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Step right up, folks, for a public dissection
The greatest autopsy on Earth?
The LOTME staff would like to apologize in advance. The following item contains historical facts.
P.T. Barnum is a rather controversial figure in American history. The greatest show on Earth was certainly popular in its day. However, Barnum got his start in 1835 by leasing a slave named Joyce Heth, an elderly Black woman who told vivid stories of caring for a young George Washington. He toured her around the country, advertising her as a 160-year-old woman who served as George Washington’s nanny. When Ms. Heth died the next year, Barnum sold tickets to the autopsy, charging the equivalent of $30 in today’s money.
When a doctor announced that Ms. Heth was actually 75-80 when she died, it caused great controversy in the press and ruined Barnum’s career. Wait, no, that’s not right. The opposite, actually. He weathered the storm, built his famous circus, and never again committed a hoax.
It’s difficult to quantify how wrong publicly dissecting a person and charging people to see said dissection is, but that was almost 200 years ago. At the very least, we can say that such terrible behavior is firmly in the distant past.
Oh wait.
David Saunders, a 98-year-old veteran of World War II and the Korean War, donated his body to science. His body, however, was purchased by DeathScience.org from a medical lab – with the buyer supposedly misleading the medical lab about its intentions, which was for use at the traveling Oddities and Curiosities Expo. Tickets went for up to $500 each to witness the public autopsy of Mr. Saunders’ body, which took place at a Marriott in Portland, Ore. It promised to be an exciting, all-day event from 9 a.m. to 4 p.m., with a break for lunch, of course. You can’t have an autopsy without a catered lunch.
Another public autopsy event was scheduled in Seattle but canceled after news of the first event broke. Oh, and for that extra little kick, Mr. Saunders died from COVID-19, meaning that all those paying customers were exposed.
P.T. Barnum is probably rolling over in his grave right now. His autopsy tickets were a bargain.
Go ahead, have that soda before math
We should all know by now that sugary drinks are bad, even artificially sweetened ones. It might not always stop us from drinking them, but we know the deal. But what if sugary drinks like soda could be helpful for girls in school?
You read that right. We said girls. A soda before class might have boys bouncing off the walls, but not girls. A recent study showed that not only was girls’ behavior unaffected by having a sugary drink, their math skills even improved.
Researchers analyzed the behavior of 4- to 6-year-old children before and after having a sugary drink. The sugar rush was actually calming for girls and helped them perform better with numerical skills, but the opposite was true for boys. “Our study is the first to provide large-scale experimental evidence on the impact of sugary drinks on preschool children. The results clearly indicate a causal impact of sugary drinks on children’s behavior and test scores,” Fritz Schiltz, PhD, said in a written statement.
This probably isn’t the green light to have as many sugary drinks as you want, but it might be interesting to see how your work is affected after a soda.
Chicken nuggets and the meat paradox
Two young children are fighting over the last chicken nugget when an adult comes in to see what’s going on.
Liam: Vegetable!
Olivia: Meat!
Liam: Chicken nuggets are vegetables!
Olivia: No, dorkface! They’re meat.
Caregiver: Good news, kids. You’re both right.
Olivia: How can we both be right?
At this point, a woman enters the room. She’s wearing a white lab coat, so she must be a scientist.
Dr. Scientist: You can’t both be right, Olivia. You are being fed a serving of the meat paradox. That’s why Liam here doesn’t know that chicken nuggets are made of chicken, which is a form of meat. Sadly, he’s not the only one.
In a recent study, scientists from Furman University in Greenville, S.C., found that 38% of 176 children aged 4-7 years thought that chicken nuggets were vegetables and more than 46% identified French fries as animal based.
Olivia: Did our caregiver lie to us, Dr. Scientist?
Dr. Scientist: Yes, Olivia. The researchers I mentioned explained that “many people experience unease while eating meat. Omnivores eat foods that entail animal suffering and death while at the same time endorsing the compassionate treatment of animals.” That’s the meat paradox.
Liam: What else did they say, Dr. Scientist?
Dr. Scientist: Over 70% of those children said that cows and pigs were not edible and 5% thought that cats and horses were. The investigators wrote “that children and youth should be viewed as agents of environmental change” in the future, but suggested that parents need to bring honesty to the table.
Caregiver: How did you get in here anyway? And how do you know their names?
Dr. Scientist: I’ve been rooting through your garbage for years. All in the name of science, of course.
Bedtimes aren’t just for children
There are multiple ways to prevent heart disease, but what if it could be as easy as switching your bedtime? A recent study in European Heart Journal–Digital Health suggests that there’s a sweet spot when it comes to sleep timing.
Through smartwatch-like devices, researchers measured the sleep-onset and wake-up times for 7 days in 88,026 participants aged 43-79 years. After 5.7 years of follow-up to see if anyone had a heart attack, stroke, or any other cardiovascular event, 3.6% developed some kind of cardiovascular disease.
Those who went to bed between 10 p.m. and 11 p.m. had a lower risk of developing heart disease. The risk was 25% higher for subjects who went to bed at midnight or later, 24% higher for bedtimes before 10 p.m., and 12% higher for bedtimes between 11 p.m. and midnight.
So, why can you go to bed before “The Tonight Show” and lower your cardiovascular risk but not before the nightly news? Well, it has something to do with your body’s natural clock.
“The optimum time to go to sleep is at a specific point in the body’s 24-hour cycle and deviations may be detrimental to health. The riskiest time was after midnight, potentially because it may reduce the likelihood of seeing morning light, which resets the body clock,” said study author Dr. David Plans of the University of Exeter, England.
Although a sleep schedule is preferred, it isn’t realistic all the time for those in certain occupations who might have to resort to other methods to keep their circadian clocks ticking optimally for their health. But if all it takes is prescribing a sleep time to reduce heart disease on a massive scale it would make a great “low-cost public health target.”
So bedtimes aren’t just for children.
The greatest autopsy on Earth?
The LOTME staff would like to apologize in advance. The following item contains historical facts.
P.T. Barnum is a rather controversial figure in American history. The greatest show on Earth was certainly popular in its day. However, Barnum got his start in 1835 by leasing a slave named Joyce Heth, an elderly Black woman who told vivid stories of caring for a young George Washington. He toured her around the country, advertising her as a 160-year-old woman who served as George Washington’s nanny. When Ms. Heth died the next year, Barnum sold tickets to the autopsy, charging the equivalent of $30 in today’s money.
When a doctor announced that Ms. Heth was actually 75-80 when she died, it caused great controversy in the press and ruined Barnum’s career. Wait, no, that’s not right. The opposite, actually. He weathered the storm, built his famous circus, and never again committed a hoax.
It’s difficult to quantify how wrong publicly dissecting a person and charging people to see said dissection is, but that was almost 200 years ago. At the very least, we can say that such terrible behavior is firmly in the distant past.
Oh wait.
David Saunders, a 98-year-old veteran of World War II and the Korean War, donated his body to science. His body, however, was purchased by DeathScience.org from a medical lab – with the buyer supposedly misleading the medical lab about its intentions, which was for use at the traveling Oddities and Curiosities Expo. Tickets went for up to $500 each to witness the public autopsy of Mr. Saunders’ body, which took place at a Marriott in Portland, Ore. It promised to be an exciting, all-day event from 9 a.m. to 4 p.m., with a break for lunch, of course. You can’t have an autopsy without a catered lunch.
Another public autopsy event was scheduled in Seattle but canceled after news of the first event broke. Oh, and for that extra little kick, Mr. Saunders died from COVID-19, meaning that all those paying customers were exposed.
P.T. Barnum is probably rolling over in his grave right now. His autopsy tickets were a bargain.
Go ahead, have that soda before math
We should all know by now that sugary drinks are bad, even artificially sweetened ones. It might not always stop us from drinking them, but we know the deal. But what if sugary drinks like soda could be helpful for girls in school?
You read that right. We said girls. A soda before class might have boys bouncing off the walls, but not girls. A recent study showed that not only was girls’ behavior unaffected by having a sugary drink, their math skills even improved.
Researchers analyzed the behavior of 4- to 6-year-old children before and after having a sugary drink. The sugar rush was actually calming for girls and helped them perform better with numerical skills, but the opposite was true for boys. “Our study is the first to provide large-scale experimental evidence on the impact of sugary drinks on preschool children. The results clearly indicate a causal impact of sugary drinks on children’s behavior and test scores,” Fritz Schiltz, PhD, said in a written statement.
This probably isn’t the green light to have as many sugary drinks as you want, but it might be interesting to see how your work is affected after a soda.
Chicken nuggets and the meat paradox
Two young children are fighting over the last chicken nugget when an adult comes in to see what’s going on.
Liam: Vegetable!
Olivia: Meat!
Liam: Chicken nuggets are vegetables!
Olivia: No, dorkface! They’re meat.
Caregiver: Good news, kids. You’re both right.
Olivia: How can we both be right?
At this point, a woman enters the room. She’s wearing a white lab coat, so she must be a scientist.
Dr. Scientist: You can’t both be right, Olivia. You are being fed a serving of the meat paradox. That’s why Liam here doesn’t know that chicken nuggets are made of chicken, which is a form of meat. Sadly, he’s not the only one.
In a recent study, scientists from Furman University in Greenville, S.C., found that 38% of 176 children aged 4-7 years thought that chicken nuggets were vegetables and more than 46% identified French fries as animal based.
Olivia: Did our caregiver lie to us, Dr. Scientist?
Dr. Scientist: Yes, Olivia. The researchers I mentioned explained that “many people experience unease while eating meat. Omnivores eat foods that entail animal suffering and death while at the same time endorsing the compassionate treatment of animals.” That’s the meat paradox.
Liam: What else did they say, Dr. Scientist?
Dr. Scientist: Over 70% of those children said that cows and pigs were not edible and 5% thought that cats and horses were. The investigators wrote “that children and youth should be viewed as agents of environmental change” in the future, but suggested that parents need to bring honesty to the table.
Caregiver: How did you get in here anyway? And how do you know their names?
Dr. Scientist: I’ve been rooting through your garbage for years. All in the name of science, of course.
Bedtimes aren’t just for children
There are multiple ways to prevent heart disease, but what if it could be as easy as switching your bedtime? A recent study in European Heart Journal–Digital Health suggests that there’s a sweet spot when it comes to sleep timing.
Through smartwatch-like devices, researchers measured the sleep-onset and wake-up times for 7 days in 88,026 participants aged 43-79 years. After 5.7 years of follow-up to see if anyone had a heart attack, stroke, or any other cardiovascular event, 3.6% developed some kind of cardiovascular disease.
Those who went to bed between 10 p.m. and 11 p.m. had a lower risk of developing heart disease. The risk was 25% higher for subjects who went to bed at midnight or later, 24% higher for bedtimes before 10 p.m., and 12% higher for bedtimes between 11 p.m. and midnight.
So, why can you go to bed before “The Tonight Show” and lower your cardiovascular risk but not before the nightly news? Well, it has something to do with your body’s natural clock.
“The optimum time to go to sleep is at a specific point in the body’s 24-hour cycle and deviations may be detrimental to health. The riskiest time was after midnight, potentially because it may reduce the likelihood of seeing morning light, which resets the body clock,” said study author Dr. David Plans of the University of Exeter, England.
Although a sleep schedule is preferred, it isn’t realistic all the time for those in certain occupations who might have to resort to other methods to keep their circadian clocks ticking optimally for their health. But if all it takes is prescribing a sleep time to reduce heart disease on a massive scale it would make a great “low-cost public health target.”
So bedtimes aren’t just for children.
The greatest autopsy on Earth?
The LOTME staff would like to apologize in advance. The following item contains historical facts.
P.T. Barnum is a rather controversial figure in American history. The greatest show on Earth was certainly popular in its day. However, Barnum got his start in 1835 by leasing a slave named Joyce Heth, an elderly Black woman who told vivid stories of caring for a young George Washington. He toured her around the country, advertising her as a 160-year-old woman who served as George Washington’s nanny. When Ms. Heth died the next year, Barnum sold tickets to the autopsy, charging the equivalent of $30 in today’s money.
When a doctor announced that Ms. Heth was actually 75-80 when she died, it caused great controversy in the press and ruined Barnum’s career. Wait, no, that’s not right. The opposite, actually. He weathered the storm, built his famous circus, and never again committed a hoax.
It’s difficult to quantify how wrong publicly dissecting a person and charging people to see said dissection is, but that was almost 200 years ago. At the very least, we can say that such terrible behavior is firmly in the distant past.
Oh wait.
David Saunders, a 98-year-old veteran of World War II and the Korean War, donated his body to science. His body, however, was purchased by DeathScience.org from a medical lab – with the buyer supposedly misleading the medical lab about its intentions, which was for use at the traveling Oddities and Curiosities Expo. Tickets went for up to $500 each to witness the public autopsy of Mr. Saunders’ body, which took place at a Marriott in Portland, Ore. It promised to be an exciting, all-day event from 9 a.m. to 4 p.m., with a break for lunch, of course. You can’t have an autopsy without a catered lunch.
Another public autopsy event was scheduled in Seattle but canceled after news of the first event broke. Oh, and for that extra little kick, Mr. Saunders died from COVID-19, meaning that all those paying customers were exposed.
P.T. Barnum is probably rolling over in his grave right now. His autopsy tickets were a bargain.
Go ahead, have that soda before math
We should all know by now that sugary drinks are bad, even artificially sweetened ones. It might not always stop us from drinking them, but we know the deal. But what if sugary drinks like soda could be helpful for girls in school?
You read that right. We said girls. A soda before class might have boys bouncing off the walls, but not girls. A recent study showed that not only was girls’ behavior unaffected by having a sugary drink, their math skills even improved.
Researchers analyzed the behavior of 4- to 6-year-old children before and after having a sugary drink. The sugar rush was actually calming for girls and helped them perform better with numerical skills, but the opposite was true for boys. “Our study is the first to provide large-scale experimental evidence on the impact of sugary drinks on preschool children. The results clearly indicate a causal impact of sugary drinks on children’s behavior and test scores,” Fritz Schiltz, PhD, said in a written statement.
This probably isn’t the green light to have as many sugary drinks as you want, but it might be interesting to see how your work is affected after a soda.
Chicken nuggets and the meat paradox
Two young children are fighting over the last chicken nugget when an adult comes in to see what’s going on.
Liam: Vegetable!
Olivia: Meat!
Liam: Chicken nuggets are vegetables!
Olivia: No, dorkface! They’re meat.
Caregiver: Good news, kids. You’re both right.
Olivia: How can we both be right?
At this point, a woman enters the room. She’s wearing a white lab coat, so she must be a scientist.
Dr. Scientist: You can’t both be right, Olivia. You are being fed a serving of the meat paradox. That’s why Liam here doesn’t know that chicken nuggets are made of chicken, which is a form of meat. Sadly, he’s not the only one.
In a recent study, scientists from Furman University in Greenville, S.C., found that 38% of 176 children aged 4-7 years thought that chicken nuggets were vegetables and more than 46% identified French fries as animal based.
Olivia: Did our caregiver lie to us, Dr. Scientist?
Dr. Scientist: Yes, Olivia. The researchers I mentioned explained that “many people experience unease while eating meat. Omnivores eat foods that entail animal suffering and death while at the same time endorsing the compassionate treatment of animals.” That’s the meat paradox.
Liam: What else did they say, Dr. Scientist?
Dr. Scientist: Over 70% of those children said that cows and pigs were not edible and 5% thought that cats and horses were. The investigators wrote “that children and youth should be viewed as agents of environmental change” in the future, but suggested that parents need to bring honesty to the table.
Caregiver: How did you get in here anyway? And how do you know their names?
Dr. Scientist: I’ve been rooting through your garbage for years. All in the name of science, of course.
Bedtimes aren’t just for children
There are multiple ways to prevent heart disease, but what if it could be as easy as switching your bedtime? A recent study in European Heart Journal–Digital Health suggests that there’s a sweet spot when it comes to sleep timing.
Through smartwatch-like devices, researchers measured the sleep-onset and wake-up times for 7 days in 88,026 participants aged 43-79 years. After 5.7 years of follow-up to see if anyone had a heart attack, stroke, or any other cardiovascular event, 3.6% developed some kind of cardiovascular disease.
Those who went to bed between 10 p.m. and 11 p.m. had a lower risk of developing heart disease. The risk was 25% higher for subjects who went to bed at midnight or later, 24% higher for bedtimes before 10 p.m., and 12% higher for bedtimes between 11 p.m. and midnight.
So, why can you go to bed before “The Tonight Show” and lower your cardiovascular risk but not before the nightly news? Well, it has something to do with your body’s natural clock.
“The optimum time to go to sleep is at a specific point in the body’s 24-hour cycle and deviations may be detrimental to health. The riskiest time was after midnight, potentially because it may reduce the likelihood of seeing morning light, which resets the body clock,” said study author Dr. David Plans of the University of Exeter, England.
Although a sleep schedule is preferred, it isn’t realistic all the time for those in certain occupations who might have to resort to other methods to keep their circadian clocks ticking optimally for their health. But if all it takes is prescribing a sleep time to reduce heart disease on a massive scale it would make a great “low-cost public health target.”
So bedtimes aren’t just for children.
Should you tell your doctor that you’re a doctor?
The question drew spirited debate when urologist Ashley Winter, MD, made a simple, straightforward request on Twitter: “If you are a doctor & you come to an appointment please tell me you are a doctor, not because I will treat you differently but because it’s easier to speak in jargon.”
She later added, “This doesn’t’ mean I would be less patient-focused or emotional with a physician or other [healthcare worker]. Just means that, instead of saying ‘you will have a catheter draining your urine to a bag,’ I can say, ‘you will have a Foley.’ ”
The Tweet followed an encounter with a patient who told Dr. Winter that he was a doctor only after she had gone to some length explaining a surgical procedure in lay terms.
“I explained the surgery, obviously assuming he was an intelligent adult, but using fully layman’s terms,” she said in an interview. The patient then told her that he was a doctor. “I guess I felt this embarrassment — I wouldn’t have treated him differently, but I just could have discussed the procedure with him in more professional terms.”
“To some extent, it was my own fault,” she commented in an interview. “I didn’t take the time to ask [about his work] at the beginning of the consultation, but that’s a fine line, also,” added Dr. Winter, a urologist and sexual medicine physician in Portland, Ore.
“You know that patient is there because they want care from you and it’s not necessarily always at the forefront of importance to be asking them what they do for their work, but alternatively, if you don’t ask then you put them in this position where they have to find a way to go ahead and tell you.”
Several people chimed in on the thread to voice their thoughts on the matter. Some commiserated with Dr. Winter’s experience:
“I took care of a retired cardiologist in the hospital as a second-year resident and honest to god he let me ramble on ‘explaining’ his echo result and never told me. I found out a couple days later and wanted to die,” posted @MaddyAndrewsMD.
Another recalled a similarly embarrassing experience when she “went on and on” discussing headaches with a patient whose husband “was in the corner smirking.”
“They told my attending later [that the] husband was a retired FM doc who practiced medicine longer than I’ve been alive. I wanted to die,” posted @JSinghDO.
Many on the thread, though, were doctors and other healthcare professionals speaking as patients. Some said they didn’t want to disclose their status as a healthcare provider because they felt it affected the care they received.
For example, @drhelenrainford commented: “In my experience my care is less ‘caring’ when they know I am a [doctor]. I get spoken to like they are discussing a patient with me — no empathy just facts and difficult results just blurted out without consideration. Awful awful time as an inpatient …but that’s another story!”
@Dr_B_Ring said: “Nope – You and I speak different jargon – I would want you to speak to me like a human that doesn’t know your jargon. My ego would get in the way of asking about the acronyms I don’t know if you knew I was a fellow physician.”
Conversely, @lozzlemcfozzle said: “Honestly I prefer not to tell my Doctors — I’ve found people skip explanations assuming I ‘know,’ or seem a little nervous when I tell them!”
Others said they felt uncomfortable — pretentious, even — in announcing their status, or worried that they might come across as expecting special care.
“It’s such a tough needle to thread. Want to tell people early but not come off as demanding special treatment, but don’t want to wait too long and it seems like a trap,” said @MDaware.
Twitter user @MsBabyCatcher wrote: “I have a hard time doing this because I don’t want people to think I’m being pretentious or going to micromanage/dictate care.”
Replying to @MsBabyCatcher, @RedStethoscope wrote: “I used to think this too until I got [very poor] care a few times, and was advised by other doctor moms to ‘play the doctor card.’ I have gotten better/more compassionate care by making sure it’s clear that I’m a physician (which is junk, but here we are).”
Several of those responding used the words “tricky” and “awkward,” suggesting a common theme for doctors presenting as patients.
“I struggle with this. My 5-year-old broke her arm this weekend, we spent hours in the ED, of my own hospital, I never mentioned it because I didn’t want to get preferential care. But as they were explaining her type of fracture, it felt awkward and inefficient,” said @lindsay_petty.
To avoid the awkwardness, a number of respondents said they purposefully use medical jargon to open up a conversation rather than just offering up the information that they are a doctor.
Still others offered suggestions on how to broach the subject more directly when presenting as a patient:
‘”Just FYI I’m a X doc but I’m here because I really want your help and advice!” That’s what I usually do,” wrote @drcakefm.
@BeeSting14618 Tweeted: “I usually say ‘I know some of this but I’m here because I want YOUR guidance. Also I may ask dumb questions, and I’ll tell you if a question is asking your opinion or making a request.’”
A few others injected a bit of humor: “I just do the 14-part handshake that only doctors know. Is that not customary?” quipped @Branmiz25.
“Ah yes, that transmits the entire [history of present illness],” replied Dr. Winter.
Jokes aside, the topic is obviously one that touched on a shared experience among healthcare providers, Dr. Winter commented. The Twitter thread she started just “blew up.”
That’s typically a sign that the Tweet is relatable for a lot of people, she said.
“It’s definitely something that all of us as care providers and as patients understand. It’s a funny, awkward thing that can really change an interaction, so we probably all feel pretty strongly about our experiences related to that,” she added.
The debate begs the question: Is there a duty or ethical reason to disclose?
“I definitely think it is very reasonable to disclose that one is a medical professional to another doctor,” medical ethicist Charlotte Blease, PhD, said in an interview. “There are good reasons to believe doing so might make a difference to the quality of communication and transparency.”
If the ability to use medical terminology or jargon more freely improves patient understanding, autonomy, and shared decision-making, then it may be of benefit, said Dr. Blease, a Keane OpenNotes Scholar at Beth Israel Deaconess Medical Center in Boston.
“Since doctors should strive to communicate effectively with every patient and to respect their unique needs and level of understanding, then I see no reason to deny that one is a medic,” she added.”
Knowing how to share the information is another story.
“This is something that affects all of us as physicians — we’re going to be patients at some point, right?” Dr. Winter commented. “But I don’t think how to disclose that is something that was ever brought up in my medical training.”
“Maybe there should just be a discussion of this one day when people are in medical school — maybe in a professionalism course — to broach this topic or look at if there’s any literature on outcomes related to disclosure of status or what are best practices,” she suggested.
A version of this article first appeared on Medscape.com.
The question drew spirited debate when urologist Ashley Winter, MD, made a simple, straightforward request on Twitter: “If you are a doctor & you come to an appointment please tell me you are a doctor, not because I will treat you differently but because it’s easier to speak in jargon.”
She later added, “This doesn’t’ mean I would be less patient-focused or emotional with a physician or other [healthcare worker]. Just means that, instead of saying ‘you will have a catheter draining your urine to a bag,’ I can say, ‘you will have a Foley.’ ”
The Tweet followed an encounter with a patient who told Dr. Winter that he was a doctor only after she had gone to some length explaining a surgical procedure in lay terms.
“I explained the surgery, obviously assuming he was an intelligent adult, but using fully layman’s terms,” she said in an interview. The patient then told her that he was a doctor. “I guess I felt this embarrassment — I wouldn’t have treated him differently, but I just could have discussed the procedure with him in more professional terms.”
“To some extent, it was my own fault,” she commented in an interview. “I didn’t take the time to ask [about his work] at the beginning of the consultation, but that’s a fine line, also,” added Dr. Winter, a urologist and sexual medicine physician in Portland, Ore.
“You know that patient is there because they want care from you and it’s not necessarily always at the forefront of importance to be asking them what they do for their work, but alternatively, if you don’t ask then you put them in this position where they have to find a way to go ahead and tell you.”
Several people chimed in on the thread to voice their thoughts on the matter. Some commiserated with Dr. Winter’s experience:
“I took care of a retired cardiologist in the hospital as a second-year resident and honest to god he let me ramble on ‘explaining’ his echo result and never told me. I found out a couple days later and wanted to die,” posted @MaddyAndrewsMD.
Another recalled a similarly embarrassing experience when she “went on and on” discussing headaches with a patient whose husband “was in the corner smirking.”
“They told my attending later [that the] husband was a retired FM doc who practiced medicine longer than I’ve been alive. I wanted to die,” posted @JSinghDO.
Many on the thread, though, were doctors and other healthcare professionals speaking as patients. Some said they didn’t want to disclose their status as a healthcare provider because they felt it affected the care they received.
For example, @drhelenrainford commented: “In my experience my care is less ‘caring’ when they know I am a [doctor]. I get spoken to like they are discussing a patient with me — no empathy just facts and difficult results just blurted out without consideration. Awful awful time as an inpatient …but that’s another story!”
@Dr_B_Ring said: “Nope – You and I speak different jargon – I would want you to speak to me like a human that doesn’t know your jargon. My ego would get in the way of asking about the acronyms I don’t know if you knew I was a fellow physician.”
Conversely, @lozzlemcfozzle said: “Honestly I prefer not to tell my Doctors — I’ve found people skip explanations assuming I ‘know,’ or seem a little nervous when I tell them!”
Others said they felt uncomfortable — pretentious, even — in announcing their status, or worried that they might come across as expecting special care.
“It’s such a tough needle to thread. Want to tell people early but not come off as demanding special treatment, but don’t want to wait too long and it seems like a trap,” said @MDaware.
Twitter user @MsBabyCatcher wrote: “I have a hard time doing this because I don’t want people to think I’m being pretentious or going to micromanage/dictate care.”
Replying to @MsBabyCatcher, @RedStethoscope wrote: “I used to think this too until I got [very poor] care a few times, and was advised by other doctor moms to ‘play the doctor card.’ I have gotten better/more compassionate care by making sure it’s clear that I’m a physician (which is junk, but here we are).”
Several of those responding used the words “tricky” and “awkward,” suggesting a common theme for doctors presenting as patients.
“I struggle with this. My 5-year-old broke her arm this weekend, we spent hours in the ED, of my own hospital, I never mentioned it because I didn’t want to get preferential care. But as they were explaining her type of fracture, it felt awkward and inefficient,” said @lindsay_petty.
To avoid the awkwardness, a number of respondents said they purposefully use medical jargon to open up a conversation rather than just offering up the information that they are a doctor.
Still others offered suggestions on how to broach the subject more directly when presenting as a patient:
‘”Just FYI I’m a X doc but I’m here because I really want your help and advice!” That’s what I usually do,” wrote @drcakefm.
@BeeSting14618 Tweeted: “I usually say ‘I know some of this but I’m here because I want YOUR guidance. Also I may ask dumb questions, and I’ll tell you if a question is asking your opinion or making a request.’”
A few others injected a bit of humor: “I just do the 14-part handshake that only doctors know. Is that not customary?” quipped @Branmiz25.
“Ah yes, that transmits the entire [history of present illness],” replied Dr. Winter.
Jokes aside, the topic is obviously one that touched on a shared experience among healthcare providers, Dr. Winter commented. The Twitter thread she started just “blew up.”
That’s typically a sign that the Tweet is relatable for a lot of people, she said.
“It’s definitely something that all of us as care providers and as patients understand. It’s a funny, awkward thing that can really change an interaction, so we probably all feel pretty strongly about our experiences related to that,” she added.
The debate begs the question: Is there a duty or ethical reason to disclose?
“I definitely think it is very reasonable to disclose that one is a medical professional to another doctor,” medical ethicist Charlotte Blease, PhD, said in an interview. “There are good reasons to believe doing so might make a difference to the quality of communication and transparency.”
If the ability to use medical terminology or jargon more freely improves patient understanding, autonomy, and shared decision-making, then it may be of benefit, said Dr. Blease, a Keane OpenNotes Scholar at Beth Israel Deaconess Medical Center in Boston.
“Since doctors should strive to communicate effectively with every patient and to respect their unique needs and level of understanding, then I see no reason to deny that one is a medic,” she added.”
Knowing how to share the information is another story.
“This is something that affects all of us as physicians — we’re going to be patients at some point, right?” Dr. Winter commented. “But I don’t think how to disclose that is something that was ever brought up in my medical training.”
“Maybe there should just be a discussion of this one day when people are in medical school — maybe in a professionalism course — to broach this topic or look at if there’s any literature on outcomes related to disclosure of status or what are best practices,” she suggested.
A version of this article first appeared on Medscape.com.
The question drew spirited debate when urologist Ashley Winter, MD, made a simple, straightforward request on Twitter: “If you are a doctor & you come to an appointment please tell me you are a doctor, not because I will treat you differently but because it’s easier to speak in jargon.”
She later added, “This doesn’t’ mean I would be less patient-focused or emotional with a physician or other [healthcare worker]. Just means that, instead of saying ‘you will have a catheter draining your urine to a bag,’ I can say, ‘you will have a Foley.’ ”
The Tweet followed an encounter with a patient who told Dr. Winter that he was a doctor only after she had gone to some length explaining a surgical procedure in lay terms.
“I explained the surgery, obviously assuming he was an intelligent adult, but using fully layman’s terms,” she said in an interview. The patient then told her that he was a doctor. “I guess I felt this embarrassment — I wouldn’t have treated him differently, but I just could have discussed the procedure with him in more professional terms.”
“To some extent, it was my own fault,” she commented in an interview. “I didn’t take the time to ask [about his work] at the beginning of the consultation, but that’s a fine line, also,” added Dr. Winter, a urologist and sexual medicine physician in Portland, Ore.
“You know that patient is there because they want care from you and it’s not necessarily always at the forefront of importance to be asking them what they do for their work, but alternatively, if you don’t ask then you put them in this position where they have to find a way to go ahead and tell you.”
Several people chimed in on the thread to voice their thoughts on the matter. Some commiserated with Dr. Winter’s experience:
“I took care of a retired cardiologist in the hospital as a second-year resident and honest to god he let me ramble on ‘explaining’ his echo result and never told me. I found out a couple days later and wanted to die,” posted @MaddyAndrewsMD.
Another recalled a similarly embarrassing experience when she “went on and on” discussing headaches with a patient whose husband “was in the corner smirking.”
“They told my attending later [that the] husband was a retired FM doc who practiced medicine longer than I’ve been alive. I wanted to die,” posted @JSinghDO.
Many on the thread, though, were doctors and other healthcare professionals speaking as patients. Some said they didn’t want to disclose their status as a healthcare provider because they felt it affected the care they received.
For example, @drhelenrainford commented: “In my experience my care is less ‘caring’ when they know I am a [doctor]. I get spoken to like they are discussing a patient with me — no empathy just facts and difficult results just blurted out without consideration. Awful awful time as an inpatient …but that’s another story!”
@Dr_B_Ring said: “Nope – You and I speak different jargon – I would want you to speak to me like a human that doesn’t know your jargon. My ego would get in the way of asking about the acronyms I don’t know if you knew I was a fellow physician.”
Conversely, @lozzlemcfozzle said: “Honestly I prefer not to tell my Doctors — I’ve found people skip explanations assuming I ‘know,’ or seem a little nervous when I tell them!”
Others said they felt uncomfortable — pretentious, even — in announcing their status, or worried that they might come across as expecting special care.
“It’s such a tough needle to thread. Want to tell people early but not come off as demanding special treatment, but don’t want to wait too long and it seems like a trap,” said @MDaware.
Twitter user @MsBabyCatcher wrote: “I have a hard time doing this because I don’t want people to think I’m being pretentious or going to micromanage/dictate care.”
Replying to @MsBabyCatcher, @RedStethoscope wrote: “I used to think this too until I got [very poor] care a few times, and was advised by other doctor moms to ‘play the doctor card.’ I have gotten better/more compassionate care by making sure it’s clear that I’m a physician (which is junk, but here we are).”
Several of those responding used the words “tricky” and “awkward,” suggesting a common theme for doctors presenting as patients.
“I struggle with this. My 5-year-old broke her arm this weekend, we spent hours in the ED, of my own hospital, I never mentioned it because I didn’t want to get preferential care. But as they were explaining her type of fracture, it felt awkward and inefficient,” said @lindsay_petty.
To avoid the awkwardness, a number of respondents said they purposefully use medical jargon to open up a conversation rather than just offering up the information that they are a doctor.
Still others offered suggestions on how to broach the subject more directly when presenting as a patient:
‘”Just FYI I’m a X doc but I’m here because I really want your help and advice!” That’s what I usually do,” wrote @drcakefm.
@BeeSting14618 Tweeted: “I usually say ‘I know some of this but I’m here because I want YOUR guidance. Also I may ask dumb questions, and I’ll tell you if a question is asking your opinion or making a request.’”
A few others injected a bit of humor: “I just do the 14-part handshake that only doctors know. Is that not customary?” quipped @Branmiz25.
“Ah yes, that transmits the entire [history of present illness],” replied Dr. Winter.
Jokes aside, the topic is obviously one that touched on a shared experience among healthcare providers, Dr. Winter commented. The Twitter thread she started just “blew up.”
That’s typically a sign that the Tweet is relatable for a lot of people, she said.
“It’s definitely something that all of us as care providers and as patients understand. It’s a funny, awkward thing that can really change an interaction, so we probably all feel pretty strongly about our experiences related to that,” she added.
The debate begs the question: Is there a duty or ethical reason to disclose?
“I definitely think it is very reasonable to disclose that one is a medical professional to another doctor,” medical ethicist Charlotte Blease, PhD, said in an interview. “There are good reasons to believe doing so might make a difference to the quality of communication and transparency.”
If the ability to use medical terminology or jargon more freely improves patient understanding, autonomy, and shared decision-making, then it may be of benefit, said Dr. Blease, a Keane OpenNotes Scholar at Beth Israel Deaconess Medical Center in Boston.
“Since doctors should strive to communicate effectively with every patient and to respect their unique needs and level of understanding, then I see no reason to deny that one is a medic,” she added.”
Knowing how to share the information is another story.
“This is something that affects all of us as physicians — we’re going to be patients at some point, right?” Dr. Winter commented. “But I don’t think how to disclose that is something that was ever brought up in my medical training.”
“Maybe there should just be a discussion of this one day when people are in medical school — maybe in a professionalism course — to broach this topic or look at if there’s any literature on outcomes related to disclosure of status or what are best practices,” she suggested.
A version of this article first appeared on Medscape.com.
Liraglutide effective against weight regain after gastric bypass
The glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide (Saxenda, Novo Nordisk) was safe and effective for treating weight regain after Roux-en-Y gastric bypass (RYGB), in a randomized controlled trial.
That is, 132 patients who had lost at least 25% of their initial weight after RYGB and then gained at least 10% back were randomized 2:1 to receive liraglutide plus frequent lifestyle advice from a registered dietitian or lifestyle advice alone.
After a year, 69%, 48%, and 24% of patients who had received liraglutide lost at least 5%, 10%, and 15% of their study entry weight, respectively. In contrast, only 5% of patients in the control group lost at least 5% of their weight and none lost at least 10% of their weight.
“Liraglutide 3.0 mg/day, with lifestyle modification, was significantly more effective than placebo in treating weight regain after RYGB without increased risk of serious adverse events,” Holly F. Lofton, MD, summarized this week in an oral session at ObesityWeek®, the annual meeting of The Obesity Society.
Dr. Lofton, a clinical associate professor of surgery and medicine, and director, weight management program, NYU, Langone Health, explained to this news organization that she initiated the study after attending a “packed” session about post bariatric surgery weight regain at a prior American Society of Metabolic and Bariatric Surgery conference.
“The lecturers recommended conservative measures (such as reiterating the diet recommendations, exercise, [and] counseling), and revisional surgeries,” she said in an email, but at the time “there was no literature that provided direction on which pharmacotherapies are best for this population.”
It was known that decreases in endogenous GLP-1 levels coincide with weight regain, and liraglutide (Saxenda) was the only GLP-1 agonist approved for chronic weight management at the time, so she devised the current study protocol.
The findings are especially helpful for patients who are not candidates for bariatric surgery revisions, she noted. Further research is needed to investigate the effect of newer GLP-1 agonists, such as semaglutide (Wegovy), on weight regain following different types of bariatric surgery.
Asked to comment, Wendy C. King, PhD, who was not involved with this research, said that more than two-thirds of patients treated with 3 mg/day subcutaneous liraglutide injections in the current study lost at least 5% of their initial weight a year later, and 20% of them attained a weight as low as, or lower than, their lowest weight after bariatric surgery (nadir weight).
“The fact that both groups received lifestyle counseling from registered dietitians for just over a year, but only patients in the liraglutide group lost weight, on average, speaks to the difficulty of losing weight following weight regain post–bariatric surgery,” added Dr. King, an associate professor of epidemiology at the University of Pittsburgh, Pennsylvania.
This study “provides data that may help clinicians and patients understand the potential effect of adding liraglutide 3.0 mg/day to their weight loss efforts,” she told this news organization in an email.
However, “given that 42% of those on liraglutide reported gastrointestinal-related side effects, patients should also be counseled on this potential outcome and given suggestions for how to minimize such side effects,” Dr. King suggested.
Weight regain common, repeat surgery entails risk
Weight regain is common even years after bariatric surgery. Repeat surgery entails some risk, and lifestyle approaches alone are rarely successful in reversing weight regain, Dr. Lofton told the audience.
The researchers enrolled 132 adults who had a mean weight of 134 kg (295 pounds) when they underwent RYGB, and who lost at least 25% of their initial weight (mean weight loss of 38%) after the surgery, but who also regained at least 10% of their initial weight.
At enrollment of the current study (baseline), the patients had had RYGB 18 months to 10 years earlier (mean 5.7 years earlier) and now had a mean weight of 99 kg (218 pounds) and a mean BMI of 35.6 kg/m2. None of the patients had diabetes.
The patients were randomized to receive liraglutide (n = 89, 84% women) or placebo (n = 43, 88% women) for 56 weeks.
They were a mean age of 48 years, and about 59% were White and 25% were Black.
All patients had clinic visits every 3 months where they received lifestyle counseling from a registered dietitian.
At 12 months, patients in the liraglutide group had lost a mean of 8.8% of their baseline weight, whereas those in the placebo group had gained a mean of 1.48% of their baseline weight.
There were no significant between-group differences in cardiometabolic variables.
None of the patients in the control group attained a weight that was as low as their nadir weight after RYGB.
The rates of nausea (25%), constipation (16%), and abdominal pain (10%) in the liraglutide group were higher than in the placebo group (7%, 14%, and 5%, respectively) but similar to rates of gastrointestinal side effects in other trials of this agent.
Dr. Lofton has disclosed receiving consulting fees and being on a speaker bureau for Novo Nordisk and receiving research funds from Boehringer Ingelheim, Eli Lilly, and Novo Nordisk. Dr. King has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide (Saxenda, Novo Nordisk) was safe and effective for treating weight regain after Roux-en-Y gastric bypass (RYGB), in a randomized controlled trial.
That is, 132 patients who had lost at least 25% of their initial weight after RYGB and then gained at least 10% back were randomized 2:1 to receive liraglutide plus frequent lifestyle advice from a registered dietitian or lifestyle advice alone.
After a year, 69%, 48%, and 24% of patients who had received liraglutide lost at least 5%, 10%, and 15% of their study entry weight, respectively. In contrast, only 5% of patients in the control group lost at least 5% of their weight and none lost at least 10% of their weight.
“Liraglutide 3.0 mg/day, with lifestyle modification, was significantly more effective than placebo in treating weight regain after RYGB without increased risk of serious adverse events,” Holly F. Lofton, MD, summarized this week in an oral session at ObesityWeek®, the annual meeting of The Obesity Society.
Dr. Lofton, a clinical associate professor of surgery and medicine, and director, weight management program, NYU, Langone Health, explained to this news organization that she initiated the study after attending a “packed” session about post bariatric surgery weight regain at a prior American Society of Metabolic and Bariatric Surgery conference.
“The lecturers recommended conservative measures (such as reiterating the diet recommendations, exercise, [and] counseling), and revisional surgeries,” she said in an email, but at the time “there was no literature that provided direction on which pharmacotherapies are best for this population.”
It was known that decreases in endogenous GLP-1 levels coincide with weight regain, and liraglutide (Saxenda) was the only GLP-1 agonist approved for chronic weight management at the time, so she devised the current study protocol.
The findings are especially helpful for patients who are not candidates for bariatric surgery revisions, she noted. Further research is needed to investigate the effect of newer GLP-1 agonists, such as semaglutide (Wegovy), on weight regain following different types of bariatric surgery.
Asked to comment, Wendy C. King, PhD, who was not involved with this research, said that more than two-thirds of patients treated with 3 mg/day subcutaneous liraglutide injections in the current study lost at least 5% of their initial weight a year later, and 20% of them attained a weight as low as, or lower than, their lowest weight after bariatric surgery (nadir weight).
“The fact that both groups received lifestyle counseling from registered dietitians for just over a year, but only patients in the liraglutide group lost weight, on average, speaks to the difficulty of losing weight following weight regain post–bariatric surgery,” added Dr. King, an associate professor of epidemiology at the University of Pittsburgh, Pennsylvania.
This study “provides data that may help clinicians and patients understand the potential effect of adding liraglutide 3.0 mg/day to their weight loss efforts,” she told this news organization in an email.
However, “given that 42% of those on liraglutide reported gastrointestinal-related side effects, patients should also be counseled on this potential outcome and given suggestions for how to minimize such side effects,” Dr. King suggested.
Weight regain common, repeat surgery entails risk
Weight regain is common even years after bariatric surgery. Repeat surgery entails some risk, and lifestyle approaches alone are rarely successful in reversing weight regain, Dr. Lofton told the audience.
The researchers enrolled 132 adults who had a mean weight of 134 kg (295 pounds) when they underwent RYGB, and who lost at least 25% of their initial weight (mean weight loss of 38%) after the surgery, but who also regained at least 10% of their initial weight.
At enrollment of the current study (baseline), the patients had had RYGB 18 months to 10 years earlier (mean 5.7 years earlier) and now had a mean weight of 99 kg (218 pounds) and a mean BMI of 35.6 kg/m2. None of the patients had diabetes.
The patients were randomized to receive liraglutide (n = 89, 84% women) or placebo (n = 43, 88% women) for 56 weeks.
They were a mean age of 48 years, and about 59% were White and 25% were Black.
All patients had clinic visits every 3 months where they received lifestyle counseling from a registered dietitian.
At 12 months, patients in the liraglutide group had lost a mean of 8.8% of their baseline weight, whereas those in the placebo group had gained a mean of 1.48% of their baseline weight.
There were no significant between-group differences in cardiometabolic variables.
None of the patients in the control group attained a weight that was as low as their nadir weight after RYGB.
The rates of nausea (25%), constipation (16%), and abdominal pain (10%) in the liraglutide group were higher than in the placebo group (7%, 14%, and 5%, respectively) but similar to rates of gastrointestinal side effects in other trials of this agent.
Dr. Lofton has disclosed receiving consulting fees and being on a speaker bureau for Novo Nordisk and receiving research funds from Boehringer Ingelheim, Eli Lilly, and Novo Nordisk. Dr. King has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide (Saxenda, Novo Nordisk) was safe and effective for treating weight regain after Roux-en-Y gastric bypass (RYGB), in a randomized controlled trial.
That is, 132 patients who had lost at least 25% of their initial weight after RYGB and then gained at least 10% back were randomized 2:1 to receive liraglutide plus frequent lifestyle advice from a registered dietitian or lifestyle advice alone.
After a year, 69%, 48%, and 24% of patients who had received liraglutide lost at least 5%, 10%, and 15% of their study entry weight, respectively. In contrast, only 5% of patients in the control group lost at least 5% of their weight and none lost at least 10% of their weight.
“Liraglutide 3.0 mg/day, with lifestyle modification, was significantly more effective than placebo in treating weight regain after RYGB without increased risk of serious adverse events,” Holly F. Lofton, MD, summarized this week in an oral session at ObesityWeek®, the annual meeting of The Obesity Society.
Dr. Lofton, a clinical associate professor of surgery and medicine, and director, weight management program, NYU, Langone Health, explained to this news organization that she initiated the study after attending a “packed” session about post bariatric surgery weight regain at a prior American Society of Metabolic and Bariatric Surgery conference.
“The lecturers recommended conservative measures (such as reiterating the diet recommendations, exercise, [and] counseling), and revisional surgeries,” she said in an email, but at the time “there was no literature that provided direction on which pharmacotherapies are best for this population.”
It was known that decreases in endogenous GLP-1 levels coincide with weight regain, and liraglutide (Saxenda) was the only GLP-1 agonist approved for chronic weight management at the time, so she devised the current study protocol.
The findings are especially helpful for patients who are not candidates for bariatric surgery revisions, she noted. Further research is needed to investigate the effect of newer GLP-1 agonists, such as semaglutide (Wegovy), on weight regain following different types of bariatric surgery.
Asked to comment, Wendy C. King, PhD, who was not involved with this research, said that more than two-thirds of patients treated with 3 mg/day subcutaneous liraglutide injections in the current study lost at least 5% of their initial weight a year later, and 20% of them attained a weight as low as, or lower than, their lowest weight after bariatric surgery (nadir weight).
“The fact that both groups received lifestyle counseling from registered dietitians for just over a year, but only patients in the liraglutide group lost weight, on average, speaks to the difficulty of losing weight following weight regain post–bariatric surgery,” added Dr. King, an associate professor of epidemiology at the University of Pittsburgh, Pennsylvania.
This study “provides data that may help clinicians and patients understand the potential effect of adding liraglutide 3.0 mg/day to their weight loss efforts,” she told this news organization in an email.
However, “given that 42% of those on liraglutide reported gastrointestinal-related side effects, patients should also be counseled on this potential outcome and given suggestions for how to minimize such side effects,” Dr. King suggested.
Weight regain common, repeat surgery entails risk
Weight regain is common even years after bariatric surgery. Repeat surgery entails some risk, and lifestyle approaches alone are rarely successful in reversing weight regain, Dr. Lofton told the audience.
The researchers enrolled 132 adults who had a mean weight of 134 kg (295 pounds) when they underwent RYGB, and who lost at least 25% of their initial weight (mean weight loss of 38%) after the surgery, but who also regained at least 10% of their initial weight.
At enrollment of the current study (baseline), the patients had had RYGB 18 months to 10 years earlier (mean 5.7 years earlier) and now had a mean weight of 99 kg (218 pounds) and a mean BMI of 35.6 kg/m2. None of the patients had diabetes.
The patients were randomized to receive liraglutide (n = 89, 84% women) or placebo (n = 43, 88% women) for 56 weeks.
They were a mean age of 48 years, and about 59% were White and 25% were Black.
All patients had clinic visits every 3 months where they received lifestyle counseling from a registered dietitian.
At 12 months, patients in the liraglutide group had lost a mean of 8.8% of their baseline weight, whereas those in the placebo group had gained a mean of 1.48% of their baseline weight.
There were no significant between-group differences in cardiometabolic variables.
None of the patients in the control group attained a weight that was as low as their nadir weight after RYGB.
The rates of nausea (25%), constipation (16%), and abdominal pain (10%) in the liraglutide group were higher than in the placebo group (7%, 14%, and 5%, respectively) but similar to rates of gastrointestinal side effects in other trials of this agent.
Dr. Lofton has disclosed receiving consulting fees and being on a speaker bureau for Novo Nordisk and receiving research funds from Boehringer Ingelheim, Eli Lilly, and Novo Nordisk. Dr. King has reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM OBESITY WEEK 2021
Management of Acute and Chronic Pain Associated With Hidradenitis Suppurativa: A Comprehensive Review of Pharmacologic and Therapeutic Considerations in Clinical Practice
Hidradenitis suppurativa (HS) is a chronic inflammatory, androgen gland disorder characterized by recurrent rupture of the hair follicles with a vigorous inflammatory response. This response results in abscess formation and development of draining sinus tracts and hypertrophic fibrous scars.1,2 Pain, discomfort, and odorous discharge from the recalcitrant lesions have a profound impact on patient quality of life.3,4
The morbidity and disease burden associated with HS are particularly underestimated, as patients frequently report debilitating pain that often is overlooked.5,6 Additionally, the quality and intensity of perceived pain are compounded by frequently associated depression and anxiety.7-9 Pain has been reported by patients with HS to be the highest cause of morbidity, despite the disfiguring nature of the disease and its associated psychosocial distress.7,10 Nonetheless, HS lacks an accepted pain management algorithm similar to those that have been developed for the treatment of other acute or chronic pain disorders, such as back pain and sickle cell disease.4,11-13
Given the lack of formal studies regarding pain management in patients with HS, clinicians are limited to general pain guidelines, expert opinion, small trials, and patient preference.3 Furthermore, effective pain management in HS necessitates the treatment of both chronic pain affecting daily function and acute pain present during disease flares, surgical interventions, and dressing changes.3 The result is a wide array of strategies used for HS-associated pain.3,4
Epidemiology and Pathophysiology
Hidradenitis suppurativa historically has been an overlooked and underdiagnosed disease, which limits epidemiology data.5 Current estimates are that HS affects approximately 1% of the general population; however, prevalence rates range from 0.03% to 4.1%.14-16
The exact etiology of HS remains unclear, but it is thought that genetic factors, immune dysregulation, and environmental/behavioral influences all contribute to its pathophysiology.1,17 Up to 40% of patients with HS report a positive family history of the disease.18-20 Hidradenitis suppurativa has been associated with other inflammatory disease states, such as inflammatory bowel disease, spondyloarthropathies, and pyoderma gangrenosum.16,21,22
It is thought that HS is the result of some defect in keratin clearance that leads to follicular hyperkeratinization and occlusion.1 Resultant rupture of pilosebaceous units and spillage of contents (including keratin and bacteria) into the surrounding dermis triggers a vigorous inflammatory response. Sinus tracts and fistulas become the targets of bacterial colonization, biofilm formation, and secondary infection. The result is suppuration and extension of the lesions as well as sustained chronic inflammation.23,24
Although the etiology of HS is complex, several modifiable risk factors for the disease have been identified, most prominently cigarette smoking and obesity. Approximately 70% of patients with HS smoke cigarettes.2,15,25,26 Obesity has a well-known association with HS, and it is possible that weight reduction lowers disease severity.27-30
Clinical Presentation and Diagnosis
Establishing a diagnosis of HS necessitates recognition of disease morphology, topography, and chronicity. Hidradenitis suppurativa most commonly occurs in the axillae, inguinal and anogenital region, perineal region, and inframammary region.5,31 A typical history involves a prolonged disease course with recurrent lesions and intermittent periods of improvement or remission. Primary lesions are deep, inflamed, painful, and sterile. Ultimately, these lesions rupture and track subcutaneously.15,25 Intercommunicating sinus tracts form from multiple recurrent nodules in close proximity and may ultimately lead to fibrotic scarring and local architectural distortion.32 The Hurley staging system helps to guide treatment interventions based on disease severity. Approach to pain management is discussed below.
Pain Management in HS: General Principles
Pain management is complex for clinicians, as there are limited studies from which to draw treatment recommendations. Incomplete understanding of the etiology and pathophysiology of the disease contributes to the lack of established management guidelines.
A PubMed search of articles indexed for MEDLINE using the terms hidradenitis, suppurativa, pain, and management revealed 61 different results dating back to 1980, 52 of which had been published in the last 5 years. When the word acute was added to the search, there were only 6 results identified. These results clearly reflect a better understanding of HS-mediated pain as well as clinical unmet needs and evolving strategies in pain management therapeutics. However, many of these studies reflect therapies focused on the mediation or modulation of HS pathogenesis rather than potential pain management therapies.
In addition, the heterogenous nature of the pain experience in HS poses a challenge for clinicians. Patients may experience multiple pain types concurrently, including inflammatory, noninflammatory, nociceptive, neuropathic, and ischemic, as well as pain related to arthritis.3,33,34 Pain perception is further complicated by the observation that patients with HS have high rates of psychiatric comorbidities such as depression and anxiety, both of which profoundly alter perception of both the strength and quality of pain.7,8,22,35 A suggested algorithm for treatment of pain in HS is described in the eTable.36
Chronicity is a hallmark of HS. Patients experience a prolonged disease course involving acute painful exacerbations superimposed on chronic pain that affects all aspects of daily life. Changes in self-perception, daily living activities, mood state, physical functioning, and physical comfort frequently are reported to have a major impact on quality of life.1,3,37
In 2018, Thorlacius et al38 created a multistakeholder consensus on a core outcome set of domains detailing what to measure in clinical trials for HS. The authors hoped that the routine adoption of these core domains would promote the collection of consistent and relevant information, bolster the strength of evidence synthesis, and minimize the risk for outcome reporting bias among studies.38 It is important to ascertain the patient’s description of his/her pain to distinguish between stimulus-dependent nociceptive pain vs spontaneous neuropathic pain.3,7,10 The most common pain descriptors used by patients are “shooting,” “itchy,” “blinding,” “cutting,” and “exhausting.”10 In addition to obtaining descriptive factors, it is important for the clinician to obtain information on the timing of the pain, whether or not the pain is relieved with spontaneous or surgical drainage, and if the patient is experiencing chronic background pain secondary to scarring or skin contraction.3 With the routine utilization of a consistent set of core domains, advances in our understanding of the different elements of HS pain, and increased provider awareness of the disease, the future of pain management in patients with HS seems promising.
Acute and Perioperative Pain Management
Acute Pain Management—The pain in HS can range from mild to excruciating.3,7 The difference between acute and chronic pain in this condition may be hard to delineate, as patients may have intense acute flares on top of a baseline level of chronic pain.3,7,14 These factors, in combination with various pain types of differing etiologies, make the treatment of HS-associated pain a therapeutic challenge.
The first-line treatments for acute pain in HS are oral acetaminophen, oral nonsteroidal anti-inflammatory drugs (NSAIDs), and topical analgesics.3 These treatment modalities are especially helpful for nociceptive pain, which often is described as having an aching or tender quality.3 Topical treatment for acute pain episodes includes diclofenac gel and liposomal lidocaine cream.39 Topical lidocaine in particular has the benefit of being rapid acting, and its effect can last 1 to 2 hours. Ketamine has been anecdotally used as a topical treatment. Treatment options for neuropathic pain include topical amitriptyline, gabapentin, and pregabalin.39 Dressings and ice packs may be used in cases of mild acute pain, depending on patient preference.3
First-line therapies may not provide adequate pain control in many patients.3,40,41 Should the first-line treatments fail, oral opiates can be considered as a treatment option, especially if the patient has a history of recurrent pain unresponsive to milder methods of pain control.3,40,41 However, prudence should be exercised, as patients with HS have a higher risk for opioid abuse, and referral to a pain specialist is advisable.40 Generally, use of opioids should be limited to the smallest period of time possible.40,41 Codeine can be used as a first opioid option, with hydromorphone available as an alternative.41
Pain caused by inflamed abscesses and nodules can be treated with either intralesional corticosteroids or incision and drainage. Intralesional triamcinolone has been found to cause substantial pain relief within 1 day of injection in patients with HS.3,42
Prompt discussion about the remitting course of HS will prepare patients for flares. Although the therapies discussed here aim to reduce the clinical severity and inflammation associated with HS, achieving pain-free remission can be challenging. Barriers to developing a long-term treatment regimen include intolerable side effects or simply nonresponsive disease.36,43
Management of Perioperative Pain—Medical treatment of HS often yields only transient or mild results. Hurley stage II or III lesions typically require surgical removal of affected tissues.32,44-46 Surgery may dramatically reduce the primary disease burden and provide substantial pain relief.3,4,44 Complete resection of the affected tissue by wide excision is the most common surgical procedure used.46-48 However, various tissue-sparing techniques, such as skin-tissue-sparing excision with electrosurgical peeling, also have been utilized. Tissue-sparing surgical techniques may lead to shorter healing times and less postoperative pain.48
There currently is little guidance available on the perioperative management of pain as it relates to surgical procedures for HS. The pain experienced from surgery varies based on the area and location of affected tissue; extent of disease; surgical technique used; and whether primary closure, closure by secondary intention, or skin grafting is utilized.47,49 Medical treatment aimed at reducing inflammation prior to surgical intervention may improve postoperative pain and complications.
The use of general vs local anesthesia during surgery depends on the extent of the disease and the amount of tissue being removed; however, the use of local anesthesia has been associated with a higher recurrence of disease, possibly owing to less aggressive tissue removal.50 Intraoperatively, the injection of 0.5% bupivacaine around the wound edges may lead to less postoperative pain.3,48 Postoperative pain usually is managed with acetaminophen and NSAIDs.48 In cases of severe postoperative pain, short- and long-acting opioid oxycodone preparations may be used. The combination of diclofenac and tramadol also has been used postoperatively.3 Patients who do not undergo extensive surgery often can leave the hospital the same day.
Effective strategies for mitigating HS-associated pain must address the chronic pain component of the disease. Long-term management involves lifestyle modifications and pharmacologic agents.
Chronic Pain Management
Although HS is not a curable disease, there are treatments available to minimize symptoms. Long-term management of HS is essential to minimize the effects of chronic pain and physical scarring associated with inflammation.31 In one study from the French Society of Dermatology, pain reported by patients with HS was directly associated with severity and duration of disease, emotional symptoms, and reduced functionality.51 For these reasons, many treatments for HS target reducing clinical severity and achieving remission, often defined as more than 6 months without any recurrence of lesions.52 In addition to lifestyle management, therapies available to manage HS include topical and systemic medications as well as procedures such as surgical excision.36,43,52,53
Lifestyle Modifications
Regardless of the severity of HS, all patients may benefit from basic education on the pathogenesis of the disease.36 The associations with smoking and obesity have been well documented, and treatment of these comorbid conditions is indicated.36,43,52 For example, in relation to obesity, the use of metformin is very well tolerated and seems to positively impact HS symptoms.43 Several studies have suggested that weight reduction lowers disease severity.28-30 Patients should be counseled on the importance of smoking cessation and weight loss.
Finally, the emotional impact of HS is not to be discounted, both the physical and social discomfort as well as the chronicity of the disease and frustration with treatment.51 Chronic pain has been associated with increased rates of depression, and 43% of patients with HS specifically have been diagnosed with major depressive disorder.7 For these reasons, clinician guidance, social support, and websites can improve patient understanding of the disease, adherence to treatment, and comorbid anxiety and depression.52
Topical Therapy
Topical therapy generally is limited to mild disease and is geared at decreasing inflammation or superimposed infection.36,52 Some of the earliest therapies used were topical antibiotics.43 Topical clindamycin has been shown to be as effective as oral tetracyclines in reducing the number of abscesses, but neither treatment substantially reduces pain associated with smaller nodules.54 Intralesional corticosteroids such as triamcinolone acetonide have been shown to decrease both patient-reported pain and physician-assessed severity within 1 to 7 days.42 Routine injection, however, is not a feasible means of long-term treatment both because of inconvenience and the potential adverse effects of corticosteroids.36,52 Both topical clindamycin and intralesional steroids are helpful in reducing inflammation prior to planned surgical intervention.36,52,53
Newer topical therapies include resorcinol peels and combination antimicrobials, such as 2% triclosan and oral zinc gluconate.52,53 Data surrounding the use of resorcinol in mild to moderate HS are promising and have shown decreased severity of both new and long-standing nodules. Fifteen-percent resorcinol peels are helpful tools that allow for self-administration by patients during exacerbations to decrease pain and flare duration.55,56 In a 2016 clinical trial, a combination of oral zinc gluconate with topical triclosan was shown to reduce flare-ups and nodules in mild HS.57 Oral zinc alone may have anti-inflammatory properties and generally is well tolerated.43,53 Topical therapies have a role in reducing HS-associated pain but often are limited to milder disease.
Systemic Agents
Several therapeutic options exist for the treatment of HS; however, a detailed description of their mechanisms and efficacies is beyond the scope of this review, which is focused on pain. Briefly, these systemic agents include antibiotics, retinoids, corticosteroids, antiandrogens, and biologics.43,52,53
Treatment with antibiotics such as tetracyclines or a combination of clindamycin plus rifampin has been shown to produce complete remission in 60% to 80% of users; however, this treatment requires more than 6 months of antibiotic therapy, which can be difficult to tolerate.52,53,58 Relapse is common after antibiotic cessation.2,43,52 Antibiotics have demonstrated efficacy during acute flares and in reducing inflammatory activity prior to surgery.52
Retinoids have been utilized in the treatment of HS because of their action on sebaceous glands and hair follicles.43,53 Acitretin has been shown to be the most effective oral retinoid available in the United States.43 Unfortunately, many of the studies investigating the use of retinoids for treatment of HS are limited by small sample size.36,43,52
Because HS is predominantly an inflammatory condition, immunosuppressants have been adapted to manage patients when antibiotics and topicals have failed. Systemic steroids rarely are used for long-term therapy because of the severe side effects and are preferred only for acute management.36,52 Cyclosporine and dapsone have demonstrated efficacy in treating moderate to severe HS, whereas methotrexate and colchicine have shown little efficacy.52 Both cyclosporine and dapsone are difficult to tolerate, require laboratory monitoring, and lead to only conservative improvement rather than remission in most patients.43
Immune dysregulation in HS involves elevated levels of proinflammatory cytokines such as tumor necrosis factor α (TNF-α), which is a key mediator of inflammation and a stimulator of other inflammatory cytokines.59,60 The first approved biologic treatment of HS was adalimumab, a TNF-α inhibitor, which showed a 50% reduction in total abscess and inflammatory nodule count in 60% of patients with moderate to severe HS.61-63 Of course, TNF-α inhibitor therapy is not without risks, specifically those of infection.43,53,61,62 Maintenance therapy may be required if patients relapse.53,61
Various interleukin inhibitors also have emerged as potential therapies for HS, such as ustekinumab and anakinra.36,64 Both have been subject to numerous small case trials that have reported improvements in clinical severity and pain; however, both drugs were associated with a fair number of nonresponders.36,64,65
Surgical Procedures
Although HS lesions may regress on their own in a matter of weeks, surgical drainage allows an acute alleviation of the severe burning pain associated with HS flares.36,52,53 Because of improved understanding of the disease pathophysiology, recent therapies targeting the hair follicle have been developed and have shown promising results. These therapies include laser- and light-based procedures. Long-pulsed Nd:YAG laser therapy reduces the number of hair follicles and sebaceous glands and has been effective for Hurley stage I or II disease.36,43,52,53,66 Photodynamic therapy offers a less-invasive option compared to surgery and laser therapy.52,53,66 Both Nd:YAG and CO2 laser therapy offer low recurrence rates (<30%) due to destruction of the apocrine unit.43,53 Photodynamic therapy for mild disease offers a less-invasive option compared to surgery and laser therapy.53 There is a need for larger randomized controlled trials involving laser, light, and CO2 therapies.66
Conclusion
Hidradenitis suppurativa is a debilitating condition with an underestimated disease burden. Although the pathophysiology of the disease is not completely understood, it is evident that pain is a major cause of morbidity. Patients experience a multitude of acute and chronic pain types: inflammatory, noninflammatory, nociceptive, neuropathic, and ischemic. Pain perception and quality of life are further impacted by psychiatric conditions such as depression and anxiety, both of which are common comorbidities in patients with HS. Several pharmacologic agents have been used to treat HS-associated pain with mixed results. First-line treatment of acute pain episodes includes oral acetaminophen, NSAIDs, and topical analgesics. Management of chronic pain includes utilization of topical agents, systemic agents, and biologics, as well as addressing lifestyle (eg, obesity, smoking status) and psychiatric comorbidities. Although these therapies have roles in HS pain management, the most effective pain remedies developed thus far are limited to surgery and TNF-α inhibitors. Optimization of pain control in patients with HS requires multidisciplinary collaboration among dermatologists, pain specialists, psychiatrists, and other members of the health care team. Further large-scale studies are needed to create an evidence-based treatment algorithm for the management of pain in HS.
- Napolitano M, Megna M, Timoshchuk EA, et al. Hidradenitis suppurativa: from pathogenesis to diagnosis and treatment. Clin Cosmet Investig Dermatol. 2017;10:105-115. doi:10.2147/CCID.S111019
- Revuz J. Hidradenitis suppurativa. J Eur Acad Dermatology Venereol. 2009;23:985-998. doi:10.1111/j.1468-3083.2009.03356.x
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- Puza CJ, Wolfe SA, Jaleel T. Pain management in patients with hidradenitis suppurativa requiring surgery. Dermatolog Surg. 2019;45:1327-1330. doi:10.1097/DSS.0000000000001693
- Kurzen H, Kurokawa I, Jemec GBE, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17:455-456. doi:10.1111/j.1600-0625.2008.00712_1.x
- Kelly G, Sweeney CM, Tobin AM, et al. Hidradenitis suppurativa: the role of immune dysregulation. Int J Dermatol. 2014;53:1186-1196. doi:10.1111/ijd.12550
- Patel ZS, Hoffman LK, Buse DC, et al. Pain, psychological comorbidities, disability, and impaired quality of life in hidradenitis suppurativa. Curr Pain Headache Rep. 2017;21:49. doi:10.1007/s11916-017-0647-3
- Sist TC, Florio GA, Miner MF, et al. The relationship between depression and pain language in cancer and chronic non-cancer pain patients. J Pain Symptom Manage. 1998;15:350-358. doi:10.1016/S0885-3924(98)00006-2
- Jemec GBE. Hidradenitis suppurativa. N Engl J Med. 2012;366:158-164. doi:10.1056/NEJMcp1014163
- Nielsen RM, Lindsø Andersen P, Sigsgaard V, et al. Pain perception in patients with hidradenitis suppurativa. Br J Dermatol. 2019;182:bjd.17935. doi:10.1111/bjd.17935
- Tanabe P, Myers R, Zosel A, et al. Emergency department management of acute pain episodes in sickle cell disease. Acad Emerg Med. 2007;14:419-425. doi:10.1197/j.aem.2006.11.033
- Chou R, Loeser JD, Owens DK, et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: an evidence-based clinical practice guideline from the American Pain Society. Spine (Phila Pa 1976). 2009;34:1066-1077. doi:10.1097/BRS.0b013e3181a1390d
- Enamandram M, Rathmell JP, Kimball AB. Chronic pain management in dermatology: a guide to assessment and nonopioid pharmacotherapy. J Am Acad Dermatol. 2015;73:563-573; quiz 573-574. doi:10.1016/j.jaad.2014.11.039
- Jemec GBE, Kimball AB. Hidradenitis suppurativa: epidemiology and scope of the problem. J Am Acad Dermatol. 2015;73(5 suppl 1):S4-S7. doi:10.1016/j.jaad.2015.07.052
- Vinkel C, Thomsen SF. Hidradenitis suppurativa: causes, features, and current treatments. J Clin Aesthet Dermatol. 2018;11:17-23.
- Patil S, Apurwa A, Nadkarni N, et al. Hidradenitis suppurativa: inside and out. Indian J Dermatol. 2018;63:91-98. doi:10.4103/ijd.IJD_412_16
- Woodruff CM, Charlie AM, Leslie KS. Hidradenitis suppurativa: a guide for the practicing physician. Mayo Clin Proc. 2015;90:1679-1693. doi:10.1016/j.mayocp.2015.08.020
- Pink AE, Simpson MA, Desai N, et al. Mutations in the γ-secretase genes NCSTN, PSENEN, and PSEN1 underlie rare forms of hidradenitis suppurativa (acne inversa). J Invest Dermatol. 2012;132:2459-2461. doi:10.1038/jid.2012.162
- Jemec GBE, Heidenheim M, Nielsen NH. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol. 1996;35:191-194. doi:10.1016/s0190-9622(96)90321-7
- Fitzsimmons JS, Guilbert PR. A family study of hidradenitis suppurativa. J Med Genet. 1985;22:367-373. doi:10.1136/jmg.22.5.367
- Kelly G, Prens EP. Inflammatory mechanisms in hidradenitis suppurativa. Dermatol Clin. 2016;34:51-58. doi:10.1016/j.det.2015.08.004
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- Kathju S, Lasko LA, Stoodley P. Considering hidradenitis suppurativa as a bacterial biofilm disease. FEMS Immunol Med Microbiol. 2012;65:385-389. doi:10.1111/j.1574-695X.2012.00946.x
- Jahns AC, Killasli H, Nosek D, et al. Microbiology of hidradenitis suppurativa (acne inversa): a histological study of 27 patients. APMIS. 2014;122:804-809. doi:10.1111/apm.12220
- Ralf Paus L, Kurzen H, Kurokawa I, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17:455-456. doi:10.1111/j.1600-0625.2008.00712_1.x
- Vazquez BG, Alikhan A, Weaver AL, et al. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;133:97-103. doi:10.1038/jid.2012.255
- Kromann CB, Ibler KS, Kristiansen VB, et al. The influence of body weight on the prevalence and severity of hidradenitis suppurativa. Acta Derm Venereol. 2014;94:553-557. doi:10.2340/00015555-1800
- Lindsø Andersen P, Kromann C, Fonvig CE, et al. Hidradenitis suppurativa in a cohort of overweight and obese children and adolescents. Int J Dermatol. 2020;59:47-51. doi:10.1111/ijd.14639
- Revuz JE, Canoui-Poitrine F, Wolkenstein P, et al. Prevalence and factors associated with hidradenitis suppurativa: results from two case-control studies. J Am Acad Dermatol. 2008;59:596-601. doi:10.1016/j.jaad.2008.06.020
- Kromann CB, Deckers IE, Esmann S, et al. Risk factors, clinical course and long-term prognosis in hidradenitis suppurativa: a cross-sectional study. Br J Dermatol. 2014;171:819-824. doi:10.1111/bjd.13090
- Wieczorek M, Walecka I. Hidradenitis suppurativa—known and unknown disease. Reumatologia. 2018;56:337-339. doi:10.5114/reum.2018.80709
- Hsiao J, Leslie K, McMichael A, et al. Folliculitis and other follicular disorders. In: Bolognia J, Schaffer J, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:615-632.
- Scheinfeld N. Treatment of hidradenitis suppurativa associated pain with nonsteroidal anti-inflammatory drugs, acetaminophen, celecoxib, gapapentin, pegabalin, duloxetine, and venlafaxine. Dermatol Online J. 2013;19:20616.
- Scheinfeld N. Hidradenitis suppurativa: a practical review of possible medical treatments based on over 350 hidradenitis patients. Dermatol Online J. 2013;19:1.
- Rajmohan V, Suresh Kumar S. Psychiatric morbidity, pain perception, and functional status of chronic pain patients in palliative care. Indian J Palliat Care. 2013;19:146-151. doi:10.4103/0973-1075.121527
- Saunte DML, Jemec GBE. Hidradenitis suppurativa: advances in diagnosis and treatment. JAMA. 2017;318:2019-2032. doi:10.1001/jama.2017.16691
- Wang B, Yang W, Wen W, et al. Gamma-secretase gene mutations in familial acne inversa. Science. 2010;330:1065. doi:10.1126/science.1196284
- Thorlacius L, Ingram JR, Villumsen B, et al. A core domain set for hidradenitis suppurativa trial outcomes: an international Delphi process. Br J Dermatol. 2018;179:642-650. doi:10.1111/bjd.16672
- Scheinfeld N. Topical treatments of skin pain: a general review with a focus on hidradenitis suppurativa with topical agents. Dermatol Online J. 2014;20:13030/qt4m57506k.
- Reddy S, Orenstein LAV, Strunk A, et al. Incidence of long-term opioid use among opioid-naive patients with hidradenitis suppurativa in the United States. JAMA Dermatol. 2019;155:1284-1290. doi:10.1001/jamadermatol.2019.2610
- Zouboulis CC, Desai N, Emtestam L, et al. European S1 guideline for the treatment of hidradenitis suppurativa/acne inversa. J Eur Acad Dermatology Venereol. 2015;29:619-644. doi:10.1111/jdv.12966
- Riis PT, Boer J, Prens EP, et al. Intralesional triamcinolone for flares of hidradenitis suppurativa (HS): a case series. J Am Acad Dermatol. 2016;75:1151-1155. doi:10.1016/j.jaad.2016.06.049
- Robert E, Bodin F, Paul C, et al. Non-surgical treatments for hidradenitis suppurativa: a systematic review. Ann Chir Plast Esthet. 2017;62:274-294. doi:10.1016/j.anplas.2017.03.012
- Menderes A, Sunay O, Vayvada H, et al. Surgical management of hidradenitis suppurativa. Int J Med Sci. 2010;7:240-247. doi:10.7150/ijms.7.240
- Alharbi Z, Kauczok J, Pallua N. A review of wide surgical excision of hidradenitis suppurativa. BMC Dermatol. 2012;12:9. doi:10.1186/1471-5945-12-9
- Burney RE. 35-year experience with surgical treatment of hidradenitis suppurativa. World J Surg. 2017;41:2723-2730. doi:10.1007/s00268-017-4091-7
- Bocchini SF, Habr-Gama A, Kiss DR, et al. Gluteal and perianal hidradenitis suppurativa: surgical treatment by wide excision. Dis Colon Rectum. 2003;46:944-949. doi:10.1007/s10350-004-6691-1
- Blok JL, Spoo JR, Leeman FWJ, et al. Skin-tissue-sparing excision with electrosurgical peeling (STEEP): a surgical treatment option for severe hidradenitis suppurativa Hurley stage II/III. J Eur Acad Dermatol Venereol. 2015;29:379-382. doi:10.1111/jdv.12376
- Bilali S, Todi V, Lila A, et al. Surgical treatment of chronic hidradenitis suppurativa in the gluteal and perianal regions. Acta Chir Iugosl. 2012;59:91-95. doi:10.2298/ACI1202091B
- Walter AC, Meissner M, Kaufmann R, et al. Hidradenitis suppurativa after radical surgery-long-term follow-up for recurrences and associated factors. Dermatol Surg. 2018;44:1323-1331. doi:10.1097/DSS.0000000000001668.
- Wolkenstein P, Loundou A, Barrau K, et al. Quality of life impairment in hidradenitis suppurativa: a study of 61 cases. J Am Acad Dermatol. 2007;56:621-623. doi:10.1016/j.jaad.2006.08.061
- Alavi A, Lynde C, Alhusayen R, et al. Approach to the management of patients with hidradenitis suppurativa: a consensus document. J Cutan Med Surg. 2017;21:513-524. doi:10.1177/1203475417716117
- Duran C, Baumeister A. Recognition, diagnosis, and treatment of hidradenitis suppurativa. J Am Acad Physician Assist. 2019;32:36-42. doi:10.1097/01.JAA.0000578768.62051.13
- Jemec GBE, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of hidradenitis suppurativa. J Am Acad Dermatol. 1998;39:971-974. doi:10.1016/S0190-9622(98)70272-5
- Pascual JC, Encabo B, Ruiz de Apodaca RF, et al. Topical 15% resorcinol for hidradenitis suppurativa: an uncontrolled prospective trial with clinical and ultrasonographic follow-up. J Am Acad Dermatol. 2017;77:1175-1178. doi:10.1016/j.jaad.2017.07.008
- Boer J, Jemec GBE. Resorcinol peels as a possible self-treatment of painful nodules in hidradenitis suppurativa. Clin Exp Dermatol. 2010;35:36-40. doi:10.1111/j.1365-2230.2009.03377.x
- Hessam S, Sand M, Meier NM, et al. Combination of oral zinc gluconate and topical triclosan: an anti-inflammatory treatment modality for initial hidradenitis suppurativa. J Dermatol Sci. 2016;84:197-202. doi:10.1016/j.jdermsci.2016.08.010
- Gener G, Canoui-Poitrine F, Revuz JE, et al. Combination therapy with clindamycin and rifampicin for hidradenitis suppurativa: a series of 116 consecutive patients. Dermatology. 2009;219:148-154. doi:10.1159/000228334
- Vossen ARJV, van der Zee HH, Prens EP. Hidradenitis suppurativa: a systematic review integrating inflammatory pathways into a cohesive pathogenic model. Front Immunol. 2018;9:2965. doi:10.3389/fimmu.2018.02965
- Chu WM. Tumor necrosis factor. Cancer Lett. 2013;328:222-225. doi:10.1016/j.canlet.2012.10.014
- Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375:422-434. doi:10.1056/NEJMoa1504370
- Morita A, Takahashi H, Ozawa K, et al. Twenty-four-week interim analysis from a phase 3 open-label trial of adalimumab in Japanese patients with moderate to severe hidradenitis suppurativa. J Dermatol. 2019;46:745-751. doi:10.1111/1346-8138.14997
- Ghias MH, Johnston AD, Kutner AJ, et al. High-dose, high-frequency infliximab: a novel treatment paradigm for hidradenitis suppurativa. J Am Acad Dermatol. 2020;82:1094-1101. doi:10.1016/j.jaad.2019.09.071
- Tzanetakou V, Kanni T, Giatrakou S, et al. Safety and efficacy of anakinra in severe hidradenitis suppurativa a randomized clinical trial. JAMA Dermatol. 2016;152:52-59. doi:10.1001/jamadermatol.2015.3903
- Blok JL, Li K, Brodmerkel C, et al. Ustekinumab in hidradenitis suppurativa: clinical results and a search for potential biomarkers in serum. Br J Dermatol. 2016;174:839-846. doi:10.1111/bjd.14338
- John H, Manoloudakis N, Stephen Sinclair J. A systematic review of the use of lasers for the treatment of hidradenitis suppurativa. J Plast Reconstr Aesthet Surg. 2016;69:1374-1381. doi:10.1016/j.bjps.2016.05.029
Hidradenitis suppurativa (HS) is a chronic inflammatory, androgen gland disorder characterized by recurrent rupture of the hair follicles with a vigorous inflammatory response. This response results in abscess formation and development of draining sinus tracts and hypertrophic fibrous scars.1,2 Pain, discomfort, and odorous discharge from the recalcitrant lesions have a profound impact on patient quality of life.3,4
The morbidity and disease burden associated with HS are particularly underestimated, as patients frequently report debilitating pain that often is overlooked.5,6 Additionally, the quality and intensity of perceived pain are compounded by frequently associated depression and anxiety.7-9 Pain has been reported by patients with HS to be the highest cause of morbidity, despite the disfiguring nature of the disease and its associated psychosocial distress.7,10 Nonetheless, HS lacks an accepted pain management algorithm similar to those that have been developed for the treatment of other acute or chronic pain disorders, such as back pain and sickle cell disease.4,11-13
Given the lack of formal studies regarding pain management in patients with HS, clinicians are limited to general pain guidelines, expert opinion, small trials, and patient preference.3 Furthermore, effective pain management in HS necessitates the treatment of both chronic pain affecting daily function and acute pain present during disease flares, surgical interventions, and dressing changes.3 The result is a wide array of strategies used for HS-associated pain.3,4
Epidemiology and Pathophysiology
Hidradenitis suppurativa historically has been an overlooked and underdiagnosed disease, which limits epidemiology data.5 Current estimates are that HS affects approximately 1% of the general population; however, prevalence rates range from 0.03% to 4.1%.14-16
The exact etiology of HS remains unclear, but it is thought that genetic factors, immune dysregulation, and environmental/behavioral influences all contribute to its pathophysiology.1,17 Up to 40% of patients with HS report a positive family history of the disease.18-20 Hidradenitis suppurativa has been associated with other inflammatory disease states, such as inflammatory bowel disease, spondyloarthropathies, and pyoderma gangrenosum.16,21,22
It is thought that HS is the result of some defect in keratin clearance that leads to follicular hyperkeratinization and occlusion.1 Resultant rupture of pilosebaceous units and spillage of contents (including keratin and bacteria) into the surrounding dermis triggers a vigorous inflammatory response. Sinus tracts and fistulas become the targets of bacterial colonization, biofilm formation, and secondary infection. The result is suppuration and extension of the lesions as well as sustained chronic inflammation.23,24
Although the etiology of HS is complex, several modifiable risk factors for the disease have been identified, most prominently cigarette smoking and obesity. Approximately 70% of patients with HS smoke cigarettes.2,15,25,26 Obesity has a well-known association with HS, and it is possible that weight reduction lowers disease severity.27-30
Clinical Presentation and Diagnosis
Establishing a diagnosis of HS necessitates recognition of disease morphology, topography, and chronicity. Hidradenitis suppurativa most commonly occurs in the axillae, inguinal and anogenital region, perineal region, and inframammary region.5,31 A typical history involves a prolonged disease course with recurrent lesions and intermittent periods of improvement or remission. Primary lesions are deep, inflamed, painful, and sterile. Ultimately, these lesions rupture and track subcutaneously.15,25 Intercommunicating sinus tracts form from multiple recurrent nodules in close proximity and may ultimately lead to fibrotic scarring and local architectural distortion.32 The Hurley staging system helps to guide treatment interventions based on disease severity. Approach to pain management is discussed below.
Pain Management in HS: General Principles
Pain management is complex for clinicians, as there are limited studies from which to draw treatment recommendations. Incomplete understanding of the etiology and pathophysiology of the disease contributes to the lack of established management guidelines.
A PubMed search of articles indexed for MEDLINE using the terms hidradenitis, suppurativa, pain, and management revealed 61 different results dating back to 1980, 52 of which had been published in the last 5 years. When the word acute was added to the search, there were only 6 results identified. These results clearly reflect a better understanding of HS-mediated pain as well as clinical unmet needs and evolving strategies in pain management therapeutics. However, many of these studies reflect therapies focused on the mediation or modulation of HS pathogenesis rather than potential pain management therapies.
In addition, the heterogenous nature of the pain experience in HS poses a challenge for clinicians. Patients may experience multiple pain types concurrently, including inflammatory, noninflammatory, nociceptive, neuropathic, and ischemic, as well as pain related to arthritis.3,33,34 Pain perception is further complicated by the observation that patients with HS have high rates of psychiatric comorbidities such as depression and anxiety, both of which profoundly alter perception of both the strength and quality of pain.7,8,22,35 A suggested algorithm for treatment of pain in HS is described in the eTable.36
Chronicity is a hallmark of HS. Patients experience a prolonged disease course involving acute painful exacerbations superimposed on chronic pain that affects all aspects of daily life. Changes in self-perception, daily living activities, mood state, physical functioning, and physical comfort frequently are reported to have a major impact on quality of life.1,3,37
In 2018, Thorlacius et al38 created a multistakeholder consensus on a core outcome set of domains detailing what to measure in clinical trials for HS. The authors hoped that the routine adoption of these core domains would promote the collection of consistent and relevant information, bolster the strength of evidence synthesis, and minimize the risk for outcome reporting bias among studies.38 It is important to ascertain the patient’s description of his/her pain to distinguish between stimulus-dependent nociceptive pain vs spontaneous neuropathic pain.3,7,10 The most common pain descriptors used by patients are “shooting,” “itchy,” “blinding,” “cutting,” and “exhausting.”10 In addition to obtaining descriptive factors, it is important for the clinician to obtain information on the timing of the pain, whether or not the pain is relieved with spontaneous or surgical drainage, and if the patient is experiencing chronic background pain secondary to scarring or skin contraction.3 With the routine utilization of a consistent set of core domains, advances in our understanding of the different elements of HS pain, and increased provider awareness of the disease, the future of pain management in patients with HS seems promising.
Acute and Perioperative Pain Management
Acute Pain Management—The pain in HS can range from mild to excruciating.3,7 The difference between acute and chronic pain in this condition may be hard to delineate, as patients may have intense acute flares on top of a baseline level of chronic pain.3,7,14 These factors, in combination with various pain types of differing etiologies, make the treatment of HS-associated pain a therapeutic challenge.
The first-line treatments for acute pain in HS are oral acetaminophen, oral nonsteroidal anti-inflammatory drugs (NSAIDs), and topical analgesics.3 These treatment modalities are especially helpful for nociceptive pain, which often is described as having an aching or tender quality.3 Topical treatment for acute pain episodes includes diclofenac gel and liposomal lidocaine cream.39 Topical lidocaine in particular has the benefit of being rapid acting, and its effect can last 1 to 2 hours. Ketamine has been anecdotally used as a topical treatment. Treatment options for neuropathic pain include topical amitriptyline, gabapentin, and pregabalin.39 Dressings and ice packs may be used in cases of mild acute pain, depending on patient preference.3
First-line therapies may not provide adequate pain control in many patients.3,40,41 Should the first-line treatments fail, oral opiates can be considered as a treatment option, especially if the patient has a history of recurrent pain unresponsive to milder methods of pain control.3,40,41 However, prudence should be exercised, as patients with HS have a higher risk for opioid abuse, and referral to a pain specialist is advisable.40 Generally, use of opioids should be limited to the smallest period of time possible.40,41 Codeine can be used as a first opioid option, with hydromorphone available as an alternative.41
Pain caused by inflamed abscesses and nodules can be treated with either intralesional corticosteroids or incision and drainage. Intralesional triamcinolone has been found to cause substantial pain relief within 1 day of injection in patients with HS.3,42
Prompt discussion about the remitting course of HS will prepare patients for flares. Although the therapies discussed here aim to reduce the clinical severity and inflammation associated with HS, achieving pain-free remission can be challenging. Barriers to developing a long-term treatment regimen include intolerable side effects or simply nonresponsive disease.36,43
Management of Perioperative Pain—Medical treatment of HS often yields only transient or mild results. Hurley stage II or III lesions typically require surgical removal of affected tissues.32,44-46 Surgery may dramatically reduce the primary disease burden and provide substantial pain relief.3,4,44 Complete resection of the affected tissue by wide excision is the most common surgical procedure used.46-48 However, various tissue-sparing techniques, such as skin-tissue-sparing excision with electrosurgical peeling, also have been utilized. Tissue-sparing surgical techniques may lead to shorter healing times and less postoperative pain.48
There currently is little guidance available on the perioperative management of pain as it relates to surgical procedures for HS. The pain experienced from surgery varies based on the area and location of affected tissue; extent of disease; surgical technique used; and whether primary closure, closure by secondary intention, or skin grafting is utilized.47,49 Medical treatment aimed at reducing inflammation prior to surgical intervention may improve postoperative pain and complications.
The use of general vs local anesthesia during surgery depends on the extent of the disease and the amount of tissue being removed; however, the use of local anesthesia has been associated with a higher recurrence of disease, possibly owing to less aggressive tissue removal.50 Intraoperatively, the injection of 0.5% bupivacaine around the wound edges may lead to less postoperative pain.3,48 Postoperative pain usually is managed with acetaminophen and NSAIDs.48 In cases of severe postoperative pain, short- and long-acting opioid oxycodone preparations may be used. The combination of diclofenac and tramadol also has been used postoperatively.3 Patients who do not undergo extensive surgery often can leave the hospital the same day.
Effective strategies for mitigating HS-associated pain must address the chronic pain component of the disease. Long-term management involves lifestyle modifications and pharmacologic agents.
Chronic Pain Management
Although HS is not a curable disease, there are treatments available to minimize symptoms. Long-term management of HS is essential to minimize the effects of chronic pain and physical scarring associated with inflammation.31 In one study from the French Society of Dermatology, pain reported by patients with HS was directly associated with severity and duration of disease, emotional symptoms, and reduced functionality.51 For these reasons, many treatments for HS target reducing clinical severity and achieving remission, often defined as more than 6 months without any recurrence of lesions.52 In addition to lifestyle management, therapies available to manage HS include topical and systemic medications as well as procedures such as surgical excision.36,43,52,53
Lifestyle Modifications
Regardless of the severity of HS, all patients may benefit from basic education on the pathogenesis of the disease.36 The associations with smoking and obesity have been well documented, and treatment of these comorbid conditions is indicated.36,43,52 For example, in relation to obesity, the use of metformin is very well tolerated and seems to positively impact HS symptoms.43 Several studies have suggested that weight reduction lowers disease severity.28-30 Patients should be counseled on the importance of smoking cessation and weight loss.
Finally, the emotional impact of HS is not to be discounted, both the physical and social discomfort as well as the chronicity of the disease and frustration with treatment.51 Chronic pain has been associated with increased rates of depression, and 43% of patients with HS specifically have been diagnosed with major depressive disorder.7 For these reasons, clinician guidance, social support, and websites can improve patient understanding of the disease, adherence to treatment, and comorbid anxiety and depression.52
Topical Therapy
Topical therapy generally is limited to mild disease and is geared at decreasing inflammation or superimposed infection.36,52 Some of the earliest therapies used were topical antibiotics.43 Topical clindamycin has been shown to be as effective as oral tetracyclines in reducing the number of abscesses, but neither treatment substantially reduces pain associated with smaller nodules.54 Intralesional corticosteroids such as triamcinolone acetonide have been shown to decrease both patient-reported pain and physician-assessed severity within 1 to 7 days.42 Routine injection, however, is not a feasible means of long-term treatment both because of inconvenience and the potential adverse effects of corticosteroids.36,52 Both topical clindamycin and intralesional steroids are helpful in reducing inflammation prior to planned surgical intervention.36,52,53
Newer topical therapies include resorcinol peels and combination antimicrobials, such as 2% triclosan and oral zinc gluconate.52,53 Data surrounding the use of resorcinol in mild to moderate HS are promising and have shown decreased severity of both new and long-standing nodules. Fifteen-percent resorcinol peels are helpful tools that allow for self-administration by patients during exacerbations to decrease pain and flare duration.55,56 In a 2016 clinical trial, a combination of oral zinc gluconate with topical triclosan was shown to reduce flare-ups and nodules in mild HS.57 Oral zinc alone may have anti-inflammatory properties and generally is well tolerated.43,53 Topical therapies have a role in reducing HS-associated pain but often are limited to milder disease.
Systemic Agents
Several therapeutic options exist for the treatment of HS; however, a detailed description of their mechanisms and efficacies is beyond the scope of this review, which is focused on pain. Briefly, these systemic agents include antibiotics, retinoids, corticosteroids, antiandrogens, and biologics.43,52,53
Treatment with antibiotics such as tetracyclines or a combination of clindamycin plus rifampin has been shown to produce complete remission in 60% to 80% of users; however, this treatment requires more than 6 months of antibiotic therapy, which can be difficult to tolerate.52,53,58 Relapse is common after antibiotic cessation.2,43,52 Antibiotics have demonstrated efficacy during acute flares and in reducing inflammatory activity prior to surgery.52
Retinoids have been utilized in the treatment of HS because of their action on sebaceous glands and hair follicles.43,53 Acitretin has been shown to be the most effective oral retinoid available in the United States.43 Unfortunately, many of the studies investigating the use of retinoids for treatment of HS are limited by small sample size.36,43,52
Because HS is predominantly an inflammatory condition, immunosuppressants have been adapted to manage patients when antibiotics and topicals have failed. Systemic steroids rarely are used for long-term therapy because of the severe side effects and are preferred only for acute management.36,52 Cyclosporine and dapsone have demonstrated efficacy in treating moderate to severe HS, whereas methotrexate and colchicine have shown little efficacy.52 Both cyclosporine and dapsone are difficult to tolerate, require laboratory monitoring, and lead to only conservative improvement rather than remission in most patients.43
Immune dysregulation in HS involves elevated levels of proinflammatory cytokines such as tumor necrosis factor α (TNF-α), which is a key mediator of inflammation and a stimulator of other inflammatory cytokines.59,60 The first approved biologic treatment of HS was adalimumab, a TNF-α inhibitor, which showed a 50% reduction in total abscess and inflammatory nodule count in 60% of patients with moderate to severe HS.61-63 Of course, TNF-α inhibitor therapy is not without risks, specifically those of infection.43,53,61,62 Maintenance therapy may be required if patients relapse.53,61
Various interleukin inhibitors also have emerged as potential therapies for HS, such as ustekinumab and anakinra.36,64 Both have been subject to numerous small case trials that have reported improvements in clinical severity and pain; however, both drugs were associated with a fair number of nonresponders.36,64,65
Surgical Procedures
Although HS lesions may regress on their own in a matter of weeks, surgical drainage allows an acute alleviation of the severe burning pain associated with HS flares.36,52,53 Because of improved understanding of the disease pathophysiology, recent therapies targeting the hair follicle have been developed and have shown promising results. These therapies include laser- and light-based procedures. Long-pulsed Nd:YAG laser therapy reduces the number of hair follicles and sebaceous glands and has been effective for Hurley stage I or II disease.36,43,52,53,66 Photodynamic therapy offers a less-invasive option compared to surgery and laser therapy.52,53,66 Both Nd:YAG and CO2 laser therapy offer low recurrence rates (<30%) due to destruction of the apocrine unit.43,53 Photodynamic therapy for mild disease offers a less-invasive option compared to surgery and laser therapy.53 There is a need for larger randomized controlled trials involving laser, light, and CO2 therapies.66
Conclusion
Hidradenitis suppurativa is a debilitating condition with an underestimated disease burden. Although the pathophysiology of the disease is not completely understood, it is evident that pain is a major cause of morbidity. Patients experience a multitude of acute and chronic pain types: inflammatory, noninflammatory, nociceptive, neuropathic, and ischemic. Pain perception and quality of life are further impacted by psychiatric conditions such as depression and anxiety, both of which are common comorbidities in patients with HS. Several pharmacologic agents have been used to treat HS-associated pain with mixed results. First-line treatment of acute pain episodes includes oral acetaminophen, NSAIDs, and topical analgesics. Management of chronic pain includes utilization of topical agents, systemic agents, and biologics, as well as addressing lifestyle (eg, obesity, smoking status) and psychiatric comorbidities. Although these therapies have roles in HS pain management, the most effective pain remedies developed thus far are limited to surgery and TNF-α inhibitors. Optimization of pain control in patients with HS requires multidisciplinary collaboration among dermatologists, pain specialists, psychiatrists, and other members of the health care team. Further large-scale studies are needed to create an evidence-based treatment algorithm for the management of pain in HS.
Hidradenitis suppurativa (HS) is a chronic inflammatory, androgen gland disorder characterized by recurrent rupture of the hair follicles with a vigorous inflammatory response. This response results in abscess formation and development of draining sinus tracts and hypertrophic fibrous scars.1,2 Pain, discomfort, and odorous discharge from the recalcitrant lesions have a profound impact on patient quality of life.3,4
The morbidity and disease burden associated with HS are particularly underestimated, as patients frequently report debilitating pain that often is overlooked.5,6 Additionally, the quality and intensity of perceived pain are compounded by frequently associated depression and anxiety.7-9 Pain has been reported by patients with HS to be the highest cause of morbidity, despite the disfiguring nature of the disease and its associated psychosocial distress.7,10 Nonetheless, HS lacks an accepted pain management algorithm similar to those that have been developed for the treatment of other acute or chronic pain disorders, such as back pain and sickle cell disease.4,11-13
Given the lack of formal studies regarding pain management in patients with HS, clinicians are limited to general pain guidelines, expert opinion, small trials, and patient preference.3 Furthermore, effective pain management in HS necessitates the treatment of both chronic pain affecting daily function and acute pain present during disease flares, surgical interventions, and dressing changes.3 The result is a wide array of strategies used for HS-associated pain.3,4
Epidemiology and Pathophysiology
Hidradenitis suppurativa historically has been an overlooked and underdiagnosed disease, which limits epidemiology data.5 Current estimates are that HS affects approximately 1% of the general population; however, prevalence rates range from 0.03% to 4.1%.14-16
The exact etiology of HS remains unclear, but it is thought that genetic factors, immune dysregulation, and environmental/behavioral influences all contribute to its pathophysiology.1,17 Up to 40% of patients with HS report a positive family history of the disease.18-20 Hidradenitis suppurativa has been associated with other inflammatory disease states, such as inflammatory bowel disease, spondyloarthropathies, and pyoderma gangrenosum.16,21,22
It is thought that HS is the result of some defect in keratin clearance that leads to follicular hyperkeratinization and occlusion.1 Resultant rupture of pilosebaceous units and spillage of contents (including keratin and bacteria) into the surrounding dermis triggers a vigorous inflammatory response. Sinus tracts and fistulas become the targets of bacterial colonization, biofilm formation, and secondary infection. The result is suppuration and extension of the lesions as well as sustained chronic inflammation.23,24
Although the etiology of HS is complex, several modifiable risk factors for the disease have been identified, most prominently cigarette smoking and obesity. Approximately 70% of patients with HS smoke cigarettes.2,15,25,26 Obesity has a well-known association with HS, and it is possible that weight reduction lowers disease severity.27-30
Clinical Presentation and Diagnosis
Establishing a diagnosis of HS necessitates recognition of disease morphology, topography, and chronicity. Hidradenitis suppurativa most commonly occurs in the axillae, inguinal and anogenital region, perineal region, and inframammary region.5,31 A typical history involves a prolonged disease course with recurrent lesions and intermittent periods of improvement or remission. Primary lesions are deep, inflamed, painful, and sterile. Ultimately, these lesions rupture and track subcutaneously.15,25 Intercommunicating sinus tracts form from multiple recurrent nodules in close proximity and may ultimately lead to fibrotic scarring and local architectural distortion.32 The Hurley staging system helps to guide treatment interventions based on disease severity. Approach to pain management is discussed below.
Pain Management in HS: General Principles
Pain management is complex for clinicians, as there are limited studies from which to draw treatment recommendations. Incomplete understanding of the etiology and pathophysiology of the disease contributes to the lack of established management guidelines.
A PubMed search of articles indexed for MEDLINE using the terms hidradenitis, suppurativa, pain, and management revealed 61 different results dating back to 1980, 52 of which had been published in the last 5 years. When the word acute was added to the search, there were only 6 results identified. These results clearly reflect a better understanding of HS-mediated pain as well as clinical unmet needs and evolving strategies in pain management therapeutics. However, many of these studies reflect therapies focused on the mediation or modulation of HS pathogenesis rather than potential pain management therapies.
In addition, the heterogenous nature of the pain experience in HS poses a challenge for clinicians. Patients may experience multiple pain types concurrently, including inflammatory, noninflammatory, nociceptive, neuropathic, and ischemic, as well as pain related to arthritis.3,33,34 Pain perception is further complicated by the observation that patients with HS have high rates of psychiatric comorbidities such as depression and anxiety, both of which profoundly alter perception of both the strength and quality of pain.7,8,22,35 A suggested algorithm for treatment of pain in HS is described in the eTable.36
Chronicity is a hallmark of HS. Patients experience a prolonged disease course involving acute painful exacerbations superimposed on chronic pain that affects all aspects of daily life. Changes in self-perception, daily living activities, mood state, physical functioning, and physical comfort frequently are reported to have a major impact on quality of life.1,3,37
In 2018, Thorlacius et al38 created a multistakeholder consensus on a core outcome set of domains detailing what to measure in clinical trials for HS. The authors hoped that the routine adoption of these core domains would promote the collection of consistent and relevant information, bolster the strength of evidence synthesis, and minimize the risk for outcome reporting bias among studies.38 It is important to ascertain the patient’s description of his/her pain to distinguish between stimulus-dependent nociceptive pain vs spontaneous neuropathic pain.3,7,10 The most common pain descriptors used by patients are “shooting,” “itchy,” “blinding,” “cutting,” and “exhausting.”10 In addition to obtaining descriptive factors, it is important for the clinician to obtain information on the timing of the pain, whether or not the pain is relieved with spontaneous or surgical drainage, and if the patient is experiencing chronic background pain secondary to scarring or skin contraction.3 With the routine utilization of a consistent set of core domains, advances in our understanding of the different elements of HS pain, and increased provider awareness of the disease, the future of pain management in patients with HS seems promising.
Acute and Perioperative Pain Management
Acute Pain Management—The pain in HS can range from mild to excruciating.3,7 The difference between acute and chronic pain in this condition may be hard to delineate, as patients may have intense acute flares on top of a baseline level of chronic pain.3,7,14 These factors, in combination with various pain types of differing etiologies, make the treatment of HS-associated pain a therapeutic challenge.
The first-line treatments for acute pain in HS are oral acetaminophen, oral nonsteroidal anti-inflammatory drugs (NSAIDs), and topical analgesics.3 These treatment modalities are especially helpful for nociceptive pain, which often is described as having an aching or tender quality.3 Topical treatment for acute pain episodes includes diclofenac gel and liposomal lidocaine cream.39 Topical lidocaine in particular has the benefit of being rapid acting, and its effect can last 1 to 2 hours. Ketamine has been anecdotally used as a topical treatment. Treatment options for neuropathic pain include topical amitriptyline, gabapentin, and pregabalin.39 Dressings and ice packs may be used in cases of mild acute pain, depending on patient preference.3
First-line therapies may not provide adequate pain control in many patients.3,40,41 Should the first-line treatments fail, oral opiates can be considered as a treatment option, especially if the patient has a history of recurrent pain unresponsive to milder methods of pain control.3,40,41 However, prudence should be exercised, as patients with HS have a higher risk for opioid abuse, and referral to a pain specialist is advisable.40 Generally, use of opioids should be limited to the smallest period of time possible.40,41 Codeine can be used as a first opioid option, with hydromorphone available as an alternative.41
Pain caused by inflamed abscesses and nodules can be treated with either intralesional corticosteroids or incision and drainage. Intralesional triamcinolone has been found to cause substantial pain relief within 1 day of injection in patients with HS.3,42
Prompt discussion about the remitting course of HS will prepare patients for flares. Although the therapies discussed here aim to reduce the clinical severity and inflammation associated with HS, achieving pain-free remission can be challenging. Barriers to developing a long-term treatment regimen include intolerable side effects or simply nonresponsive disease.36,43
Management of Perioperative Pain—Medical treatment of HS often yields only transient or mild results. Hurley stage II or III lesions typically require surgical removal of affected tissues.32,44-46 Surgery may dramatically reduce the primary disease burden and provide substantial pain relief.3,4,44 Complete resection of the affected tissue by wide excision is the most common surgical procedure used.46-48 However, various tissue-sparing techniques, such as skin-tissue-sparing excision with electrosurgical peeling, also have been utilized. Tissue-sparing surgical techniques may lead to shorter healing times and less postoperative pain.48
There currently is little guidance available on the perioperative management of pain as it relates to surgical procedures for HS. The pain experienced from surgery varies based on the area and location of affected tissue; extent of disease; surgical technique used; and whether primary closure, closure by secondary intention, or skin grafting is utilized.47,49 Medical treatment aimed at reducing inflammation prior to surgical intervention may improve postoperative pain and complications.
The use of general vs local anesthesia during surgery depends on the extent of the disease and the amount of tissue being removed; however, the use of local anesthesia has been associated with a higher recurrence of disease, possibly owing to less aggressive tissue removal.50 Intraoperatively, the injection of 0.5% bupivacaine around the wound edges may lead to less postoperative pain.3,48 Postoperative pain usually is managed with acetaminophen and NSAIDs.48 In cases of severe postoperative pain, short- and long-acting opioid oxycodone preparations may be used. The combination of diclofenac and tramadol also has been used postoperatively.3 Patients who do not undergo extensive surgery often can leave the hospital the same day.
Effective strategies for mitigating HS-associated pain must address the chronic pain component of the disease. Long-term management involves lifestyle modifications and pharmacologic agents.
Chronic Pain Management
Although HS is not a curable disease, there are treatments available to minimize symptoms. Long-term management of HS is essential to minimize the effects of chronic pain and physical scarring associated with inflammation.31 In one study from the French Society of Dermatology, pain reported by patients with HS was directly associated with severity and duration of disease, emotional symptoms, and reduced functionality.51 For these reasons, many treatments for HS target reducing clinical severity and achieving remission, often defined as more than 6 months without any recurrence of lesions.52 In addition to lifestyle management, therapies available to manage HS include topical and systemic medications as well as procedures such as surgical excision.36,43,52,53
Lifestyle Modifications
Regardless of the severity of HS, all patients may benefit from basic education on the pathogenesis of the disease.36 The associations with smoking and obesity have been well documented, and treatment of these comorbid conditions is indicated.36,43,52 For example, in relation to obesity, the use of metformin is very well tolerated and seems to positively impact HS symptoms.43 Several studies have suggested that weight reduction lowers disease severity.28-30 Patients should be counseled on the importance of smoking cessation and weight loss.
Finally, the emotional impact of HS is not to be discounted, both the physical and social discomfort as well as the chronicity of the disease and frustration with treatment.51 Chronic pain has been associated with increased rates of depression, and 43% of patients with HS specifically have been diagnosed with major depressive disorder.7 For these reasons, clinician guidance, social support, and websites can improve patient understanding of the disease, adherence to treatment, and comorbid anxiety and depression.52
Topical Therapy
Topical therapy generally is limited to mild disease and is geared at decreasing inflammation or superimposed infection.36,52 Some of the earliest therapies used were topical antibiotics.43 Topical clindamycin has been shown to be as effective as oral tetracyclines in reducing the number of abscesses, but neither treatment substantially reduces pain associated with smaller nodules.54 Intralesional corticosteroids such as triamcinolone acetonide have been shown to decrease both patient-reported pain and physician-assessed severity within 1 to 7 days.42 Routine injection, however, is not a feasible means of long-term treatment both because of inconvenience and the potential adverse effects of corticosteroids.36,52 Both topical clindamycin and intralesional steroids are helpful in reducing inflammation prior to planned surgical intervention.36,52,53
Newer topical therapies include resorcinol peels and combination antimicrobials, such as 2% triclosan and oral zinc gluconate.52,53 Data surrounding the use of resorcinol in mild to moderate HS are promising and have shown decreased severity of both new and long-standing nodules. Fifteen-percent resorcinol peels are helpful tools that allow for self-administration by patients during exacerbations to decrease pain and flare duration.55,56 In a 2016 clinical trial, a combination of oral zinc gluconate with topical triclosan was shown to reduce flare-ups and nodules in mild HS.57 Oral zinc alone may have anti-inflammatory properties and generally is well tolerated.43,53 Topical therapies have a role in reducing HS-associated pain but often are limited to milder disease.
Systemic Agents
Several therapeutic options exist for the treatment of HS; however, a detailed description of their mechanisms and efficacies is beyond the scope of this review, which is focused on pain. Briefly, these systemic agents include antibiotics, retinoids, corticosteroids, antiandrogens, and biologics.43,52,53
Treatment with antibiotics such as tetracyclines or a combination of clindamycin plus rifampin has been shown to produce complete remission in 60% to 80% of users; however, this treatment requires more than 6 months of antibiotic therapy, which can be difficult to tolerate.52,53,58 Relapse is common after antibiotic cessation.2,43,52 Antibiotics have demonstrated efficacy during acute flares and in reducing inflammatory activity prior to surgery.52
Retinoids have been utilized in the treatment of HS because of their action on sebaceous glands and hair follicles.43,53 Acitretin has been shown to be the most effective oral retinoid available in the United States.43 Unfortunately, many of the studies investigating the use of retinoids for treatment of HS are limited by small sample size.36,43,52
Because HS is predominantly an inflammatory condition, immunosuppressants have been adapted to manage patients when antibiotics and topicals have failed. Systemic steroids rarely are used for long-term therapy because of the severe side effects and are preferred only for acute management.36,52 Cyclosporine and dapsone have demonstrated efficacy in treating moderate to severe HS, whereas methotrexate and colchicine have shown little efficacy.52 Both cyclosporine and dapsone are difficult to tolerate, require laboratory monitoring, and lead to only conservative improvement rather than remission in most patients.43
Immune dysregulation in HS involves elevated levels of proinflammatory cytokines such as tumor necrosis factor α (TNF-α), which is a key mediator of inflammation and a stimulator of other inflammatory cytokines.59,60 The first approved biologic treatment of HS was adalimumab, a TNF-α inhibitor, which showed a 50% reduction in total abscess and inflammatory nodule count in 60% of patients with moderate to severe HS.61-63 Of course, TNF-α inhibitor therapy is not without risks, specifically those of infection.43,53,61,62 Maintenance therapy may be required if patients relapse.53,61
Various interleukin inhibitors also have emerged as potential therapies for HS, such as ustekinumab and anakinra.36,64 Both have been subject to numerous small case trials that have reported improvements in clinical severity and pain; however, both drugs were associated with a fair number of nonresponders.36,64,65
Surgical Procedures
Although HS lesions may regress on their own in a matter of weeks, surgical drainage allows an acute alleviation of the severe burning pain associated with HS flares.36,52,53 Because of improved understanding of the disease pathophysiology, recent therapies targeting the hair follicle have been developed and have shown promising results. These therapies include laser- and light-based procedures. Long-pulsed Nd:YAG laser therapy reduces the number of hair follicles and sebaceous glands and has been effective for Hurley stage I or II disease.36,43,52,53,66 Photodynamic therapy offers a less-invasive option compared to surgery and laser therapy.52,53,66 Both Nd:YAG and CO2 laser therapy offer low recurrence rates (<30%) due to destruction of the apocrine unit.43,53 Photodynamic therapy for mild disease offers a less-invasive option compared to surgery and laser therapy.53 There is a need for larger randomized controlled trials involving laser, light, and CO2 therapies.66
Conclusion
Hidradenitis suppurativa is a debilitating condition with an underestimated disease burden. Although the pathophysiology of the disease is not completely understood, it is evident that pain is a major cause of morbidity. Patients experience a multitude of acute and chronic pain types: inflammatory, noninflammatory, nociceptive, neuropathic, and ischemic. Pain perception and quality of life are further impacted by psychiatric conditions such as depression and anxiety, both of which are common comorbidities in patients with HS. Several pharmacologic agents have been used to treat HS-associated pain with mixed results. First-line treatment of acute pain episodes includes oral acetaminophen, NSAIDs, and topical analgesics. Management of chronic pain includes utilization of topical agents, systemic agents, and biologics, as well as addressing lifestyle (eg, obesity, smoking status) and psychiatric comorbidities. Although these therapies have roles in HS pain management, the most effective pain remedies developed thus far are limited to surgery and TNF-α inhibitors. Optimization of pain control in patients with HS requires multidisciplinary collaboration among dermatologists, pain specialists, psychiatrists, and other members of the health care team. Further large-scale studies are needed to create an evidence-based treatment algorithm for the management of pain in HS.
- Napolitano M, Megna M, Timoshchuk EA, et al. Hidradenitis suppurativa: from pathogenesis to diagnosis and treatment. Clin Cosmet Investig Dermatol. 2017;10:105-115. doi:10.2147/CCID.S111019
- Revuz J. Hidradenitis suppurativa. J Eur Acad Dermatology Venereol. 2009;23:985-998. doi:10.1111/j.1468-3083.2009.03356.x
- Horváth B, Janse IC, Sibbald GR. Pain management in patients with hidradenitis suppurativa. J Am Acad Dermatol. 2015;73(5 suppl 1):S47-S51. doi:10.1016/j.jaad.2015.07.046
- Puza CJ, Wolfe SA, Jaleel T. Pain management in patients with hidradenitis suppurativa requiring surgery. Dermatolog Surg. 2019;45:1327-1330. doi:10.1097/DSS.0000000000001693
- Kurzen H, Kurokawa I, Jemec GBE, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17:455-456. doi:10.1111/j.1600-0625.2008.00712_1.x
- Kelly G, Sweeney CM, Tobin AM, et al. Hidradenitis suppurativa: the role of immune dysregulation. Int J Dermatol. 2014;53:1186-1196. doi:10.1111/ijd.12550
- Patel ZS, Hoffman LK, Buse DC, et al. Pain, psychological comorbidities, disability, and impaired quality of life in hidradenitis suppurativa. Curr Pain Headache Rep. 2017;21:49. doi:10.1007/s11916-017-0647-3
- Sist TC, Florio GA, Miner MF, et al. The relationship between depression and pain language in cancer and chronic non-cancer pain patients. J Pain Symptom Manage. 1998;15:350-358. doi:10.1016/S0885-3924(98)00006-2
- Jemec GBE. Hidradenitis suppurativa. N Engl J Med. 2012;366:158-164. doi:10.1056/NEJMcp1014163
- Nielsen RM, Lindsø Andersen P, Sigsgaard V, et al. Pain perception in patients with hidradenitis suppurativa. Br J Dermatol. 2019;182:bjd.17935. doi:10.1111/bjd.17935
- Tanabe P, Myers R, Zosel A, et al. Emergency department management of acute pain episodes in sickle cell disease. Acad Emerg Med. 2007;14:419-425. doi:10.1197/j.aem.2006.11.033
- Chou R, Loeser JD, Owens DK, et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: an evidence-based clinical practice guideline from the American Pain Society. Spine (Phila Pa 1976). 2009;34:1066-1077. doi:10.1097/BRS.0b013e3181a1390d
- Enamandram M, Rathmell JP, Kimball AB. Chronic pain management in dermatology: a guide to assessment and nonopioid pharmacotherapy. J Am Acad Dermatol. 2015;73:563-573; quiz 573-574. doi:10.1016/j.jaad.2014.11.039
- Jemec GBE, Kimball AB. Hidradenitis suppurativa: epidemiology and scope of the problem. J Am Acad Dermatol. 2015;73(5 suppl 1):S4-S7. doi:10.1016/j.jaad.2015.07.052
- Vinkel C, Thomsen SF. Hidradenitis suppurativa: causes, features, and current treatments. J Clin Aesthet Dermatol. 2018;11:17-23.
- Patil S, Apurwa A, Nadkarni N, et al. Hidradenitis suppurativa: inside and out. Indian J Dermatol. 2018;63:91-98. doi:10.4103/ijd.IJD_412_16
- Woodruff CM, Charlie AM, Leslie KS. Hidradenitis suppurativa: a guide for the practicing physician. Mayo Clin Proc. 2015;90:1679-1693. doi:10.1016/j.mayocp.2015.08.020
- Pink AE, Simpson MA, Desai N, et al. Mutations in the γ-secretase genes NCSTN, PSENEN, and PSEN1 underlie rare forms of hidradenitis suppurativa (acne inversa). J Invest Dermatol. 2012;132:2459-2461. doi:10.1038/jid.2012.162
- Jemec GBE, Heidenheim M, Nielsen NH. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol. 1996;35:191-194. doi:10.1016/s0190-9622(96)90321-7
- Fitzsimmons JS, Guilbert PR. A family study of hidradenitis suppurativa. J Med Genet. 1985;22:367-373. doi:10.1136/jmg.22.5.367
- Kelly G, Prens EP. Inflammatory mechanisms in hidradenitis suppurativa. Dermatol Clin. 2016;34:51-58. doi:10.1016/j.det.2015.08.004
- Yazdanyar S, Jemec GB. Hidradenitis suppurativa: a review of cause and treatment. Curr Opin Infect Dis. 2011;24:118-123. doi:10.1097/QCO.0b013e3283428d07
- Kathju S, Lasko LA, Stoodley P. Considering hidradenitis suppurativa as a bacterial biofilm disease. FEMS Immunol Med Microbiol. 2012;65:385-389. doi:10.1111/j.1574-695X.2012.00946.x
- Jahns AC, Killasli H, Nosek D, et al. Microbiology of hidradenitis suppurativa (acne inversa): a histological study of 27 patients. APMIS. 2014;122:804-809. doi:10.1111/apm.12220
- Ralf Paus L, Kurzen H, Kurokawa I, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17:455-456. doi:10.1111/j.1600-0625.2008.00712_1.x
- Vazquez BG, Alikhan A, Weaver AL, et al. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;133:97-103. doi:10.1038/jid.2012.255
- Kromann CB, Ibler KS, Kristiansen VB, et al. The influence of body weight on the prevalence and severity of hidradenitis suppurativa. Acta Derm Venereol. 2014;94:553-557. doi:10.2340/00015555-1800
- Lindsø Andersen P, Kromann C, Fonvig CE, et al. Hidradenitis suppurativa in a cohort of overweight and obese children and adolescents. Int J Dermatol. 2020;59:47-51. doi:10.1111/ijd.14639
- Revuz JE, Canoui-Poitrine F, Wolkenstein P, et al. Prevalence and factors associated with hidradenitis suppurativa: results from two case-control studies. J Am Acad Dermatol. 2008;59:596-601. doi:10.1016/j.jaad.2008.06.020
- Kromann CB, Deckers IE, Esmann S, et al. Risk factors, clinical course and long-term prognosis in hidradenitis suppurativa: a cross-sectional study. Br J Dermatol. 2014;171:819-824. doi:10.1111/bjd.13090
- Wieczorek M, Walecka I. Hidradenitis suppurativa—known and unknown disease. Reumatologia. 2018;56:337-339. doi:10.5114/reum.2018.80709
- Hsiao J, Leslie K, McMichael A, et al. Folliculitis and other follicular disorders. In: Bolognia J, Schaffer J, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:615-632.
- Scheinfeld N. Treatment of hidradenitis suppurativa associated pain with nonsteroidal anti-inflammatory drugs, acetaminophen, celecoxib, gapapentin, pegabalin, duloxetine, and venlafaxine. Dermatol Online J. 2013;19:20616.
- Scheinfeld N. Hidradenitis suppurativa: a practical review of possible medical treatments based on over 350 hidradenitis patients. Dermatol Online J. 2013;19:1.
- Rajmohan V, Suresh Kumar S. Psychiatric morbidity, pain perception, and functional status of chronic pain patients in palliative care. Indian J Palliat Care. 2013;19:146-151. doi:10.4103/0973-1075.121527
- Saunte DML, Jemec GBE. Hidradenitis suppurativa: advances in diagnosis and treatment. JAMA. 2017;318:2019-2032. doi:10.1001/jama.2017.16691
- Wang B, Yang W, Wen W, et al. Gamma-secretase gene mutations in familial acne inversa. Science. 2010;330:1065. doi:10.1126/science.1196284
- Thorlacius L, Ingram JR, Villumsen B, et al. A core domain set for hidradenitis suppurativa trial outcomes: an international Delphi process. Br J Dermatol. 2018;179:642-650. doi:10.1111/bjd.16672
- Scheinfeld N. Topical treatments of skin pain: a general review with a focus on hidradenitis suppurativa with topical agents. Dermatol Online J. 2014;20:13030/qt4m57506k.
- Reddy S, Orenstein LAV, Strunk A, et al. Incidence of long-term opioid use among opioid-naive patients with hidradenitis suppurativa in the United States. JAMA Dermatol. 2019;155:1284-1290. doi:10.1001/jamadermatol.2019.2610
- Zouboulis CC, Desai N, Emtestam L, et al. European S1 guideline for the treatment of hidradenitis suppurativa/acne inversa. J Eur Acad Dermatology Venereol. 2015;29:619-644. doi:10.1111/jdv.12966
- Riis PT, Boer J, Prens EP, et al. Intralesional triamcinolone for flares of hidradenitis suppurativa (HS): a case series. J Am Acad Dermatol. 2016;75:1151-1155. doi:10.1016/j.jaad.2016.06.049
- Robert E, Bodin F, Paul C, et al. Non-surgical treatments for hidradenitis suppurativa: a systematic review. Ann Chir Plast Esthet. 2017;62:274-294. doi:10.1016/j.anplas.2017.03.012
- Menderes A, Sunay O, Vayvada H, et al. Surgical management of hidradenitis suppurativa. Int J Med Sci. 2010;7:240-247. doi:10.7150/ijms.7.240
- Alharbi Z, Kauczok J, Pallua N. A review of wide surgical excision of hidradenitis suppurativa. BMC Dermatol. 2012;12:9. doi:10.1186/1471-5945-12-9
- Burney RE. 35-year experience with surgical treatment of hidradenitis suppurativa. World J Surg. 2017;41:2723-2730. doi:10.1007/s00268-017-4091-7
- Bocchini SF, Habr-Gama A, Kiss DR, et al. Gluteal and perianal hidradenitis suppurativa: surgical treatment by wide excision. Dis Colon Rectum. 2003;46:944-949. doi:10.1007/s10350-004-6691-1
- Blok JL, Spoo JR, Leeman FWJ, et al. Skin-tissue-sparing excision with electrosurgical peeling (STEEP): a surgical treatment option for severe hidradenitis suppurativa Hurley stage II/III. J Eur Acad Dermatol Venereol. 2015;29:379-382. doi:10.1111/jdv.12376
- Bilali S, Todi V, Lila A, et al. Surgical treatment of chronic hidradenitis suppurativa in the gluteal and perianal regions. Acta Chir Iugosl. 2012;59:91-95. doi:10.2298/ACI1202091B
- Walter AC, Meissner M, Kaufmann R, et al. Hidradenitis suppurativa after radical surgery-long-term follow-up for recurrences and associated factors. Dermatol Surg. 2018;44:1323-1331. doi:10.1097/DSS.0000000000001668.
- Wolkenstein P, Loundou A, Barrau K, et al. Quality of life impairment in hidradenitis suppurativa: a study of 61 cases. J Am Acad Dermatol. 2007;56:621-623. doi:10.1016/j.jaad.2006.08.061
- Alavi A, Lynde C, Alhusayen R, et al. Approach to the management of patients with hidradenitis suppurativa: a consensus document. J Cutan Med Surg. 2017;21:513-524. doi:10.1177/1203475417716117
- Duran C, Baumeister A. Recognition, diagnosis, and treatment of hidradenitis suppurativa. J Am Acad Physician Assist. 2019;32:36-42. doi:10.1097/01.JAA.0000578768.62051.13
- Jemec GBE, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of hidradenitis suppurativa. J Am Acad Dermatol. 1998;39:971-974. doi:10.1016/S0190-9622(98)70272-5
- Pascual JC, Encabo B, Ruiz de Apodaca RF, et al. Topical 15% resorcinol for hidradenitis suppurativa: an uncontrolled prospective trial with clinical and ultrasonographic follow-up. J Am Acad Dermatol. 2017;77:1175-1178. doi:10.1016/j.jaad.2017.07.008
- Boer J, Jemec GBE. Resorcinol peels as a possible self-treatment of painful nodules in hidradenitis suppurativa. Clin Exp Dermatol. 2010;35:36-40. doi:10.1111/j.1365-2230.2009.03377.x
- Hessam S, Sand M, Meier NM, et al. Combination of oral zinc gluconate and topical triclosan: an anti-inflammatory treatment modality for initial hidradenitis suppurativa. J Dermatol Sci. 2016;84:197-202. doi:10.1016/j.jdermsci.2016.08.010
- Gener G, Canoui-Poitrine F, Revuz JE, et al. Combination therapy with clindamycin and rifampicin for hidradenitis suppurativa: a series of 116 consecutive patients. Dermatology. 2009;219:148-154. doi:10.1159/000228334
- Vossen ARJV, van der Zee HH, Prens EP. Hidradenitis suppurativa: a systematic review integrating inflammatory pathways into a cohesive pathogenic model. Front Immunol. 2018;9:2965. doi:10.3389/fimmu.2018.02965
- Chu WM. Tumor necrosis factor. Cancer Lett. 2013;328:222-225. doi:10.1016/j.canlet.2012.10.014
- Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375:422-434. doi:10.1056/NEJMoa1504370
- Morita A, Takahashi H, Ozawa K, et al. Twenty-four-week interim analysis from a phase 3 open-label trial of adalimumab in Japanese patients with moderate to severe hidradenitis suppurativa. J Dermatol. 2019;46:745-751. doi:10.1111/1346-8138.14997
- Ghias MH, Johnston AD, Kutner AJ, et al. High-dose, high-frequency infliximab: a novel treatment paradigm for hidradenitis suppurativa. J Am Acad Dermatol. 2020;82:1094-1101. doi:10.1016/j.jaad.2019.09.071
- Tzanetakou V, Kanni T, Giatrakou S, et al. Safety and efficacy of anakinra in severe hidradenitis suppurativa a randomized clinical trial. JAMA Dermatol. 2016;152:52-59. doi:10.1001/jamadermatol.2015.3903
- Blok JL, Li K, Brodmerkel C, et al. Ustekinumab in hidradenitis suppurativa: clinical results and a search for potential biomarkers in serum. Br J Dermatol. 2016;174:839-846. doi:10.1111/bjd.14338
- John H, Manoloudakis N, Stephen Sinclair J. A systematic review of the use of lasers for the treatment of hidradenitis suppurativa. J Plast Reconstr Aesthet Surg. 2016;69:1374-1381. doi:10.1016/j.bjps.2016.05.029
- Napolitano M, Megna M, Timoshchuk EA, et al. Hidradenitis suppurativa: from pathogenesis to diagnosis and treatment. Clin Cosmet Investig Dermatol. 2017;10:105-115. doi:10.2147/CCID.S111019
- Revuz J. Hidradenitis suppurativa. J Eur Acad Dermatology Venereol. 2009;23:985-998. doi:10.1111/j.1468-3083.2009.03356.x
- Horváth B, Janse IC, Sibbald GR. Pain management in patients with hidradenitis suppurativa. J Am Acad Dermatol. 2015;73(5 suppl 1):S47-S51. doi:10.1016/j.jaad.2015.07.046
- Puza CJ, Wolfe SA, Jaleel T. Pain management in patients with hidradenitis suppurativa requiring surgery. Dermatolog Surg. 2019;45:1327-1330. doi:10.1097/DSS.0000000000001693
- Kurzen H, Kurokawa I, Jemec GBE, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17:455-456. doi:10.1111/j.1600-0625.2008.00712_1.x
- Kelly G, Sweeney CM, Tobin AM, et al. Hidradenitis suppurativa: the role of immune dysregulation. Int J Dermatol. 2014;53:1186-1196. doi:10.1111/ijd.12550
- Patel ZS, Hoffman LK, Buse DC, et al. Pain, psychological comorbidities, disability, and impaired quality of life in hidradenitis suppurativa. Curr Pain Headache Rep. 2017;21:49. doi:10.1007/s11916-017-0647-3
- Sist TC, Florio GA, Miner MF, et al. The relationship between depression and pain language in cancer and chronic non-cancer pain patients. J Pain Symptom Manage. 1998;15:350-358. doi:10.1016/S0885-3924(98)00006-2
- Jemec GBE. Hidradenitis suppurativa. N Engl J Med. 2012;366:158-164. doi:10.1056/NEJMcp1014163
- Nielsen RM, Lindsø Andersen P, Sigsgaard V, et al. Pain perception in patients with hidradenitis suppurativa. Br J Dermatol. 2019;182:bjd.17935. doi:10.1111/bjd.17935
- Tanabe P, Myers R, Zosel A, et al. Emergency department management of acute pain episodes in sickle cell disease. Acad Emerg Med. 2007;14:419-425. doi:10.1197/j.aem.2006.11.033
- Chou R, Loeser JD, Owens DK, et al. Interventional therapies, surgery, and interdisciplinary rehabilitation for low back pain: an evidence-based clinical practice guideline from the American Pain Society. Spine (Phila Pa 1976). 2009;34:1066-1077. doi:10.1097/BRS.0b013e3181a1390d
- Enamandram M, Rathmell JP, Kimball AB. Chronic pain management in dermatology: a guide to assessment and nonopioid pharmacotherapy. J Am Acad Dermatol. 2015;73:563-573; quiz 573-574. doi:10.1016/j.jaad.2014.11.039
- Jemec GBE, Kimball AB. Hidradenitis suppurativa: epidemiology and scope of the problem. J Am Acad Dermatol. 2015;73(5 suppl 1):S4-S7. doi:10.1016/j.jaad.2015.07.052
- Vinkel C, Thomsen SF. Hidradenitis suppurativa: causes, features, and current treatments. J Clin Aesthet Dermatol. 2018;11:17-23.
- Patil S, Apurwa A, Nadkarni N, et al. Hidradenitis suppurativa: inside and out. Indian J Dermatol. 2018;63:91-98. doi:10.4103/ijd.IJD_412_16
- Woodruff CM, Charlie AM, Leslie KS. Hidradenitis suppurativa: a guide for the practicing physician. Mayo Clin Proc. 2015;90:1679-1693. doi:10.1016/j.mayocp.2015.08.020
- Pink AE, Simpson MA, Desai N, et al. Mutations in the γ-secretase genes NCSTN, PSENEN, and PSEN1 underlie rare forms of hidradenitis suppurativa (acne inversa). J Invest Dermatol. 2012;132:2459-2461. doi:10.1038/jid.2012.162
- Jemec GBE, Heidenheim M, Nielsen NH. The prevalence of hidradenitis suppurativa and its potential precursor lesions. J Am Acad Dermatol. 1996;35:191-194. doi:10.1016/s0190-9622(96)90321-7
- Fitzsimmons JS, Guilbert PR. A family study of hidradenitis suppurativa. J Med Genet. 1985;22:367-373. doi:10.1136/jmg.22.5.367
- Kelly G, Prens EP. Inflammatory mechanisms in hidradenitis suppurativa. Dermatol Clin. 2016;34:51-58. doi:10.1016/j.det.2015.08.004
- Yazdanyar S, Jemec GB. Hidradenitis suppurativa: a review of cause and treatment. Curr Opin Infect Dis. 2011;24:118-123. doi:10.1097/QCO.0b013e3283428d07
- Kathju S, Lasko LA, Stoodley P. Considering hidradenitis suppurativa as a bacterial biofilm disease. FEMS Immunol Med Microbiol. 2012;65:385-389. doi:10.1111/j.1574-695X.2012.00946.x
- Jahns AC, Killasli H, Nosek D, et al. Microbiology of hidradenitis suppurativa (acne inversa): a histological study of 27 patients. APMIS. 2014;122:804-809. doi:10.1111/apm.12220
- Ralf Paus L, Kurzen H, Kurokawa I, et al. What causes hidradenitis suppurativa? Exp Dermatol. 2008;17:455-456. doi:10.1111/j.1600-0625.2008.00712_1.x
- Vazquez BG, Alikhan A, Weaver AL, et al. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;133:97-103. doi:10.1038/jid.2012.255
- Kromann CB, Ibler KS, Kristiansen VB, et al. The influence of body weight on the prevalence and severity of hidradenitis suppurativa. Acta Derm Venereol. 2014;94:553-557. doi:10.2340/00015555-1800
- Lindsø Andersen P, Kromann C, Fonvig CE, et al. Hidradenitis suppurativa in a cohort of overweight and obese children and adolescents. Int J Dermatol. 2020;59:47-51. doi:10.1111/ijd.14639
- Revuz JE, Canoui-Poitrine F, Wolkenstein P, et al. Prevalence and factors associated with hidradenitis suppurativa: results from two case-control studies. J Am Acad Dermatol. 2008;59:596-601. doi:10.1016/j.jaad.2008.06.020
- Kromann CB, Deckers IE, Esmann S, et al. Risk factors, clinical course and long-term prognosis in hidradenitis suppurativa: a cross-sectional study. Br J Dermatol. 2014;171:819-824. doi:10.1111/bjd.13090
- Wieczorek M, Walecka I. Hidradenitis suppurativa—known and unknown disease. Reumatologia. 2018;56:337-339. doi:10.5114/reum.2018.80709
- Hsiao J, Leslie K, McMichael A, et al. Folliculitis and other follicular disorders. In: Bolognia J, Schaffer J, Cerroni L, eds. Dermatology. 4th ed. Elsevier; 2018:615-632.
- Scheinfeld N. Treatment of hidradenitis suppurativa associated pain with nonsteroidal anti-inflammatory drugs, acetaminophen, celecoxib, gapapentin, pegabalin, duloxetine, and venlafaxine. Dermatol Online J. 2013;19:20616.
- Scheinfeld N. Hidradenitis suppurativa: a practical review of possible medical treatments based on over 350 hidradenitis patients. Dermatol Online J. 2013;19:1.
- Rajmohan V, Suresh Kumar S. Psychiatric morbidity, pain perception, and functional status of chronic pain patients in palliative care. Indian J Palliat Care. 2013;19:146-151. doi:10.4103/0973-1075.121527
- Saunte DML, Jemec GBE. Hidradenitis suppurativa: advances in diagnosis and treatment. JAMA. 2017;318:2019-2032. doi:10.1001/jama.2017.16691
- Wang B, Yang W, Wen W, et al. Gamma-secretase gene mutations in familial acne inversa. Science. 2010;330:1065. doi:10.1126/science.1196284
- Thorlacius L, Ingram JR, Villumsen B, et al. A core domain set for hidradenitis suppurativa trial outcomes: an international Delphi process. Br J Dermatol. 2018;179:642-650. doi:10.1111/bjd.16672
- Scheinfeld N. Topical treatments of skin pain: a general review with a focus on hidradenitis suppurativa with topical agents. Dermatol Online J. 2014;20:13030/qt4m57506k.
- Reddy S, Orenstein LAV, Strunk A, et al. Incidence of long-term opioid use among opioid-naive patients with hidradenitis suppurativa in the United States. JAMA Dermatol. 2019;155:1284-1290. doi:10.1001/jamadermatol.2019.2610
- Zouboulis CC, Desai N, Emtestam L, et al. European S1 guideline for the treatment of hidradenitis suppurativa/acne inversa. J Eur Acad Dermatology Venereol. 2015;29:619-644. doi:10.1111/jdv.12966
- Riis PT, Boer J, Prens EP, et al. Intralesional triamcinolone for flares of hidradenitis suppurativa (HS): a case series. J Am Acad Dermatol. 2016;75:1151-1155. doi:10.1016/j.jaad.2016.06.049
- Robert E, Bodin F, Paul C, et al. Non-surgical treatments for hidradenitis suppurativa: a systematic review. Ann Chir Plast Esthet. 2017;62:274-294. doi:10.1016/j.anplas.2017.03.012
- Menderes A, Sunay O, Vayvada H, et al. Surgical management of hidradenitis suppurativa. Int J Med Sci. 2010;7:240-247. doi:10.7150/ijms.7.240
- Alharbi Z, Kauczok J, Pallua N. A review of wide surgical excision of hidradenitis suppurativa. BMC Dermatol. 2012;12:9. doi:10.1186/1471-5945-12-9
- Burney RE. 35-year experience with surgical treatment of hidradenitis suppurativa. World J Surg. 2017;41:2723-2730. doi:10.1007/s00268-017-4091-7
- Bocchini SF, Habr-Gama A, Kiss DR, et al. Gluteal and perianal hidradenitis suppurativa: surgical treatment by wide excision. Dis Colon Rectum. 2003;46:944-949. doi:10.1007/s10350-004-6691-1
- Blok JL, Spoo JR, Leeman FWJ, et al. Skin-tissue-sparing excision with electrosurgical peeling (STEEP): a surgical treatment option for severe hidradenitis suppurativa Hurley stage II/III. J Eur Acad Dermatol Venereol. 2015;29:379-382. doi:10.1111/jdv.12376
- Bilali S, Todi V, Lila A, et al. Surgical treatment of chronic hidradenitis suppurativa in the gluteal and perianal regions. Acta Chir Iugosl. 2012;59:91-95. doi:10.2298/ACI1202091B
- Walter AC, Meissner M, Kaufmann R, et al. Hidradenitis suppurativa after radical surgery-long-term follow-up for recurrences and associated factors. Dermatol Surg. 2018;44:1323-1331. doi:10.1097/DSS.0000000000001668.
- Wolkenstein P, Loundou A, Barrau K, et al. Quality of life impairment in hidradenitis suppurativa: a study of 61 cases. J Am Acad Dermatol. 2007;56:621-623. doi:10.1016/j.jaad.2006.08.061
- Alavi A, Lynde C, Alhusayen R, et al. Approach to the management of patients with hidradenitis suppurativa: a consensus document. J Cutan Med Surg. 2017;21:513-524. doi:10.1177/1203475417716117
- Duran C, Baumeister A. Recognition, diagnosis, and treatment of hidradenitis suppurativa. J Am Acad Physician Assist. 2019;32:36-42. doi:10.1097/01.JAA.0000578768.62051.13
- Jemec GBE, Wendelboe P. Topical clindamycin versus systemic tetracycline in the treatment of hidradenitis suppurativa. J Am Acad Dermatol. 1998;39:971-974. doi:10.1016/S0190-9622(98)70272-5
- Pascual JC, Encabo B, Ruiz de Apodaca RF, et al. Topical 15% resorcinol for hidradenitis suppurativa: an uncontrolled prospective trial with clinical and ultrasonographic follow-up. J Am Acad Dermatol. 2017;77:1175-1178. doi:10.1016/j.jaad.2017.07.008
- Boer J, Jemec GBE. Resorcinol peels as a possible self-treatment of painful nodules in hidradenitis suppurativa. Clin Exp Dermatol. 2010;35:36-40. doi:10.1111/j.1365-2230.2009.03377.x
- Hessam S, Sand M, Meier NM, et al. Combination of oral zinc gluconate and topical triclosan: an anti-inflammatory treatment modality for initial hidradenitis suppurativa. J Dermatol Sci. 2016;84:197-202. doi:10.1016/j.jdermsci.2016.08.010
- Gener G, Canoui-Poitrine F, Revuz JE, et al. Combination therapy with clindamycin and rifampicin for hidradenitis suppurativa: a series of 116 consecutive patients. Dermatology. 2009;219:148-154. doi:10.1159/000228334
- Vossen ARJV, van der Zee HH, Prens EP. Hidradenitis suppurativa: a systematic review integrating inflammatory pathways into a cohesive pathogenic model. Front Immunol. 2018;9:2965. doi:10.3389/fimmu.2018.02965
- Chu WM. Tumor necrosis factor. Cancer Lett. 2013;328:222-225. doi:10.1016/j.canlet.2012.10.014
- Kimball AB, Okun MM, Williams DA, et al. Two phase 3 trials of adalimumab for hidradenitis suppurativa. N Engl J Med. 2016;375:422-434. doi:10.1056/NEJMoa1504370
- Morita A, Takahashi H, Ozawa K, et al. Twenty-four-week interim analysis from a phase 3 open-label trial of adalimumab in Japanese patients with moderate to severe hidradenitis suppurativa. J Dermatol. 2019;46:745-751. doi:10.1111/1346-8138.14997
- Ghias MH, Johnston AD, Kutner AJ, et al. High-dose, high-frequency infliximab: a novel treatment paradigm for hidradenitis suppurativa. J Am Acad Dermatol. 2020;82:1094-1101. doi:10.1016/j.jaad.2019.09.071
- Tzanetakou V, Kanni T, Giatrakou S, et al. Safety and efficacy of anakinra in severe hidradenitis suppurativa a randomized clinical trial. JAMA Dermatol. 2016;152:52-59. doi:10.1001/jamadermatol.2015.3903
- Blok JL, Li K, Brodmerkel C, et al. Ustekinumab in hidradenitis suppurativa: clinical results and a search for potential biomarkers in serum. Br J Dermatol. 2016;174:839-846. doi:10.1111/bjd.14338
- John H, Manoloudakis N, Stephen Sinclair J. A systematic review of the use of lasers for the treatment of hidradenitis suppurativa. J Plast Reconstr Aesthet Surg. 2016;69:1374-1381. doi:10.1016/j.bjps.2016.05.029
Practice Points
- First-line therapies may not provide adequate pain control in many patients with hidradenitis suppurativa.
- Pain caused by inflamed abscesses and nodules can be treated with either intralesional corticosteroids or incision and drainage. Tissue-sparing surgical techniques may lead to shorter healing times and less postoperative pain.
- Long-term management involves lifestyle modifications and pharmacologic agents.
- The most effective pain remedies developed thus far are limited to surgery and tumor necrosis factor α inhibitors.
Detransitioners received poor evaluation when transitioning
Over half of people who believed they were transgender, transitioned to the opposite sex, but then regretted it and transitioned back – known as detransitioners – felt they did not receive adequate evaluation from a doctor or mental health professional before starting transition, new research indicates.
In what is thought to be the first study to ask whether detransitioners informed their original clinicians of their regret at transitioning, only 24 of the 100 surveyed said they had done so.
This strongly suggests that records on detransition may understate the real numbers, said Lisa Littman, MD, MPH, president of The Institute for Comprehensive Gender Dysphoria Research (ICGDR), who is the sole author of the study, published in Archives of Sexual Behavior.
She stressed that the findings illustrate the complexity surrounding gender dysphoria. “We need to recognize that there are many different types of experiences around gender dysphoria, transition, and detransition,” she told this news organization.
She said there is some resistance among certain health care professionals, and in society in general, to the idea that transitioning is not always successful.
‘We need to understand why this is happening’
“Detransition exists and we need to understand why this is happening,” Dr. Littman emphasized.
She observed that some supporters of “rapid transition” do not want to accept that transitioning helps some individuals but harms others.
“In the end, our goals should be providing the right treatment for the right patient, and without a thorough evaluation, clinicians are at serious risk of giving patients the wrong treatment,” she urged.
She noted that, despite some individuals feeling better after transition, these people still felt inclined to detransition because of discrimination and pressure.
“Individuals should not be pressured to detransition, nor should they be pressured to transition. Both types of pressure were reported by respondents.”
The recently recognized shift from mostly natal males to natal females seeking to transition was borne out by her study data, with the proportion of natal girls who detransitioned at 69%.
‘Shedding light’ on often ignored population
Asked to comment on the study, Laura Edwards-Leeper, PhD, a clinical psychologist from Beaverton, Ore., who specializes in gender-diverse and transgender children, welcomed Dr. Littman’s study.
It is, said Dr. Edwards-Leeper, a “critical preliminary step toward shedding light on this often-ignored and dismissed population of individuals who deserve support, compassion, and sometimes medical intervention from health care providers.”
She added that multiple online reports attest to detransitioners feeling they had not received adequate evaluation prior to medically transitioning, as well as many who expressed feeling too ashamed or angry to return to their same clinicians to detransition.
“Littman’s study provides quantitative support for both of these reported experiences, further emphasizing the importance of the field taking a closer look at the processes currently in place for those experiencing gender dysphoria,” said Dr. Edwards-Leeper.
And Miroslav L. Djordjevic, MD, PhD, professor of surgery/urology, University of Belgrade (Serbia), who is a specialist in urogenital reconstructive surgery and has performed over 2,000 gender-reassignment surgeries in transgender individuals, has recently seen many cases of regret after such surgeries, with requests for reversal operations.
“Despite the fact that medical detransition is relatively safe and without severe consequences, surgical detransition presents one of the most difficult issues in transgender medicine,” Dr. Djordjevic told this news organization.
Commending Dr. Littman on her study, he drew attention to some of the bioethical questions that arise relating to those who detransition.
“I ask what happened in the period before medical transitioning? Was there proper psychological care during medical transitioning? Who confirmed their desire for detransition – the same professionals who did the transition?” or someone else, he continued. “And who accepted these individuals for gender-affirming surgery and what were the criteria for this decision?”
Substantial study of reasons for both transitioning and detransitioning
In her article, Dr. Littman describes a 100-strong population of individuals (66 Americans, 9 British, 9 Canadian, 4 Australians, and 12 from “other” nations), ranging in age from 18 years to over 60 years with a mean age of 29.2 years, who had experienced gender dysphoria, chosen to undergo medical and/or surgical transition, and then detransitioned by discontinuing medications, having reversal surgery, or both.
Participants completed a 115-question survey providing data including age at first experience of gender dysphoria, when participants first sought transitioning care and from whom, and whether they felt pressured to do so. Friendship group dynamics were also explored.
Various narratives of participants’ transitioning-detransitioning experiences were gathered and grouped, for example, those related to discrimination pressures, experiences of trauma or mental health conditions prior to transition, and reports of internalized homophobia.
Dr. Edwards-Leeper observed that the study offers a more extensive assessment of reasons for detransitioning than any other prior research in the field, which has been sparse.
A survey published in April found that detransitioners report significant unmet medical and psychological needs, and a lack of compassion and help from medical and mental health practitioners.
But another 2021 study concluded most detransitioners only reverted to their birth sex because of societal or family pressure, discrimination, or shift to a nonbinary identity.
“However, [Dr.] Littman’s study found that only a small percentage actually detransitioned for that reason [23%], whereas the majority detransitioned because of a change in how the individual understood being a male or female, resulting in becoming comfortable in their assigned gender [60%],” noted Dr. Edwards-Leeper.
Reasons for detransitioning
Asked to expand upon the motives for detransition identified in her study, Dr. Littman told this news organization: “We found remarkable breadth in the reasons given for detransitioning.”
“I believe that we were able to capture the diversity of experiences around detransition because we reached out to communities that were strongly ‘protransition’ – like the World Professional Association for Transgender Health – and communities where individuals might be more skeptical about transition being universally beneficial, like detransition forums,” she said.
Speaking to the complexity of the experiences, 87% selected more than one reason for detransitioning.
The most common reason (60%) was becoming more comfortable identifying with their birth sex, followed by having concerns about potential medical complications from transitioning (49.0%).
Regarding those who became more comfortable with their natal sex, Dr. Littman noted that the finding adds “further support that gender dysphoria is not always permanent.”
She added that, “because most gender-dysphoric youth who are allowed to go through puberty grow up to be lesbian, gay, or bisexual (LGB) nontransgender adults, intervening too soon with medical treatments risks derailing their development as LGB individuals.”
Internalized homophobia or difficulty accepting themselves as lesbian, gay, or bisexual was reported by 23% of participants as a reason for transition and subsequent detransition.
“For these people, transitioning could be interpreted as an attempt to escape the reality of being same-sex attracted and detransitioning was part of accepting themselves as homosexual or bisexual,” explained Dr. Littman.
“Exploring their distress and discomfort around sexual orientation issues may have been more helpful to them than medical and surgical transition or at least an important part of exploration,” she added in the article.
Societal pressure, friends, and social media also play a role
The latest first-hand reports also support prior work by Dr. Littman when she first identified the concept she termed rapid-onset gender dysphoria (ROGD) to describe a sudden transgender identification, usually in the early teenage years, and with no prior indication of any gender questioning.
ROGD, Dr. Littman believes, is strongly related to psychosocial factors, such as trauma, mental health problems, or social influence contributing to the development of gender dysphoria.
The current study found that 58% of respondents expressed the belief that the cause of their gender dysphoria was something specific, such as trauma, abuse, or a mental health condition, with respondents suggesting that transitioning prevented, or delayed, them from addressing their underlying mental health conditions.
One participant is quoted as saying: “I was deeply uncomfortable with my secondary sex characteristics, which I now understand was a result of childhood trauma and associating my secondary sex characteristics with those events.”
Reflecting on their previous identification as transgender, more than a third of respondents reported that someone else told them their feelings meant they were transgender, and they believed them.
“This speaks to the effect social influence can have on people’s interpretation of their own feelings and their development of a transgender identity,” Dr. Littman remarked.
“Participants also listed several social media sources that encouraged them to believe that transitioning would help them,” she added.
Several friendship group dynamics suggestive of social influence were reported by a subset of respondents, including the fact that their friendship groups mocked people who were not transgender and their popularity increased when they announced they were going to transition.
Pendulum has swung too far the other way
Natal females, who in recent years have made up most referrals, were younger than natal males when they sought transition and decided to detransition; and they stayed “transitioned” for a shorter period than natal males. They were also more likely to have experienced a trauma less than 1 year before the onset of gender dysphoria and were more likely to have felt pressured to transition.
“Because the females in the study transitioned more recently than the males, they may have experienced a culture where there is more of a ‘push’ to transition,” Dr. Littman pointed out.
She added that, “20 years ago, gender-dysphoric patients were most likely to be underdiagnosed and undertreated. Now, the pendulum has swung the other way and patients are, in my opinion, more likely to be overdiagnosed and overtreated. I think we need to aim for somewhere between these two extremes and prioritize people getting the right treatment for the right reason for their distress.”
Dr. Djordjevic added that, with colleagues from Belgrade and the Netherlands, he has published accounts of the experiences of seven individuals who showed regret after gender-affirming surgery.
All of them were born male, “and we confirmed the very poor evaluation and transition process they underwent. We conclude that clinicians should be aware that not everyone with gender identity disorders need or want all elements of hormonal or surgical therapy,” he told this news organization.
Dr. Edwards-Leeper said that more long-term longitudinal studies are needed that follow individuals who undergo transition under different models of care.
“My prediction is that those who first engage in supportive, gender exploratory therapy, followed by comprehensive assessment, will have the best outcomes, perhaps even if they ultimately detransition, as these individuals will know that they did not jump into irreversible interventions too quickly and had time to make the best decision for themselves at the time,” she concluded.
A version of this article first appeared on Medscape.com.
Over half of people who believed they were transgender, transitioned to the opposite sex, but then regretted it and transitioned back – known as detransitioners – felt they did not receive adequate evaluation from a doctor or mental health professional before starting transition, new research indicates.
In what is thought to be the first study to ask whether detransitioners informed their original clinicians of their regret at transitioning, only 24 of the 100 surveyed said they had done so.
This strongly suggests that records on detransition may understate the real numbers, said Lisa Littman, MD, MPH, president of The Institute for Comprehensive Gender Dysphoria Research (ICGDR), who is the sole author of the study, published in Archives of Sexual Behavior.
She stressed that the findings illustrate the complexity surrounding gender dysphoria. “We need to recognize that there are many different types of experiences around gender dysphoria, transition, and detransition,” she told this news organization.
She said there is some resistance among certain health care professionals, and in society in general, to the idea that transitioning is not always successful.
‘We need to understand why this is happening’
“Detransition exists and we need to understand why this is happening,” Dr. Littman emphasized.
She observed that some supporters of “rapid transition” do not want to accept that transitioning helps some individuals but harms others.
“In the end, our goals should be providing the right treatment for the right patient, and without a thorough evaluation, clinicians are at serious risk of giving patients the wrong treatment,” she urged.
She noted that, despite some individuals feeling better after transition, these people still felt inclined to detransition because of discrimination and pressure.
“Individuals should not be pressured to detransition, nor should they be pressured to transition. Both types of pressure were reported by respondents.”
The recently recognized shift from mostly natal males to natal females seeking to transition was borne out by her study data, with the proportion of natal girls who detransitioned at 69%.
‘Shedding light’ on often ignored population
Asked to comment on the study, Laura Edwards-Leeper, PhD, a clinical psychologist from Beaverton, Ore., who specializes in gender-diverse and transgender children, welcomed Dr. Littman’s study.
It is, said Dr. Edwards-Leeper, a “critical preliminary step toward shedding light on this often-ignored and dismissed population of individuals who deserve support, compassion, and sometimes medical intervention from health care providers.”
She added that multiple online reports attest to detransitioners feeling they had not received adequate evaluation prior to medically transitioning, as well as many who expressed feeling too ashamed or angry to return to their same clinicians to detransition.
“Littman’s study provides quantitative support for both of these reported experiences, further emphasizing the importance of the field taking a closer look at the processes currently in place for those experiencing gender dysphoria,” said Dr. Edwards-Leeper.
And Miroslav L. Djordjevic, MD, PhD, professor of surgery/urology, University of Belgrade (Serbia), who is a specialist in urogenital reconstructive surgery and has performed over 2,000 gender-reassignment surgeries in transgender individuals, has recently seen many cases of regret after such surgeries, with requests for reversal operations.
“Despite the fact that medical detransition is relatively safe and without severe consequences, surgical detransition presents one of the most difficult issues in transgender medicine,” Dr. Djordjevic told this news organization.
Commending Dr. Littman on her study, he drew attention to some of the bioethical questions that arise relating to those who detransition.
“I ask what happened in the period before medical transitioning? Was there proper psychological care during medical transitioning? Who confirmed their desire for detransition – the same professionals who did the transition?” or someone else, he continued. “And who accepted these individuals for gender-affirming surgery and what were the criteria for this decision?”
Substantial study of reasons for both transitioning and detransitioning
In her article, Dr. Littman describes a 100-strong population of individuals (66 Americans, 9 British, 9 Canadian, 4 Australians, and 12 from “other” nations), ranging in age from 18 years to over 60 years with a mean age of 29.2 years, who had experienced gender dysphoria, chosen to undergo medical and/or surgical transition, and then detransitioned by discontinuing medications, having reversal surgery, or both.
Participants completed a 115-question survey providing data including age at first experience of gender dysphoria, when participants first sought transitioning care and from whom, and whether they felt pressured to do so. Friendship group dynamics were also explored.
Various narratives of participants’ transitioning-detransitioning experiences were gathered and grouped, for example, those related to discrimination pressures, experiences of trauma or mental health conditions prior to transition, and reports of internalized homophobia.
Dr. Edwards-Leeper observed that the study offers a more extensive assessment of reasons for detransitioning than any other prior research in the field, which has been sparse.
A survey published in April found that detransitioners report significant unmet medical and psychological needs, and a lack of compassion and help from medical and mental health practitioners.
But another 2021 study concluded most detransitioners only reverted to their birth sex because of societal or family pressure, discrimination, or shift to a nonbinary identity.
“However, [Dr.] Littman’s study found that only a small percentage actually detransitioned for that reason [23%], whereas the majority detransitioned because of a change in how the individual understood being a male or female, resulting in becoming comfortable in their assigned gender [60%],” noted Dr. Edwards-Leeper.
Reasons for detransitioning
Asked to expand upon the motives for detransition identified in her study, Dr. Littman told this news organization: “We found remarkable breadth in the reasons given for detransitioning.”
“I believe that we were able to capture the diversity of experiences around detransition because we reached out to communities that were strongly ‘protransition’ – like the World Professional Association for Transgender Health – and communities where individuals might be more skeptical about transition being universally beneficial, like detransition forums,” she said.
Speaking to the complexity of the experiences, 87% selected more than one reason for detransitioning.
The most common reason (60%) was becoming more comfortable identifying with their birth sex, followed by having concerns about potential medical complications from transitioning (49.0%).
Regarding those who became more comfortable with their natal sex, Dr. Littman noted that the finding adds “further support that gender dysphoria is not always permanent.”
She added that, “because most gender-dysphoric youth who are allowed to go through puberty grow up to be lesbian, gay, or bisexual (LGB) nontransgender adults, intervening too soon with medical treatments risks derailing their development as LGB individuals.”
Internalized homophobia or difficulty accepting themselves as lesbian, gay, or bisexual was reported by 23% of participants as a reason for transition and subsequent detransition.
“For these people, transitioning could be interpreted as an attempt to escape the reality of being same-sex attracted and detransitioning was part of accepting themselves as homosexual or bisexual,” explained Dr. Littman.
“Exploring their distress and discomfort around sexual orientation issues may have been more helpful to them than medical and surgical transition or at least an important part of exploration,” she added in the article.
Societal pressure, friends, and social media also play a role
The latest first-hand reports also support prior work by Dr. Littman when she first identified the concept she termed rapid-onset gender dysphoria (ROGD) to describe a sudden transgender identification, usually in the early teenage years, and with no prior indication of any gender questioning.
ROGD, Dr. Littman believes, is strongly related to psychosocial factors, such as trauma, mental health problems, or social influence contributing to the development of gender dysphoria.
The current study found that 58% of respondents expressed the belief that the cause of their gender dysphoria was something specific, such as trauma, abuse, or a mental health condition, with respondents suggesting that transitioning prevented, or delayed, them from addressing their underlying mental health conditions.
One participant is quoted as saying: “I was deeply uncomfortable with my secondary sex characteristics, which I now understand was a result of childhood trauma and associating my secondary sex characteristics with those events.”
Reflecting on their previous identification as transgender, more than a third of respondents reported that someone else told them their feelings meant they were transgender, and they believed them.
“This speaks to the effect social influence can have on people’s interpretation of their own feelings and their development of a transgender identity,” Dr. Littman remarked.
“Participants also listed several social media sources that encouraged them to believe that transitioning would help them,” she added.
Several friendship group dynamics suggestive of social influence were reported by a subset of respondents, including the fact that their friendship groups mocked people who were not transgender and their popularity increased when they announced they were going to transition.
Pendulum has swung too far the other way
Natal females, who in recent years have made up most referrals, were younger than natal males when they sought transition and decided to detransition; and they stayed “transitioned” for a shorter period than natal males. They were also more likely to have experienced a trauma less than 1 year before the onset of gender dysphoria and were more likely to have felt pressured to transition.
“Because the females in the study transitioned more recently than the males, they may have experienced a culture where there is more of a ‘push’ to transition,” Dr. Littman pointed out.
She added that, “20 years ago, gender-dysphoric patients were most likely to be underdiagnosed and undertreated. Now, the pendulum has swung the other way and patients are, in my opinion, more likely to be overdiagnosed and overtreated. I think we need to aim for somewhere between these two extremes and prioritize people getting the right treatment for the right reason for their distress.”
Dr. Djordjevic added that, with colleagues from Belgrade and the Netherlands, he has published accounts of the experiences of seven individuals who showed regret after gender-affirming surgery.
All of them were born male, “and we confirmed the very poor evaluation and transition process they underwent. We conclude that clinicians should be aware that not everyone with gender identity disorders need or want all elements of hormonal or surgical therapy,” he told this news organization.
Dr. Edwards-Leeper said that more long-term longitudinal studies are needed that follow individuals who undergo transition under different models of care.
“My prediction is that those who first engage in supportive, gender exploratory therapy, followed by comprehensive assessment, will have the best outcomes, perhaps even if they ultimately detransition, as these individuals will know that they did not jump into irreversible interventions too quickly and had time to make the best decision for themselves at the time,” she concluded.
A version of this article first appeared on Medscape.com.
Over half of people who believed they were transgender, transitioned to the opposite sex, but then regretted it and transitioned back – known as detransitioners – felt they did not receive adequate evaluation from a doctor or mental health professional before starting transition, new research indicates.
In what is thought to be the first study to ask whether detransitioners informed their original clinicians of their regret at transitioning, only 24 of the 100 surveyed said they had done so.
This strongly suggests that records on detransition may understate the real numbers, said Lisa Littman, MD, MPH, president of The Institute for Comprehensive Gender Dysphoria Research (ICGDR), who is the sole author of the study, published in Archives of Sexual Behavior.
She stressed that the findings illustrate the complexity surrounding gender dysphoria. “We need to recognize that there are many different types of experiences around gender dysphoria, transition, and detransition,” she told this news organization.
She said there is some resistance among certain health care professionals, and in society in general, to the idea that transitioning is not always successful.
‘We need to understand why this is happening’
“Detransition exists and we need to understand why this is happening,” Dr. Littman emphasized.
She observed that some supporters of “rapid transition” do not want to accept that transitioning helps some individuals but harms others.
“In the end, our goals should be providing the right treatment for the right patient, and without a thorough evaluation, clinicians are at serious risk of giving patients the wrong treatment,” she urged.
She noted that, despite some individuals feeling better after transition, these people still felt inclined to detransition because of discrimination and pressure.
“Individuals should not be pressured to detransition, nor should they be pressured to transition. Both types of pressure were reported by respondents.”
The recently recognized shift from mostly natal males to natal females seeking to transition was borne out by her study data, with the proportion of natal girls who detransitioned at 69%.
‘Shedding light’ on often ignored population
Asked to comment on the study, Laura Edwards-Leeper, PhD, a clinical psychologist from Beaverton, Ore., who specializes in gender-diverse and transgender children, welcomed Dr. Littman’s study.
It is, said Dr. Edwards-Leeper, a “critical preliminary step toward shedding light on this often-ignored and dismissed population of individuals who deserve support, compassion, and sometimes medical intervention from health care providers.”
She added that multiple online reports attest to detransitioners feeling they had not received adequate evaluation prior to medically transitioning, as well as many who expressed feeling too ashamed or angry to return to their same clinicians to detransition.
“Littman’s study provides quantitative support for both of these reported experiences, further emphasizing the importance of the field taking a closer look at the processes currently in place for those experiencing gender dysphoria,” said Dr. Edwards-Leeper.
And Miroslav L. Djordjevic, MD, PhD, professor of surgery/urology, University of Belgrade (Serbia), who is a specialist in urogenital reconstructive surgery and has performed over 2,000 gender-reassignment surgeries in transgender individuals, has recently seen many cases of regret after such surgeries, with requests for reversal operations.
“Despite the fact that medical detransition is relatively safe and without severe consequences, surgical detransition presents one of the most difficult issues in transgender medicine,” Dr. Djordjevic told this news organization.
Commending Dr. Littman on her study, he drew attention to some of the bioethical questions that arise relating to those who detransition.
“I ask what happened in the period before medical transitioning? Was there proper psychological care during medical transitioning? Who confirmed their desire for detransition – the same professionals who did the transition?” or someone else, he continued. “And who accepted these individuals for gender-affirming surgery and what were the criteria for this decision?”
Substantial study of reasons for both transitioning and detransitioning
In her article, Dr. Littman describes a 100-strong population of individuals (66 Americans, 9 British, 9 Canadian, 4 Australians, and 12 from “other” nations), ranging in age from 18 years to over 60 years with a mean age of 29.2 years, who had experienced gender dysphoria, chosen to undergo medical and/or surgical transition, and then detransitioned by discontinuing medications, having reversal surgery, or both.
Participants completed a 115-question survey providing data including age at first experience of gender dysphoria, when participants first sought transitioning care and from whom, and whether they felt pressured to do so. Friendship group dynamics were also explored.
Various narratives of participants’ transitioning-detransitioning experiences were gathered and grouped, for example, those related to discrimination pressures, experiences of trauma or mental health conditions prior to transition, and reports of internalized homophobia.
Dr. Edwards-Leeper observed that the study offers a more extensive assessment of reasons for detransitioning than any other prior research in the field, which has been sparse.
A survey published in April found that detransitioners report significant unmet medical and psychological needs, and a lack of compassion and help from medical and mental health practitioners.
But another 2021 study concluded most detransitioners only reverted to their birth sex because of societal or family pressure, discrimination, or shift to a nonbinary identity.
“However, [Dr.] Littman’s study found that only a small percentage actually detransitioned for that reason [23%], whereas the majority detransitioned because of a change in how the individual understood being a male or female, resulting in becoming comfortable in their assigned gender [60%],” noted Dr. Edwards-Leeper.
Reasons for detransitioning
Asked to expand upon the motives for detransition identified in her study, Dr. Littman told this news organization: “We found remarkable breadth in the reasons given for detransitioning.”
“I believe that we were able to capture the diversity of experiences around detransition because we reached out to communities that were strongly ‘protransition’ – like the World Professional Association for Transgender Health – and communities where individuals might be more skeptical about transition being universally beneficial, like detransition forums,” she said.
Speaking to the complexity of the experiences, 87% selected more than one reason for detransitioning.
The most common reason (60%) was becoming more comfortable identifying with their birth sex, followed by having concerns about potential medical complications from transitioning (49.0%).
Regarding those who became more comfortable with their natal sex, Dr. Littman noted that the finding adds “further support that gender dysphoria is not always permanent.”
She added that, “because most gender-dysphoric youth who are allowed to go through puberty grow up to be lesbian, gay, or bisexual (LGB) nontransgender adults, intervening too soon with medical treatments risks derailing their development as LGB individuals.”
Internalized homophobia or difficulty accepting themselves as lesbian, gay, or bisexual was reported by 23% of participants as a reason for transition and subsequent detransition.
“For these people, transitioning could be interpreted as an attempt to escape the reality of being same-sex attracted and detransitioning was part of accepting themselves as homosexual or bisexual,” explained Dr. Littman.
“Exploring their distress and discomfort around sexual orientation issues may have been more helpful to them than medical and surgical transition or at least an important part of exploration,” she added in the article.
Societal pressure, friends, and social media also play a role
The latest first-hand reports also support prior work by Dr. Littman when she first identified the concept she termed rapid-onset gender dysphoria (ROGD) to describe a sudden transgender identification, usually in the early teenage years, and with no prior indication of any gender questioning.
ROGD, Dr. Littman believes, is strongly related to psychosocial factors, such as trauma, mental health problems, or social influence contributing to the development of gender dysphoria.
The current study found that 58% of respondents expressed the belief that the cause of their gender dysphoria was something specific, such as trauma, abuse, or a mental health condition, with respondents suggesting that transitioning prevented, or delayed, them from addressing their underlying mental health conditions.
One participant is quoted as saying: “I was deeply uncomfortable with my secondary sex characteristics, which I now understand was a result of childhood trauma and associating my secondary sex characteristics with those events.”
Reflecting on their previous identification as transgender, more than a third of respondents reported that someone else told them their feelings meant they were transgender, and they believed them.
“This speaks to the effect social influence can have on people’s interpretation of their own feelings and their development of a transgender identity,” Dr. Littman remarked.
“Participants also listed several social media sources that encouraged them to believe that transitioning would help them,” she added.
Several friendship group dynamics suggestive of social influence were reported by a subset of respondents, including the fact that their friendship groups mocked people who were not transgender and their popularity increased when they announced they were going to transition.
Pendulum has swung too far the other way
Natal females, who in recent years have made up most referrals, were younger than natal males when they sought transition and decided to detransition; and they stayed “transitioned” for a shorter period than natal males. They were also more likely to have experienced a trauma less than 1 year before the onset of gender dysphoria and were more likely to have felt pressured to transition.
“Because the females in the study transitioned more recently than the males, they may have experienced a culture where there is more of a ‘push’ to transition,” Dr. Littman pointed out.
She added that, “20 years ago, gender-dysphoric patients were most likely to be underdiagnosed and undertreated. Now, the pendulum has swung the other way and patients are, in my opinion, more likely to be overdiagnosed and overtreated. I think we need to aim for somewhere between these two extremes and prioritize people getting the right treatment for the right reason for their distress.”
Dr. Djordjevic added that, with colleagues from Belgrade and the Netherlands, he has published accounts of the experiences of seven individuals who showed regret after gender-affirming surgery.
All of them were born male, “and we confirmed the very poor evaluation and transition process they underwent. We conclude that clinicians should be aware that not everyone with gender identity disorders need or want all elements of hormonal or surgical therapy,” he told this news organization.
Dr. Edwards-Leeper said that more long-term longitudinal studies are needed that follow individuals who undergo transition under different models of care.
“My prediction is that those who first engage in supportive, gender exploratory therapy, followed by comprehensive assessment, will have the best outcomes, perhaps even if they ultimately detransition, as these individuals will know that they did not jump into irreversible interventions too quickly and had time to make the best decision for themselves at the time,” she concluded.
A version of this article first appeared on Medscape.com.
FFR-guided PCI falls short vs. surgery in multivessel disease: FAME 3
Coronary stenting guided by fractional flow reserve (FFR) readings, considered to reflect the targeted lesion’s functional impact, was no match for coronary bypass surgery (CABG) in patients with multivessel disease (MVD) in a major international randomized trial.
Indeed, FFR-guided percutaneous coronary intervention (PCI) using one of the latest drug-eluting stents (DES) seemed to perform poorly in the trial, compared with surgery, apparently upping the risk for clinical events by 50% over 1 year.
Designed statistically for noninferiority, the third Fractional Flow Reserve Versus Angiography for Multivessel Evaluation (FAME 3) trial, with 1,500 randomized patients, showed that FFR-guided PCI was “not noninferior” to CABG. Of those randomized to PCI, 10.6% met the 1-year primary endpoint of major adverse cardiac or cerebrovascular events (MACCE), compared with only 6.9% of patients assigned to CABG.
The trial enrolled only patients with three-vessel coronary disease with no left-main coronary artery involvement, who were declared by their institution’s multidisciplinary heart team to be appropriate for either form of revascularization.
One of the roles of FFR for PCI guidance is to identify significant lesions “that are underrecognized by the angiogram,” which is less likely to happen in patients with very complex coronary anatomy, study chair William F. Fearon, MD, Stanford (Calif.) University, said in an interview.
“That’s what we saw in a subgroup analysis based on SYNTAX score,” an index of lesion complexity. “In patients with very high SYNTAX scores, CABG outperformed FFR-guided PCI. But if you look at patients with low SYNTAX scores, actually, FFR-guided PCI outperformed CABG for 1-year MACCE.”
Dr. Fearon is lead author on the study’s Nov. 4, 2021, publication in the New England Journal of Medicine, its release timed to coincide with his presentation of the trial at the Transcatheter Cardiovascular Therapeutics annual meeting, held virtually and live in Orlando and sponsored by the Cardiovascular Research Foundation.
He noted that FAME-3 “wasn’t designed or powered to test for superiority,” so its results do not imply CABG is superior to FFR-PCI in patients with MVD, and remains “inconclusive” on that question.
“I think what this study does is provide both the physician and patients more contemporary data and information on options and expected outcomes in multivessel disease. So if you are a patient who has less complex disease, I think you can feel comfortable that you will get an equivalent result with FFR-guided PCI.” But, at least based on FAME-3, Dr. Fearon said, CABG provides better outcomes in patients with more complex disease.
“I think there are still patients that look at trade-offs. Some patients will accept a higher event rate in order to avoid a long recovery, and vice versa.” So the trial may allow patients and physicians to make more informed decisions, he said.
A main message of FAME-3 “is that we’re getting very good results with three-vessel PCI, but better results with surgery,” Ran Kornowski, MD, Rabin Medical Center, Petah Tikva, Israel, and Tel Aviv University, said as a discussant following Dr. Fearon’s presentation of the trial. The subanalysis by SYNTAX score, he agreed, probably could be used as part of shared decision-making with patients.
Not all that surprising
“It’s a well-designed study, with a lot of patients,” said surgeon Frank W. Sellke, MD, of Rhode Island Hospital, Miriam Hospital, and Brown University, all in Providence.
“I don’t think it’s all that surprising,” he said in an interview. “It’s very consistent with what other studies have shown, that for three-vessel disease, surgery tends to have the edge,” even when pitted against FFR-guided PCI.
Indeed, pressure-wire FFR-PCI has a spotty history, even as an alternative to standard angiography-based PCI. For example, it has performed well in registry and other cohort studies but showed no advantage in the all-comers RIPCORD-2 trial or in the setting of complete revascularization PCI for acute MI in FLOWER-MI. And it emitted an increased-mortality signal in the prematurely halted FUTURE trial.
In FAME-3, “the 1-year follow-up was the best chance for FFR-PCI to be noninferior to CABG. The CABG advantage is only going to get better with time if prior experience and pathobiology is true,” Sanjay Kaul, MD, Cedars-Sinai Medical Center, Los Angeles, said in an interview.
Overall, “the quality and quantity of evidence is insufficient to support FFR-guided PCI” in patients with complex coronary artery disease (CAD), he said. “I would also argue that the evidence for FFR-guided PCI for simple CAD is also not high quality.”
Dr. Kaul also blasted the claim that FFR-PCI was seen to perform better against CABG in patients with low SYNTAX scores. “In general, one cannot use a positive subgroup in a null or negative trial, as is the case with FAME-3, to ‘rescue’ the treatment intervention.” Such a positive subgroup finding, he said, “would at best be deemed hypothesis-generating and not hypothesis validating.”
Dr. Fearon agreed that the subgroup analysis by SYNTAX score, though prespecified, was only hypothesis generating. “But I think that other studies have shown the same thing – that in less complex disease, the two strategies appear to perform in a similar fashion.”
The FAME-3 trial’s 1,500 patients were randomly assigned at 48 centers to undergo standard CABG or FFR-guided PCI with Resolute Integrity (Medtronic) zotarolimus-eluting DES. Lesions with a pressure-wire FFR of 0.80 or less were stented and those with higher FFR readings were deferred.
The 1-year hazard ratio for the primary endpoint—a composite of death from any cause, MI, stroke, or repeat revascularization – was 1.5 (95% confidence interval, 1.1-2.2) with a noninferiority P value of .35 for the comparison of FFR-PCI versus CABG.
FFR-guided PCI fared significantly better than CABG for some safety endpoints, including major bleeding (1.6% vs 3.8%, P < .01), arrhythmia including atrial fibrillation (2.4% vs. 14.1%, P < .001), acute kidney injury (0.1% vs 0.9%, P < .04), and 30-day rehospitalization (5.5% vs 10.2%, P < .001).
Did the primary endpoint favor CABG?
At a media briefing prior to Dr. Fearon’s TCT 2021 presentation of the trail, Roxana Mehran, MD, Icahn School of Medicine at Mount Sinai, New York, proposed that the inclusion of repeat revascularization in the trial’s composite primary endpoint tilted the outcome in favor of CABG. “To me, the FAME-3 results are predictable because repeat revascularization is in the equation.”
It’s well recognized that the endpoint is less likely after CABG than PCI. The latter treats focal lesions that are a limited part of a coronary artery in which CAD is still likely progressing. CABG, on the other hand, can bypass longer segments of diseased artery.
Indeed, as Dr. Fearon reported, the rates of death, MI, or stroke excluding repeat revascularization were 7.3% with FFR-PCI and 5.2% for CABG, for an HR of 1.4 (95% CI, 0.9-2.1).
Dr. Mehran also proposed that intravascular-ultrasound (IVUS) guidance, had it been part of the trial, could potentially have boosted the performance of FFR-PCI.
Repeat revascularization, Dr. Kaul agreed, “should not have been included” in the trial’s primary endpoint. It had been added “to amplify events and to minimize sample size. Not including revascularization would render the sample size prohibitive. There is always give and take in designing clinical trials.”
And he agreed that “IVUS-based PCI optimization would have further improved PCI outcomes.” However, “IVUS plus FFR adds to the procedural burden and limited resources available.” Dr. Fearon said when interviewed that the trial’s definition of procedural MI, a component of the primary endpoint, might potentially be seen as controversial. Procedural MIs in both the PCI and CABG groups were required to meet the standards of CABG-related type-5 MI according to the third and fourth Universal Definitions. The had also had to be accompanied by “a significant finding like new Q waves or a new wall-motion abnormality on echocardiography,” he said.
“That’s fairly strict. Because of that, we had a low rate of periprocedural MI and it was similar between the two groups, around 1.5% in both arms.”
FAME-3 was funded by Medtronic and Abbott Vascular. Dr. Kaul disclosed no relevant financial relationships. Dr. Kornowsky receives royalties from or holds intellectual property rights with CathWorks. Dr. Mehran disclosed financial ties to numerous pharmaceutical and device companies, and that she, her spouse, or her institution hold equity in Elixir Medical, Applied Therapeutics, and ControlRad.
A version of this article first appeared on Medscape.com.
Coronary stenting guided by fractional flow reserve (FFR) readings, considered to reflect the targeted lesion’s functional impact, was no match for coronary bypass surgery (CABG) in patients with multivessel disease (MVD) in a major international randomized trial.
Indeed, FFR-guided percutaneous coronary intervention (PCI) using one of the latest drug-eluting stents (DES) seemed to perform poorly in the trial, compared with surgery, apparently upping the risk for clinical events by 50% over 1 year.
Designed statistically for noninferiority, the third Fractional Flow Reserve Versus Angiography for Multivessel Evaluation (FAME 3) trial, with 1,500 randomized patients, showed that FFR-guided PCI was “not noninferior” to CABG. Of those randomized to PCI, 10.6% met the 1-year primary endpoint of major adverse cardiac or cerebrovascular events (MACCE), compared with only 6.9% of patients assigned to CABG.
The trial enrolled only patients with three-vessel coronary disease with no left-main coronary artery involvement, who were declared by their institution’s multidisciplinary heart team to be appropriate for either form of revascularization.
One of the roles of FFR for PCI guidance is to identify significant lesions “that are underrecognized by the angiogram,” which is less likely to happen in patients with very complex coronary anatomy, study chair William F. Fearon, MD, Stanford (Calif.) University, said in an interview.
“That’s what we saw in a subgroup analysis based on SYNTAX score,” an index of lesion complexity. “In patients with very high SYNTAX scores, CABG outperformed FFR-guided PCI. But if you look at patients with low SYNTAX scores, actually, FFR-guided PCI outperformed CABG for 1-year MACCE.”
Dr. Fearon is lead author on the study’s Nov. 4, 2021, publication in the New England Journal of Medicine, its release timed to coincide with his presentation of the trial at the Transcatheter Cardiovascular Therapeutics annual meeting, held virtually and live in Orlando and sponsored by the Cardiovascular Research Foundation.
He noted that FAME-3 “wasn’t designed or powered to test for superiority,” so its results do not imply CABG is superior to FFR-PCI in patients with MVD, and remains “inconclusive” on that question.
“I think what this study does is provide both the physician and patients more contemporary data and information on options and expected outcomes in multivessel disease. So if you are a patient who has less complex disease, I think you can feel comfortable that you will get an equivalent result with FFR-guided PCI.” But, at least based on FAME-3, Dr. Fearon said, CABG provides better outcomes in patients with more complex disease.
“I think there are still patients that look at trade-offs. Some patients will accept a higher event rate in order to avoid a long recovery, and vice versa.” So the trial may allow patients and physicians to make more informed decisions, he said.
A main message of FAME-3 “is that we’re getting very good results with three-vessel PCI, but better results with surgery,” Ran Kornowski, MD, Rabin Medical Center, Petah Tikva, Israel, and Tel Aviv University, said as a discussant following Dr. Fearon’s presentation of the trial. The subanalysis by SYNTAX score, he agreed, probably could be used as part of shared decision-making with patients.
Not all that surprising
“It’s a well-designed study, with a lot of patients,” said surgeon Frank W. Sellke, MD, of Rhode Island Hospital, Miriam Hospital, and Brown University, all in Providence.
“I don’t think it’s all that surprising,” he said in an interview. “It’s very consistent with what other studies have shown, that for three-vessel disease, surgery tends to have the edge,” even when pitted against FFR-guided PCI.
Indeed, pressure-wire FFR-PCI has a spotty history, even as an alternative to standard angiography-based PCI. For example, it has performed well in registry and other cohort studies but showed no advantage in the all-comers RIPCORD-2 trial or in the setting of complete revascularization PCI for acute MI in FLOWER-MI. And it emitted an increased-mortality signal in the prematurely halted FUTURE trial.
In FAME-3, “the 1-year follow-up was the best chance for FFR-PCI to be noninferior to CABG. The CABG advantage is only going to get better with time if prior experience and pathobiology is true,” Sanjay Kaul, MD, Cedars-Sinai Medical Center, Los Angeles, said in an interview.
Overall, “the quality and quantity of evidence is insufficient to support FFR-guided PCI” in patients with complex coronary artery disease (CAD), he said. “I would also argue that the evidence for FFR-guided PCI for simple CAD is also not high quality.”
Dr. Kaul also blasted the claim that FFR-PCI was seen to perform better against CABG in patients with low SYNTAX scores. “In general, one cannot use a positive subgroup in a null or negative trial, as is the case with FAME-3, to ‘rescue’ the treatment intervention.” Such a positive subgroup finding, he said, “would at best be deemed hypothesis-generating and not hypothesis validating.”
Dr. Fearon agreed that the subgroup analysis by SYNTAX score, though prespecified, was only hypothesis generating. “But I think that other studies have shown the same thing – that in less complex disease, the two strategies appear to perform in a similar fashion.”
The FAME-3 trial’s 1,500 patients were randomly assigned at 48 centers to undergo standard CABG or FFR-guided PCI with Resolute Integrity (Medtronic) zotarolimus-eluting DES. Lesions with a pressure-wire FFR of 0.80 or less were stented and those with higher FFR readings were deferred.
The 1-year hazard ratio for the primary endpoint—a composite of death from any cause, MI, stroke, or repeat revascularization – was 1.5 (95% confidence interval, 1.1-2.2) with a noninferiority P value of .35 for the comparison of FFR-PCI versus CABG.
FFR-guided PCI fared significantly better than CABG for some safety endpoints, including major bleeding (1.6% vs 3.8%, P < .01), arrhythmia including atrial fibrillation (2.4% vs. 14.1%, P < .001), acute kidney injury (0.1% vs 0.9%, P < .04), and 30-day rehospitalization (5.5% vs 10.2%, P < .001).
Did the primary endpoint favor CABG?
At a media briefing prior to Dr. Fearon’s TCT 2021 presentation of the trail, Roxana Mehran, MD, Icahn School of Medicine at Mount Sinai, New York, proposed that the inclusion of repeat revascularization in the trial’s composite primary endpoint tilted the outcome in favor of CABG. “To me, the FAME-3 results are predictable because repeat revascularization is in the equation.”
It’s well recognized that the endpoint is less likely after CABG than PCI. The latter treats focal lesions that are a limited part of a coronary artery in which CAD is still likely progressing. CABG, on the other hand, can bypass longer segments of diseased artery.
Indeed, as Dr. Fearon reported, the rates of death, MI, or stroke excluding repeat revascularization were 7.3% with FFR-PCI and 5.2% for CABG, for an HR of 1.4 (95% CI, 0.9-2.1).
Dr. Mehran also proposed that intravascular-ultrasound (IVUS) guidance, had it been part of the trial, could potentially have boosted the performance of FFR-PCI.
Repeat revascularization, Dr. Kaul agreed, “should not have been included” in the trial’s primary endpoint. It had been added “to amplify events and to minimize sample size. Not including revascularization would render the sample size prohibitive. There is always give and take in designing clinical trials.”
And he agreed that “IVUS-based PCI optimization would have further improved PCI outcomes.” However, “IVUS plus FFR adds to the procedural burden and limited resources available.” Dr. Fearon said when interviewed that the trial’s definition of procedural MI, a component of the primary endpoint, might potentially be seen as controversial. Procedural MIs in both the PCI and CABG groups were required to meet the standards of CABG-related type-5 MI according to the third and fourth Universal Definitions. The had also had to be accompanied by “a significant finding like new Q waves or a new wall-motion abnormality on echocardiography,” he said.
“That’s fairly strict. Because of that, we had a low rate of periprocedural MI and it was similar between the two groups, around 1.5% in both arms.”
FAME-3 was funded by Medtronic and Abbott Vascular. Dr. Kaul disclosed no relevant financial relationships. Dr. Kornowsky receives royalties from or holds intellectual property rights with CathWorks. Dr. Mehran disclosed financial ties to numerous pharmaceutical and device companies, and that she, her spouse, or her institution hold equity in Elixir Medical, Applied Therapeutics, and ControlRad.
A version of this article first appeared on Medscape.com.
Coronary stenting guided by fractional flow reserve (FFR) readings, considered to reflect the targeted lesion’s functional impact, was no match for coronary bypass surgery (CABG) in patients with multivessel disease (MVD) in a major international randomized trial.
Indeed, FFR-guided percutaneous coronary intervention (PCI) using one of the latest drug-eluting stents (DES) seemed to perform poorly in the trial, compared with surgery, apparently upping the risk for clinical events by 50% over 1 year.
Designed statistically for noninferiority, the third Fractional Flow Reserve Versus Angiography for Multivessel Evaluation (FAME 3) trial, with 1,500 randomized patients, showed that FFR-guided PCI was “not noninferior” to CABG. Of those randomized to PCI, 10.6% met the 1-year primary endpoint of major adverse cardiac or cerebrovascular events (MACCE), compared with only 6.9% of patients assigned to CABG.
The trial enrolled only patients with three-vessel coronary disease with no left-main coronary artery involvement, who were declared by their institution’s multidisciplinary heart team to be appropriate for either form of revascularization.
One of the roles of FFR for PCI guidance is to identify significant lesions “that are underrecognized by the angiogram,” which is less likely to happen in patients with very complex coronary anatomy, study chair William F. Fearon, MD, Stanford (Calif.) University, said in an interview.
“That’s what we saw in a subgroup analysis based on SYNTAX score,” an index of lesion complexity. “In patients with very high SYNTAX scores, CABG outperformed FFR-guided PCI. But if you look at patients with low SYNTAX scores, actually, FFR-guided PCI outperformed CABG for 1-year MACCE.”
Dr. Fearon is lead author on the study’s Nov. 4, 2021, publication in the New England Journal of Medicine, its release timed to coincide with his presentation of the trial at the Transcatheter Cardiovascular Therapeutics annual meeting, held virtually and live in Orlando and sponsored by the Cardiovascular Research Foundation.
He noted that FAME-3 “wasn’t designed or powered to test for superiority,” so its results do not imply CABG is superior to FFR-PCI in patients with MVD, and remains “inconclusive” on that question.
“I think what this study does is provide both the physician and patients more contemporary data and information on options and expected outcomes in multivessel disease. So if you are a patient who has less complex disease, I think you can feel comfortable that you will get an equivalent result with FFR-guided PCI.” But, at least based on FAME-3, Dr. Fearon said, CABG provides better outcomes in patients with more complex disease.
“I think there are still patients that look at trade-offs. Some patients will accept a higher event rate in order to avoid a long recovery, and vice versa.” So the trial may allow patients and physicians to make more informed decisions, he said.
A main message of FAME-3 “is that we’re getting very good results with three-vessel PCI, but better results with surgery,” Ran Kornowski, MD, Rabin Medical Center, Petah Tikva, Israel, and Tel Aviv University, said as a discussant following Dr. Fearon’s presentation of the trial. The subanalysis by SYNTAX score, he agreed, probably could be used as part of shared decision-making with patients.
Not all that surprising
“It’s a well-designed study, with a lot of patients,” said surgeon Frank W. Sellke, MD, of Rhode Island Hospital, Miriam Hospital, and Brown University, all in Providence.
“I don’t think it’s all that surprising,” he said in an interview. “It’s very consistent with what other studies have shown, that for three-vessel disease, surgery tends to have the edge,” even when pitted against FFR-guided PCI.
Indeed, pressure-wire FFR-PCI has a spotty history, even as an alternative to standard angiography-based PCI. For example, it has performed well in registry and other cohort studies but showed no advantage in the all-comers RIPCORD-2 trial or in the setting of complete revascularization PCI for acute MI in FLOWER-MI. And it emitted an increased-mortality signal in the prematurely halted FUTURE trial.
In FAME-3, “the 1-year follow-up was the best chance for FFR-PCI to be noninferior to CABG. The CABG advantage is only going to get better with time if prior experience and pathobiology is true,” Sanjay Kaul, MD, Cedars-Sinai Medical Center, Los Angeles, said in an interview.
Overall, “the quality and quantity of evidence is insufficient to support FFR-guided PCI” in patients with complex coronary artery disease (CAD), he said. “I would also argue that the evidence for FFR-guided PCI for simple CAD is also not high quality.”
Dr. Kaul also blasted the claim that FFR-PCI was seen to perform better against CABG in patients with low SYNTAX scores. “In general, one cannot use a positive subgroup in a null or negative trial, as is the case with FAME-3, to ‘rescue’ the treatment intervention.” Such a positive subgroup finding, he said, “would at best be deemed hypothesis-generating and not hypothesis validating.”
Dr. Fearon agreed that the subgroup analysis by SYNTAX score, though prespecified, was only hypothesis generating. “But I think that other studies have shown the same thing – that in less complex disease, the two strategies appear to perform in a similar fashion.”
The FAME-3 trial’s 1,500 patients were randomly assigned at 48 centers to undergo standard CABG or FFR-guided PCI with Resolute Integrity (Medtronic) zotarolimus-eluting DES. Lesions with a pressure-wire FFR of 0.80 or less were stented and those with higher FFR readings were deferred.
The 1-year hazard ratio for the primary endpoint—a composite of death from any cause, MI, stroke, or repeat revascularization – was 1.5 (95% confidence interval, 1.1-2.2) with a noninferiority P value of .35 for the comparison of FFR-PCI versus CABG.
FFR-guided PCI fared significantly better than CABG for some safety endpoints, including major bleeding (1.6% vs 3.8%, P < .01), arrhythmia including atrial fibrillation (2.4% vs. 14.1%, P < .001), acute kidney injury (0.1% vs 0.9%, P < .04), and 30-day rehospitalization (5.5% vs 10.2%, P < .001).
Did the primary endpoint favor CABG?
At a media briefing prior to Dr. Fearon’s TCT 2021 presentation of the trail, Roxana Mehran, MD, Icahn School of Medicine at Mount Sinai, New York, proposed that the inclusion of repeat revascularization in the trial’s composite primary endpoint tilted the outcome in favor of CABG. “To me, the FAME-3 results are predictable because repeat revascularization is in the equation.”
It’s well recognized that the endpoint is less likely after CABG than PCI. The latter treats focal lesions that are a limited part of a coronary artery in which CAD is still likely progressing. CABG, on the other hand, can bypass longer segments of diseased artery.
Indeed, as Dr. Fearon reported, the rates of death, MI, or stroke excluding repeat revascularization were 7.3% with FFR-PCI and 5.2% for CABG, for an HR of 1.4 (95% CI, 0.9-2.1).
Dr. Mehran also proposed that intravascular-ultrasound (IVUS) guidance, had it been part of the trial, could potentially have boosted the performance of FFR-PCI.
Repeat revascularization, Dr. Kaul agreed, “should not have been included” in the trial’s primary endpoint. It had been added “to amplify events and to minimize sample size. Not including revascularization would render the sample size prohibitive. There is always give and take in designing clinical trials.”
And he agreed that “IVUS-based PCI optimization would have further improved PCI outcomes.” However, “IVUS plus FFR adds to the procedural burden and limited resources available.” Dr. Fearon said when interviewed that the trial’s definition of procedural MI, a component of the primary endpoint, might potentially be seen as controversial. Procedural MIs in both the PCI and CABG groups were required to meet the standards of CABG-related type-5 MI according to the third and fourth Universal Definitions. The had also had to be accompanied by “a significant finding like new Q waves or a new wall-motion abnormality on echocardiography,” he said.
“That’s fairly strict. Because of that, we had a low rate of periprocedural MI and it was similar between the two groups, around 1.5% in both arms.”
FAME-3 was funded by Medtronic and Abbott Vascular. Dr. Kaul disclosed no relevant financial relationships. Dr. Kornowsky receives royalties from or holds intellectual property rights with CathWorks. Dr. Mehran disclosed financial ties to numerous pharmaceutical and device companies, and that she, her spouse, or her institution hold equity in Elixir Medical, Applied Therapeutics, and ControlRad.
A version of this article first appeared on Medscape.com.
James Bond taken down by an epidemiologist
No, Mr. Bond, I expect you to die
Movie watching usually requires a certain suspension of disbelief, and it’s safe to say James Bond movies require this more than most. Between the impossible gadgets and ludicrous doomsday plans, very few have ever stopped to consider the health risks of the James Bond universe.
Now, however, Bond, James Bond, has met his most formidable opponent: Wouter Graumans, a graduate student in epidemiology from the Netherlands. During a foray to Burkina Faso to study infectious diseases, Mr. Graumans came down with a case of food poisoning, which led him to wonder how 007 is able to trot across this big world of ours without contracting so much as a sinus infection.
Because Mr. Graumans is a man of science and conviction, mere speculation wasn’t enough. He and a group of coauthors wrote an entire paper on the health risks of the James Bond universe.
Doing so required watching over 3,000 minutes of numerous movies and analyzing Bond’s 86 total trips to 46 different countries based on current Centers for Disease Control and Prevention advice for travel to those countries. Time which, the authors state in the abstract, “could easily have been spent on more pressing societal issues or forms of relaxation that are more acceptable in academic circles.”
Naturally, Mr. Bond’s line of work entails exposure to unpleasant things, such as poison, dehydration, heatstroke, and dangerous wildlife (everything from ticks to crocodiles), though oddly enough he never succumbs to any of it. He’s also curiously immune to hangovers, despite rarely drinking anything nonalcoholic. There are also less obvious risks: For one, 007 rarely washes his hands. During one movie, he handles raw chicken to lure away a pack of crocodiles but fails to wash his hands afterward, leaving him at risk for multiple food-borne illnesses.
Of course, we must address the elephant in the bedroom: Mr. Bond’s numerous, er, encounters with women. One would imagine the biggest risk to those women would be from the various STDs that likely course through Bond’s body, but of the 27% who died shortly after … encountering … him, all involved violence, with disease playing no obvious role. Who knows, maybe he’s clean? Stranger things have happened.
The timing of this article may seem a bit suspicious. Was it a PR stunt by the studio? Rest assured, the authors addressed this, noting that they received no funding for the study, and that, “given the futility of its academic value, this is deemed entirely appropriate by all authors.” We love when a punchline writes itself.
How to see Atlanta on $688.35 a day
The world is always changing, so we have to change with it. This week, LOTME becomes a travel guide, and our first stop is the Big A, the Big Peach, Dogwood City, Empire City of the South, Wakanda.
There’s lots to do in Atlanta: Celebrate a World Series win, visit the College Football Hall of Fame or the World of Coca Cola, or take the Stranger Things/Upside Down film locations tour. Serious adventurers, however, get out of the city and go to Emory Decatur Hospital in – you guessed it – Decatur (unofficial motto: “Everything is Greater in Decatur”).
Find the emergency room and ask for Taylor Davis, who will be your personal guide. She’ll show you how to check in at the desk, sit in the waiting room for 7 hours, and then leave without seeing any medical personnel or receiving any sort of attention whatsoever. All the things she did when she went there in July for a head injury.
Ms. Davis told Fox5 Atlanta: “I didn’t get my vitals taken, nobody called my name. I wasn’t seen at all.”
But wait! There’s more! By booking your trip through LOTMEgo* and using the code “Decatur,” you’ll get the Taylor Davis special, which includes a bill/cover charge for $688.35 from the hospital. An Emory Healthcare patient financial services employee told Ms. Davis that “you get charged before you are seen. Not for being seen.”
If all this has you ready to hop in your car (really?), then check out LOTMEgo* on Twittbook and InstaTok. You’ll also find trick-or-treating tips and discounts on haunted hospital tours.
*Does not actually exist
Breaking down the hot flash
Do you ever wonder why we scramble for cold things when we’re feeling nauseous? Whether it’s the cool air that needs to hit your face in the car or a cold, damp towel on the back of your neck, scientists think it could possibly be an evolutionary mechanism at the cellular level.
Motion sickness it’s actually a battle of body temperature, according to an article from LiveScience. Capillaries in the skin dilate, allowing for more blood flow near the skin’s surface and causing core temperature to fall. Once body temperature drops, the hypothalamus, which regulates temperature, tries to do its job by raising body temperature. Thus the hot flash!
The cold compress and cool air help fight the battle by counteracting the hypothalamus, but why the drop in body temperature to begin with?
There are a few theories. Dr. Robert Glatter, an emergency physician at Lenox Hill Hospital in New York, told LiveScience that the lack of oxygen needed in body tissue to survive at lower temperatures could be making it difficult to get oxygen to the body when a person is ill, and is “more likely an adaptive response influenced by poorly understood mechanisms at the cellular level.”
Another theory is that the nausea and body temperature shift is the body’s natural response to help people vomit.
Then there’s the theory of “defensive hypothermia,” which suggests that cold sweats are a possible mechanism to conserve energy so the body can fight off an intruder, which was supported by a 2014 study and a 2016 review.
It’s another one of the body’s many survival tricks.
Teachers were right: Pupils can do the math
Teachers liked to preach that we wouldn’t have calculators with us all the time, but that wound up not being true. Our phones have calculators at the press of a button. But maybe even calculators aren’t always needed because our pupils do more math than you think.
The pupil light reflex – constrict in light and dilate in darkness – is well known, but recent work shows that pupil size is also regulated by cognitive and perceptual factors. By presenting subjects with images of various numbers of dots and measuring pupil size, the investigators were able to show “that numerical information is intrinsically related to perception,” lead author Dr. Elisa Castaldi of Florence University noted in a written statement.
The researchers found that pupils are responsible for important survival techniques. Coauthor David Burr of the University of Sydney and the University of Florence gave an evolutionary perspective: “When we look around, we spontaneously perceive the form, size, movement and colour of a scene. Equally spontaneously, we perceive the number of items before us. This ability, shared with most other animals, is an evolutionary fundamental: It reveals immediately important quantities, such as how many apples there are on the tree, or how many enemies are attacking.”
Useful information, indeed, but our pupils seem to be more interested in the quantity of beers in the refrigerator.
No, Mr. Bond, I expect you to die
Movie watching usually requires a certain suspension of disbelief, and it’s safe to say James Bond movies require this more than most. Between the impossible gadgets and ludicrous doomsday plans, very few have ever stopped to consider the health risks of the James Bond universe.
Now, however, Bond, James Bond, has met his most formidable opponent: Wouter Graumans, a graduate student in epidemiology from the Netherlands. During a foray to Burkina Faso to study infectious diseases, Mr. Graumans came down with a case of food poisoning, which led him to wonder how 007 is able to trot across this big world of ours without contracting so much as a sinus infection.
Because Mr. Graumans is a man of science and conviction, mere speculation wasn’t enough. He and a group of coauthors wrote an entire paper on the health risks of the James Bond universe.
Doing so required watching over 3,000 minutes of numerous movies and analyzing Bond’s 86 total trips to 46 different countries based on current Centers for Disease Control and Prevention advice for travel to those countries. Time which, the authors state in the abstract, “could easily have been spent on more pressing societal issues or forms of relaxation that are more acceptable in academic circles.”
Naturally, Mr. Bond’s line of work entails exposure to unpleasant things, such as poison, dehydration, heatstroke, and dangerous wildlife (everything from ticks to crocodiles), though oddly enough he never succumbs to any of it. He’s also curiously immune to hangovers, despite rarely drinking anything nonalcoholic. There are also less obvious risks: For one, 007 rarely washes his hands. During one movie, he handles raw chicken to lure away a pack of crocodiles but fails to wash his hands afterward, leaving him at risk for multiple food-borne illnesses.
Of course, we must address the elephant in the bedroom: Mr. Bond’s numerous, er, encounters with women. One would imagine the biggest risk to those women would be from the various STDs that likely course through Bond’s body, but of the 27% who died shortly after … encountering … him, all involved violence, with disease playing no obvious role. Who knows, maybe he’s clean? Stranger things have happened.
The timing of this article may seem a bit suspicious. Was it a PR stunt by the studio? Rest assured, the authors addressed this, noting that they received no funding for the study, and that, “given the futility of its academic value, this is deemed entirely appropriate by all authors.” We love when a punchline writes itself.
How to see Atlanta on $688.35 a day
The world is always changing, so we have to change with it. This week, LOTME becomes a travel guide, and our first stop is the Big A, the Big Peach, Dogwood City, Empire City of the South, Wakanda.
There’s lots to do in Atlanta: Celebrate a World Series win, visit the College Football Hall of Fame or the World of Coca Cola, or take the Stranger Things/Upside Down film locations tour. Serious adventurers, however, get out of the city and go to Emory Decatur Hospital in – you guessed it – Decatur (unofficial motto: “Everything is Greater in Decatur”).
Find the emergency room and ask for Taylor Davis, who will be your personal guide. She’ll show you how to check in at the desk, sit in the waiting room for 7 hours, and then leave without seeing any medical personnel or receiving any sort of attention whatsoever. All the things she did when she went there in July for a head injury.
Ms. Davis told Fox5 Atlanta: “I didn’t get my vitals taken, nobody called my name. I wasn’t seen at all.”
But wait! There’s more! By booking your trip through LOTMEgo* and using the code “Decatur,” you’ll get the Taylor Davis special, which includes a bill/cover charge for $688.35 from the hospital. An Emory Healthcare patient financial services employee told Ms. Davis that “you get charged before you are seen. Not for being seen.”
If all this has you ready to hop in your car (really?), then check out LOTMEgo* on Twittbook and InstaTok. You’ll also find trick-or-treating tips and discounts on haunted hospital tours.
*Does not actually exist
Breaking down the hot flash
Do you ever wonder why we scramble for cold things when we’re feeling nauseous? Whether it’s the cool air that needs to hit your face in the car or a cold, damp towel on the back of your neck, scientists think it could possibly be an evolutionary mechanism at the cellular level.
Motion sickness it’s actually a battle of body temperature, according to an article from LiveScience. Capillaries in the skin dilate, allowing for more blood flow near the skin’s surface and causing core temperature to fall. Once body temperature drops, the hypothalamus, which regulates temperature, tries to do its job by raising body temperature. Thus the hot flash!
The cold compress and cool air help fight the battle by counteracting the hypothalamus, but why the drop in body temperature to begin with?
There are a few theories. Dr. Robert Glatter, an emergency physician at Lenox Hill Hospital in New York, told LiveScience that the lack of oxygen needed in body tissue to survive at lower temperatures could be making it difficult to get oxygen to the body when a person is ill, and is “more likely an adaptive response influenced by poorly understood mechanisms at the cellular level.”
Another theory is that the nausea and body temperature shift is the body’s natural response to help people vomit.
Then there’s the theory of “defensive hypothermia,” which suggests that cold sweats are a possible mechanism to conserve energy so the body can fight off an intruder, which was supported by a 2014 study and a 2016 review.
It’s another one of the body’s many survival tricks.
Teachers were right: Pupils can do the math
Teachers liked to preach that we wouldn’t have calculators with us all the time, but that wound up not being true. Our phones have calculators at the press of a button. But maybe even calculators aren’t always needed because our pupils do more math than you think.
The pupil light reflex – constrict in light and dilate in darkness – is well known, but recent work shows that pupil size is also regulated by cognitive and perceptual factors. By presenting subjects with images of various numbers of dots and measuring pupil size, the investigators were able to show “that numerical information is intrinsically related to perception,” lead author Dr. Elisa Castaldi of Florence University noted in a written statement.
The researchers found that pupils are responsible for important survival techniques. Coauthor David Burr of the University of Sydney and the University of Florence gave an evolutionary perspective: “When we look around, we spontaneously perceive the form, size, movement and colour of a scene. Equally spontaneously, we perceive the number of items before us. This ability, shared with most other animals, is an evolutionary fundamental: It reveals immediately important quantities, such as how many apples there are on the tree, or how many enemies are attacking.”
Useful information, indeed, but our pupils seem to be more interested in the quantity of beers in the refrigerator.
No, Mr. Bond, I expect you to die
Movie watching usually requires a certain suspension of disbelief, and it’s safe to say James Bond movies require this more than most. Between the impossible gadgets and ludicrous doomsday plans, very few have ever stopped to consider the health risks of the James Bond universe.
Now, however, Bond, James Bond, has met his most formidable opponent: Wouter Graumans, a graduate student in epidemiology from the Netherlands. During a foray to Burkina Faso to study infectious diseases, Mr. Graumans came down with a case of food poisoning, which led him to wonder how 007 is able to trot across this big world of ours without contracting so much as a sinus infection.
Because Mr. Graumans is a man of science and conviction, mere speculation wasn’t enough. He and a group of coauthors wrote an entire paper on the health risks of the James Bond universe.
Doing so required watching over 3,000 minutes of numerous movies and analyzing Bond’s 86 total trips to 46 different countries based on current Centers for Disease Control and Prevention advice for travel to those countries. Time which, the authors state in the abstract, “could easily have been spent on more pressing societal issues or forms of relaxation that are more acceptable in academic circles.”
Naturally, Mr. Bond’s line of work entails exposure to unpleasant things, such as poison, dehydration, heatstroke, and dangerous wildlife (everything from ticks to crocodiles), though oddly enough he never succumbs to any of it. He’s also curiously immune to hangovers, despite rarely drinking anything nonalcoholic. There are also less obvious risks: For one, 007 rarely washes his hands. During one movie, he handles raw chicken to lure away a pack of crocodiles but fails to wash his hands afterward, leaving him at risk for multiple food-borne illnesses.
Of course, we must address the elephant in the bedroom: Mr. Bond’s numerous, er, encounters with women. One would imagine the biggest risk to those women would be from the various STDs that likely course through Bond’s body, but of the 27% who died shortly after … encountering … him, all involved violence, with disease playing no obvious role. Who knows, maybe he’s clean? Stranger things have happened.
The timing of this article may seem a bit suspicious. Was it a PR stunt by the studio? Rest assured, the authors addressed this, noting that they received no funding for the study, and that, “given the futility of its academic value, this is deemed entirely appropriate by all authors.” We love when a punchline writes itself.
How to see Atlanta on $688.35 a day
The world is always changing, so we have to change with it. This week, LOTME becomes a travel guide, and our first stop is the Big A, the Big Peach, Dogwood City, Empire City of the South, Wakanda.
There’s lots to do in Atlanta: Celebrate a World Series win, visit the College Football Hall of Fame or the World of Coca Cola, or take the Stranger Things/Upside Down film locations tour. Serious adventurers, however, get out of the city and go to Emory Decatur Hospital in – you guessed it – Decatur (unofficial motto: “Everything is Greater in Decatur”).
Find the emergency room and ask for Taylor Davis, who will be your personal guide. She’ll show you how to check in at the desk, sit in the waiting room for 7 hours, and then leave without seeing any medical personnel or receiving any sort of attention whatsoever. All the things she did when she went there in July for a head injury.
Ms. Davis told Fox5 Atlanta: “I didn’t get my vitals taken, nobody called my name. I wasn’t seen at all.”
But wait! There’s more! By booking your trip through LOTMEgo* and using the code “Decatur,” you’ll get the Taylor Davis special, which includes a bill/cover charge for $688.35 from the hospital. An Emory Healthcare patient financial services employee told Ms. Davis that “you get charged before you are seen. Not for being seen.”
If all this has you ready to hop in your car (really?), then check out LOTMEgo* on Twittbook and InstaTok. You’ll also find trick-or-treating tips and discounts on haunted hospital tours.
*Does not actually exist
Breaking down the hot flash
Do you ever wonder why we scramble for cold things when we’re feeling nauseous? Whether it’s the cool air that needs to hit your face in the car or a cold, damp towel on the back of your neck, scientists think it could possibly be an evolutionary mechanism at the cellular level.
Motion sickness it’s actually a battle of body temperature, according to an article from LiveScience. Capillaries in the skin dilate, allowing for more blood flow near the skin’s surface and causing core temperature to fall. Once body temperature drops, the hypothalamus, which regulates temperature, tries to do its job by raising body temperature. Thus the hot flash!
The cold compress and cool air help fight the battle by counteracting the hypothalamus, but why the drop in body temperature to begin with?
There are a few theories. Dr. Robert Glatter, an emergency physician at Lenox Hill Hospital in New York, told LiveScience that the lack of oxygen needed in body tissue to survive at lower temperatures could be making it difficult to get oxygen to the body when a person is ill, and is “more likely an adaptive response influenced by poorly understood mechanisms at the cellular level.”
Another theory is that the nausea and body temperature shift is the body’s natural response to help people vomit.
Then there’s the theory of “defensive hypothermia,” which suggests that cold sweats are a possible mechanism to conserve energy so the body can fight off an intruder, which was supported by a 2014 study and a 2016 review.
It’s another one of the body’s many survival tricks.
Teachers were right: Pupils can do the math
Teachers liked to preach that we wouldn’t have calculators with us all the time, but that wound up not being true. Our phones have calculators at the press of a button. But maybe even calculators aren’t always needed because our pupils do more math than you think.
The pupil light reflex – constrict in light and dilate in darkness – is well known, but recent work shows that pupil size is also regulated by cognitive and perceptual factors. By presenting subjects with images of various numbers of dots and measuring pupil size, the investigators were able to show “that numerical information is intrinsically related to perception,” lead author Dr. Elisa Castaldi of Florence University noted in a written statement.
The researchers found that pupils are responsible for important survival techniques. Coauthor David Burr of the University of Sydney and the University of Florence gave an evolutionary perspective: “When we look around, we spontaneously perceive the form, size, movement and colour of a scene. Equally spontaneously, we perceive the number of items before us. This ability, shared with most other animals, is an evolutionary fundamental: It reveals immediately important quantities, such as how many apples there are on the tree, or how many enemies are attacking.”
Useful information, indeed, but our pupils seem to be more interested in the quantity of beers in the refrigerator.
FDA class I recall of CardioSave hybrid/rescue IABPs
Datascope/Getinge/Maquet is recalling CardioSave Hybrid and Rescue intra-aortic balloon pumps (IABPs) because some battery packs may have a shortened run time and fail unexpectedly, according to a medical device recall notice posted on the U.S. Food and Drug Administration website.
The FDA has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.
The recalled IABPs have substandard batteries that do not meet performance specifications and were mistakenly released to a limited number of customers.
If a patient requires life-supporting therapy with an IABP and the device does not work or stops working during use because of battery failure, the patient will be at risk for serious injury, including death, the FDA cautions.
Both IABP monitors display battery life and have low battery alarms when alternative power sources are needed.
Datascope/Getting/Maquet has received six complaints but no reports of injury or death related to this issue.
“However, there is a potential for underreporting since the end user reporting a failed battery or short battery run time cannot be aware that they originally received a substandard battery,” the FDA said.
The recall involves 137 battery packs distributed in the United States between Sept. 23, 2017, and Aug. 17, 2021. Product codes and lot numbers are available in the recall notice.
The company sent an urgent medical device removal letter to customers requesting that they check inventory to determine if there are any CardioSave LiIon battery packs with part number/reference number 0146-00-0097 and with serial numbers listed in the letter.
Customers are asked to replace any affected battery with an unaffected battery and remove the affected product from areas of use.
The company will issue credit or a replacement battery at no cost to the facility upon receipt of the response form attached to the letter.
Distributors who shipped any affected product to customers are asked to forward the device removal letter to customers.
All customers, regardless of whether or not they have defective batteries, are asked to complete and sign the response form to acknowledge that they received the notification and disposed of the affected batteries.
Completed forms can be scanned and emailed to Datascope/Getinge/Maquet at [email protected] or by FAX to 1-877-446-3360.
Customers who have questions about this recall should contact their Datascope/Getinge/Maquet sales representative or, for technical questions, customer service (1-888-943-8872, option 2), Monday through Friday, 8:00 a.m. to 6:00 p.m. ET.
Any adverse events or suspected adverse events related to the recalled CardioSave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
A version of this article first appeared on Medscape.com.
Datascope/Getinge/Maquet is recalling CardioSave Hybrid and Rescue intra-aortic balloon pumps (IABPs) because some battery packs may have a shortened run time and fail unexpectedly, according to a medical device recall notice posted on the U.S. Food and Drug Administration website.
The FDA has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.
The recalled IABPs have substandard batteries that do not meet performance specifications and were mistakenly released to a limited number of customers.
If a patient requires life-supporting therapy with an IABP and the device does not work or stops working during use because of battery failure, the patient will be at risk for serious injury, including death, the FDA cautions.
Both IABP monitors display battery life and have low battery alarms when alternative power sources are needed.
Datascope/Getting/Maquet has received six complaints but no reports of injury or death related to this issue.
“However, there is a potential for underreporting since the end user reporting a failed battery or short battery run time cannot be aware that they originally received a substandard battery,” the FDA said.
The recall involves 137 battery packs distributed in the United States between Sept. 23, 2017, and Aug. 17, 2021. Product codes and lot numbers are available in the recall notice.
The company sent an urgent medical device removal letter to customers requesting that they check inventory to determine if there are any CardioSave LiIon battery packs with part number/reference number 0146-00-0097 and with serial numbers listed in the letter.
Customers are asked to replace any affected battery with an unaffected battery and remove the affected product from areas of use.
The company will issue credit or a replacement battery at no cost to the facility upon receipt of the response form attached to the letter.
Distributors who shipped any affected product to customers are asked to forward the device removal letter to customers.
All customers, regardless of whether or not they have defective batteries, are asked to complete and sign the response form to acknowledge that they received the notification and disposed of the affected batteries.
Completed forms can be scanned and emailed to Datascope/Getinge/Maquet at [email protected] or by FAX to 1-877-446-3360.
Customers who have questions about this recall should contact their Datascope/Getinge/Maquet sales representative or, for technical questions, customer service (1-888-943-8872, option 2), Monday through Friday, 8:00 a.m. to 6:00 p.m. ET.
Any adverse events or suspected adverse events related to the recalled CardioSave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
A version of this article first appeared on Medscape.com.
Datascope/Getinge/Maquet is recalling CardioSave Hybrid and Rescue intra-aortic balloon pumps (IABPs) because some battery packs may have a shortened run time and fail unexpectedly, according to a medical device recall notice posted on the U.S. Food and Drug Administration website.
The FDA has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.
The recalled IABPs have substandard batteries that do not meet performance specifications and were mistakenly released to a limited number of customers.
If a patient requires life-supporting therapy with an IABP and the device does not work or stops working during use because of battery failure, the patient will be at risk for serious injury, including death, the FDA cautions.
Both IABP monitors display battery life and have low battery alarms when alternative power sources are needed.
Datascope/Getting/Maquet has received six complaints but no reports of injury or death related to this issue.
“However, there is a potential for underreporting since the end user reporting a failed battery or short battery run time cannot be aware that they originally received a substandard battery,” the FDA said.
The recall involves 137 battery packs distributed in the United States between Sept. 23, 2017, and Aug. 17, 2021. Product codes and lot numbers are available in the recall notice.
The company sent an urgent medical device removal letter to customers requesting that they check inventory to determine if there are any CardioSave LiIon battery packs with part number/reference number 0146-00-0097 and with serial numbers listed in the letter.
Customers are asked to replace any affected battery with an unaffected battery and remove the affected product from areas of use.
The company will issue credit or a replacement battery at no cost to the facility upon receipt of the response form attached to the letter.
Distributors who shipped any affected product to customers are asked to forward the device removal letter to customers.
All customers, regardless of whether or not they have defective batteries, are asked to complete and sign the response form to acknowledge that they received the notification and disposed of the affected batteries.
Completed forms can be scanned and emailed to Datascope/Getinge/Maquet at [email protected] or by FAX to 1-877-446-3360.
Customers who have questions about this recall should contact their Datascope/Getinge/Maquet sales representative or, for technical questions, customer service (1-888-943-8872, option 2), Monday through Friday, 8:00 a.m. to 6:00 p.m. ET.
Any adverse events or suspected adverse events related to the recalled CardioSave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
A version of this article first appeared on Medscape.com.
Overall survival for metastatic urothelial carcinoma approaching 2 years
This is according to a review of the recent therapeutic advances and ongoing clinical trials in metastatic urothelial carcinoma.
“Survival in the metastatic setting is 12-15 months with cisplatin-based combination chemotherapy, but only 3-6 months if left untreated,” wrote Srikala S. Sridhar, MD, of the University of Toronto, and colleagues. Their report is in Therapeutic Advances in Medical Oncology. “More recently, with the advent of immunotherapy, antibody-drug conjugates, and targeted agents, the treatment landscape has changed significantly, with overall survival now approaching two years.”
Both the incidence and mortality from bladder cancer have risen over the past few decades. Around 5% of patients are metastatic at presentation, but nearly half of patients with muscle-invasive bladder cancer will eventually relapse and develop metastatic disease.
For first-line treatment in metastatic urothelial carcinoma, cisplatin-based chemotherapy remains the preferred option with response rates up to 72%, but durability is an issue with most patients experiencing disease progression. In patients with locally advanced or metastatic disease, who are not eligible for cisplatin-based chemotherapy and whose tumors express PD-L1, or patients who are not eligible for any platinum-based regimen regardless of PD-L1 status, the immune checkpoint inhibitors atezolizumab and pembrolizumab have received accelerated Food and Drug administration approval. More recently, pembrolizumab gained full FDA approval for use in patients not eligible to receive platinum-based chemotherapy.
While phase 3 studies are evaluating chemotherapy combined with atezolizumab or pembrolizumab, the results have not been promising. Moreover, the decreased survival observed in the immunotherapy-alone arms of these trials led the FDA to issue a warning that single agent immunotherapy should be used only in patients who are not eligible for cisplatin-based therapy and have PD-L1 expression, or in those not eligible for any platinum-based regimens regardless of PD-L1 expression.
“More intensive treatment in metastatic urothelial carcinoma is not always better,” the authors wrote. “Some of the reasons for this could be that chemotherapy and immunotherapy are targeting a similar population of cells, or that chemotherapy and immunotherapy are antagonistic on some level.”
Maintenance strategies are considered standard of care for other advanced solid tumors. In patients with bladder cancer without disease progression after a first line platinum-based chemotherapy, maintenance avelumab, an anti PD-L1, has shown an overall survival of 21.4 months versus 14.3 months with best supportive care, a finding that the authors described as “practice changing.” Meanwhile, a separate trial showed increased progression-free survival with maintenance pembrolizumab, but no increased overall survival.
For second-line treatment, immunotherapy is currently the standard of care in patients with disease progression during or after platinum-based chemotherapy. While the efficiency of five anti PD-1 and PD-L1 antibodies has been reported in the second-line setting, pembrolizumab is the only immune checkpoint inhibitor to receive full FDA approval. Atezolizumab, nivolumab, avelumab, and durvalumab have received accelerated approval.
“In urothelial carcinomas, PD-1 appears to have an advantage over anti PD-L1 in the second-line setting, but in the maintenance setting, it seems to be the opposite,” the authors wrote.
Erdafitinib is the only fibroblast growth factor receptor (FGFR) inhibitor approved for locally advanced or metastatic urothelial carcinoma, progressing on platinum-based chemotherapy. The oral potent tyrosine kinase inhibitor of FGFR 1-4 is approved for use only in patients with susceptible FGFR3 gene mutations or FGFR2/3 gene fusions. Despite being approved for second-line treatment, erdafitinib is used mainly in third-line treatment after progression on immunotherapy.
The antibody drug conjugates sacituzumab govitecan and enfortumab vedotin, which have gained accelerated FDA approval, provide other options for patients with metastatic urothelial carcinoma resistant to chemotherapy and checkpoint inhibitors. As these antibody drug conjugates have different mechanisms of action and toxicity profiles, they could be used in the same patient throughout the disease course, but further research is needed. Meanwhile, many chemotherapy options, including docetaxel, gemcitabine, ifosfamide, and pemetrexed, have been tested in metastatic urothelial carcinoma with some response after platinum-based treatment.
“A number of studies evaluating promising therapeutic strategies are still ongoing and will hopefully provide information for some important unanswered questions and further guide treatment sequencing in advanced urothelial carcinoma,” the authors wrote.
They declared that there are no conflicts of interest.
This is according to a review of the recent therapeutic advances and ongoing clinical trials in metastatic urothelial carcinoma.
“Survival in the metastatic setting is 12-15 months with cisplatin-based combination chemotherapy, but only 3-6 months if left untreated,” wrote Srikala S. Sridhar, MD, of the University of Toronto, and colleagues. Their report is in Therapeutic Advances in Medical Oncology. “More recently, with the advent of immunotherapy, antibody-drug conjugates, and targeted agents, the treatment landscape has changed significantly, with overall survival now approaching two years.”
Both the incidence and mortality from bladder cancer have risen over the past few decades. Around 5% of patients are metastatic at presentation, but nearly half of patients with muscle-invasive bladder cancer will eventually relapse and develop metastatic disease.
For first-line treatment in metastatic urothelial carcinoma, cisplatin-based chemotherapy remains the preferred option with response rates up to 72%, but durability is an issue with most patients experiencing disease progression. In patients with locally advanced or metastatic disease, who are not eligible for cisplatin-based chemotherapy and whose tumors express PD-L1, or patients who are not eligible for any platinum-based regimen regardless of PD-L1 status, the immune checkpoint inhibitors atezolizumab and pembrolizumab have received accelerated Food and Drug administration approval. More recently, pembrolizumab gained full FDA approval for use in patients not eligible to receive platinum-based chemotherapy.
While phase 3 studies are evaluating chemotherapy combined with atezolizumab or pembrolizumab, the results have not been promising. Moreover, the decreased survival observed in the immunotherapy-alone arms of these trials led the FDA to issue a warning that single agent immunotherapy should be used only in patients who are not eligible for cisplatin-based therapy and have PD-L1 expression, or in those not eligible for any platinum-based regimens regardless of PD-L1 expression.
“More intensive treatment in metastatic urothelial carcinoma is not always better,” the authors wrote. “Some of the reasons for this could be that chemotherapy and immunotherapy are targeting a similar population of cells, or that chemotherapy and immunotherapy are antagonistic on some level.”
Maintenance strategies are considered standard of care for other advanced solid tumors. In patients with bladder cancer without disease progression after a first line platinum-based chemotherapy, maintenance avelumab, an anti PD-L1, has shown an overall survival of 21.4 months versus 14.3 months with best supportive care, a finding that the authors described as “practice changing.” Meanwhile, a separate trial showed increased progression-free survival with maintenance pembrolizumab, but no increased overall survival.
For second-line treatment, immunotherapy is currently the standard of care in patients with disease progression during or after platinum-based chemotherapy. While the efficiency of five anti PD-1 and PD-L1 antibodies has been reported in the second-line setting, pembrolizumab is the only immune checkpoint inhibitor to receive full FDA approval. Atezolizumab, nivolumab, avelumab, and durvalumab have received accelerated approval.
“In urothelial carcinomas, PD-1 appears to have an advantage over anti PD-L1 in the second-line setting, but in the maintenance setting, it seems to be the opposite,” the authors wrote.
Erdafitinib is the only fibroblast growth factor receptor (FGFR) inhibitor approved for locally advanced or metastatic urothelial carcinoma, progressing on platinum-based chemotherapy. The oral potent tyrosine kinase inhibitor of FGFR 1-4 is approved for use only in patients with susceptible FGFR3 gene mutations or FGFR2/3 gene fusions. Despite being approved for second-line treatment, erdafitinib is used mainly in third-line treatment after progression on immunotherapy.
The antibody drug conjugates sacituzumab govitecan and enfortumab vedotin, which have gained accelerated FDA approval, provide other options for patients with metastatic urothelial carcinoma resistant to chemotherapy and checkpoint inhibitors. As these antibody drug conjugates have different mechanisms of action and toxicity profiles, they could be used in the same patient throughout the disease course, but further research is needed. Meanwhile, many chemotherapy options, including docetaxel, gemcitabine, ifosfamide, and pemetrexed, have been tested in metastatic urothelial carcinoma with some response after platinum-based treatment.
“A number of studies evaluating promising therapeutic strategies are still ongoing and will hopefully provide information for some important unanswered questions and further guide treatment sequencing in advanced urothelial carcinoma,” the authors wrote.
They declared that there are no conflicts of interest.
This is according to a review of the recent therapeutic advances and ongoing clinical trials in metastatic urothelial carcinoma.
“Survival in the metastatic setting is 12-15 months with cisplatin-based combination chemotherapy, but only 3-6 months if left untreated,” wrote Srikala S. Sridhar, MD, of the University of Toronto, and colleagues. Their report is in Therapeutic Advances in Medical Oncology. “More recently, with the advent of immunotherapy, antibody-drug conjugates, and targeted agents, the treatment landscape has changed significantly, with overall survival now approaching two years.”
Both the incidence and mortality from bladder cancer have risen over the past few decades. Around 5% of patients are metastatic at presentation, but nearly half of patients with muscle-invasive bladder cancer will eventually relapse and develop metastatic disease.
For first-line treatment in metastatic urothelial carcinoma, cisplatin-based chemotherapy remains the preferred option with response rates up to 72%, but durability is an issue with most patients experiencing disease progression. In patients with locally advanced or metastatic disease, who are not eligible for cisplatin-based chemotherapy and whose tumors express PD-L1, or patients who are not eligible for any platinum-based regimen regardless of PD-L1 status, the immune checkpoint inhibitors atezolizumab and pembrolizumab have received accelerated Food and Drug administration approval. More recently, pembrolizumab gained full FDA approval for use in patients not eligible to receive platinum-based chemotherapy.
While phase 3 studies are evaluating chemotherapy combined with atezolizumab or pembrolizumab, the results have not been promising. Moreover, the decreased survival observed in the immunotherapy-alone arms of these trials led the FDA to issue a warning that single agent immunotherapy should be used only in patients who are not eligible for cisplatin-based therapy and have PD-L1 expression, or in those not eligible for any platinum-based regimens regardless of PD-L1 expression.
“More intensive treatment in metastatic urothelial carcinoma is not always better,” the authors wrote. “Some of the reasons for this could be that chemotherapy and immunotherapy are targeting a similar population of cells, or that chemotherapy and immunotherapy are antagonistic on some level.”
Maintenance strategies are considered standard of care for other advanced solid tumors. In patients with bladder cancer without disease progression after a first line platinum-based chemotherapy, maintenance avelumab, an anti PD-L1, has shown an overall survival of 21.4 months versus 14.3 months with best supportive care, a finding that the authors described as “practice changing.” Meanwhile, a separate trial showed increased progression-free survival with maintenance pembrolizumab, but no increased overall survival.
For second-line treatment, immunotherapy is currently the standard of care in patients with disease progression during or after platinum-based chemotherapy. While the efficiency of five anti PD-1 and PD-L1 antibodies has been reported in the second-line setting, pembrolizumab is the only immune checkpoint inhibitor to receive full FDA approval. Atezolizumab, nivolumab, avelumab, and durvalumab have received accelerated approval.
“In urothelial carcinomas, PD-1 appears to have an advantage over anti PD-L1 in the second-line setting, but in the maintenance setting, it seems to be the opposite,” the authors wrote.
Erdafitinib is the only fibroblast growth factor receptor (FGFR) inhibitor approved for locally advanced or metastatic urothelial carcinoma, progressing on platinum-based chemotherapy. The oral potent tyrosine kinase inhibitor of FGFR 1-4 is approved for use only in patients with susceptible FGFR3 gene mutations or FGFR2/3 gene fusions. Despite being approved for second-line treatment, erdafitinib is used mainly in third-line treatment after progression on immunotherapy.
The antibody drug conjugates sacituzumab govitecan and enfortumab vedotin, which have gained accelerated FDA approval, provide other options for patients with metastatic urothelial carcinoma resistant to chemotherapy and checkpoint inhibitors. As these antibody drug conjugates have different mechanisms of action and toxicity profiles, they could be used in the same patient throughout the disease course, but further research is needed. Meanwhile, many chemotherapy options, including docetaxel, gemcitabine, ifosfamide, and pemetrexed, have been tested in metastatic urothelial carcinoma with some response after platinum-based treatment.
“A number of studies evaluating promising therapeutic strategies are still ongoing and will hopefully provide information for some important unanswered questions and further guide treatment sequencing in advanced urothelial carcinoma,” the authors wrote.
They declared that there are no conflicts of interest.
FROM THERAPEUTIC ADVANCES IN MEDICAL ONCOLOGY
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.