic in November and December 2020. More recent troubling rises in COVID cases, particularly in areas with lower vaccination rates – suggest that the challenges of the pandemic are still not behind us.
“By no means is the crisis done in rural America,” said Alan Morgan, CEO of the National Rural Health Association, in a Virtual Rural Health Journalism workshop on rural health care sponsored by the Association of Health Care Journalists.2
Mr. Morgan’s colleague, Brock Slabach, NRHA’s chief operations officer, said in an interview that, while 453 of the 1,800 hospitals in rural areas fit NRHA’s criteria as being vulnerable to closure, the rest are not, and are fulfilling their missions for their communities. Hospitalists are becoming more common in these hospitals, he said, and rural hospitalists can be an important asset in attracting primary care physicians – who might not appreciate being perpetually on call for their hospitalized patients – to rural communities.
In many cases, traveling doctors like Dr. Mandal or telemedicine backup, particularly for after-hours coverage or ICU beds, are important pieces of the puzzle for smaller hospitals. There are different ways to use the spectrum of telemedicine services to interact with a hospital’s daytime and night routines. In some isolated locations, nurse practitioners or physician assistants provide on-the-ground coverage with virtual backup. Rural hospitals often affiliate with telemedicine networks within health systems – or else contract with independent specialized providers of telemedicine consultation.
Mr. Slabach said another alternative for staffing hospitals with smaller ED and inpatient volumes is to have one doctor on duty who can cover both departments simultaneously. Meanwhile, the new federal Rural Emergency Hospital Program proposes to allow rural hospitals to become essentially freestanding EDs – starting Jan. 1, 2023 – that can manage patients for a maximum of 24 hours.3
Community connections and proactive staffing
Lisa Kaufmann, MD, works as a hospitalist for a two-hospital system in North Carolina, Appalachian Regional Health Care. She practices at Watauga Medical Center, with 100 licensed beds in Boone, and at Cannon Memorial Hospital, a critical access hospital in unincorporated Linville. “We are proud of what we have been able to accomplish during the pandemic,” she said.
A former critical care unit at Watauga had been shut down, but its wiring remained intact. “We turned it into a COVID unit in three days. Then we opened another COVID unit with 18 beds, but that still wasn’t enough. We converted half of our med/surg capacity into a COVID unit. At one point almost half of all of our acute beds were for COVID patients. We made plans for what we would do if it got worse, since we had almost run out of beds,” she said. Demand peaked at the end of January 2021.
“The biggest barrier for us was if someone needed to be transferred, for example, if they needed ECMO [extracorporeal membrane oxygenation], and we couldn’t find another hospital to provide that technology.” In ARHC’s mountainous region – known as the “High Country” – weather can also make it difficult to transport patients. “Sometimes the ambulance can’t make it off the mountain, and half of the time the medical helicopter can’t fly. So we have to be prepared to keep people who we might think ought to be transferred,” she said.
Like many rural communities, the High Country is tightly knit, and its hospitals are really connected to their communities, Dr. Kaufmann said. The health system already had a lot of community connections beyond acute care, and that meant the pandemic wasn’t experienced as severely as it was in some other rural communities. “But without hospitalists in our hospitals, it would have been much more difficult.”
Proactive supply fulfillment meant that her hospitals never ran out of personal protective equipment. “Staffing was a challenge, but we were proactive in getting traveling doctors to come here. We also utilized extra doctors from the local community,” she said. Another key was well-established disaster planning, with regular drills, and a robust incident command structure, which just needed to be activated in the crisis. “Small hospitals need to be prepared for disaster,” Dr. Kaufmann said.
For Dale Wiersma, MD, a hospitalist with Spectrum Health, a 14-hospital system in western Michigan, telemedicine services are coordinated across 8 rural regional hospitals. “We don’t tend to use it for direct hospitalist work during daytime hours, unless a facility is swamped, in which case we can cross-cover. We do more telemedicine at night. But during daytime hours we have access to stroke neurology, cardiology, psychiatry, critical care and infectious disease specialists who are able to offer virtual consults,” Dr. Wiersma said. A virtual critical care team of doctor and nurse is often the only intensivist service covering Spectrum’s rural hospitals.
“In our system, the pandemic accelerated the adoption of telemedicine,” Dr. Wiersma said. “We had been working on the tele-ICU program, trying to get it rolled out. When the pandemic hit, we launched it in just 6 weeks.”
There have been several COVID surges in Michigan, he said. “We were stretched pretty close to our limit several times, but never to the breaking point. For our physicians, it was the protracted nature of the pandemic that was fatiguing for everyone involved. Our system worked hard to staff up as well as it could, to make sure our people didn’t go over the edge.” It was also hard for hospitals that typically might see one or two deaths in a month to suddenly have five in a week.
Another Spectrum hospitalist, Christopher Skinner, MD, works at two rural Michigan hospitals 15 minutes apart in Big Rapids and Reed City. “I prefer working in rural areas. I’ve never had an ambition to be a top dog. I like the style of practice where you don’t have all of the medical subspecialties on site. It frees you up to use all your skills,” Dr. Skinner said.
But that approach was put to the test by the pandemic, since it was harder to transfer those patients who normally would not have stayed at these rural hospitals. “We had to make do,” he said, although virtual backup and second opinions from Spectrum’s virtual critical care team helped.
“It was a great collaboration, which helped us to handle critical care cases that we hadn’t had to manage pre-COVID. We’ve gotten used to it, with the backup, so I expect we’ll still be taking care of these kind of sick ventilator patients even after the pandemic ends,” Dr. Skinner said. “We’ve gotten pretty good at it.”
Sukhbir Pannu, MD, a hospitalist in Denver and CEO and founder of Rural Physicians Group, said the pandemic was highly impactful, operationally and logistically, for his firm, which contracts with 54 hospitals to provide their hospitalist staffing. “There was no preparation. Everything had to be done on the fly. Initially, it was felt that rural areas weren’t at as great a risk for COVID, but that proved not to be true. Many experienced a sudden increase in very sick patients. We set up a task force to manage daily census in all of our contracted facilities.”
How did Rural Physicians Group manage through the crisis? “The short answer is telemedicine,” he said. “We had physicians on the ground in these hospitals. But we needed intensivists at the other end of the line to support them.” A lot of conversations about telemedicine were already going on in the company, but the pandemic provided the impetus to launch its network, which has grown to include rheumatologists, pulmonologists, cardiologists, infection medicine, neurology, and psychiatry, all reachable through a central command structure.
Telemedicine is not a cure-all, Dr. Pannu said. It doesn’t work in a vacuum. It requires both a provider on the ground and specialists available remotely. “But it can be a massive multiplier.”
Critical medicine
Other hospitals, including small and rural ones, have reported taking on the challenge of covering critical care with nonintensivist physicians because the pandemic demanded it. David Aymond, MD, a hospitalist at 60-bed Byrd Regional Hospital in Leesville, La., population 6,612, has advocated for years for expanded training and credentialing opportunities in intensive care medicine beyond the traditional path of becoming a board-certified intensivist. Some rural hospitalists were already experienced in providing critical care for ICU patients even before the pandemic hit.
“What COVID did was to highlight the problem that there aren’t enough intensivists in this country, particular for smaller hospitals,” Dr. Aymond said. Some hospitalists who stepped into crisis roles in ICUs during COVID surges showed that they could take care of COVID patients very well.
Dr. Aymond, who is a fellowship-trained hospitalist with primary training in family medicine, has used his ICU experience in both fellowship and practice to make a thorough study of critical care medicine, which he put to good use when the seven-bed ICU at Byrd Memorial filled with COVID patients. “Early on, we were managing multiple ventilators throughout the hospital,” he said. “But we were having good outcomes. Our COVID patients were surviving.” That led to Dr. Aymond being interviewed by local news media, which led to other patients across the state asking to be transferred to “the COVID specialist who practices at Byrd.”
Dr. Aymond would like to see opportunities for abbreviated 1-year critical care fellowships for hospitalists who have amassed enough ICU experience in practice or in residency, and to make room for family medicine physicians in such programs. He is also working through SHM with the Society of Critical Care Medicine to generate educational ICU content. SHM now has a critical care lecture series at: www.hospitalmedicine.org/clinical-topics/critical-care/.
Dr. Mandal, who also works as a pediatric hospitalist, said that experience gave her more familiarity with using noninvasive methods for delivering respiratory therapies like high-flow oxygen. “When I saw a COVID patient who had hypoxia but was still able to talk, I didn’t hesitate to deliver oxygen through noninvasive means.” Eventually hospital practice generally for COVID caught up with this approach.
But she ran into personal difficulties because N95 face masks didn’t fit her face. Instead, she had to wear a portable respirator, which made it hard to hear what her patients were saying. “I formulated a lot of workarounds, such as interviewing the patient over the phone before going into the room for the physical exam.”
Throughout the pandemic, she never wavered in her commitment to rural hospital medicine and its opportunities for working in a small and wonderful community, where she could practice at the top of her license, with a degree of autonomy not granted in other settings. For doctors who want that kind of practice, she said, “the rewards will be paid back in spades. That’s been my experience.”
For more information on SHM’s Rural SIG and its supports for rural hospitalists, contact its executive chair, Kenneth Simone, DO, at ksimone911@gmail.com.
References
1. Personal communication from Peiyin Hung, June 2021.
2. Association of Health Care Journalists. Rural Health Journalism Workshop 2021. June 21, 2021. https://healthjournalism.org/calendar-details.php?id=2369.
3. Congress Establishes New Medicare Provider Category and Reimbursement for Rural Emergency Hospitals. National Law Review. Jan. 5, 2021. https://www.natlawreview.com/article/congress-establishes-new-medicare-provider-category-and-reimbursement-rural.
In 2018, Atashi Mandal, MD, a hospitalist residing in Orange County, Calif., was recruited along with several other doctors to fill hospitalist positions in rural Bishop, Calif. She has since driven 600 miles round trip every month for a week of hospital medicine shifts at Northern Inyo Hospital.
Dr. Mandal said she has really enjoyed her time at the small rural hospital and found it professionally fulfilling to participate so fully in the health of its local community. She was building personal bonds and calling the experience the pinnacle of her career when the COVID-19 pandemic swept across America and the world, even reaching up into Bishop, population 3,760, in the isolated Owens Valley.
The 25-bed hospital has seen at least 100 COVID patients in the past year and some months. Responsibility for taking care of these patients has been both humbling and gratifying, Dr. Mandal said. The facility’s hospitalists made a commitment to keep working through the pandemic. “We were able to come together (around COVID) as a team and our teamwork really made a difference,” she said.
“One of the advantages in a smaller hospital is you can have greater cohesiveness and your communication can be tighter. That played a big role in how we were able to accomplish so much with fewer resources as a rural hospital.” But staffing shortages, recruitment, and retention remain a perennial challenge for rural hospitals. “And COVID only exacerbated the problems,” she said. “I’ve had my challenges trying to make proper treatment plans without access to specialists.”
It was also difficult to witness so many patients severely ill or dying from COVID, Dr. Mandal said, especially since patients were not allowed family visitors – even though that was for a good reason, to minimize the virus’s spread.
HM in rural communities
Hospital medicine continues to extend into rural communities and small rural hospitals. In 2018, 35.7% of all rural counties in America had hospitals staffed with hospitalists, and 63.3% of rural hospitals had hospitalist programs (compared with 79.2% of urban hospitals). These numbers come from Medicare resources files from the Department of Health & Human Services, analyzed by Peiyin Hung, PhD, assistant professor of health services management and policy at the University of South Carolina, Columbia.1 Hospitalist penetration rates rose steadily from 2011 to 2017, with a slight dip in 2018, Dr. Hung said in an interview.
A total of 138 rural hospitals have closed since 2010, according to the Cecil G. Sheps Center for Health Services Research in Chapel Hill, N.C. Nineteen rural hospitals closed in 2020 alone, although many of those were caused by factors predating the pandemic. Only one has closed so far in 2021. But financial pressures, including low patient volumes and loss of revenue from canceled routine services like elective surgeries during the pandemic, have added to hospitals’ difficulties. Pandemic relief funding may have helped some hospitals stay open, but that support eventually will go away.
Experts emphasize the diversity of rural America and its health care systems. Rural economies are volatile and more diverse than is often appreciated. The hospital may be a cornerstone of the local economy; when one closes, it can devastate the community. Workforce is one of the chief components of a hospital’s ability to meet its strategic vision, and hospitalists are a big part in that. But while hospitalists are valued and appreciated, if the hospital is suffering severe financial problems, that will impact its doctors’ jobs and livelihoods.
“Bandwidth” varies widely for rural hospitalists and their hospitalist groups, said Ken Simone, DO, SFHM, executive chair of SHM’s Rural Special Interest Group and founder and principal of KGS Consultants, a Hospital Medicine and Primary Care Practice Management Consulting company. They may face scarce resources, scarce clinical staffing, lack of support staff to help operations run smoothly, lack of access to specialists locally, and lack of technology. While practicing in a rural setting presents various challenges, it can be rewarding for those clinicians who embrace its autonomy and broad scope of services, Dr. Simone said.
SHM’s Rural SIG focuses on the unique needs of rural hospitalists, providing them with an opportunity to share their concerns, challenges and solutions through roundtable discussions every other month and a special interest forum held in conjunction with the SHM Converge annual conference, Dr. Simone said. (The next SHM Converge will be April 7-10, 2022, in Nashville, Tenn.) The Rural SIG also collaborates with other hospital medicine SIGs and committees and is working on a white paper, “Key Principles and Characteristics of an Effective Rural Hospital Medicine Group.” It is also looking to develop a rural mentorship exchange program.
COVID reaches rural America
Early COVID caseloads tended to be in urban areas, but subsequent surges of infections have spread to many rural areas. Some rural settings became epicenters for the pandemic in November and December 2020. More recent troubling rises in COVID cases, particularly in areas with lower vaccination rates – suggest that the challenges of the pandemic are still not behind us.
“By no means is the crisis done in rural America,” said Alan Morgan, CEO of the National Rural Health Association, in a Virtual Rural Health Journalism workshop on rural health care sponsored by the Association of Health Care Journalists.2
Mr. Morgan’s colleague, Brock Slabach, NRHA’s chief operations officer, said in an interview that, while 453 of the 1,800 hospitals in rural areas fit NRHA’s criteria as being vulnerable to closure, the rest are not, and are fulfilling their missions for their communities. Hospitalists are becoming more common in these hospitals, he said, and rural hospitalists can be an important asset in attracting primary care physicians – who might not appreciate being perpetually on call for their hospitalized patients – to rural communities.
In many cases, traveling doctors like Dr. Mandal or telemedicine backup, particularly for after-hours coverage or ICU beds, are important pieces of the puzzle for smaller hospitals. There are different ways to use the spectrum of telemedicine services to interact with a hospital’s daytime and night routines. In some isolated locations, nurse practitioners or physician assistants provide on-the-ground coverage with virtual backup. Rural hospitals often affiliate with telemedicine networks within health systems – or else contract with independent specialized providers of telemedicine consultation.
Mr. Slabach said another alternative for staffing hospitals with smaller ED and inpatient volumes is to have one doctor on duty who can cover both departments simultaneously. Meanwhile, the new federal Rural Emergency Hospital Program proposes to allow rural hospitals to become essentially freestanding EDs – starting Jan. 1, 2023 – that can manage patients for a maximum of 24 hours.3
Community connections and proactive staffing
Lisa Kaufmann, MD, works as a hospitalist for a two-hospital system in North Carolina, Appalachian Regional Health Care. She practices at Watauga Medical Center, with 100 licensed beds in Boone, and at Cannon Memorial Hospital, a critical access hospital in unincorporated Linville. “We are proud of what we have been able to accomplish during the pandemic,” she said.
A former critical care unit at Watauga had been shut down, but its wiring remained intact. “We turned it into a COVID unit in three days. Then we opened another COVID unit with 18 beds, but that still wasn’t enough. We converted half of our med/surg capacity into a COVID unit. At one point almost half of all of our acute beds were for COVID patients. We made plans for what we would do if it got worse, since we had almost run out of beds,” she said. Demand peaked at the end of January 2021.
“The biggest barrier for us was if someone needed to be transferred, for example, if they needed ECMO [extracorporeal membrane oxygenation], and we couldn’t find another hospital to provide that technology.” In ARHC’s mountainous region – known as the “High Country” – weather can also make it difficult to transport patients. “Sometimes the ambulance can’t make it off the mountain, and half of the time the medical helicopter can’t fly. So we have to be prepared to keep people who we might think ought to be transferred,” she said.
Like many rural communities, the High Country is tightly knit, and its hospitals are really connected to their communities, Dr. Kaufmann said. The health system already had a lot of community connections beyond acute care, and that meant the pandemic wasn’t experienced as severely as it was in some other rural communities. “But without hospitalists in our hospitals, it would have been much more difficult.”
Proactive supply fulfillment meant that her hospitals never ran out of personal protective equipment. “Staffing was a challenge, but we were proactive in getting traveling doctors to come here. We also utilized extra doctors from the local community,” she said. Another key was well-established disaster planning, with regular drills, and a robust incident command structure, which just needed to be activated in the crisis. “Small hospitals need to be prepared for disaster,” Dr. Kaufmann said.
For Dale Wiersma, MD, a hospitalist with Spectrum Health, a 14-hospital system in western Michigan, telemedicine services are coordinated across 8 rural regional hospitals. “We don’t tend to use it for direct hospitalist work during daytime hours, unless a facility is swamped, in which case we can cross-cover. We do more telemedicine at night. But during daytime hours we have access to stroke neurology, cardiology, psychiatry, critical care and infectious disease specialists who are able to offer virtual consults,” Dr. Wiersma said. A virtual critical care team of doctor and nurse is often the only intensivist service covering Spectrum’s rural hospitals.
“In our system, the pandemic accelerated the adoption of telemedicine,” Dr. Wiersma said. “We had been working on the tele-ICU program, trying to get it rolled out. When the pandemic hit, we launched it in just 6 weeks.”
There have been several COVID surges in Michigan, he said. “We were stretched pretty close to our limit several times, but never to the breaking point. For our physicians, it was the protracted nature of the pandemic that was fatiguing for everyone involved. Our system worked hard to staff up as well as it could, to make sure our people didn’t go over the edge.” It was also hard for hospitals that typically might see one or two deaths in a month to suddenly have five in a week.
Another Spectrum hospitalist, Christopher Skinner, MD, works at two rural Michigan hospitals 15 minutes apart in Big Rapids and Reed City. “I prefer working in rural areas. I’ve never had an ambition to be a top dog. I like the style of practice where you don’t have all of the medical subspecialties on site. It frees you up to use all your skills,” Dr. Skinner said.
But that approach was put to the test by the pandemic, since it was harder to transfer those patients who normally would not have stayed at these rural hospitals. “We had to make do,” he said, although virtual backup and second opinions from Spectrum’s virtual critical care team helped.
“It was a great collaboration, which helped us to handle critical care cases that we hadn’t had to manage pre-COVID. We’ve gotten used to it, with the backup, so I expect we’ll still be taking care of these kind of sick ventilator patients even after the pandemic ends,” Dr. Skinner said. “We’ve gotten pretty good at it.”
Sukhbir Pannu, MD, a hospitalist in Denver and CEO and founder of Rural Physicians Group, said the pandemic was highly impactful, operationally and logistically, for his firm, which contracts with 54 hospitals to provide their hospitalist staffing. “There was no preparation. Everything had to be done on the fly. Initially, it was felt that rural areas weren’t at as great a risk for COVID, but that proved not to be true. Many experienced a sudden increase in very sick patients. We set up a task force to manage daily census in all of our contracted facilities.”
How did Rural Physicians Group manage through the crisis? “The short answer is telemedicine,” he said. “We had physicians on the ground in these hospitals. But we needed intensivists at the other end of the line to support them.” A lot of conversations about telemedicine were already going on in the company, but the pandemic provided the impetus to launch its network, which has grown to include rheumatologists, pulmonologists, cardiologists, infection medicine, neurology, and psychiatry, all reachable through a central command structure.
Telemedicine is not a cure-all, Dr. Pannu said. It doesn’t work in a vacuum. It requires both a provider on the ground and specialists available remotely. “But it can be a massive multiplier.”
Critical medicine
Other hospitals, including small and rural ones, have reported taking on the challenge of covering critical care with nonintensivist physicians because the pandemic demanded it. David Aymond, MD, a hospitalist at 60-bed Byrd Regional Hospital in Leesville, La., population 6,612, has advocated for years for expanded training and credentialing opportunities in intensive care medicine beyond the traditional path of becoming a board-certified intensivist. Some rural hospitalists were already experienced in providing critical care for ICU patients even before the pandemic hit.
“What COVID did was to highlight the problem that there aren’t enough intensivists in this country, particular for smaller hospitals,” Dr. Aymond said. Some hospitalists who stepped into crisis roles in ICUs during COVID surges showed that they could take care of COVID patients very well.
Dr. Aymond, who is a fellowship-trained hospitalist with primary training in family medicine, has used his ICU experience in both fellowship and practice to make a thorough study of critical care medicine, which he put to good use when the seven-bed ICU at Byrd Memorial filled with COVID patients. “Early on, we were managing multiple ventilators throughout the hospital,” he said. “But we were having good outcomes. Our COVID patients were surviving.” That led to Dr. Aymond being interviewed by local news media, which led to other patients across the state asking to be transferred to “the COVID specialist who practices at Byrd.”
Dr. Aymond would like to see opportunities for abbreviated 1-year critical care fellowships for hospitalists who have amassed enough ICU experience in practice or in residency, and to make room for family medicine physicians in such programs. He is also working through SHM with the Society of Critical Care Medicine to generate educational ICU content. SHM now has a critical care lecture series at: www.hospitalmedicine.org/clinical-topics/critical-care/.
Dr. Mandal, who also works as a pediatric hospitalist, said that experience gave her more familiarity with using noninvasive methods for delivering respiratory therapies like high-flow oxygen. “When I saw a COVID patient who had hypoxia but was still able to talk, I didn’t hesitate to deliver oxygen through noninvasive means.” Eventually hospital practice generally for COVID caught up with this approach.
But she ran into personal difficulties because N95 face masks didn’t fit her face. Instead, she had to wear a portable respirator, which made it hard to hear what her patients were saying. “I formulated a lot of workarounds, such as interviewing the patient over the phone before going into the room for the physical exam.”
Throughout the pandemic, she never wavered in her commitment to rural hospital medicine and its opportunities for working in a small and wonderful community, where she could practice at the top of her license, with a degree of autonomy not granted in other settings. For doctors who want that kind of practice, she said, “the rewards will be paid back in spades. That’s been my experience.”
For more information on SHM’s Rural SIG and its supports for rural hospitalists, contact its executive chair, Kenneth Simone, DO, at ksimone911@gmail.com.
References
1. Personal communication from Peiyin Hung, June 2021.
2. Association of Health Care Journalists. Rural Health Journalism Workshop 2021. June 21, 2021. https://healthjournalism.org/calendar-details.php?id=2369.
3. Congress Establishes New Medicare Provider Category and Reimbursement for Rural Emergency Hospitals. National Law Review. Jan. 5, 2021. https://www.natlawreview.com/article/congress-establishes-new-medicare-provider-category-and-reimbursement-rural.
Emerging realities
Dear colleagues,
Welcome to the November edition of The New Gastroenterologist! Our fall newsletter features a particularly interesting compilation of articles. As the pandemic lingers on, we are forced to face the realities of coexisting with COVID-19 as the virus certainly seems to be here to stay.
To protect against ongoing risk of exposure, health care workers and other high-risk subsets of patients are now being offered booster shots. For our patients with inflammatory bowel disease (IBD) on immune-modifying therapies, there has always been a question of vaccine efficacy. Dr. Freddy Caldera and Dr. Trevor Schell (University of Wisconsin-Madison) shed some much needed light on recommendations on the COVID-19 vaccine for IBD patients.
In April of 2021, a federal rule was implemented mandating that patients have immediate and free access to their electronic health information – which includes all documentation from their health care providers. Some physicians have been concerned about this practice, namely how patients will respond and whether this will increase the burden on clinicians. Clearly, this issue is multifaceted: Dr. Sachin Shah (University of Chicago) discusses the ethical implications from a clinical standpoint, while attorney Valerie Guttman Koch (University of Houston Law Center, MacLean Center for Clinical Medical Ethics, University of Chicago) shares a riveting legal perspective.
Colonic diverticular bleeding is the most common etiology of overt lower gastrointestinal bleeding and one of the most frequent consults we receive as gastroenterologists. However, even with the use of colonoscopy, obtaining a definitive diagnosis can often be difficult. Our “In Focus” feature for November, is an excellent piece written by Dr. Vivy Cusumano, Dr. Christopher Paiji, and Dr. Dennis Jensen (all with University of California, Los Angeles), detailing the pathophysiology, diagnosis, and treatment.
Navigating pregnancy and parental leave during training is difficult. Drs. Joy Liu, Keith Summa, Ronak Patel, Erica Donnan, Amanda Guentner, and Leila Kia (all with Northwestern University) share their program’s experience, providing incredibly helpful and practical recommendations for both gastroenterology trainees and fellowship directors.
The Association of Black Gastroenterologists and Hepatologists emerged against the backdrop of recent social and health care injustices. Dr. Kafayat Busari (Florida State University) and Dr. Alexandra Guillaume (Stony Brook University Hospital) discuss the critical importance and mission of this association and how it will help shape the field of gastroenterology in the years to come.
Medical pancreatology is a subspecialty that most gastroenterology fellows have little, if any, exposure to. In our post-fellowship pathways section, Dr. Sajan Nagpal (University of Chicago) details his own experiences in addition to discussing the important role of a medical pancreatologist within a gastroenterology division.
Lastly, our DHPA Private Practice Perspectives article, written by Dr. Sanjay Sandhir (Dayton [Ohio] Gastroenterology), discusses the importance of education and screening for nonalcoholic fatty liver disease.
If you have interest in contributing or have ideas for future TNG topics, please contact me (vijayarao@medicine.bsd.uchicago.edu), or Ryan Farrell (rfarrell@gastro.org), managing editor of TNG.
Stay well,
Vijaya L. Rao, MD
Editor-in-Chief
Assistant Professor of Medicine, University of Chicago, Section of Gastroenterology, Hepatology & Nutrition
Dear colleagues,
Welcome to the November edition of The New Gastroenterologist! Our fall newsletter features a particularly interesting compilation of articles. As the pandemic lingers on, we are forced to face the realities of coexisting with COVID-19 as the virus certainly seems to be here to stay.
To protect against ongoing risk of exposure, health care workers and other high-risk subsets of patients are now being offered booster shots. For our patients with inflammatory bowel disease (IBD) on immune-modifying therapies, there has always been a question of vaccine efficacy. Dr. Freddy Caldera and Dr. Trevor Schell (University of Wisconsin-Madison) shed some much needed light on recommendations on the COVID-19 vaccine for IBD patients.
In April of 2021, a federal rule was implemented mandating that patients have immediate and free access to their electronic health information – which includes all documentation from their health care providers. Some physicians have been concerned about this practice, namely how patients will respond and whether this will increase the burden on clinicians. Clearly, this issue is multifaceted: Dr. Sachin Shah (University of Chicago) discusses the ethical implications from a clinical standpoint, while attorney Valerie Guttman Koch (University of Houston Law Center, MacLean Center for Clinical Medical Ethics, University of Chicago) shares a riveting legal perspective.
Colonic diverticular bleeding is the most common etiology of overt lower gastrointestinal bleeding and one of the most frequent consults we receive as gastroenterologists. However, even with the use of colonoscopy, obtaining a definitive diagnosis can often be difficult. Our “In Focus” feature for November, is an excellent piece written by Dr. Vivy Cusumano, Dr. Christopher Paiji, and Dr. Dennis Jensen (all with University of California, Los Angeles), detailing the pathophysiology, diagnosis, and treatment.
Navigating pregnancy and parental leave during training is difficult. Drs. Joy Liu, Keith Summa, Ronak Patel, Erica Donnan, Amanda Guentner, and Leila Kia (all with Northwestern University) share their program’s experience, providing incredibly helpful and practical recommendations for both gastroenterology trainees and fellowship directors.
The Association of Black Gastroenterologists and Hepatologists emerged against the backdrop of recent social and health care injustices. Dr. Kafayat Busari (Florida State University) and Dr. Alexandra Guillaume (Stony Brook University Hospital) discuss the critical importance and mission of this association and how it will help shape the field of gastroenterology in the years to come.
Medical pancreatology is a subspecialty that most gastroenterology fellows have little, if any, exposure to. In our post-fellowship pathways section, Dr. Sajan Nagpal (University of Chicago) details his own experiences in addition to discussing the important role of a medical pancreatologist within a gastroenterology division.
Lastly, our DHPA Private Practice Perspectives article, written by Dr. Sanjay Sandhir (Dayton [Ohio] Gastroenterology), discusses the importance of education and screening for nonalcoholic fatty liver disease.
If you have interest in contributing or have ideas for future TNG topics, please contact me (vijayarao@medicine.bsd.uchicago.edu), or Ryan Farrell (rfarrell@gastro.org), managing editor of TNG.
Stay well,
Vijaya L. Rao, MD
Editor-in-Chief
Assistant Professor of Medicine, University of Chicago, Section of Gastroenterology, Hepatology & Nutrition
Dear colleagues,
Welcome to the November edition of The New Gastroenterologist! Our fall newsletter features a particularly interesting compilation of articles. As the pandemic lingers on, we are forced to face the realities of coexisting with COVID-19 as the virus certainly seems to be here to stay.
To protect against ongoing risk of exposure, health care workers and other high-risk subsets of patients are now being offered booster shots. For our patients with inflammatory bowel disease (IBD) on immune-modifying therapies, there has always been a question of vaccine efficacy. Dr. Freddy Caldera and Dr. Trevor Schell (University of Wisconsin-Madison) shed some much needed light on recommendations on the COVID-19 vaccine for IBD patients.
In April of 2021, a federal rule was implemented mandating that patients have immediate and free access to their electronic health information – which includes all documentation from their health care providers. Some physicians have been concerned about this practice, namely how patients will respond and whether this will increase the burden on clinicians. Clearly, this issue is multifaceted: Dr. Sachin Shah (University of Chicago) discusses the ethical implications from a clinical standpoint, while attorney Valerie Guttman Koch (University of Houston Law Center, MacLean Center for Clinical Medical Ethics, University of Chicago) shares a riveting legal perspective.
Colonic diverticular bleeding is the most common etiology of overt lower gastrointestinal bleeding and one of the most frequent consults we receive as gastroenterologists. However, even with the use of colonoscopy, obtaining a definitive diagnosis can often be difficult. Our “In Focus” feature for November, is an excellent piece written by Dr. Vivy Cusumano, Dr. Christopher Paiji, and Dr. Dennis Jensen (all with University of California, Los Angeles), detailing the pathophysiology, diagnosis, and treatment.
Navigating pregnancy and parental leave during training is difficult. Drs. Joy Liu, Keith Summa, Ronak Patel, Erica Donnan, Amanda Guentner, and Leila Kia (all with Northwestern University) share their program’s experience, providing incredibly helpful and practical recommendations for both gastroenterology trainees and fellowship directors.
The Association of Black Gastroenterologists and Hepatologists emerged against the backdrop of recent social and health care injustices. Dr. Kafayat Busari (Florida State University) and Dr. Alexandra Guillaume (Stony Brook University Hospital) discuss the critical importance and mission of this association and how it will help shape the field of gastroenterology in the years to come.
Medical pancreatology is a subspecialty that most gastroenterology fellows have little, if any, exposure to. In our post-fellowship pathways section, Dr. Sajan Nagpal (University of Chicago) details his own experiences in addition to discussing the important role of a medical pancreatologist within a gastroenterology division.
Lastly, our DHPA Private Practice Perspectives article, written by Dr. Sanjay Sandhir (Dayton [Ohio] Gastroenterology), discusses the importance of education and screening for nonalcoholic fatty liver disease.
If you have interest in contributing or have ideas for future TNG topics, please contact me (vijayarao@medicine.bsd.uchicago.edu), or Ryan Farrell (rfarrell@gastro.org), managing editor of TNG.
Stay well,
Vijaya L. Rao, MD
Editor-in-Chief
Assistant Professor of Medicine, University of Chicago, Section of Gastroenterology, Hepatology & Nutrition
Droperidol/midazolam combo curbs agitation in ED patients
a study involving 86 adult patients at a single tertiary medical care center.
Patients with acute agitation present significant safety concerns in the emergency department, according to Jessica Javed, MD, of the University of Louisville (Ky.) and colleagues.
A combination of haloperidol and lorazepam has been widely used to curb agitation in these patients, but droperidol and midazolam could be more effective, owing to faster onset of action, Dr. Javed noted in a presentation at the annual meeting of the American College of Emergency Physicians.
Dr. Javed and colleagues conducted a prospective study to compare time to adequate sedation in agitated patients in the ED. In the trial, 43 patients received droperidol 5 mg plus midazolam 5 mg, and 43 patients received haloperidol plus lorazepam 2 mg. The average age of the patients in the droperidol/midazolam group was 34 years; the average age of the patients in the haloperidol/lorazepam group was 38 years. Baseline demographics, including height, weight, body mass index, and baseline Sedation Assessment Tool (SAT) scores, were similar between the groups.
The SAT score scale ranges from +3 (combative, violent, or out of control) to –3 (no response to stimulation); zero indicates being awake and calm/cooperative. The median baseline SAT score was 3 for both treatment groups.
The primary outcome was the proportion of patients with adequate sedation (defined as SAT scores of ≤0) 10 min after treatment.
Significantly more patients in the droperidol/midazolam group met this outcome, compared with the patients in the haloperidol/lorazepam group (51.2% vs. 7%). Also, significantly more patients in the droperidol/midazolam group achieved adequate sedation at 5, 10, 15, and 30 min than in the haloperidol/lorazepam group.
Fewer patients in the haloperidol/lorazepam group required supplemental oxygen, compared with the droperidol/midazolam group (9.3% vs. 25.6%). However, none of the droperidol/midazolam patients required rescue sedation, compared with 16.3% of the haloperidol/lorazepam patients, Dr. Javed noted. None of the patients required endotracheal intubation or experienced extrapyramidal symptoms, she said.
The study was limited by the small sample size and inclusion of data from only a single center.
The results suggest that droperidol/midazolam is superior to intramuscular haloperidol/lorazepam for producing adequate sedation after 10 min in agitated patients, Dr. Javed concluded.
The study received no outside funding. The researchers have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
a study involving 86 adult patients at a single tertiary medical care center.
Patients with acute agitation present significant safety concerns in the emergency department, according to Jessica Javed, MD, of the University of Louisville (Ky.) and colleagues.
A combination of haloperidol and lorazepam has been widely used to curb agitation in these patients, but droperidol and midazolam could be more effective, owing to faster onset of action, Dr. Javed noted in a presentation at the annual meeting of the American College of Emergency Physicians.
Dr. Javed and colleagues conducted a prospective study to compare time to adequate sedation in agitated patients in the ED. In the trial, 43 patients received droperidol 5 mg plus midazolam 5 mg, and 43 patients received haloperidol plus lorazepam 2 mg. The average age of the patients in the droperidol/midazolam group was 34 years; the average age of the patients in the haloperidol/lorazepam group was 38 years. Baseline demographics, including height, weight, body mass index, and baseline Sedation Assessment Tool (SAT) scores, were similar between the groups.
The SAT score scale ranges from +3 (combative, violent, or out of control) to –3 (no response to stimulation); zero indicates being awake and calm/cooperative. The median baseline SAT score was 3 for both treatment groups.
The primary outcome was the proportion of patients with adequate sedation (defined as SAT scores of ≤0) 10 min after treatment.
Significantly more patients in the droperidol/midazolam group met this outcome, compared with the patients in the haloperidol/lorazepam group (51.2% vs. 7%). Also, significantly more patients in the droperidol/midazolam group achieved adequate sedation at 5, 10, 15, and 30 min than in the haloperidol/lorazepam group.
Fewer patients in the haloperidol/lorazepam group required supplemental oxygen, compared with the droperidol/midazolam group (9.3% vs. 25.6%). However, none of the droperidol/midazolam patients required rescue sedation, compared with 16.3% of the haloperidol/lorazepam patients, Dr. Javed noted. None of the patients required endotracheal intubation or experienced extrapyramidal symptoms, she said.
The study was limited by the small sample size and inclusion of data from only a single center.
The results suggest that droperidol/midazolam is superior to intramuscular haloperidol/lorazepam for producing adequate sedation after 10 min in agitated patients, Dr. Javed concluded.
The study received no outside funding. The researchers have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
a study involving 86 adult patients at a single tertiary medical care center.
Patients with acute agitation present significant safety concerns in the emergency department, according to Jessica Javed, MD, of the University of Louisville (Ky.) and colleagues.
A combination of haloperidol and lorazepam has been widely used to curb agitation in these patients, but droperidol and midazolam could be more effective, owing to faster onset of action, Dr. Javed noted in a presentation at the annual meeting of the American College of Emergency Physicians.
Dr. Javed and colleagues conducted a prospective study to compare time to adequate sedation in agitated patients in the ED. In the trial, 43 patients received droperidol 5 mg plus midazolam 5 mg, and 43 patients received haloperidol plus lorazepam 2 mg. The average age of the patients in the droperidol/midazolam group was 34 years; the average age of the patients in the haloperidol/lorazepam group was 38 years. Baseline demographics, including height, weight, body mass index, and baseline Sedation Assessment Tool (SAT) scores, were similar between the groups.
The SAT score scale ranges from +3 (combative, violent, or out of control) to –3 (no response to stimulation); zero indicates being awake and calm/cooperative. The median baseline SAT score was 3 for both treatment groups.
The primary outcome was the proportion of patients with adequate sedation (defined as SAT scores of ≤0) 10 min after treatment.
Significantly more patients in the droperidol/midazolam group met this outcome, compared with the patients in the haloperidol/lorazepam group (51.2% vs. 7%). Also, significantly more patients in the droperidol/midazolam group achieved adequate sedation at 5, 10, 15, and 30 min than in the haloperidol/lorazepam group.
Fewer patients in the haloperidol/lorazepam group required supplemental oxygen, compared with the droperidol/midazolam group (9.3% vs. 25.6%). However, none of the droperidol/midazolam patients required rescue sedation, compared with 16.3% of the haloperidol/lorazepam patients, Dr. Javed noted. None of the patients required endotracheal intubation or experienced extrapyramidal symptoms, she said.
The study was limited by the small sample size and inclusion of data from only a single center.
The results suggest that droperidol/midazolam is superior to intramuscular haloperidol/lorazepam for producing adequate sedation after 10 min in agitated patients, Dr. Javed concluded.
The study received no outside funding. The researchers have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Serotonin-mediated anxiety: How to recognize and treat it
Sara R. Abell, MD, and Rif S. El-Mallakh, MD
Individuals with anxiety will experience frequent or chronic excessive worry, nervousness, a sense of unease, a feeling of being unfocused, and distress, which result in functional impairment.1 Frequently, anxiety is accompanied by restlessness or muscle tension. Generalized anxiety disorder is one of the most common psychiatric diagnoses in the United States and has a prevalence of 2% to 6% globally.2 Although research has been conducted regarding anxiety’s pathogenesis, to date a firm consensus on its etiology has not been reached.3 It is likely multifactorial, with environmental and biologic components.
One area of focus has been neurotransmitters and the possible role they play in the pathogenesis of anxiety. Specifically, the monoamine neurotransmitters have been implicated in the clinical manifestations of anxiety. Among the amines, normal roles include stimulating the autonomic nervous system and regulating numerous cognitive phenomena, such as volition and emotion. Many psychiatric medications modify aminergic transmission, and many current anxiety medications target amine neurotransmitters. Medications that target histamine, serotonin, norepinephrine, and dopamine all play a role in treating anxiety.
In this article, we focus on serotonin (5-hydroxytryptamine, 5-HT) as a mediator of anxiety and on excessive synaptic 5-HT as the cause of anxiety. We discuss how 5-HT–mediated anxiety can be identified and offer some solutions for its treatment.
The amine neurotransmitters
There are 6 amine neurotransmitters in the CNS. These are derived from tyrosine (dopamine [DA], norepinephrine [NE], and epinephrine), histidine (histamine), and tryptophan (serotonin [5-HT] and melatonin). In addition to their physiologic actions, amines have been implicated in both acute and chronic anxiety. Excessive DA stimulation has been linked with fear4,5; NE elevations are central to hypervigilance and hyperarousal of posttraumatic stress disorder6; and histamine may mediate emotional memories involved in fear and anxiety.7 Understanding the normal function of 5-HT will aid in understanding its potential problematic role (Box,8-18page 38).
How serotonin-mediated anxiety presents
“Anxiety” is a collection of signs and symptoms that likely represent multiple processes and have the common characteristic of being subjectively unpleasant, with a subjective wish for the feeling to end. The expression of anxiety disorders is quite diverse and ranges from brief episodes such as panic attacks (which may be mediated, in part, by epinephrine/NE19) to lifelong stereotypic obsessions and compulsions (which may be mediated, in part, by DA and modified by 5-HT20,21). Biochemical separation of the anxiety disorders is key to achieving tailored treatment.6 Towards this end, it is important to investigate the phenomenon of serotonin-mediated anxiety.
Because clinicians are familiar with reductions of anxiety as selective serotonin reuptake inhibitors (SSRIs) increase 5-HT levels in the synapse, it is difficult to conceptualize serotonin-mediated anxiety. However, many of the effects at postsynaptic 5-HT receptors may be biphasic.15-18 Serotonin-mediated anxiety appears to occur when levels of 5-HT (or stimulation of 5-HT receptors) are particularly high. This is most frequently seen in patients who genetically have high synaptic 5-HT (by virtue of the short form of the 5-HT transporter),22 whose synaptic 5-HT is further increased by treatment with an SSRI,23 and who are experiencing a stressor that yet further increases their synaptic 5-HT.24 However, it may occur in some individuals with only 2 of these 3 conditions.Clinically, individuals with serotonin-mediated anxiety will usually appear calm. The anxiety they are experiencing is not exhibited in any way in the motor system (ie, they do not appear restless, do not pace, muscle tone is not increased, etc.). However, they will generally complain of an internal agitation, a sense of a negative internal energy. Frequently, they will use descriptions such as “I feel I could jump out of my skin.” As previously mentioned, this is usually in the setting of some environmental stress, in addition to either a pharmacologic (SSRI) or genetic (short form of the 5-HT transporter) reason for increasing synaptic 5-HT, or both.
Almost always, interventions that block multiple postsynaptic 5-HT receptors or discontinuation of the SSRI (if applicable) will alleviate the anxiety, quickly or more slowly, respectively. Sublingual asenapine, which at low doses can block 5-HT2C (Ki = 0.03 nM), 5-HT2A (Ki = 0.07 nM), 5-HT7 (Ki = 0.11 nM), 5-HT2B (Ki = 0.18 nM), and 5-HT6 (Ki = 0.25 nM),25,26 and which will produce peak plasma levels within 10 minutes,27 usually is quite effective.
Box
Serotonin (5-HT) arises from neurons in the raphe nuclei of the rostral pons and projects superiorly to the cerebral cortex and inferiorly to the spinal cord.8 It works in an inhibitory or excitatory manner depending on which receptors are activated. In the periphery, 5-HT influences intestinal peristalsis, sensory modulation, gland function, thermoregulation, blood pressure, platelet aggregation, and sexual behavior,9 all actions that produce potential adverse effects of serotonin reuptake– inhibiting antidepressants. In the CNS, 5-HT plays a role in attention bias; decision-making; sleep and wakefulness; and mood regulation. In short, serotonin can be viewed as mediating emotional motivation.10
Serotonin alters neuroplasticity. During development, 5-HT stimulates creation of new synapses and increases the density of synaptic webs. It has a direct stimulatory effect on the length of dendrites, their branching, and their myelination.11 In the CNS, it plays a role in dendritic arborization. Animal studies with rats have shown that lesioning highly concentrated 5-HT areas at early ages resulted in an adult brain with a lower number of neurons and a less complex web of dendrites.12,13 In situations of emotional stress, it is theorized that low levels of 5-HT lead to a reduced ability to deal with emotional stressors due to lower levels of complexity in synaptic connections.
Serotonin has also been implicated in mediating some aspects of dopamine-related actions, such as locomotion, reward, and threat avoidance. This is believed to contribute to the beneficial effect of 5-HT2A blockade by secondgeneration antipsychotics (SGAs).14 Blockade of other 5-HT receptors, such as 5-HT1A, 5-HT2C, 5-HT6, and 5-HT7, may also contribute to the antipsychotic action of SGAs.14
Serotonin receptors are found throughout the body, and 14 subtypes have been identified.9 Excitatory and inhibitory action of 5-HT depends on the receptor, and the actions of 5-HT can differ with the same receptor at different concentrations. This is because serotonin’s effects are biphasic and concentration-dependent, meaning that levels of 5-HT in the synapse will dictate the downstream effect of receptor agonism or antagonism. Animal models have shown that low-dose agonism of 5-HT receptors causes vasoconstriction of the coronary arteries, and high doses cause relaxation. This response has also been demonstrated in the vasculature of the kidneys and the smooth muscle of the trachea. Additionally, 5-HT works in conjunction with histamine to produce a biphasic response in the colonic arteries and veins in situations of endothelial damage.15
Most relevant to this discussion are 5-HT’s actions in mood regulation and behavior. Low 5-HT states result in less behavioral inhibition, leading to higher impulse control failures and aggression. Experiments in mice with deficient serotonergic brain regions show hypoactivity, extended daytime sleep, anxiety, and depressive behaviors.13 Serotonin’s behavioral effects are also biphasic. For example, lowdose antagonism with trazodone of 5-HT receptors demonstrated a pro-aggressive behavioral effect, while high-dose antagonism is anti-aggressive.15 Similar biphasic effects may result in either induction or reduction of anxiety with agents that block or excite certain 5-HT receptors.16-18
Continue to: A key difference: No motor system involvement...
A key difference: No motor system involvement
What distinguishes 5-HT from the other amine transmitters as a mediator of anxiety is the lack of involvement of the motor system. Multiple studies in rats illustrate that exogenously augmenting 5-HT has no effect on levels of locomotor activity. Dopamine depletion is well-characterized in the motor dysfunction of Parkinson’s disease, and DA excess can cause repetitive, stereotyped movements, such as seen in tardive dyskinesia or Huntington’s disease.8 In humans, serotonin-mediated anxiety is usually without a motoric component; patients appear calm but complain of extreme anxiety or agitation. Agitation has been reported after initiation of an SSRI,29 and is more likely to occur in patients with the short form of the 5-HT transporter.30 Motoric activation has been reported in some of these studies, but does not seem to cluster with the complaint of agitation.29 The reduced number of available transporters means a chronic steady-state elevation of serotonin, because less serotonin is being removed from the synapse after it is released. This is one of the reasons patients with the short form of the 5-HT transporter may be more susceptible to serotonin-mediated anxiety.
What you need to keep in mind
Pharmacologic treatment of anxiety begins with an SSRI, a serotonin-norepinephrine reuptake inhibitor (SNRI), or buspirone. Second-line treatments include hydroxyzine, gabapentin, pregabalin, and quetiapine.3,31 However, clinicians need to be aware that a fraction of their patients will report anxiety that will not have any external manifestations, but will be experienced as an unpleasant internal energy. These patients may report an increase in their anxiety levels when started on an SSRI or SNRI.29,30 This anxiety is most likely mediated by increases of synaptic 5-HT. This occurs because many serotonergic receptors may have a biphasic response, so that too much stimulation is experienced as excessive internal energy.16-18 In such patients, blockade of key 5-HT receptors may reduce that internal agitation. The advantage of recognizing serotonin-mediated anxiety is that one can specifically tailor treatment to address the patient’s specific physiology.
It is important to note that the anxiolytic effect of asenapine is specific to patients with serotonin-mediated anxiety. Unlike quetiapine, which is effective as augmentation therapy in generalized anxiety disorder,31 asenapine does not appear to reduce anxiety in patients with schizophrenia32 or borderline personality disorder33 when administered for other reasons. However, it may reduce anxiety in patients with the short form of the 5-HT transporter.30,34
Bottom Line
Serotonin-mediated anxiety occurs when levels of synaptic serotonin (5-HT) are high. Patients with serotonin-mediated anxiety appear calm but will report experiencing an unpleasant internal energy. Interventions that block multiple postsynaptic 5-HT receptors or discontinuation of a selective serotonin reuptake inhibitor (if applicable) will alleviate the anxiety.
Related Resource
• Bhatt NV. Anxiety disorders. https://emedicine.medscape. com/article/286227-overview
Drug Brand Names
Asenapine • Saphris, Secuado
Gabapentin • Neurontin
Hydroxyzine • Vistaril
Pregabalin • Lyrica
Quetiapine • Seroquel
Trazodone • Oleptro
1. Shelton CI. Diagnosis and management of anxiety disorders. J Am Osteopath Assoc. 2004;104(3 Suppl 3):S2-S5.
2. Ruscio AM, Hallion LS, Lim CCW, et al. Cross-sectional comparison of the epidemiology of DSM-5 generalized anxiety disorder across the globe. JAMA Psychiatry. 2017;74(5):465-475.
3. Locke AB, Kirst N, Shultz CG. Diagnosis and management of generalized anxiety disorder and panic disorder in adults. Am Fam Physician. 2015;91(9):617-624.
4. Hariri AR, Mattay VS, Tessitore A, et al. Dextroamphetamine modulates the response of the human amygdala. Neuropsychopharmacology. 2002;27(6):1036-1040.
5. Colombo AC, de Oliveira AR, Reimer AE, et al. Dopaminergic mechanisms underlying catalepsy, fear and anxiety: do they interact? Behav Brain Res. 2013;257:201-207.
6. Togay B, El-Mallakh RS. Posttraumatic stress disorder: from pathophysiology to pharmacology. Curr Psychiatry. 2020;19(5):33-39.
7. Provensi G, Passani MB, Costa A, et al. Neuronal histamine and the memory of emotionally salient events. Br J Pharmacol. 2020;177(3):557-569.
8. Purves D, Augustine GJ, Fitzpatrick D, et al (eds). Neuroscience. 2nd ed. Sinauer Associates; 2001.
9. Pytliak M, Vargová V, Mechírová V, et al. Serotonin receptors – from molecular biology to clinical applications. Physiol Res. 2011;60(1):15-25.
10. Meneses A, Liy-Salmeron G. Serotonin and emotion, learning and memory. Rev Neurosci. 2012;23(5-6):543-553.
11. Whitaker-Azmitia PM. Serotonin and brain development: role in human developmental diseases. Brain Res Bull. 2001;56(5):479-485.
12. Towle AC, Breese GR, Mueller RA, et al. Early postnatal administration of 5,7-DHT: effects on serotonergic neurons and terminals. Brain Res. 1984;310(1):67-75.
13. Rok-Bujko P, Krzs´cik P, Szyndler J, et al. The influence of neonatal serotonin depletion on emotional and exploratory behaviours in rats. Behav Brain Res. 2012;226(1):87-95.
14. Meltzer HY. The role of serotonin in antipsychotic drug action. Neuropsychopharmacology. 1999;21(2 Suppl):106S-115S.
15. Calabrese EJ. 5-Hydroxytryptamine (serotonin): biphasic dose responses. Crit Rev Toxicol. 2001;31(4-5):553-561.
16. Zuardi AW. 5-HT-related drugs and human experimental anxiety. Neurosci Biobehav Rev. 1990;14(4):507-510.
17. Sánchez C, Meier E. Behavioral profiles of SSRIs in animal models of depression, anxiety and aggression. Are they all alike? Psychopharmacology (Berl). 1997;129(3):197-205.
18. Koek W, Mitchell NC, Daws LC. Biphasic effects of selective serotonin reuptake inhibitors on anxiety: rapid reversal of escitalopram’s anxiogenic effects in the novelty-induced hypophagia test in mice? Behav Pharmacol. 2018;29(4):365-369.
19. van Zijderveld GA, Veltman DJ, van Dyck R, et al. Epinephrine-induced panic attacks and hyperventilation. J Psychiatr Res. 1999;33(1):73-78.
20. Ho EV, Thompson SL, Katzka WR, et al. Clinically effective OCD treatment prevents 5-HT1B receptor-induced repetitive behavior and striatal activation. Psychopharmacology (Berl). 2016;233(1):57-70.
21. Stein DJ, Costa DLC, Lochner C, et al. Obsessive-compulsive disorder. Nat Rev Dis Primers. 2019;5(1):52.
22. Luddington NS, Mandadapu A, Husk M, et al. Clinical implications of genetic variation in the serotonin transporter promoter region: a review. Prim Care Companion J Clin Psychiatry. 2009;11(3):93-102.
23. Stahl SM. Mechanism of action of serotonin selective reuptake inhibitors. Serotonin receptors and pathways mediate therapeutic effects and side effects. J Affect Disord. 1998;51(3):215-235.
24. Chaouloff F, Berton O, Mormède P. Serotonin and stress. Neuropsychopharmacology. 1999;21(2 Suppl):28S-32S.
25. Siafis S, Tzachanis D, Samara M, et al. Antipsychotic drugs: From receptor-binding profiles to metabolic side effects. Curr Neuropharmacol. 2018;16(8):1210-1223.
26. Carrithers B, El-Mallakh RS. Transdermal asenapine in schizophrenia: a systematic review. Patient Prefer Adherence. 2020;14:1541-1551.
27. Citrome L. Asenapine review, part I: chemistry, receptor affinity profile, pharmacokinetics and metabolism. Expert Opin Drug Metab Toxicol. 2014;10(6):893-903.
28. Pratts M, Citrome L, Grant W, et al. A single-dose, randomized, double-blind, placebo-controlled trial of sublingual asenapine for acute agitation. Acta Psychiatr Scand. 2014;130(1):61-68.
29. Biswas AB, Bhaumik S, Branford D. Treatment-emergent behavioural side effects with selective serotonin re-uptake inhibitors in adults with learning disabilities. Hum Psychopharmacol. 2001;16(2):133-137.
30. Perlis RH, Mischoulon D, Smoller JW, et al. Serotonin transporter polymorphisms and adverse effects with fluoxetine treatment. Biol Psychiatry. 2003;54(9):879-883.
31. Ipser JC, Carey P, Dhansay Y, et al. Pharmacotherapy augmentation strategies in treatment-resistant anxiety disorders. Cochrane Database Syst Rev. 2006;(4):CD005473.
32. Kane JM, Mackle M, Snow-Adami L, et al. A randomized placebo-controlled trial of asenapine for the prevention of relapse of schizophrenia after long-term treatment. J Clin Psychiatry. 2011;72(3):349-355.
33. Bozzatello P, Rocca P, Uscinska M, et al. Efficacy and tolerability of asenapine compared with olanzapine in borderline personality disorder: an open-label randomized controlled trial. CNS Drugs. 2017;31(9):809-819.
34. El-Mallakh RS, Nuss S, Gao D, et al. Asenapine in the treatment of bipolar depression. Psychopharmacol Bull. 2020;50(1):8-18.
Sara R. Abell, MD, and Rif S. El-Mallakh, MD
Individuals with anxiety will experience frequent or chronic excessive worry, nervousness, a sense of unease, a feeling of being unfocused, and distress, which result in functional impairment.1 Frequently, anxiety is accompanied by restlessness or muscle tension. Generalized anxiety disorder is one of the most common psychiatric diagnoses in the United States and has a prevalence of 2% to 6% globally.2 Although research has been conducted regarding anxiety’s pathogenesis, to date a firm consensus on its etiology has not been reached.3 It is likely multifactorial, with environmental and biologic components.
One area of focus has been neurotransmitters and the possible role they play in the pathogenesis of anxiety. Specifically, the monoamine neurotransmitters have been implicated in the clinical manifestations of anxiety. Among the amines, normal roles include stimulating the autonomic nervous system and regulating numerous cognitive phenomena, such as volition and emotion. Many psychiatric medications modify aminergic transmission, and many current anxiety medications target amine neurotransmitters. Medications that target histamine, serotonin, norepinephrine, and dopamine all play a role in treating anxiety.
In this article, we focus on serotonin (5-hydroxytryptamine, 5-HT) as a mediator of anxiety and on excessive synaptic 5-HT as the cause of anxiety. We discuss how 5-HT–mediated anxiety can be identified and offer some solutions for its treatment.
The amine neurotransmitters
There are 6 amine neurotransmitters in the CNS. These are derived from tyrosine (dopamine [DA], norepinephrine [NE], and epinephrine), histidine (histamine), and tryptophan (serotonin [5-HT] and melatonin). In addition to their physiologic actions, amines have been implicated in both acute and chronic anxiety. Excessive DA stimulation has been linked with fear4,5; NE elevations are central to hypervigilance and hyperarousal of posttraumatic stress disorder6; and histamine may mediate emotional memories involved in fear and anxiety.7 Understanding the normal function of 5-HT will aid in understanding its potential problematic role (Box,8-18page 38).
How serotonin-mediated anxiety presents
“Anxiety” is a collection of signs and symptoms that likely represent multiple processes and have the common characteristic of being subjectively unpleasant, with a subjective wish for the feeling to end. The expression of anxiety disorders is quite diverse and ranges from brief episodes such as panic attacks (which may be mediated, in part, by epinephrine/NE19) to lifelong stereotypic obsessions and compulsions (which may be mediated, in part, by DA and modified by 5-HT20,21). Biochemical separation of the anxiety disorders is key to achieving tailored treatment.6 Towards this end, it is important to investigate the phenomenon of serotonin-mediated anxiety.
Because clinicians are familiar with reductions of anxiety as selective serotonin reuptake inhibitors (SSRIs) increase 5-HT levels in the synapse, it is difficult to conceptualize serotonin-mediated anxiety. However, many of the effects at postsynaptic 5-HT receptors may be biphasic.15-18 Serotonin-mediated anxiety appears to occur when levels of 5-HT (or stimulation of 5-HT receptors) are particularly high. This is most frequently seen in patients who genetically have high synaptic 5-HT (by virtue of the short form of the 5-HT transporter),22 whose synaptic 5-HT is further increased by treatment with an SSRI,23 and who are experiencing a stressor that yet further increases their synaptic 5-HT.24 However, it may occur in some individuals with only 2 of these 3 conditions.Clinically, individuals with serotonin-mediated anxiety will usually appear calm. The anxiety they are experiencing is not exhibited in any way in the motor system (ie, they do not appear restless, do not pace, muscle tone is not increased, etc.). However, they will generally complain of an internal agitation, a sense of a negative internal energy. Frequently, they will use descriptions such as “I feel I could jump out of my skin.” As previously mentioned, this is usually in the setting of some environmental stress, in addition to either a pharmacologic (SSRI) or genetic (short form of the 5-HT transporter) reason for increasing synaptic 5-HT, or both.
Almost always, interventions that block multiple postsynaptic 5-HT receptors or discontinuation of the SSRI (if applicable) will alleviate the anxiety, quickly or more slowly, respectively. Sublingual asenapine, which at low doses can block 5-HT2C (Ki = 0.03 nM), 5-HT2A (Ki = 0.07 nM), 5-HT7 (Ki = 0.11 nM), 5-HT2B (Ki = 0.18 nM), and 5-HT6 (Ki = 0.25 nM),25,26 and which will produce peak plasma levels within 10 minutes,27 usually is quite effective.
Box
Serotonin (5-HT) arises from neurons in the raphe nuclei of the rostral pons and projects superiorly to the cerebral cortex and inferiorly to the spinal cord.8 It works in an inhibitory or excitatory manner depending on which receptors are activated. In the periphery, 5-HT influences intestinal peristalsis, sensory modulation, gland function, thermoregulation, blood pressure, platelet aggregation, and sexual behavior,9 all actions that produce potential adverse effects of serotonin reuptake– inhibiting antidepressants. In the CNS, 5-HT plays a role in attention bias; decision-making; sleep and wakefulness; and mood regulation. In short, serotonin can be viewed as mediating emotional motivation.10
Serotonin alters neuroplasticity. During development, 5-HT stimulates creation of new synapses and increases the density of synaptic webs. It has a direct stimulatory effect on the length of dendrites, their branching, and their myelination.11 In the CNS, it plays a role in dendritic arborization. Animal studies with rats have shown that lesioning highly concentrated 5-HT areas at early ages resulted in an adult brain with a lower number of neurons and a less complex web of dendrites.12,13 In situations of emotional stress, it is theorized that low levels of 5-HT lead to a reduced ability to deal with emotional stressors due to lower levels of complexity in synaptic connections.
Serotonin has also been implicated in mediating some aspects of dopamine-related actions, such as locomotion, reward, and threat avoidance. This is believed to contribute to the beneficial effect of 5-HT2A blockade by secondgeneration antipsychotics (SGAs).14 Blockade of other 5-HT receptors, such as 5-HT1A, 5-HT2C, 5-HT6, and 5-HT7, may also contribute to the antipsychotic action of SGAs.14
Serotonin receptors are found throughout the body, and 14 subtypes have been identified.9 Excitatory and inhibitory action of 5-HT depends on the receptor, and the actions of 5-HT can differ with the same receptor at different concentrations. This is because serotonin’s effects are biphasic and concentration-dependent, meaning that levels of 5-HT in the synapse will dictate the downstream effect of receptor agonism or antagonism. Animal models have shown that low-dose agonism of 5-HT receptors causes vasoconstriction of the coronary arteries, and high doses cause relaxation. This response has also been demonstrated in the vasculature of the kidneys and the smooth muscle of the trachea. Additionally, 5-HT works in conjunction with histamine to produce a biphasic response in the colonic arteries and veins in situations of endothelial damage.15
Most relevant to this discussion are 5-HT’s actions in mood regulation and behavior. Low 5-HT states result in less behavioral inhibition, leading to higher impulse control failures and aggression. Experiments in mice with deficient serotonergic brain regions show hypoactivity, extended daytime sleep, anxiety, and depressive behaviors.13 Serotonin’s behavioral effects are also biphasic. For example, lowdose antagonism with trazodone of 5-HT receptors demonstrated a pro-aggressive behavioral effect, while high-dose antagonism is anti-aggressive.15 Similar biphasic effects may result in either induction or reduction of anxiety with agents that block or excite certain 5-HT receptors.16-18
Continue to: A key difference: No motor system involvement...
A key difference: No motor system involvement
What distinguishes 5-HT from the other amine transmitters as a mediator of anxiety is the lack of involvement of the motor system. Multiple studies in rats illustrate that exogenously augmenting 5-HT has no effect on levels of locomotor activity. Dopamine depletion is well-characterized in the motor dysfunction of Parkinson’s disease, and DA excess can cause repetitive, stereotyped movements, such as seen in tardive dyskinesia or Huntington’s disease.8 In humans, serotonin-mediated anxiety is usually without a motoric component; patients appear calm but complain of extreme anxiety or agitation. Agitation has been reported after initiation of an SSRI,29 and is more likely to occur in patients with the short form of the 5-HT transporter.30 Motoric activation has been reported in some of these studies, but does not seem to cluster with the complaint of agitation.29 The reduced number of available transporters means a chronic steady-state elevation of serotonin, because less serotonin is being removed from the synapse after it is released. This is one of the reasons patients with the short form of the 5-HT transporter may be more susceptible to serotonin-mediated anxiety.
What you need to keep in mind
Pharmacologic treatment of anxiety begins with an SSRI, a serotonin-norepinephrine reuptake inhibitor (SNRI), or buspirone. Second-line treatments include hydroxyzine, gabapentin, pregabalin, and quetiapine.3,31 However, clinicians need to be aware that a fraction of their patients will report anxiety that will not have any external manifestations, but will be experienced as an unpleasant internal energy. These patients may report an increase in their anxiety levels when started on an SSRI or SNRI.29,30 This anxiety is most likely mediated by increases of synaptic 5-HT. This occurs because many serotonergic receptors may have a biphasic response, so that too much stimulation is experienced as excessive internal energy.16-18 In such patients, blockade of key 5-HT receptors may reduce that internal agitation. The advantage of recognizing serotonin-mediated anxiety is that one can specifically tailor treatment to address the patient’s specific physiology.
It is important to note that the anxiolytic effect of asenapine is specific to patients with serotonin-mediated anxiety. Unlike quetiapine, which is effective as augmentation therapy in generalized anxiety disorder,31 asenapine does not appear to reduce anxiety in patients with schizophrenia32 or borderline personality disorder33 when administered for other reasons. However, it may reduce anxiety in patients with the short form of the 5-HT transporter.30,34
Bottom Line
Serotonin-mediated anxiety occurs when levels of synaptic serotonin (5-HT) are high. Patients with serotonin-mediated anxiety appear calm but will report experiencing an unpleasant internal energy. Interventions that block multiple postsynaptic 5-HT receptors or discontinuation of a selective serotonin reuptake inhibitor (if applicable) will alleviate the anxiety.
Related Resource
• Bhatt NV. Anxiety disorders. https://emedicine.medscape. com/article/286227-overview
Drug Brand Names
Asenapine • Saphris, Secuado
Gabapentin • Neurontin
Hydroxyzine • Vistaril
Pregabalin • Lyrica
Quetiapine • Seroquel
Trazodone • Oleptro
Sara R. Abell, MD, and Rif S. El-Mallakh, MD
Individuals with anxiety will experience frequent or chronic excessive worry, nervousness, a sense of unease, a feeling of being unfocused, and distress, which result in functional impairment.1 Frequently, anxiety is accompanied by restlessness or muscle tension. Generalized anxiety disorder is one of the most common psychiatric diagnoses in the United States and has a prevalence of 2% to 6% globally.2 Although research has been conducted regarding anxiety’s pathogenesis, to date a firm consensus on its etiology has not been reached.3 It is likely multifactorial, with environmental and biologic components.
One area of focus has been neurotransmitters and the possible role they play in the pathogenesis of anxiety. Specifically, the monoamine neurotransmitters have been implicated in the clinical manifestations of anxiety. Among the amines, normal roles include stimulating the autonomic nervous system and regulating numerous cognitive phenomena, such as volition and emotion. Many psychiatric medications modify aminergic transmission, and many current anxiety medications target amine neurotransmitters. Medications that target histamine, serotonin, norepinephrine, and dopamine all play a role in treating anxiety.
In this article, we focus on serotonin (5-hydroxytryptamine, 5-HT) as a mediator of anxiety and on excessive synaptic 5-HT as the cause of anxiety. We discuss how 5-HT–mediated anxiety can be identified and offer some solutions for its treatment.
The amine neurotransmitters
There are 6 amine neurotransmitters in the CNS. These are derived from tyrosine (dopamine [DA], norepinephrine [NE], and epinephrine), histidine (histamine), and tryptophan (serotonin [5-HT] and melatonin). In addition to their physiologic actions, amines have been implicated in both acute and chronic anxiety. Excessive DA stimulation has been linked with fear4,5; NE elevations are central to hypervigilance and hyperarousal of posttraumatic stress disorder6; and histamine may mediate emotional memories involved in fear and anxiety.7 Understanding the normal function of 5-HT will aid in understanding its potential problematic role (Box,8-18page 38).
How serotonin-mediated anxiety presents
“Anxiety” is a collection of signs and symptoms that likely represent multiple processes and have the common characteristic of being subjectively unpleasant, with a subjective wish for the feeling to end. The expression of anxiety disorders is quite diverse and ranges from brief episodes such as panic attacks (which may be mediated, in part, by epinephrine/NE19) to lifelong stereotypic obsessions and compulsions (which may be mediated, in part, by DA and modified by 5-HT20,21). Biochemical separation of the anxiety disorders is key to achieving tailored treatment.6 Towards this end, it is important to investigate the phenomenon of serotonin-mediated anxiety.
Because clinicians are familiar with reductions of anxiety as selective serotonin reuptake inhibitors (SSRIs) increase 5-HT levels in the synapse, it is difficult to conceptualize serotonin-mediated anxiety. However, many of the effects at postsynaptic 5-HT receptors may be biphasic.15-18 Serotonin-mediated anxiety appears to occur when levels of 5-HT (or stimulation of 5-HT receptors) are particularly high. This is most frequently seen in patients who genetically have high synaptic 5-HT (by virtue of the short form of the 5-HT transporter),22 whose synaptic 5-HT is further increased by treatment with an SSRI,23 and who are experiencing a stressor that yet further increases their synaptic 5-HT.24 However, it may occur in some individuals with only 2 of these 3 conditions.Clinically, individuals with serotonin-mediated anxiety will usually appear calm. The anxiety they are experiencing is not exhibited in any way in the motor system (ie, they do not appear restless, do not pace, muscle tone is not increased, etc.). However, they will generally complain of an internal agitation, a sense of a negative internal energy. Frequently, they will use descriptions such as “I feel I could jump out of my skin.” As previously mentioned, this is usually in the setting of some environmental stress, in addition to either a pharmacologic (SSRI) or genetic (short form of the 5-HT transporter) reason for increasing synaptic 5-HT, or both.
Almost always, interventions that block multiple postsynaptic 5-HT receptors or discontinuation of the SSRI (if applicable) will alleviate the anxiety, quickly or more slowly, respectively. Sublingual asenapine, which at low doses can block 5-HT2C (Ki = 0.03 nM), 5-HT2A (Ki = 0.07 nM), 5-HT7 (Ki = 0.11 nM), 5-HT2B (Ki = 0.18 nM), and 5-HT6 (Ki = 0.25 nM),25,26 and which will produce peak plasma levels within 10 minutes,27 usually is quite effective.
Box
Serotonin (5-HT) arises from neurons in the raphe nuclei of the rostral pons and projects superiorly to the cerebral cortex and inferiorly to the spinal cord.8 It works in an inhibitory or excitatory manner depending on which receptors are activated. In the periphery, 5-HT influences intestinal peristalsis, sensory modulation, gland function, thermoregulation, blood pressure, platelet aggregation, and sexual behavior,9 all actions that produce potential adverse effects of serotonin reuptake– inhibiting antidepressants. In the CNS, 5-HT plays a role in attention bias; decision-making; sleep and wakefulness; and mood regulation. In short, serotonin can be viewed as mediating emotional motivation.10
Serotonin alters neuroplasticity. During development, 5-HT stimulates creation of new synapses and increases the density of synaptic webs. It has a direct stimulatory effect on the length of dendrites, their branching, and their myelination.11 In the CNS, it plays a role in dendritic arborization. Animal studies with rats have shown that lesioning highly concentrated 5-HT areas at early ages resulted in an adult brain with a lower number of neurons and a less complex web of dendrites.12,13 In situations of emotional stress, it is theorized that low levels of 5-HT lead to a reduced ability to deal with emotional stressors due to lower levels of complexity in synaptic connections.
Serotonin has also been implicated in mediating some aspects of dopamine-related actions, such as locomotion, reward, and threat avoidance. This is believed to contribute to the beneficial effect of 5-HT2A blockade by secondgeneration antipsychotics (SGAs).14 Blockade of other 5-HT receptors, such as 5-HT1A, 5-HT2C, 5-HT6, and 5-HT7, may also contribute to the antipsychotic action of SGAs.14
Serotonin receptors are found throughout the body, and 14 subtypes have been identified.9 Excitatory and inhibitory action of 5-HT depends on the receptor, and the actions of 5-HT can differ with the same receptor at different concentrations. This is because serotonin’s effects are biphasic and concentration-dependent, meaning that levels of 5-HT in the synapse will dictate the downstream effect of receptor agonism or antagonism. Animal models have shown that low-dose agonism of 5-HT receptors causes vasoconstriction of the coronary arteries, and high doses cause relaxation. This response has also been demonstrated in the vasculature of the kidneys and the smooth muscle of the trachea. Additionally, 5-HT works in conjunction with histamine to produce a biphasic response in the colonic arteries and veins in situations of endothelial damage.15
Most relevant to this discussion are 5-HT’s actions in mood regulation and behavior. Low 5-HT states result in less behavioral inhibition, leading to higher impulse control failures and aggression. Experiments in mice with deficient serotonergic brain regions show hypoactivity, extended daytime sleep, anxiety, and depressive behaviors.13 Serotonin’s behavioral effects are also biphasic. For example, lowdose antagonism with trazodone of 5-HT receptors demonstrated a pro-aggressive behavioral effect, while high-dose antagonism is anti-aggressive.15 Similar biphasic effects may result in either induction or reduction of anxiety with agents that block or excite certain 5-HT receptors.16-18
Continue to: A key difference: No motor system involvement...
A key difference: No motor system involvement
What distinguishes 5-HT from the other amine transmitters as a mediator of anxiety is the lack of involvement of the motor system. Multiple studies in rats illustrate that exogenously augmenting 5-HT has no effect on levels of locomotor activity. Dopamine depletion is well-characterized in the motor dysfunction of Parkinson’s disease, and DA excess can cause repetitive, stereotyped movements, such as seen in tardive dyskinesia or Huntington’s disease.8 In humans, serotonin-mediated anxiety is usually without a motoric component; patients appear calm but complain of extreme anxiety or agitation. Agitation has been reported after initiation of an SSRI,29 and is more likely to occur in patients with the short form of the 5-HT transporter.30 Motoric activation has been reported in some of these studies, but does not seem to cluster with the complaint of agitation.29 The reduced number of available transporters means a chronic steady-state elevation of serotonin, because less serotonin is being removed from the synapse after it is released. This is one of the reasons patients with the short form of the 5-HT transporter may be more susceptible to serotonin-mediated anxiety.
What you need to keep in mind
Pharmacologic treatment of anxiety begins with an SSRI, a serotonin-norepinephrine reuptake inhibitor (SNRI), or buspirone. Second-line treatments include hydroxyzine, gabapentin, pregabalin, and quetiapine.3,31 However, clinicians need to be aware that a fraction of their patients will report anxiety that will not have any external manifestations, but will be experienced as an unpleasant internal energy. These patients may report an increase in their anxiety levels when started on an SSRI or SNRI.29,30 This anxiety is most likely mediated by increases of synaptic 5-HT. This occurs because many serotonergic receptors may have a biphasic response, so that too much stimulation is experienced as excessive internal energy.16-18 In such patients, blockade of key 5-HT receptors may reduce that internal agitation. The advantage of recognizing serotonin-mediated anxiety is that one can specifically tailor treatment to address the patient’s specific physiology.
It is important to note that the anxiolytic effect of asenapine is specific to patients with serotonin-mediated anxiety. Unlike quetiapine, which is effective as augmentation therapy in generalized anxiety disorder,31 asenapine does not appear to reduce anxiety in patients with schizophrenia32 or borderline personality disorder33 when administered for other reasons. However, it may reduce anxiety in patients with the short form of the 5-HT transporter.30,34
Bottom Line
Serotonin-mediated anxiety occurs when levels of synaptic serotonin (5-HT) are high. Patients with serotonin-mediated anxiety appear calm but will report experiencing an unpleasant internal energy. Interventions that block multiple postsynaptic 5-HT receptors or discontinuation of a selective serotonin reuptake inhibitor (if applicable) will alleviate the anxiety.
Related Resource
• Bhatt NV. Anxiety disorders. https://emedicine.medscape. com/article/286227-overview
Drug Brand Names
Asenapine • Saphris, Secuado
Gabapentin • Neurontin
Hydroxyzine • Vistaril
Pregabalin • Lyrica
Quetiapine • Seroquel
Trazodone • Oleptro
1. Shelton CI. Diagnosis and management of anxiety disorders. J Am Osteopath Assoc. 2004;104(3 Suppl 3):S2-S5.
2. Ruscio AM, Hallion LS, Lim CCW, et al. Cross-sectional comparison of the epidemiology of DSM-5 generalized anxiety disorder across the globe. JAMA Psychiatry. 2017;74(5):465-475.
3. Locke AB, Kirst N, Shultz CG. Diagnosis and management of generalized anxiety disorder and panic disorder in adults. Am Fam Physician. 2015;91(9):617-624.
4. Hariri AR, Mattay VS, Tessitore A, et al. Dextroamphetamine modulates the response of the human amygdala. Neuropsychopharmacology. 2002;27(6):1036-1040.
5. Colombo AC, de Oliveira AR, Reimer AE, et al. Dopaminergic mechanisms underlying catalepsy, fear and anxiety: do they interact? Behav Brain Res. 2013;257:201-207.
6. Togay B, El-Mallakh RS. Posttraumatic stress disorder: from pathophysiology to pharmacology. Curr Psychiatry. 2020;19(5):33-39.
7. Provensi G, Passani MB, Costa A, et al. Neuronal histamine and the memory of emotionally salient events. Br J Pharmacol. 2020;177(3):557-569.
8. Purves D, Augustine GJ, Fitzpatrick D, et al (eds). Neuroscience. 2nd ed. Sinauer Associates; 2001.
9. Pytliak M, Vargová V, Mechírová V, et al. Serotonin receptors – from molecular biology to clinical applications. Physiol Res. 2011;60(1):15-25.
10. Meneses A, Liy-Salmeron G. Serotonin and emotion, learning and memory. Rev Neurosci. 2012;23(5-6):543-553.
11. Whitaker-Azmitia PM. Serotonin and brain development: role in human developmental diseases. Brain Res Bull. 2001;56(5):479-485.
12. Towle AC, Breese GR, Mueller RA, et al. Early postnatal administration of 5,7-DHT: effects on serotonergic neurons and terminals. Brain Res. 1984;310(1):67-75.
13. Rok-Bujko P, Krzs´cik P, Szyndler J, et al. The influence of neonatal serotonin depletion on emotional and exploratory behaviours in rats. Behav Brain Res. 2012;226(1):87-95.
14. Meltzer HY. The role of serotonin in antipsychotic drug action. Neuropsychopharmacology. 1999;21(2 Suppl):106S-115S.
15. Calabrese EJ. 5-Hydroxytryptamine (serotonin): biphasic dose responses. Crit Rev Toxicol. 2001;31(4-5):553-561.
16. Zuardi AW. 5-HT-related drugs and human experimental anxiety. Neurosci Biobehav Rev. 1990;14(4):507-510.
17. Sánchez C, Meier E. Behavioral profiles of SSRIs in animal models of depression, anxiety and aggression. Are they all alike? Psychopharmacology (Berl). 1997;129(3):197-205.
18. Koek W, Mitchell NC, Daws LC. Biphasic effects of selective serotonin reuptake inhibitors on anxiety: rapid reversal of escitalopram’s anxiogenic effects in the novelty-induced hypophagia test in mice? Behav Pharmacol. 2018;29(4):365-369.
19. van Zijderveld GA, Veltman DJ, van Dyck R, et al. Epinephrine-induced panic attacks and hyperventilation. J Psychiatr Res. 1999;33(1):73-78.
20. Ho EV, Thompson SL, Katzka WR, et al. Clinically effective OCD treatment prevents 5-HT1B receptor-induced repetitive behavior and striatal activation. Psychopharmacology (Berl). 2016;233(1):57-70.
21. Stein DJ, Costa DLC, Lochner C, et al. Obsessive-compulsive disorder. Nat Rev Dis Primers. 2019;5(1):52.
22. Luddington NS, Mandadapu A, Husk M, et al. Clinical implications of genetic variation in the serotonin transporter promoter region: a review. Prim Care Companion J Clin Psychiatry. 2009;11(3):93-102.
23. Stahl SM. Mechanism of action of serotonin selective reuptake inhibitors. Serotonin receptors and pathways mediate therapeutic effects and side effects. J Affect Disord. 1998;51(3):215-235.
24. Chaouloff F, Berton O, Mormède P. Serotonin and stress. Neuropsychopharmacology. 1999;21(2 Suppl):28S-32S.
25. Siafis S, Tzachanis D, Samara M, et al. Antipsychotic drugs: From receptor-binding profiles to metabolic side effects. Curr Neuropharmacol. 2018;16(8):1210-1223.
26. Carrithers B, El-Mallakh RS. Transdermal asenapine in schizophrenia: a systematic review. Patient Prefer Adherence. 2020;14:1541-1551.
27. Citrome L. Asenapine review, part I: chemistry, receptor affinity profile, pharmacokinetics and metabolism. Expert Opin Drug Metab Toxicol. 2014;10(6):893-903.
28. Pratts M, Citrome L, Grant W, et al. A single-dose, randomized, double-blind, placebo-controlled trial of sublingual asenapine for acute agitation. Acta Psychiatr Scand. 2014;130(1):61-68.
29. Biswas AB, Bhaumik S, Branford D. Treatment-emergent behavioural side effects with selective serotonin re-uptake inhibitors in adults with learning disabilities. Hum Psychopharmacol. 2001;16(2):133-137.
30. Perlis RH, Mischoulon D, Smoller JW, et al. Serotonin transporter polymorphisms and adverse effects with fluoxetine treatment. Biol Psychiatry. 2003;54(9):879-883.
31. Ipser JC, Carey P, Dhansay Y, et al. Pharmacotherapy augmentation strategies in treatment-resistant anxiety disorders. Cochrane Database Syst Rev. 2006;(4):CD005473.
32. Kane JM, Mackle M, Snow-Adami L, et al. A randomized placebo-controlled trial of asenapine for the prevention of relapse of schizophrenia after long-term treatment. J Clin Psychiatry. 2011;72(3):349-355.
33. Bozzatello P, Rocca P, Uscinska M, et al. Efficacy and tolerability of asenapine compared with olanzapine in borderline personality disorder: an open-label randomized controlled trial. CNS Drugs. 2017;31(9):809-819.
34. El-Mallakh RS, Nuss S, Gao D, et al. Asenapine in the treatment of bipolar depression. Psychopharmacol Bull. 2020;50(1):8-18.
1. Shelton CI. Diagnosis and management of anxiety disorders. J Am Osteopath Assoc. 2004;104(3 Suppl 3):S2-S5.
2. Ruscio AM, Hallion LS, Lim CCW, et al. Cross-sectional comparison of the epidemiology of DSM-5 generalized anxiety disorder across the globe. JAMA Psychiatry. 2017;74(5):465-475.
3. Locke AB, Kirst N, Shultz CG. Diagnosis and management of generalized anxiety disorder and panic disorder in adults. Am Fam Physician. 2015;91(9):617-624.
4. Hariri AR, Mattay VS, Tessitore A, et al. Dextroamphetamine modulates the response of the human amygdala. Neuropsychopharmacology. 2002;27(6):1036-1040.
5. Colombo AC, de Oliveira AR, Reimer AE, et al. Dopaminergic mechanisms underlying catalepsy, fear and anxiety: do they interact? Behav Brain Res. 2013;257:201-207.
6. Togay B, El-Mallakh RS. Posttraumatic stress disorder: from pathophysiology to pharmacology. Curr Psychiatry. 2020;19(5):33-39.
7. Provensi G, Passani MB, Costa A, et al. Neuronal histamine and the memory of emotionally salient events. Br J Pharmacol. 2020;177(3):557-569.
8. Purves D, Augustine GJ, Fitzpatrick D, et al (eds). Neuroscience. 2nd ed. Sinauer Associates; 2001.
9. Pytliak M, Vargová V, Mechírová V, et al. Serotonin receptors – from molecular biology to clinical applications. Physiol Res. 2011;60(1):15-25.
10. Meneses A, Liy-Salmeron G. Serotonin and emotion, learning and memory. Rev Neurosci. 2012;23(5-6):543-553.
11. Whitaker-Azmitia PM. Serotonin and brain development: role in human developmental diseases. Brain Res Bull. 2001;56(5):479-485.
12. Towle AC, Breese GR, Mueller RA, et al. Early postnatal administration of 5,7-DHT: effects on serotonergic neurons and terminals. Brain Res. 1984;310(1):67-75.
13. Rok-Bujko P, Krzs´cik P, Szyndler J, et al. The influence of neonatal serotonin depletion on emotional and exploratory behaviours in rats. Behav Brain Res. 2012;226(1):87-95.
14. Meltzer HY. The role of serotonin in antipsychotic drug action. Neuropsychopharmacology. 1999;21(2 Suppl):106S-115S.
15. Calabrese EJ. 5-Hydroxytryptamine (serotonin): biphasic dose responses. Crit Rev Toxicol. 2001;31(4-5):553-561.
16. Zuardi AW. 5-HT-related drugs and human experimental anxiety. Neurosci Biobehav Rev. 1990;14(4):507-510.
17. Sánchez C, Meier E. Behavioral profiles of SSRIs in animal models of depression, anxiety and aggression. Are they all alike? Psychopharmacology (Berl). 1997;129(3):197-205.
18. Koek W, Mitchell NC, Daws LC. Biphasic effects of selective serotonin reuptake inhibitors on anxiety: rapid reversal of escitalopram’s anxiogenic effects in the novelty-induced hypophagia test in mice? Behav Pharmacol. 2018;29(4):365-369.
19. van Zijderveld GA, Veltman DJ, van Dyck R, et al. Epinephrine-induced panic attacks and hyperventilation. J Psychiatr Res. 1999;33(1):73-78.
20. Ho EV, Thompson SL, Katzka WR, et al. Clinically effective OCD treatment prevents 5-HT1B receptor-induced repetitive behavior and striatal activation. Psychopharmacology (Berl). 2016;233(1):57-70.
21. Stein DJ, Costa DLC, Lochner C, et al. Obsessive-compulsive disorder. Nat Rev Dis Primers. 2019;5(1):52.
22. Luddington NS, Mandadapu A, Husk M, et al. Clinical implications of genetic variation in the serotonin transporter promoter region: a review. Prim Care Companion J Clin Psychiatry. 2009;11(3):93-102.
23. Stahl SM. Mechanism of action of serotonin selective reuptake inhibitors. Serotonin receptors and pathways mediate therapeutic effects and side effects. J Affect Disord. 1998;51(3):215-235.
24. Chaouloff F, Berton O, Mormède P. Serotonin and stress. Neuropsychopharmacology. 1999;21(2 Suppl):28S-32S.
25. Siafis S, Tzachanis D, Samara M, et al. Antipsychotic drugs: From receptor-binding profiles to metabolic side effects. Curr Neuropharmacol. 2018;16(8):1210-1223.
26. Carrithers B, El-Mallakh RS. Transdermal asenapine in schizophrenia: a systematic review. Patient Prefer Adherence. 2020;14:1541-1551.
27. Citrome L. Asenapine review, part I: chemistry, receptor affinity profile, pharmacokinetics and metabolism. Expert Opin Drug Metab Toxicol. 2014;10(6):893-903.
28. Pratts M, Citrome L, Grant W, et al. A single-dose, randomized, double-blind, placebo-controlled trial of sublingual asenapine for acute agitation. Acta Psychiatr Scand. 2014;130(1):61-68.
29. Biswas AB, Bhaumik S, Branford D. Treatment-emergent behavioural side effects with selective serotonin re-uptake inhibitors in adults with learning disabilities. Hum Psychopharmacol. 2001;16(2):133-137.
30. Perlis RH, Mischoulon D, Smoller JW, et al. Serotonin transporter polymorphisms and adverse effects with fluoxetine treatment. Biol Psychiatry. 2003;54(9):879-883.
31. Ipser JC, Carey P, Dhansay Y, et al. Pharmacotherapy augmentation strategies in treatment-resistant anxiety disorders. Cochrane Database Syst Rev. 2006;(4):CD005473.
32. Kane JM, Mackle M, Snow-Adami L, et al. A randomized placebo-controlled trial of asenapine for the prevention of relapse of schizophrenia after long-term treatment. J Clin Psychiatry. 2011;72(3):349-355.
33. Bozzatello P, Rocca P, Uscinska M, et al. Efficacy and tolerability of asenapine compared with olanzapine in borderline personality disorder: an open-label randomized controlled trial. CNS Drugs. 2017;31(9):809-819.
34. El-Mallakh RS, Nuss S, Gao D, et al. Asenapine in the treatment of bipolar depression. Psychopharmacol Bull. 2020;50(1):8-18.
Dealing with a difficult boss: A ‘bossectomy’ is rarely the cure
Ms. D is a 48-year-old administrative assistant and married mother of 2 teenagers with a history of adjustment disorder with mixed anxiety and depressed mood. She presents with increasing anxiety, poor sleep, irritability, and occasional feelings of hopelessness in the context of feeling stuck in a “dead-end job.” She describes her main issue as having an uncaring boss with unrealistic expectations. Clearly exasperated, she tells you, “If only I could get rid of my boss, everything would be just fine.”
Ms. D’s situation is common. When confronted with overbearing and demanding supervisors, the natural inclination for some employees is to flee. Symptoms of burnout (eg, emotional exhaustion, depersonalization, and decreased personal accomplishment) often occur, sometimes with more serious symptoms of adjustment disorder or even major depressive disorder or generalized anxiety disorder. To help patients such as Ms. D who are experiencing difficulties with their boss, you can use a simple approach aimed at helping them make the decision to stay at the job or leave for other opportunities, while supporting them along the way.
Clarify, then support and explore
A critical addition to the typical evaluation is a full social history, including prior employment and formative relationships, that may inform current workplace dynamics. Does the patient have a pattern of similar circumstances, or is this unusual for her? How does she view the supervisor-employee relationship, and how do power differentials, potential job loss, and subsequent financial impacts further amplify emotional friction?
Once the dynamics are clarified, support and validate her emotional reaction before exploring potential cognitive distortions and her own contributions to the relationship dysfunction. If her tendency is to lash out in anger, she could fan the flames and risk being fired. If her tendency is to cower or freeze, you can help to gradually empower her. Regardless of relationship dynamics, be careful not to medicalize what may simply be a difficult situation.1 Perhaps she is a perfectionist and minimizes her supervisor’s behaviors that affirm her work and value as a person. In such cases, you can use cognitive-behavioral therapy techniques to help her consider different points of view and nuance. Rarely are people all good or all bad.
Perhaps her perceptions are accurate, and her boss really is a jerk. If this is the case, she likely feels unfairly and helplessly persecuted. She may be suffering from demoralization, or feelings of impotence, isolation, and despair in which her self-esteem is damaged and she feels rejected because of her failure to meet her boss’s and her own expectations.2 In cases of demoralization, oddly enough, hospice literature lends some tools to help her. The Table3 provides some common terms associated with demoralization and discussion points you can use to help her move toward “remoralization.”
Regardless of the full story, it’s common for people to externalize uncomfortable emotions and attribute symptoms to an external cause. Help her develop self-efficacy by realizing she is in control of how she responds to her emotions. Have her focus on her role in the relationship with her supervisor, looking for common ground and brainstorming practical solutions. Ultimately you can help her realize that she always has choices about whether to stay at the job or look for work elsewhere. Your role is to support her regardless of her decision.
CASE CONTINUED
Over several visits, Ms. D begins to view the relationship with her supervisor in a different light. She has a conversation with him about what she needs to do personally and what she needs professionally from him to be successful at work. Her supervisor acknowledges he has been demanding and could be more supportive. Together they vow to communicate more clearly and regularly assess progress, including celebrating clear victories. Ms. D ultimately decides to stay at the job, and her symptoms resolve without a “bossectomy.”
1. Jurisic M, Bean M, Harbaugh J, et al. The personal physician’s role in helping patients with medical conditions stay at work or return to work. J Occup Environ Med. 2017;59(6):e125-e131.
2. Frank JD. Psychotherapy: the restoration of morale. Am J Psychiatry. 1974;131(3):271-274.
3. Griffith JL, Gaby L. Brief psychotherapy at the bedside: countering demoralization from medical illness. Psychosomatics. 2005;46(2):109-116.
Ms. D is a 48-year-old administrative assistant and married mother of 2 teenagers with a history of adjustment disorder with mixed anxiety and depressed mood. She presents with increasing anxiety, poor sleep, irritability, and occasional feelings of hopelessness in the context of feeling stuck in a “dead-end job.” She describes her main issue as having an uncaring boss with unrealistic expectations. Clearly exasperated, she tells you, “If only I could get rid of my boss, everything would be just fine.”
Ms. D’s situation is common. When confronted with overbearing and demanding supervisors, the natural inclination for some employees is to flee. Symptoms of burnout (eg, emotional exhaustion, depersonalization, and decreased personal accomplishment) often occur, sometimes with more serious symptoms of adjustment disorder or even major depressive disorder or generalized anxiety disorder. To help patients such as Ms. D who are experiencing difficulties with their boss, you can use a simple approach aimed at helping them make the decision to stay at the job or leave for other opportunities, while supporting them along the way.
Clarify, then support and explore
A critical addition to the typical evaluation is a full social history, including prior employment and formative relationships, that may inform current workplace dynamics. Does the patient have a pattern of similar circumstances, or is this unusual for her? How does she view the supervisor-employee relationship, and how do power differentials, potential job loss, and subsequent financial impacts further amplify emotional friction?
Once the dynamics are clarified, support and validate her emotional reaction before exploring potential cognitive distortions and her own contributions to the relationship dysfunction. If her tendency is to lash out in anger, she could fan the flames and risk being fired. If her tendency is to cower or freeze, you can help to gradually empower her. Regardless of relationship dynamics, be careful not to medicalize what may simply be a difficult situation.1 Perhaps she is a perfectionist and minimizes her supervisor’s behaviors that affirm her work and value as a person. In such cases, you can use cognitive-behavioral therapy techniques to help her consider different points of view and nuance. Rarely are people all good or all bad.
Perhaps her perceptions are accurate, and her boss really is a jerk. If this is the case, she likely feels unfairly and helplessly persecuted. She may be suffering from demoralization, or feelings of impotence, isolation, and despair in which her self-esteem is damaged and she feels rejected because of her failure to meet her boss’s and her own expectations.2 In cases of demoralization, oddly enough, hospice literature lends some tools to help her. The Table3 provides some common terms associated with demoralization and discussion points you can use to help her move toward “remoralization.”
Regardless of the full story, it’s common for people to externalize uncomfortable emotions and attribute symptoms to an external cause. Help her develop self-efficacy by realizing she is in control of how she responds to her emotions. Have her focus on her role in the relationship with her supervisor, looking for common ground and brainstorming practical solutions. Ultimately you can help her realize that she always has choices about whether to stay at the job or look for work elsewhere. Your role is to support her regardless of her decision.
CASE CONTINUED
Over several visits, Ms. D begins to view the relationship with her supervisor in a different light. She has a conversation with him about what she needs to do personally and what she needs professionally from him to be successful at work. Her supervisor acknowledges he has been demanding and could be more supportive. Together they vow to communicate more clearly and regularly assess progress, including celebrating clear victories. Ms. D ultimately decides to stay at the job, and her symptoms resolve without a “bossectomy.”
Ms. D is a 48-year-old administrative assistant and married mother of 2 teenagers with a history of adjustment disorder with mixed anxiety and depressed mood. She presents with increasing anxiety, poor sleep, irritability, and occasional feelings of hopelessness in the context of feeling stuck in a “dead-end job.” She describes her main issue as having an uncaring boss with unrealistic expectations. Clearly exasperated, she tells you, “If only I could get rid of my boss, everything would be just fine.”
Ms. D’s situation is common. When confronted with overbearing and demanding supervisors, the natural inclination for some employees is to flee. Symptoms of burnout (eg, emotional exhaustion, depersonalization, and decreased personal accomplishment) often occur, sometimes with more serious symptoms of adjustment disorder or even major depressive disorder or generalized anxiety disorder. To help patients such as Ms. D who are experiencing difficulties with their boss, you can use a simple approach aimed at helping them make the decision to stay at the job or leave for other opportunities, while supporting them along the way.
Clarify, then support and explore
A critical addition to the typical evaluation is a full social history, including prior employment and formative relationships, that may inform current workplace dynamics. Does the patient have a pattern of similar circumstances, or is this unusual for her? How does she view the supervisor-employee relationship, and how do power differentials, potential job loss, and subsequent financial impacts further amplify emotional friction?
Once the dynamics are clarified, support and validate her emotional reaction before exploring potential cognitive distortions and her own contributions to the relationship dysfunction. If her tendency is to lash out in anger, she could fan the flames and risk being fired. If her tendency is to cower or freeze, you can help to gradually empower her. Regardless of relationship dynamics, be careful not to medicalize what may simply be a difficult situation.1 Perhaps she is a perfectionist and minimizes her supervisor’s behaviors that affirm her work and value as a person. In such cases, you can use cognitive-behavioral therapy techniques to help her consider different points of view and nuance. Rarely are people all good or all bad.
Perhaps her perceptions are accurate, and her boss really is a jerk. If this is the case, she likely feels unfairly and helplessly persecuted. She may be suffering from demoralization, or feelings of impotence, isolation, and despair in which her self-esteem is damaged and she feels rejected because of her failure to meet her boss’s and her own expectations.2 In cases of demoralization, oddly enough, hospice literature lends some tools to help her. The Table3 provides some common terms associated with demoralization and discussion points you can use to help her move toward “remoralization.”
Regardless of the full story, it’s common for people to externalize uncomfortable emotions and attribute symptoms to an external cause. Help her develop self-efficacy by realizing she is in control of how she responds to her emotions. Have her focus on her role in the relationship with her supervisor, looking for common ground and brainstorming practical solutions. Ultimately you can help her realize that she always has choices about whether to stay at the job or look for work elsewhere. Your role is to support her regardless of her decision.
CASE CONTINUED
Over several visits, Ms. D begins to view the relationship with her supervisor in a different light. She has a conversation with him about what she needs to do personally and what she needs professionally from him to be successful at work. Her supervisor acknowledges he has been demanding and could be more supportive. Together they vow to communicate more clearly and regularly assess progress, including celebrating clear victories. Ms. D ultimately decides to stay at the job, and her symptoms resolve without a “bossectomy.”
1. Jurisic M, Bean M, Harbaugh J, et al. The personal physician’s role in helping patients with medical conditions stay at work or return to work. J Occup Environ Med. 2017;59(6):e125-e131.
2. Frank JD. Psychotherapy: the restoration of morale. Am J Psychiatry. 1974;131(3):271-274.
3. Griffith JL, Gaby L. Brief psychotherapy at the bedside: countering demoralization from medical illness. Psychosomatics. 2005;46(2):109-116.
1. Jurisic M, Bean M, Harbaugh J, et al. The personal physician’s role in helping patients with medical conditions stay at work or return to work. J Occup Environ Med. 2017;59(6):e125-e131.
2. Frank JD. Psychotherapy: the restoration of morale. Am J Psychiatry. 1974;131(3):271-274.
3. Griffith JL, Gaby L. Brief psychotherapy at the bedside: countering demoralization from medical illness. Psychosomatics. 2005;46(2):109-116.
ERs are swamped with seriously ill patients, although many don’t have COVID
Inside the emergency department at Sparrow Hospital in Lansing, Mich., staff members are struggling to care for patients showing up much sicker than they’ve ever seen.
Tiffani Dusang, the ER’s nursing director, practically vibrates with pent-up anxiety, looking at patients lying on a long line of stretchers pushed up against the beige walls of the hospital hallways. “It’s hard to watch,” she said in a warm Texas twang.
But there’s nothing she can do. The ER’s 72 rooms are already filled.
“I always feel very, very bad when I walk down the hallway and see that people are in pain, or needing to sleep, or needing quiet. But they have to be in the hallway with, as you can see, 10 or 15 people walking by every minute,” Ms. Dusang said.
The scene is a stark contrast to where this emergency department — and thousands of others — were at the start of the pandemic. Except for initial hot spots like New York City, in spring 2020 many ERs across the country were often eerily empty. Terrified of contracting COVID-19, people who were sick with other things did their best to stay away from hospitals. Visits to emergency rooms dropped to half their typical levels, according to the Epic Health Research Network, and didn’t fully rebound until this summer.
But now, they’re too full.
Months of treatment delays have exacerbated chronic conditions and worsened symptoms. Doctors and nurses say the severity of illness ranges widely and includes abdominal pain, respiratory problems, blood clots, heart conditions and suicide attempts, among other conditions.
But they can hardly be accommodated. Emergency departments, ideally, are meant to be brief ports in a storm, with patients staying just long enough to be sent home with instructions to follow up with primary care physicians, or sufficiently stabilized to be transferred “upstairs” to inpatient or intensive care units.
Except now those long-term care floors are full too, with a mix of covid and non-covid patients. People coming to the ER get warehoused for hours, even days, forcing ER staffers to perform long-term care roles they weren’t trained to do.
At Sparrow, space is a valuable commodity in the ER: A separate section of the hospital was turned into an overflow unit. Stretchers stack up in halls. A row of brown reclining chairs lines a wall, intended for patients who aren’t sick enough for a stretcher but are too sick to stay in the main waiting room.
Forget privacy, Alejos Perrientoz learned when he arrived. He came to the ER because his arm had been tingling and painful for over a week. He couldn’t hold a cup of coffee. A nurse gave him a full physical exam in a brown recliner, which made him self-conscious about having his shirt lifted in front of strangers. “I felt a little uncomfortable,” he whispered. “But I have no choice, you know? I’m in the hallway. There’s no rooms.
“We could have done the physical in the parking lot,” he added, managing a laugh.
Even patients who arrive by ambulance are not guaranteed a room: One nurse runs triage, screening those who absolutely need a bed, and those who can be put in the waiting area.
“I hate that we even have to make that determination,” MS. Dusang said. Lately, staff members have been pulling out some patients already in the ER’s rooms when others arrive who are more critically ill. “No one likes to take someone out of the privacy of their room and say, ‘We’re going to put you in a hallway because we need to get care to someone else.’”
ER patients have grown sicker
“We are hearing from members in every part of the country,” said Dr. Lisa Moreno, president of the American Academy of Emergency Medicine. “The Midwest, the South, the Northeast, the West … they are seeing this exact same phenomenon.”
Although the number of ER visits returned to pre-COVID levels this summer, admission rates, from the ER to the hospital’s inpatient floors, are still almost 20% higher. That’s according to the most recent analysis by the Epic Health Research Network, which pulls data from more than 120 million patients across the country.
“It’s an early indicator that what’s happening in the ED is that we’re seeing more acute cases than we were pre-pandemic,” said Caleb Cox, a data scientist at Epic.
Less acute cases, such as people with health issues like rashes or conjunctivitis, still aren’t going to the ER as much as they used to. Instead, they may be opting for an urgent care center or their primary care doctor, Mr. Cox explained. Meanwhile, there has been an increase in people coming to the ER with more serious conditions, like strokes and heart attacks.
So, even though the total number of patients coming to ERs is about the same as before the pandemic, “that’s absolutely going to feel like [if I’m an ER doctor or nurse] I’m seeing more patients and I’m seeing more acute patients,” Mr. Cox said.
Dr. Moreno, the AAEM president, works at an emergency department in New Orleans. She said the level of illness, and the inability to admit patients quickly and move them to beds upstairs, has created a level of chaos she described as “not even humane.”
At the beginning of a recent shift, she heard a patient crying nearby and went to investigate. It was a paraplegic man who’d recently had surgery for colon cancer. His large post-operative wound was sealed with a device called a wound vac, which pulls fluid from the wound into a drainage tube attached to a portable vacuum pump.
But the wound vac had malfunctioned, which is why he had come to the ER. Staffers were so busy, however, that by the time Dr. Moreno came in, the fluid from his wound was leaking everywhere.
“When I went in, the bed was covered,” she recalled. “I mean, he was lying in a puddle of secretions from this wound. And he was crying, because he said to me, ‘I’m paralyzed. I can’t move to get away from all these secretions, and I know I’m going to end up getting an infection. I know I’m going to end up getting an ulcer. I’ve been laying in this for, like, eight or nine hours.’”
The nurse in charge of his care told Dr. Moreno she simply hadn’t had time to help this patient yet. “She said, ‘I’ve had so many patients to take care of, and so many critical patients. I started [an IV] drip on this person. This person is on a cardiac monitor. I just didn’t have time to get in there.’”
“This is not humane care,” Dr. Moreno said. “This is horrible care.”
But it’s what can happen when emergency department staffers don’t have the resources they need to deal with the onslaught of competing demands.
“All the nurses and doctors had the highest level of intent to do the right thing for the person,” Dr. Moreno said. “But because of the high acuity of … a large number of patients, the staffing ratio of nurse to patient, even the staffing ratio of doctor to patient, this guy did not get the care that he deserved to get, just as a human being.”
The instance of unintended neglect that Dr. Moreno saw is extreme, and not the experience of most patients who arrive at ERs these days. But the problem is not new: Even before the pandemic, ER overcrowding had been a “widespread problem and a source of patient harm, according to a recent commentary in NEJM Catalyst Innovations in Care Delivery.
“ED crowding is not an issue of inconvenience,” the authors wrote. “There is incontrovertible evidence that ED crowding leads to significant patient harm, including morbidity and mortality related to consequential delays of treatment for both high- and low-acuity patients.”
And already-overwhelmed staffers are burning out.
Burnout feeds staffing shortages, and vice versa
Every morning, Tiffani Dusang wakes up and checks her Sparrow email with one singular hope: that she will not see yet another nurse resignation letter in her inbox.
“I cannot tell you how many of them [the nurses] tell me they went home crying” after their shifts, she said.
Despite Ms. Dusang’s best efforts to support her staffers, they’re leaving too fast to be replaced, either to take higher-paying gigs as a travel nurse, to try a less-stressful type of nursing, or simply walking away from the profession entirely.
Kelly Spitz has been an emergency department nurse at Sparrow for 10 years. But, lately, she has also fantasized about leaving. “It has crossed my mind several times,” she said, and yet she continues to come back. “Because I have a team here. And I love what I do.” But then she started to cry. The issue is not the hard work, or even the stress. She struggles with not being able to give her patients the kind of care and attention she wants to give them, and that they need and deserve, she said.
She often thinks about a patient whose test results revealed terminal cancer, she said. Ms. Spitz spent all day working the phones, hustling case managers, trying to get hospice care set up in the man’s home. He was going to die, and she just didn’t want him to have to die in the hospital, where only one visitor was allowed. She wanted to get him home, and back with his family.
Finally, after many hours, they found an ambulance to take him home.
Three days later, the man’s family members called Ms. Spitz: He had died surrounded by family. They were calling to thank her.
“I felt like I did my job there, because I got him home,” she said. But that’s a rare feeling these days. “I just hope it gets better. I hope it gets better soon.”
Around 4 p.m. at Sparrow Hospital as one shift approached its end, Ms. Dusang faced a new crisis: The overnight shift was more short-staffed than usual.
“Can we get two inpatient nurses?” she asked, hoping to borrow two nurses from one of the hospital floors upstairs.
“Already tried,” replied nurse Troy Latunski.
Without more staff, it’s going to be hard to care for new patients who come in overnight — from car crashes to seizures or other emergencies.
But Mr. Latunski had a plan: He would go home, snatch a few hours of sleep and return at 11 p.m. to work the overnight shift in the ER’s overflow unit. That meant he would be largely caring for eight patients, alone. On just a few short hours of sleep. But lately that seemed to be their only, and best, option.
Ms. Dusang considered for a moment, took a deep breath and nodded. “OK,” she said.
“Go home. Get some sleep. Thank you,” she added, shooting Mr. Latunski a grateful smile. And then she pivoted, because another nurse was approaching with an urgent question. On to the next crisis.
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation. This story is part of a partnership that includes Michigan Radio, NPR and KHN.
Inside the emergency department at Sparrow Hospital in Lansing, Mich., staff members are struggling to care for patients showing up much sicker than they’ve ever seen.
Tiffani Dusang, the ER’s nursing director, practically vibrates with pent-up anxiety, looking at patients lying on a long line of stretchers pushed up against the beige walls of the hospital hallways. “It’s hard to watch,” she said in a warm Texas twang.
But there’s nothing she can do. The ER’s 72 rooms are already filled.
“I always feel very, very bad when I walk down the hallway and see that people are in pain, or needing to sleep, or needing quiet. But they have to be in the hallway with, as you can see, 10 or 15 people walking by every minute,” Ms. Dusang said.
The scene is a stark contrast to where this emergency department — and thousands of others — were at the start of the pandemic. Except for initial hot spots like New York City, in spring 2020 many ERs across the country were often eerily empty. Terrified of contracting COVID-19, people who were sick with other things did their best to stay away from hospitals. Visits to emergency rooms dropped to half their typical levels, according to the Epic Health Research Network, and didn’t fully rebound until this summer.
But now, they’re too full.
Months of treatment delays have exacerbated chronic conditions and worsened symptoms. Doctors and nurses say the severity of illness ranges widely and includes abdominal pain, respiratory problems, blood clots, heart conditions and suicide attempts, among other conditions.
But they can hardly be accommodated. Emergency departments, ideally, are meant to be brief ports in a storm, with patients staying just long enough to be sent home with instructions to follow up with primary care physicians, or sufficiently stabilized to be transferred “upstairs” to inpatient or intensive care units.
Except now those long-term care floors are full too, with a mix of covid and non-covid patients. People coming to the ER get warehoused for hours, even days, forcing ER staffers to perform long-term care roles they weren’t trained to do.
At Sparrow, space is a valuable commodity in the ER: A separate section of the hospital was turned into an overflow unit. Stretchers stack up in halls. A row of brown reclining chairs lines a wall, intended for patients who aren’t sick enough for a stretcher but are too sick to stay in the main waiting room.
Forget privacy, Alejos Perrientoz learned when he arrived. He came to the ER because his arm had been tingling and painful for over a week. He couldn’t hold a cup of coffee. A nurse gave him a full physical exam in a brown recliner, which made him self-conscious about having his shirt lifted in front of strangers. “I felt a little uncomfortable,” he whispered. “But I have no choice, you know? I’m in the hallway. There’s no rooms.
“We could have done the physical in the parking lot,” he added, managing a laugh.
Even patients who arrive by ambulance are not guaranteed a room: One nurse runs triage, screening those who absolutely need a bed, and those who can be put in the waiting area.
“I hate that we even have to make that determination,” MS. Dusang said. Lately, staff members have been pulling out some patients already in the ER’s rooms when others arrive who are more critically ill. “No one likes to take someone out of the privacy of their room and say, ‘We’re going to put you in a hallway because we need to get care to someone else.’”
ER patients have grown sicker
“We are hearing from members in every part of the country,” said Dr. Lisa Moreno, president of the American Academy of Emergency Medicine. “The Midwest, the South, the Northeast, the West … they are seeing this exact same phenomenon.”
Although the number of ER visits returned to pre-COVID levels this summer, admission rates, from the ER to the hospital’s inpatient floors, are still almost 20% higher. That’s according to the most recent analysis by the Epic Health Research Network, which pulls data from more than 120 million patients across the country.
“It’s an early indicator that what’s happening in the ED is that we’re seeing more acute cases than we were pre-pandemic,” said Caleb Cox, a data scientist at Epic.
Less acute cases, such as people with health issues like rashes or conjunctivitis, still aren’t going to the ER as much as they used to. Instead, they may be opting for an urgent care center or their primary care doctor, Mr. Cox explained. Meanwhile, there has been an increase in people coming to the ER with more serious conditions, like strokes and heart attacks.
So, even though the total number of patients coming to ERs is about the same as before the pandemic, “that’s absolutely going to feel like [if I’m an ER doctor or nurse] I’m seeing more patients and I’m seeing more acute patients,” Mr. Cox said.
Dr. Moreno, the AAEM president, works at an emergency department in New Orleans. She said the level of illness, and the inability to admit patients quickly and move them to beds upstairs, has created a level of chaos she described as “not even humane.”
At the beginning of a recent shift, she heard a patient crying nearby and went to investigate. It was a paraplegic man who’d recently had surgery for colon cancer. His large post-operative wound was sealed with a device called a wound vac, which pulls fluid from the wound into a drainage tube attached to a portable vacuum pump.
But the wound vac had malfunctioned, which is why he had come to the ER. Staffers were so busy, however, that by the time Dr. Moreno came in, the fluid from his wound was leaking everywhere.
“When I went in, the bed was covered,” she recalled. “I mean, he was lying in a puddle of secretions from this wound. And he was crying, because he said to me, ‘I’m paralyzed. I can’t move to get away from all these secretions, and I know I’m going to end up getting an infection. I know I’m going to end up getting an ulcer. I’ve been laying in this for, like, eight or nine hours.’”
The nurse in charge of his care told Dr. Moreno she simply hadn’t had time to help this patient yet. “She said, ‘I’ve had so many patients to take care of, and so many critical patients. I started [an IV] drip on this person. This person is on a cardiac monitor. I just didn’t have time to get in there.’”
“This is not humane care,” Dr. Moreno said. “This is horrible care.”
But it’s what can happen when emergency department staffers don’t have the resources they need to deal with the onslaught of competing demands.
“All the nurses and doctors had the highest level of intent to do the right thing for the person,” Dr. Moreno said. “But because of the high acuity of … a large number of patients, the staffing ratio of nurse to patient, even the staffing ratio of doctor to patient, this guy did not get the care that he deserved to get, just as a human being.”
The instance of unintended neglect that Dr. Moreno saw is extreme, and not the experience of most patients who arrive at ERs these days. But the problem is not new: Even before the pandemic, ER overcrowding had been a “widespread problem and a source of patient harm, according to a recent commentary in NEJM Catalyst Innovations in Care Delivery.
“ED crowding is not an issue of inconvenience,” the authors wrote. “There is incontrovertible evidence that ED crowding leads to significant patient harm, including morbidity and mortality related to consequential delays of treatment for both high- and low-acuity patients.”
And already-overwhelmed staffers are burning out.
Burnout feeds staffing shortages, and vice versa
Every morning, Tiffani Dusang wakes up and checks her Sparrow email with one singular hope: that she will not see yet another nurse resignation letter in her inbox.
“I cannot tell you how many of them [the nurses] tell me they went home crying” after their shifts, she said.
Despite Ms. Dusang’s best efforts to support her staffers, they’re leaving too fast to be replaced, either to take higher-paying gigs as a travel nurse, to try a less-stressful type of nursing, or simply walking away from the profession entirely.
Kelly Spitz has been an emergency department nurse at Sparrow for 10 years. But, lately, she has also fantasized about leaving. “It has crossed my mind several times,” she said, and yet she continues to come back. “Because I have a team here. And I love what I do.” But then she started to cry. The issue is not the hard work, or even the stress. She struggles with not being able to give her patients the kind of care and attention she wants to give them, and that they need and deserve, she said.
She often thinks about a patient whose test results revealed terminal cancer, she said. Ms. Spitz spent all day working the phones, hustling case managers, trying to get hospice care set up in the man’s home. He was going to die, and she just didn’t want him to have to die in the hospital, where only one visitor was allowed. She wanted to get him home, and back with his family.
Finally, after many hours, they found an ambulance to take him home.
Three days later, the man’s family members called Ms. Spitz: He had died surrounded by family. They were calling to thank her.
“I felt like I did my job there, because I got him home,” she said. But that’s a rare feeling these days. “I just hope it gets better. I hope it gets better soon.”
Around 4 p.m. at Sparrow Hospital as one shift approached its end, Ms. Dusang faced a new crisis: The overnight shift was more short-staffed than usual.
“Can we get two inpatient nurses?” she asked, hoping to borrow two nurses from one of the hospital floors upstairs.
“Already tried,” replied nurse Troy Latunski.
Without more staff, it’s going to be hard to care for new patients who come in overnight — from car crashes to seizures or other emergencies.
But Mr. Latunski had a plan: He would go home, snatch a few hours of sleep and return at 11 p.m. to work the overnight shift in the ER’s overflow unit. That meant he would be largely caring for eight patients, alone. On just a few short hours of sleep. But lately that seemed to be their only, and best, option.
Ms. Dusang considered for a moment, took a deep breath and nodded. “OK,” she said.
“Go home. Get some sleep. Thank you,” she added, shooting Mr. Latunski a grateful smile. And then she pivoted, because another nurse was approaching with an urgent question. On to the next crisis.
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation. This story is part of a partnership that includes Michigan Radio, NPR and KHN.
Inside the emergency department at Sparrow Hospital in Lansing, Mich., staff members are struggling to care for patients showing up much sicker than they’ve ever seen.
Tiffani Dusang, the ER’s nursing director, practically vibrates with pent-up anxiety, looking at patients lying on a long line of stretchers pushed up against the beige walls of the hospital hallways. “It’s hard to watch,” she said in a warm Texas twang.
But there’s nothing she can do. The ER’s 72 rooms are already filled.
“I always feel very, very bad when I walk down the hallway and see that people are in pain, or needing to sleep, or needing quiet. But they have to be in the hallway with, as you can see, 10 or 15 people walking by every minute,” Ms. Dusang said.
The scene is a stark contrast to where this emergency department — and thousands of others — were at the start of the pandemic. Except for initial hot spots like New York City, in spring 2020 many ERs across the country were often eerily empty. Terrified of contracting COVID-19, people who were sick with other things did their best to stay away from hospitals. Visits to emergency rooms dropped to half their typical levels, according to the Epic Health Research Network, and didn’t fully rebound until this summer.
But now, they’re too full.
Months of treatment delays have exacerbated chronic conditions and worsened symptoms. Doctors and nurses say the severity of illness ranges widely and includes abdominal pain, respiratory problems, blood clots, heart conditions and suicide attempts, among other conditions.
But they can hardly be accommodated. Emergency departments, ideally, are meant to be brief ports in a storm, with patients staying just long enough to be sent home with instructions to follow up with primary care physicians, or sufficiently stabilized to be transferred “upstairs” to inpatient or intensive care units.
Except now those long-term care floors are full too, with a mix of covid and non-covid patients. People coming to the ER get warehoused for hours, even days, forcing ER staffers to perform long-term care roles they weren’t trained to do.
At Sparrow, space is a valuable commodity in the ER: A separate section of the hospital was turned into an overflow unit. Stretchers stack up in halls. A row of brown reclining chairs lines a wall, intended for patients who aren’t sick enough for a stretcher but are too sick to stay in the main waiting room.
Forget privacy, Alejos Perrientoz learned when he arrived. He came to the ER because his arm had been tingling and painful for over a week. He couldn’t hold a cup of coffee. A nurse gave him a full physical exam in a brown recliner, which made him self-conscious about having his shirt lifted in front of strangers. “I felt a little uncomfortable,” he whispered. “But I have no choice, you know? I’m in the hallway. There’s no rooms.
“We could have done the physical in the parking lot,” he added, managing a laugh.
Even patients who arrive by ambulance are not guaranteed a room: One nurse runs triage, screening those who absolutely need a bed, and those who can be put in the waiting area.
“I hate that we even have to make that determination,” MS. Dusang said. Lately, staff members have been pulling out some patients already in the ER’s rooms when others arrive who are more critically ill. “No one likes to take someone out of the privacy of their room and say, ‘We’re going to put you in a hallway because we need to get care to someone else.’”
ER patients have grown sicker
“We are hearing from members in every part of the country,” said Dr. Lisa Moreno, president of the American Academy of Emergency Medicine. “The Midwest, the South, the Northeast, the West … they are seeing this exact same phenomenon.”
Although the number of ER visits returned to pre-COVID levels this summer, admission rates, from the ER to the hospital’s inpatient floors, are still almost 20% higher. That’s according to the most recent analysis by the Epic Health Research Network, which pulls data from more than 120 million patients across the country.
“It’s an early indicator that what’s happening in the ED is that we’re seeing more acute cases than we were pre-pandemic,” said Caleb Cox, a data scientist at Epic.
Less acute cases, such as people with health issues like rashes or conjunctivitis, still aren’t going to the ER as much as they used to. Instead, they may be opting for an urgent care center or their primary care doctor, Mr. Cox explained. Meanwhile, there has been an increase in people coming to the ER with more serious conditions, like strokes and heart attacks.
So, even though the total number of patients coming to ERs is about the same as before the pandemic, “that’s absolutely going to feel like [if I’m an ER doctor or nurse] I’m seeing more patients and I’m seeing more acute patients,” Mr. Cox said.
Dr. Moreno, the AAEM president, works at an emergency department in New Orleans. She said the level of illness, and the inability to admit patients quickly and move them to beds upstairs, has created a level of chaos she described as “not even humane.”
At the beginning of a recent shift, she heard a patient crying nearby and went to investigate. It was a paraplegic man who’d recently had surgery for colon cancer. His large post-operative wound was sealed with a device called a wound vac, which pulls fluid from the wound into a drainage tube attached to a portable vacuum pump.
But the wound vac had malfunctioned, which is why he had come to the ER. Staffers were so busy, however, that by the time Dr. Moreno came in, the fluid from his wound was leaking everywhere.
“When I went in, the bed was covered,” she recalled. “I mean, he was lying in a puddle of secretions from this wound. And he was crying, because he said to me, ‘I’m paralyzed. I can’t move to get away from all these secretions, and I know I’m going to end up getting an infection. I know I’m going to end up getting an ulcer. I’ve been laying in this for, like, eight or nine hours.’”
The nurse in charge of his care told Dr. Moreno she simply hadn’t had time to help this patient yet. “She said, ‘I’ve had so many patients to take care of, and so many critical patients. I started [an IV] drip on this person. This person is on a cardiac monitor. I just didn’t have time to get in there.’”
“This is not humane care,” Dr. Moreno said. “This is horrible care.”
But it’s what can happen when emergency department staffers don’t have the resources they need to deal with the onslaught of competing demands.
“All the nurses and doctors had the highest level of intent to do the right thing for the person,” Dr. Moreno said. “But because of the high acuity of … a large number of patients, the staffing ratio of nurse to patient, even the staffing ratio of doctor to patient, this guy did not get the care that he deserved to get, just as a human being.”
The instance of unintended neglect that Dr. Moreno saw is extreme, and not the experience of most patients who arrive at ERs these days. But the problem is not new: Even before the pandemic, ER overcrowding had been a “widespread problem and a source of patient harm, according to a recent commentary in NEJM Catalyst Innovations in Care Delivery.
“ED crowding is not an issue of inconvenience,” the authors wrote. “There is incontrovertible evidence that ED crowding leads to significant patient harm, including morbidity and mortality related to consequential delays of treatment for both high- and low-acuity patients.”
And already-overwhelmed staffers are burning out.
Burnout feeds staffing shortages, and vice versa
Every morning, Tiffani Dusang wakes up and checks her Sparrow email with one singular hope: that she will not see yet another nurse resignation letter in her inbox.
“I cannot tell you how many of them [the nurses] tell me they went home crying” after their shifts, she said.
Despite Ms. Dusang’s best efforts to support her staffers, they’re leaving too fast to be replaced, either to take higher-paying gigs as a travel nurse, to try a less-stressful type of nursing, or simply walking away from the profession entirely.
Kelly Spitz has been an emergency department nurse at Sparrow for 10 years. But, lately, she has also fantasized about leaving. “It has crossed my mind several times,” she said, and yet she continues to come back. “Because I have a team here. And I love what I do.” But then she started to cry. The issue is not the hard work, or even the stress. She struggles with not being able to give her patients the kind of care and attention she wants to give them, and that they need and deserve, she said.
She often thinks about a patient whose test results revealed terminal cancer, she said. Ms. Spitz spent all day working the phones, hustling case managers, trying to get hospice care set up in the man’s home. He was going to die, and she just didn’t want him to have to die in the hospital, where only one visitor was allowed. She wanted to get him home, and back with his family.
Finally, after many hours, they found an ambulance to take him home.
Three days later, the man’s family members called Ms. Spitz: He had died surrounded by family. They were calling to thank her.
“I felt like I did my job there, because I got him home,” she said. But that’s a rare feeling these days. “I just hope it gets better. I hope it gets better soon.”
Around 4 p.m. at Sparrow Hospital as one shift approached its end, Ms. Dusang faced a new crisis: The overnight shift was more short-staffed than usual.
“Can we get two inpatient nurses?” she asked, hoping to borrow two nurses from one of the hospital floors upstairs.
“Already tried,” replied nurse Troy Latunski.
Without more staff, it’s going to be hard to care for new patients who come in overnight — from car crashes to seizures or other emergencies.
But Mr. Latunski had a plan: He would go home, snatch a few hours of sleep and return at 11 p.m. to work the overnight shift in the ER’s overflow unit. That meant he would be largely caring for eight patients, alone. On just a few short hours of sleep. But lately that seemed to be their only, and best, option.
Ms. Dusang considered for a moment, took a deep breath and nodded. “OK,” she said.
“Go home. Get some sleep. Thank you,” she added, shooting Mr. Latunski a grateful smile. And then she pivoted, because another nurse was approaching with an urgent question. On to the next crisis.
KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation. This story is part of a partnership that includes Michigan Radio, NPR and KHN.
What's your diagnosis?
Sigmoid colon perforation secondary to transcutaneous epicardial pacer wires.
A plain film image (Figure A) shows diffusely dilated loops of bowel with subdiaphragmatic air concerning for GI viscous perforation. Dedicated cross-sectional imaging confirms intra-abdominal free air, and in representative cross section, the epicardial pacing wires can be visualized within the gastrointestinal lumen (Figure D, arrows). At the time of surgical consultation, the radiology report was notable for concern regarding possible disruption of peritoneum secondary to the difficult surgical chest tube placement in a patient with a high-riding left hemidiaphragm. Urgent laparoscopic exploration secondary to these findings unexpectedly revealed that the transcutaneous epicardial pacing wires had been inadvertently placed through the sigmoid colon (Figure C). The pacer wires were cut and removed intraoperatively. Unfortunately, 4 days after removal of pacer wires, the patient continued to have ongoing distension and was found to have sigmoid volvulus necessitating endoscopic decompression. After a prolonged hospitalization and recovery, he was discharged with a normal bowel pattern and tolerating oral intake to a skilled nursing facility.
Temporary transcutaneous epicardial pacing wires are often placed after complex cardiovascular surgical procedures. Complications from wire placement are thought to be relatively rare and are typically associated with migration into local structures after wire placement and infectious complications secondary to retained wires.1,2 Perforation of local structures during placement is less common, and GI viscous perforation in particular is not a well-characterized cause of associated morbidity.3
Our case demonstrates that, in patients with hemidiaphragm elevation, epicardial wire placement risks GI viscous perforation. Furthermore, given the frequency of concomitant surgical hardware in this patient population, identification of malpositioned epicardial wires on plain film and even cross-sectional imaging can be difficult and can delay diagnosis.
References
1. Del Nido P, Goldman BS. J Card Surg. 1989 Mar;4(1):99-103.
2. Kapoor A et al. Interact Cardiovasc Thorac Surg. 2011 Jul;13(1):104-6.
3. Haba J et al. Can Assoc Radiol J. 2013 Feb;64(1):77-80.
Sigmoid colon perforation secondary to transcutaneous epicardial pacer wires.
A plain film image (Figure A) shows diffusely dilated loops of bowel with subdiaphragmatic air concerning for GI viscous perforation. Dedicated cross-sectional imaging confirms intra-abdominal free air, and in representative cross section, the epicardial pacing wires can be visualized within the gastrointestinal lumen (Figure D, arrows). At the time of surgical consultation, the radiology report was notable for concern regarding possible disruption of peritoneum secondary to the difficult surgical chest tube placement in a patient with a high-riding left hemidiaphragm. Urgent laparoscopic exploration secondary to these findings unexpectedly revealed that the transcutaneous epicardial pacing wires had been inadvertently placed through the sigmoid colon (Figure C). The pacer wires were cut and removed intraoperatively. Unfortunately, 4 days after removal of pacer wires, the patient continued to have ongoing distension and was found to have sigmoid volvulus necessitating endoscopic decompression. After a prolonged hospitalization and recovery, he was discharged with a normal bowel pattern and tolerating oral intake to a skilled nursing facility.
Temporary transcutaneous epicardial pacing wires are often placed after complex cardiovascular surgical procedures. Complications from wire placement are thought to be relatively rare and are typically associated with migration into local structures after wire placement and infectious complications secondary to retained wires.1,2 Perforation of local structures during placement is less common, and GI viscous perforation in particular is not a well-characterized cause of associated morbidity.3
Our case demonstrates that, in patients with hemidiaphragm elevation, epicardial wire placement risks GI viscous perforation. Furthermore, given the frequency of concomitant surgical hardware in this patient population, identification of malpositioned epicardial wires on plain film and even cross-sectional imaging can be difficult and can delay diagnosis.
References
1. Del Nido P, Goldman BS. J Card Surg. 1989 Mar;4(1):99-103.
2. Kapoor A et al. Interact Cardiovasc Thorac Surg. 2011 Jul;13(1):104-6.
3. Haba J et al. Can Assoc Radiol J. 2013 Feb;64(1):77-80.
Sigmoid colon perforation secondary to transcutaneous epicardial pacer wires.
A plain film image (Figure A) shows diffusely dilated loops of bowel with subdiaphragmatic air concerning for GI viscous perforation. Dedicated cross-sectional imaging confirms intra-abdominal free air, and in representative cross section, the epicardial pacing wires can be visualized within the gastrointestinal lumen (Figure D, arrows). At the time of surgical consultation, the radiology report was notable for concern regarding possible disruption of peritoneum secondary to the difficult surgical chest tube placement in a patient with a high-riding left hemidiaphragm. Urgent laparoscopic exploration secondary to these findings unexpectedly revealed that the transcutaneous epicardial pacing wires had been inadvertently placed through the sigmoid colon (Figure C). The pacer wires were cut and removed intraoperatively. Unfortunately, 4 days after removal of pacer wires, the patient continued to have ongoing distension and was found to have sigmoid volvulus necessitating endoscopic decompression. After a prolonged hospitalization and recovery, he was discharged with a normal bowel pattern and tolerating oral intake to a skilled nursing facility.
Temporary transcutaneous epicardial pacing wires are often placed after complex cardiovascular surgical procedures. Complications from wire placement are thought to be relatively rare and are typically associated with migration into local structures after wire placement and infectious complications secondary to retained wires.1,2 Perforation of local structures during placement is less common, and GI viscous perforation in particular is not a well-characterized cause of associated morbidity.3
Our case demonstrates that, in patients with hemidiaphragm elevation, epicardial wire placement risks GI viscous perforation. Furthermore, given the frequency of concomitant surgical hardware in this patient population, identification of malpositioned epicardial wires on plain film and even cross-sectional imaging can be difficult and can delay diagnosis.
References
1. Del Nido P, Goldman BS. J Card Surg. 1989 Mar;4(1):99-103.
2. Kapoor A et al. Interact Cardiovasc Thorac Surg. 2011 Jul;13(1):104-6.
3. Haba J et al. Can Assoc Radiol J. 2013 Feb;64(1):77-80.
Question: An 82-year-old man was admitted for urgent coronary artery bypass and concurrent mitral valve repair. Intraoperatively, he underwent cardiopulmonary bypass, epicardial pacing, and placement of two anterior mediastinal and one pleural chest tubes. After a relatively unremarkable initial postoperative course and nonnarcotic pain control, concern for ileus developed on postoperative day 4. A nasogastric tube was placed out of concern for worsening somnolence, nausea, and the inability to safely tolerate oral intake. The patient had been passing flatus but had yet to have a bowel movement since the operation. Physical examination at the time was notable for a soft abdomen with diffuse tenderness and voluntary guarding. Subsequent plain film imaging to confirm nasogastric tube placement (Figure A) and follow-up computed tomography imaging (Figure B) are shown.
What's the diagnosis?