Opinion

It was a quiet day. I got up around 3 o’clock in the afternoon for my shift at 6 p.m. I was shaking off the cobwebs and making coffee at our front window that overlooked Brown Street in North Philadelphia. I looked out the window and saw a man stumbling down the street, grabbing his abdomen and yelling for help. There was nobody else around so I went outside to see what was going on.

He was in his 50s or 60s, bleeding and obviously in distress. I had him sit down. Then I ran back inside and grabbed a dish towel and some exam gloves that I had in the house.

I ran back out and assessed him. A bullet had gone through one of his hands, but he had other wounds. I had to expose him, so I trauma stripped him on the sidewalk. I got his pants and his shirt off and saw a gunshot going through his lower pelvis. He was bleeding out from there.

I got the towel and started applying deep pressure down into the iliac vein in case they hit something, which I found out later, they had. I held it there. The man was just lying there begging not to die.

I’m someone who is very calm, maybe abnormally calm, as people tell me. I try to use that during my resuscitations and traumas. Just keeping everybody calm makes the situation easier. Afterwards, people asked me, “Weren’t you worried that you were going to get shot?” That does happen in North Philadelphia. But it didn’t even cross my mind.

I didn’t have to think at all about what I was doing. We saw so many gunshots, especially at Einstein Medical Center. We saw them daily. I’d sometimes get more than half a dozen gunshots in one shift.

So, I was holding pressure and some people started to come over. I got somebody to call 911 and asked the man about his medical history. I found out he had diabetes. Five or 10 minutes later, EMS showed up. They looked pretty stunned when I was able to give the handoff presentation to them. I told them what happened and his back-story. I wanted to make sure they would check his sugar and take extra precautions.

They got him on the stretcher, and he eventually made it to the hospital where he had surgery. They had to have a vascular surgeon work on him. I called later, and they told me, “Yeah, he’s alive.” But that’s about the extent of the update I got.

After the ambulance left, it was kind of chaos. All the neighbors poured out of their houses. People were panicked, talking and getting excited about it. I didn’t know, but everyone else had actually been home the whole time. They didn’t come out until then.

I went back inside and tried to get ready for work. I wasn’t planning on talking to the media, but my next door neighbor just walked the news camera crew over to my house and knocked on my door. I wasn’t exactly dressed to be on TV, but they talked to me on camera, and it was on the news later that night.

I went to work and didn’t say anything about it. To be honest, I was trying to avoid telling anyone. Our team had a close-knit bond, and we would often tease each other when we received any type of recognition.

Naturally one of my attendings saw it on the local news and told everybody. So, I got a lot of happy harassment for quite some time. Someone baked me a cake that said, “Hero of Fairmount” (the Philly neighborhood in which I live). Someone else printed out a photo of me that said, “Stop the Bleed Hero of Fairmount,” and put it on every single computer screen.

The man came to see me about 2 weeks later (a neighbor told him where I lived). The man was very tearful and gave me a big hug. We just embraced for a while, and he said how thankful he was. He brought me a bottle of wine, which I thought was really nice.

He told me what happened to him: There was a lot of construction on our street and he was the contractor overseeing a couple of home remodels and demolitions. Sometimes he paid workers in cash and carried it with him. Somebody had tipped off somebody else that he was going to be there that day. The contractor walked into one of the houses and a guy in a ski mask waited there with a gun. The guy shot him and took the cash. The bullet went through his hand into his pelvis.

I had never had to deal with something that intense before outside of work. Most of it really comes down to the basics – the ABCs and bleeding control. You do whatever you can with what you have. In this case, it was just a dish towel, gloves, and my hands to put as much pressure as possible.

It really was strange that I happened to be looking out the window at that moment. I don’t know if it was just a coincidence. The man told me he believed God had put somebody there at the right place at the right time to save his life. I just felt very fortunate to have been able to help him. I never saw him again.

I think something like this gives you a little confidence that you can actually do something and make a meaningful impact anywhere when it’s needed. It lets you know that you’re capable of doing it. You always think about it, but you don’t know until it happens.

A version of this article first appeared on Medscape.com.

It was a quiet day. I got up around 3 o’clock in the afternoon for my shift at 6 p.m. I was shaking off the cobwebs and making coffee at our front window that overlooked Brown Street in North Philadelphia. I looked out the window and saw a man stumbling down the street, grabbing his abdomen and yelling for help. There was nobody else around so I went outside to see what was going on.

He was in his 50s or 60s, bleeding and obviously in distress. I had him sit down. Then I ran back inside and grabbed a dish towel and some exam gloves that I had in the house.

I ran back out and assessed him. A bullet had gone through one of his hands, but he had other wounds. I had to expose him, so I trauma stripped him on the sidewalk. I got his pants and his shirt off and saw a gunshot going through his lower pelvis. He was bleeding out from there.

I got the towel and started applying deep pressure down into the iliac vein in case they hit something, which I found out later, they had. I held it there. The man was just lying there begging not to die.

I’m someone who is very calm, maybe abnormally calm, as people tell me. I try to use that during my resuscitations and traumas. Just keeping everybody calm makes the situation easier. Afterwards, people asked me, “Weren’t you worried that you were going to get shot?” That does happen in North Philadelphia. But it didn’t even cross my mind.

I didn’t have to think at all about what I was doing. We saw so many gunshots, especially at Einstein Medical Center. We saw them daily. I’d sometimes get more than half a dozen gunshots in one shift.

So, I was holding pressure and some people started to come over. I got somebody to call 911 and asked the man about his medical history. I found out he had diabetes. Five or 10 minutes later, EMS showed up. They looked pretty stunned when I was able to give the handoff presentation to them. I told them what happened and his back-story. I wanted to make sure they would check his sugar and take extra precautions.

They got him on the stretcher, and he eventually made it to the hospital where he had surgery. They had to have a vascular surgeon work on him. I called later, and they told me, “Yeah, he’s alive.” But that’s about the extent of the update I got.

After the ambulance left, it was kind of chaos. All the neighbors poured out of their houses. People were panicked, talking and getting excited about it. I didn’t know, but everyone else had actually been home the whole time. They didn’t come out until then.

I went back inside and tried to get ready for work. I wasn’t planning on talking to the media, but my next door neighbor just walked the news camera crew over to my house and knocked on my door. I wasn’t exactly dressed to be on TV, but they talked to me on camera, and it was on the news later that night.

I went to work and didn’t say anything about it. To be honest, I was trying to avoid telling anyone. Our team had a close-knit bond, and we would often tease each other when we received any type of recognition.

Naturally one of my attendings saw it on the local news and told everybody. So, I got a lot of happy harassment for quite some time. Someone baked me a cake that said, “Hero of Fairmount” (the Philly neighborhood in which I live). Someone else printed out a photo of me that said, “Stop the Bleed Hero of Fairmount,” and put it on every single computer screen.

The man came to see me about 2 weeks later (a neighbor told him where I lived). The man was very tearful and gave me a big hug. We just embraced for a while, and he said how thankful he was. He brought me a bottle of wine, which I thought was really nice.

He told me what happened to him: There was a lot of construction on our street and he was the contractor overseeing a couple of home remodels and demolitions. Sometimes he paid workers in cash and carried it with him. Somebody had tipped off somebody else that he was going to be there that day. The contractor walked into one of the houses and a guy in a ski mask waited there with a gun. The guy shot him and took the cash. The bullet went through his hand into his pelvis.

I had never had to deal with something that intense before outside of work. Most of it really comes down to the basics – the ABCs and bleeding control. You do whatever you can with what you have. In this case, it was just a dish towel, gloves, and my hands to put as much pressure as possible.

It really was strange that I happened to be looking out the window at that moment. I don’t know if it was just a coincidence. The man told me he believed God had put somebody there at the right place at the right time to save his life. I just felt very fortunate to have been able to help him. I never saw him again.

I think something like this gives you a little confidence that you can actually do something and make a meaningful impact anywhere when it’s needed. It lets you know that you’re capable of doing it. You always think about it, but you don’t know until it happens.

A version of this article first appeared on Medscape.com.

It was a quiet day. I got up around 3 o’clock in the afternoon for my shift at 6 p.m. I was shaking off the cobwebs and making coffee at our front window that overlooked Brown Street in North Philadelphia. I looked out the window and saw a man stumbling down the street, grabbing his abdomen and yelling for help. There was nobody else around so I went outside to see what was going on.

He was in his 50s or 60s, bleeding and obviously in distress. I had him sit down. Then I ran back inside and grabbed a dish towel and some exam gloves that I had in the house.

I ran back out and assessed him. A bullet had gone through one of his hands, but he had other wounds. I had to expose him, so I trauma stripped him on the sidewalk. I got his pants and his shirt off and saw a gunshot going through his lower pelvis. He was bleeding out from there.

I got the towel and started applying deep pressure down into the iliac vein in case they hit something, which I found out later, they had. I held it there. The man was just lying there begging not to die.

I’m someone who is very calm, maybe abnormally calm, as people tell me. I try to use that during my resuscitations and traumas. Just keeping everybody calm makes the situation easier. Afterwards, people asked me, “Weren’t you worried that you were going to get shot?” That does happen in North Philadelphia. But it didn’t even cross my mind.

I didn’t have to think at all about what I was doing. We saw so many gunshots, especially at Einstein Medical Center. We saw them daily. I’d sometimes get more than half a dozen gunshots in one shift.

So, I was holding pressure and some people started to come over. I got somebody to call 911 and asked the man about his medical history. I found out he had diabetes. Five or 10 minutes later, EMS showed up. They looked pretty stunned when I was able to give the handoff presentation to them. I told them what happened and his back-story. I wanted to make sure they would check his sugar and take extra precautions.

They got him on the stretcher, and he eventually made it to the hospital where he had surgery. They had to have a vascular surgeon work on him. I called later, and they told me, “Yeah, he’s alive.” But that’s about the extent of the update I got.

After the ambulance left, it was kind of chaos. All the neighbors poured out of their houses. People were panicked, talking and getting excited about it. I didn’t know, but everyone else had actually been home the whole time. They didn’t come out until then.

I went back inside and tried to get ready for work. I wasn’t planning on talking to the media, but my next door neighbor just walked the news camera crew over to my house and knocked on my door. I wasn’t exactly dressed to be on TV, but they talked to me on camera, and it was on the news later that night.

I went to work and didn’t say anything about it. To be honest, I was trying to avoid telling anyone. Our team had a close-knit bond, and we would often tease each other when we received any type of recognition.

Naturally one of my attendings saw it on the local news and told everybody. So, I got a lot of happy harassment for quite some time. Someone baked me a cake that said, “Hero of Fairmount” (the Philly neighborhood in which I live). Someone else printed out a photo of me that said, “Stop the Bleed Hero of Fairmount,” and put it on every single computer screen.

The man came to see me about 2 weeks later (a neighbor told him where I lived). The man was very tearful and gave me a big hug. We just embraced for a while, and he said how thankful he was. He brought me a bottle of wine, which I thought was really nice.

He told me what happened to him: There was a lot of construction on our street and he was the contractor overseeing a couple of home remodels and demolitions. Sometimes he paid workers in cash and carried it with him. Somebody had tipped off somebody else that he was going to be there that day. The contractor walked into one of the houses and a guy in a ski mask waited there with a gun. The guy shot him and took the cash. The bullet went through his hand into his pelvis.

I had never had to deal with something that intense before outside of work. Most of it really comes down to the basics – the ABCs and bleeding control. You do whatever you can with what you have. In this case, it was just a dish towel, gloves, and my hands to put as much pressure as possible.

It really was strange that I happened to be looking out the window at that moment. I don’t know if it was just a coincidence. The man told me he believed God had put somebody there at the right place at the right time to save his life. I just felt very fortunate to have been able to help him. I never saw him again.

I think something like this gives you a little confidence that you can actually do something and make a meaningful impact anywhere when it’s needed. It lets you know that you’re capable of doing it. You always think about it, but you don’t know until it happens.

A version of this article first appeared on Medscape.com.

The past few years have seen major transformations in the way health care websites operate and interact with patients. To stay competitive, it is important to ensure that your website is adapting to this changing environment, and that it continues adapting as future changes further impact its performance and ranking.

In mid-2018, a major Google algorithm change, known to the IT community as the “Medic Update,” significantly changed search criteria for most health and wellness websites. Another big update went live in late 2021. Websites that have not evolved with these changes have dropped in search rankings and provide a poorer user experience all around.

Many potential patients are searching for your services online, so your website cannot be an afterthought. Not only does it need to be designed with your target audience in mind, but it is also important to consider the metrics Google and other search engines now use when assessing the quality of your website so that patients will find it in the first place.

Here are some features that you (or your website company) need to prioritize to keep your site current and atop search results in 2023 and beyond.

Begin with an understandable URL. Search engines use URLs to determine how well your site, or a portion of it, matches search criteria. URLs also need to make sense to searchers, especially when they link specific areas of expertise (more on that in a minute). For example, a URL like “jonesdermatology.com/?p=89021” is meaningless to anyone except programmers; but “jonesdermatology.com/psoriasistreatments” obviously leads to a page about psoriasis treatments. Search engines look for not only the most relevant, but also the most helpful and user-friendly answers to a user’s query.

Incidentally, if the URL for your site is not your own name, you should register your name as a separate domain name – even if you never use it – to be sure that a trickster or troll, or someone with the same name but a bad reputation, doesn’t get it.

Continue with a good meta description. That’s the grayish text that follows the title and URL in search results. Searchers will read it to confirm that your site is what they seek, so make sure it describes exactly what you do, including any areas of special expertise.

Make your practice approachable with photos. New patients are more comfortable when they know what you look like, so real photos of you and your staff are always more effective than stock photos of models. Photos or a video tour of your office will reassure prospective patients that they will be visiting a clean, modern, professional facility.

Describe your principal services in detail. You never know which specific service a prospective patient is searching for, so describe everything you offer. Don’t try to summarize everything on a single page; relevance is determined by how deeply a topic is covered, so each principal service should have a detailed description on its own page. Not only will your skills become more visible to search engines, but you can also use the space to enumerate your qualifications and expertise in each area. Whenever possible, write your descriptions in question-and-answer form. Searchers tend to ask questions (“what is the best ... ?”), particularly in voice searches. Search engines increasingly value sites that ask and answer common questions.

Make your site interactive. “Interactivity” is a major buzzword in modern search engine parlance. Once searchers make an appointment, they stop searching. If they have to wait until the next day to call your office, they may keep looking – and might find a competitor with online scheduling. HIPAA-compliant chatbots, secure messaging, and online patient portals to access medical records, lab results, and other important information will also set your site apart.

Testimonials are essential. Amazon.com taught us that candid reviews from customers go a long way toward building the trust necessary to buy products and services, and nowhere is that truer than for medical services. According to one study, when it comes to finding a doctor, 88% of people trust online reviews as much as a personal recommendation. Loyal patients will be happy to write you glowing reviews; feature them prominently.

How does your site look on small screens? More than half of all searches are now made on smartphones, so the more mobile-friendly your site is, the higher it will be ranked. Prospective patients who are forced to scroll forever, or zoom in to tap a link, are likely to become frustrated and move on. Mobile searchers prefer sites that provide the best experience for the least amount of effort, and rankings tend to reflect that preference. You can test how easily a visitor can use your website on a mobile device with Google’s free Mobile-Friendly Test..

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

The past few years have seen major transformations in the way health care websites operate and interact with patients. To stay competitive, it is important to ensure that your website is adapting to this changing environment, and that it continues adapting as future changes further impact its performance and ranking.

In mid-2018, a major Google algorithm change, known to the IT community as the “Medic Update,” significantly changed search criteria for most health and wellness websites. Another big update went live in late 2021. Websites that have not evolved with these changes have dropped in search rankings and provide a poorer user experience all around.

Many potential patients are searching for your services online, so your website cannot be an afterthought. Not only does it need to be designed with your target audience in mind, but it is also important to consider the metrics Google and other search engines now use when assessing the quality of your website so that patients will find it in the first place.

Here are some features that you (or your website company) need to prioritize to keep your site current and atop search results in 2023 and beyond.

Begin with an understandable URL. Search engines use URLs to determine how well your site, or a portion of it, matches search criteria. URLs also need to make sense to searchers, especially when they link specific areas of expertise (more on that in a minute). For example, a URL like “jonesdermatology.com/?p=89021” is meaningless to anyone except programmers; but “jonesdermatology.com/psoriasistreatments” obviously leads to a page about psoriasis treatments. Search engines look for not only the most relevant, but also the most helpful and user-friendly answers to a user’s query.

Incidentally, if the URL for your site is not your own name, you should register your name as a separate domain name – even if you never use it – to be sure that a trickster or troll, or someone with the same name but a bad reputation, doesn’t get it.

Continue with a good meta description. That’s the grayish text that follows the title and URL in search results. Searchers will read it to confirm that your site is what they seek, so make sure it describes exactly what you do, including any areas of special expertise.

Make your practice approachable with photos. New patients are more comfortable when they know what you look like, so real photos of you and your staff are always more effective than stock photos of models. Photos or a video tour of your office will reassure prospective patients that they will be visiting a clean, modern, professional facility.

Describe your principal services in detail. You never know which specific service a prospective patient is searching for, so describe everything you offer. Don’t try to summarize everything on a single page; relevance is determined by how deeply a topic is covered, so each principal service should have a detailed description on its own page. Not only will your skills become more visible to search engines, but you can also use the space to enumerate your qualifications and expertise in each area. Whenever possible, write your descriptions in question-and-answer form. Searchers tend to ask questions (“what is the best ... ?”), particularly in voice searches. Search engines increasingly value sites that ask and answer common questions.

Make your site interactive. “Interactivity” is a major buzzword in modern search engine parlance. Once searchers make an appointment, they stop searching. If they have to wait until the next day to call your office, they may keep looking – and might find a competitor with online scheduling. HIPAA-compliant chatbots, secure messaging, and online patient portals to access medical records, lab results, and other important information will also set your site apart.

Testimonials are essential. Amazon.com taught us that candid reviews from customers go a long way toward building the trust necessary to buy products and services, and nowhere is that truer than for medical services. According to one study, when it comes to finding a doctor, 88% of people trust online reviews as much as a personal recommendation. Loyal patients will be happy to write you glowing reviews; feature them prominently.

How does your site look on small screens? More than half of all searches are now made on smartphones, so the more mobile-friendly your site is, the higher it will be ranked. Prospective patients who are forced to scroll forever, or zoom in to tap a link, are likely to become frustrated and move on. Mobile searchers prefer sites that provide the best experience for the least amount of effort, and rankings tend to reflect that preference. You can test how easily a visitor can use your website on a mobile device with Google’s free Mobile-Friendly Test..

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

The past few years have seen major transformations in the way health care websites operate and interact with patients. To stay competitive, it is important to ensure that your website is adapting to this changing environment, and that it continues adapting as future changes further impact its performance and ranking.

In mid-2018, a major Google algorithm change, known to the IT community as the “Medic Update,” significantly changed search criteria for most health and wellness websites. Another big update went live in late 2021. Websites that have not evolved with these changes have dropped in search rankings and provide a poorer user experience all around.

Many potential patients are searching for your services online, so your website cannot be an afterthought. Not only does it need to be designed with your target audience in mind, but it is also important to consider the metrics Google and other search engines now use when assessing the quality of your website so that patients will find it in the first place.

Here are some features that you (or your website company) need to prioritize to keep your site current and atop search results in 2023 and beyond.

Begin with an understandable URL. Search engines use URLs to determine how well your site, or a portion of it, matches search criteria. URLs also need to make sense to searchers, especially when they link specific areas of expertise (more on that in a minute). For example, a URL like “jonesdermatology.com/?p=89021” is meaningless to anyone except programmers; but “jonesdermatology.com/psoriasistreatments” obviously leads to a page about psoriasis treatments. Search engines look for not only the most relevant, but also the most helpful and user-friendly answers to a user’s query.

Incidentally, if the URL for your site is not your own name, you should register your name as a separate domain name – even if you never use it – to be sure that a trickster or troll, or someone with the same name but a bad reputation, doesn’t get it.

Continue with a good meta description. That’s the grayish text that follows the title and URL in search results. Searchers will read it to confirm that your site is what they seek, so make sure it describes exactly what you do, including any areas of special expertise.

Make your practice approachable with photos. New patients are more comfortable when they know what you look like, so real photos of you and your staff are always more effective than stock photos of models. Photos or a video tour of your office will reassure prospective patients that they will be visiting a clean, modern, professional facility.

Describe your principal services in detail. You never know which specific service a prospective patient is searching for, so describe everything you offer. Don’t try to summarize everything on a single page; relevance is determined by how deeply a topic is covered, so each principal service should have a detailed description on its own page. Not only will your skills become more visible to search engines, but you can also use the space to enumerate your qualifications and expertise in each area. Whenever possible, write your descriptions in question-and-answer form. Searchers tend to ask questions (“what is the best ... ?”), particularly in voice searches. Search engines increasingly value sites that ask and answer common questions.

Make your site interactive. “Interactivity” is a major buzzword in modern search engine parlance. Once searchers make an appointment, they stop searching. If they have to wait until the next day to call your office, they may keep looking – and might find a competitor with online scheduling. HIPAA-compliant chatbots, secure messaging, and online patient portals to access medical records, lab results, and other important information will also set your site apart.

Testimonials are essential. Amazon.com taught us that candid reviews from customers go a long way toward building the trust necessary to buy products and services, and nowhere is that truer than for medical services. According to one study, when it comes to finding a doctor, 88% of people trust online reviews as much as a personal recommendation. Loyal patients will be happy to write you glowing reviews; feature them prominently.

How does your site look on small screens? More than half of all searches are now made on smartphones, so the more mobile-friendly your site is, the higher it will be ranked. Prospective patients who are forced to scroll forever, or zoom in to tap a link, are likely to become frustrated and move on. Mobile searchers prefer sites that provide the best experience for the least amount of effort, and rankings tend to reflect that preference. You can test how easily a visitor can use your website on a mobile device with Google’s free Mobile-Friendly Test..

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

There’s been some recent news about medical schools gradually dropping the long-established practice of legacy admissions. This is where people related to successful alumni and/or big donors can get preferential admission, possibly over more qualified people.

All of us likely experienced this from one side or another, though realistically I haven’t thought about it years. My kids went to the same state school I did, but I’m pretty sure I had nothing to do with their being accepted. I never gave the school a single donation, nor did I call anyone there to try and get them in. Not that anyone would have known who I was if I’d tried. I’m just another one of many who went there, preserved only in some filing cabinet of transcripts somewhere.

I’m all for the legacy system ending, though, for one simple reason: It’s not fair.

If someone is qualified, great. They should be admitted on their own merits. But if they’re not, they shouldn’t get into medical school just because one (or both) of their parents went there, or is a VIP, or paid for a new library wing.

The reason I’m writing this is because the recent reporting did bring back a memory.

A long time ago, when I was in college, I hung out with other premed students. We knew we were all competing with each other for the same spots at the state medical school, but also knew that we wouldn’t all get in there. That didn’t make us enemies, it was just the truth. It’s that point in life where ANY medical school admission is all you want.

Pete (not his real name) was a nice guy, but his grades weren’t the best. His MCAT scores lagged behind the rest of us in the clique, and ... he didn’t care.

Pete’s dad had graduated from the state medical school, and was still on staff there. He was now on the teaching staff ... and on the school’s admissions board. To Pete, tests and grades didn’t matter. His admission was assured.

So it was no surprise when he got in ahead of the rest of us with better qualifications. Most of us, including me, did get in somewhere, so we were still happy. We just had to move farther and pay more, but that’s life.

I really didn’t think much about Pete again after that. I was now in medical school, I had a whole new social group, and more importantly I didn’t really have time to think of much beyond when the next exam was.

Then I moved home, and started residency. During my PGY-2 year we had a changing group of medical students assigned to my wards rotation.

And, as you probably guessed, one of them was Pete.

Pete was in his last year of medical school. But we’d both started in the same year, and now I was 2 years ahead of him. I didn’t ask him what happened, but another medical student told me he wasn’t known to be the best student, but the university refused to drop him, and just kept setting him back a class here, a year there.

Maybe they’d have done the same for anyone, but I doubt it.

I never saw Pete again after that. When I looked him up online tonight he’s not listed as being a doctor, and isn’t even in medicine. Granted, a lot of doctors have left medicine, and maybe he did too.

But the more likely reason is that Pete never should have been there in the first place. He got in as a legacy, taking a medical school slot from someone who may have been more capable and driven.

And that just doesn’t seem right to me. It didn’t then and it doesn’t now.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

There’s been some recent news about medical schools gradually dropping the long-established practice of legacy admissions. This is where people related to successful alumni and/or big donors can get preferential admission, possibly over more qualified people.

All of us likely experienced this from one side or another, though realistically I haven’t thought about it years. My kids went to the same state school I did, but I’m pretty sure I had nothing to do with their being accepted. I never gave the school a single donation, nor did I call anyone there to try and get them in. Not that anyone would have known who I was if I’d tried. I’m just another one of many who went there, preserved only in some filing cabinet of transcripts somewhere.

I’m all for the legacy system ending, though, for one simple reason: It’s not fair.

If someone is qualified, great. They should be admitted on their own merits. But if they’re not, they shouldn’t get into medical school just because one (or both) of their parents went there, or is a VIP, or paid for a new library wing.

The reason I’m writing this is because the recent reporting did bring back a memory.

A long time ago, when I was in college, I hung out with other premed students. We knew we were all competing with each other for the same spots at the state medical school, but also knew that we wouldn’t all get in there. That didn’t make us enemies, it was just the truth. It’s that point in life where ANY medical school admission is all you want.

Pete (not his real name) was a nice guy, but his grades weren’t the best. His MCAT scores lagged behind the rest of us in the clique, and ... he didn’t care.

Pete’s dad had graduated from the state medical school, and was still on staff there. He was now on the teaching staff ... and on the school’s admissions board. To Pete, tests and grades didn’t matter. His admission was assured.

So it was no surprise when he got in ahead of the rest of us with better qualifications. Most of us, including me, did get in somewhere, so we were still happy. We just had to move farther and pay more, but that’s life.

I really didn’t think much about Pete again after that. I was now in medical school, I had a whole new social group, and more importantly I didn’t really have time to think of much beyond when the next exam was.

Then I moved home, and started residency. During my PGY-2 year we had a changing group of medical students assigned to my wards rotation.

And, as you probably guessed, one of them was Pete.

Pete was in his last year of medical school. But we’d both started in the same year, and now I was 2 years ahead of him. I didn’t ask him what happened, but another medical student told me he wasn’t known to be the best student, but the university refused to drop him, and just kept setting him back a class here, a year there.

Maybe they’d have done the same for anyone, but I doubt it.

I never saw Pete again after that. When I looked him up online tonight he’s not listed as being a doctor, and isn’t even in medicine. Granted, a lot of doctors have left medicine, and maybe he did too.

But the more likely reason is that Pete never should have been there in the first place. He got in as a legacy, taking a medical school slot from someone who may have been more capable and driven.

And that just doesn’t seem right to me. It didn’t then and it doesn’t now.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

There’s been some recent news about medical schools gradually dropping the long-established practice of legacy admissions. This is where people related to successful alumni and/or big donors can get preferential admission, possibly over more qualified people.

All of us likely experienced this from one side or another, though realistically I haven’t thought about it years. My kids went to the same state school I did, but I’m pretty sure I had nothing to do with their being accepted. I never gave the school a single donation, nor did I call anyone there to try and get them in. Not that anyone would have known who I was if I’d tried. I’m just another one of many who went there, preserved only in some filing cabinet of transcripts somewhere.

I’m all for the legacy system ending, though, for one simple reason: It’s not fair.

If someone is qualified, great. They should be admitted on their own merits. But if they’re not, they shouldn’t get into medical school just because one (or both) of their parents went there, or is a VIP, or paid for a new library wing.

The reason I’m writing this is because the recent reporting did bring back a memory.

A long time ago, when I was in college, I hung out with other premed students. We knew we were all competing with each other for the same spots at the state medical school, but also knew that we wouldn’t all get in there. That didn’t make us enemies, it was just the truth. It’s that point in life where ANY medical school admission is all you want.

Pete (not his real name) was a nice guy, but his grades weren’t the best. His MCAT scores lagged behind the rest of us in the clique, and ... he didn’t care.

Pete’s dad had graduated from the state medical school, and was still on staff there. He was now on the teaching staff ... and on the school’s admissions board. To Pete, tests and grades didn’t matter. His admission was assured.

So it was no surprise when he got in ahead of the rest of us with better qualifications. Most of us, including me, did get in somewhere, so we were still happy. We just had to move farther and pay more, but that’s life.

I really didn’t think much about Pete again after that. I was now in medical school, I had a whole new social group, and more importantly I didn’t really have time to think of much beyond when the next exam was.

Then I moved home, and started residency. During my PGY-2 year we had a changing group of medical students assigned to my wards rotation.

And, as you probably guessed, one of them was Pete.

Pete was in his last year of medical school. But we’d both started in the same year, and now I was 2 years ahead of him. I didn’t ask him what happened, but another medical student told me he wasn’t known to be the best student, but the university refused to drop him, and just kept setting him back a class here, a year there.

Maybe they’d have done the same for anyone, but I doubt it.

I never saw Pete again after that. When I looked him up online tonight he’s not listed as being a doctor, and isn’t even in medicine. Granted, a lot of doctors have left medicine, and maybe he did too.

But the more likely reason is that Pete never should have been there in the first place. He got in as a legacy, taking a medical school slot from someone who may have been more capable and driven.

And that just doesn’t seem right to me. It didn’t then and it doesn’t now.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

In this patient, bacterial and viral cultures were taken and varicella zoster virus (VZV) was isolated. Additionally, Orthopox DNA by PCR and Monkeypox (mpox) virus DNA by PCR were detected. Herpes simplex virus and bacterial viral cultures were negative. Valacyclovir was started at the time of presentation and the patient’s lesions resolved without sequelae.

Mpox is a zoonotic double-stranded DNA virus that is part of the Orthopoxvirus family, including the West African and Central African variants. This disease presents similarly to smallpox, so most mpox research was conducted around the time smallpox was eradicated. It was not until 1970, when the disease was isolated from a patient with suspected smallpox in the Democratic Republic of the Congo (DRC), that human mpox was considered a distinct disease. An epidemic outbreak in the United States occurred in 2003 related to infected prairie dogs, and travel-related outbreaks have been more recently reported up until May 2022, in which mpox was reported in nonendemic areas including North America, Europe, and Australia. Most cases in this outbreak occurred in men who have sex with men (MSM), but this is not always the case, and mpox is not necessarily considered a sexually transmitted infection. Mpox presents similarly to smallpox and VZV, so using laboratory tests is important in diagnosing and tracking this disease.

Although it is not easily transmitted, the disease can spread through bodily secretions both directly and indirectly. Mpox typically begins with a prodrome that includes fever, headache, myalgia, and fatigue. This is followed by lymphadenopathy that precedes and coincides with rash development. The lymph nodes are firm, tender, may be painful, and are a defining factor in presentation that differs from smallpox and varicella. The rash typically starts on the face, then presents on the body in a centrifugal distribution. However, cases related to sexual transmission present with anogenital lesions. The lesions are characterized by a progression from maculopapular to vesiculopustular, and can vary widely in quantity.

Notably, individuals are contagious from the onset of the prodrome until the lesions have scabbed over and fallen off. The eruptive nature of the later lesions poses a threat of secondary infection, and is often accompanied by a second febrile period that signifies deterioration of the patient’s condition. Other signs of secondary infection are variable and include pulmonary symptoms, vomiting, diarrhea, ocular infections, and in rare cases, encephalitis. These sequelae are more common in unvaccinated and immunocompromised individuals. Long-term complications of mpox include pitted scarring from cutaneous lesions with children being more susceptible to severe disease. The mortality rate for the disease is very low. (As of May 10, 2023, there have been 30,395 mpox cases reported in the United States, and 42 deaths, according to the Centers for Disease Control and Prevention.)

There are a variety of diagnostic tests that can aid in mpox identification, but they are most strongly supported when combined with clinical and epidemiological data. The best, least invasive method includes collection of lesion exudate or crust on a swab, and viral DNA is best preserved by keeping the specimen in a cool, dry, and dark environment. PCR is considered the standard, and electron microscopy and immunohistochemistry are valid tests, but all modalities require sophisticated technicians with the proper laboratory equipment. This is limiting because many cases present in underserved areas that lack the facilities for proper, real-time analysis. Antigen and antibody-based tests can be used, but cross-reactivity of other orthopoxviridae limits confirmation of mpox infection. Vaccination status, history and location must be considered.

Vaccination is the chief form of prevention for mpox, although it is not considered entirely protective. Smallpox vaccination provides protection, but widespread administration of the vaccine is no longer practiced, and an estimated 70% of the global population is no longer vaccinated. Vaccination is recommended for anyone at risk of exposure, but as this is a live, attenuated vaccine, the immune status of the patient is important to keep in mind. Tecovirimat and other antiviral medications including cidofovir and brincidofovir may be considered in severe cases.

This case is unique as our patient, who had no known risk factors for mpox, presented with mpox and VZV, simultaneously. Although clinical presentation and epidemiological patterns between these diseases differ, there have been a limited number of cases of coinfection reported in the literature, mainly in the DRC where mpox is endemic. Diagnosis must be made by separate laboratory tests and there are differences in presentation between independent and coinfection for these viruses. Notably, patients with mpox/VZV coinfection may be less likely to present with lesions on the face, thorax, arms, palms, and soles than those with only mpox but experience a higher lesion burden than those afflicted by only VZV. Coinfection may be related to reactivation of dormant VZV, or increased susceptibility to secondary infection when infected with one virus.

This case and photo were submitted by Lucas Shapiro, BS, of the Dr. Kiran C. Patel College of Osteopathic Medicine at Nova Southeastern University, Fort Lauderdale, Fla., and Donna Bilu Martin, MD.

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

References

1. Macneil A et al. Clin Infect Dis. 2009 Jan 1;48(1):e6-8.

2. Di Gennaro F et al. Microorganisms. 2022 Aug 12;10(8):1633.

3. Hughes CM et al. Am J Trop Med Hyg. 2020 Dec 7;104(2):604-11.

In this patient, bacterial and viral cultures were taken and varicella zoster virus (VZV) was isolated. Additionally, Orthopox DNA by PCR and Monkeypox (mpox) virus DNA by PCR were detected. Herpes simplex virus and bacterial viral cultures were negative. Valacyclovir was started at the time of presentation and the patient’s lesions resolved without sequelae.

Mpox is a zoonotic double-stranded DNA virus that is part of the Orthopoxvirus family, including the West African and Central African variants. This disease presents similarly to smallpox, so most mpox research was conducted around the time smallpox was eradicated. It was not until 1970, when the disease was isolated from a patient with suspected smallpox in the Democratic Republic of the Congo (DRC), that human mpox was considered a distinct disease. An epidemic outbreak in the United States occurred in 2003 related to infected prairie dogs, and travel-related outbreaks have been more recently reported up until May 2022, in which mpox was reported in nonendemic areas including North America, Europe, and Australia. Most cases in this outbreak occurred in men who have sex with men (MSM), but this is not always the case, and mpox is not necessarily considered a sexually transmitted infection. Mpox presents similarly to smallpox and VZV, so using laboratory tests is important in diagnosing and tracking this disease.

Although it is not easily transmitted, the disease can spread through bodily secretions both directly and indirectly. Mpox typically begins with a prodrome that includes fever, headache, myalgia, and fatigue. This is followed by lymphadenopathy that precedes and coincides with rash development. The lymph nodes are firm, tender, may be painful, and are a defining factor in presentation that differs from smallpox and varicella. The rash typically starts on the face, then presents on the body in a centrifugal distribution. However, cases related to sexual transmission present with anogenital lesions. The lesions are characterized by a progression from maculopapular to vesiculopustular, and can vary widely in quantity.

Notably, individuals are contagious from the onset of the prodrome until the lesions have scabbed over and fallen off. The eruptive nature of the later lesions poses a threat of secondary infection, and is often accompanied by a second febrile period that signifies deterioration of the patient’s condition. Other signs of secondary infection are variable and include pulmonary symptoms, vomiting, diarrhea, ocular infections, and in rare cases, encephalitis. These sequelae are more common in unvaccinated and immunocompromised individuals. Long-term complications of mpox include pitted scarring from cutaneous lesions with children being more susceptible to severe disease. The mortality rate for the disease is very low. (As of May 10, 2023, there have been 30,395 mpox cases reported in the United States, and 42 deaths, according to the Centers for Disease Control and Prevention.)

There are a variety of diagnostic tests that can aid in mpox identification, but they are most strongly supported when combined with clinical and epidemiological data. The best, least invasive method includes collection of lesion exudate or crust on a swab, and viral DNA is best preserved by keeping the specimen in a cool, dry, and dark environment. PCR is considered the standard, and electron microscopy and immunohistochemistry are valid tests, but all modalities require sophisticated technicians with the proper laboratory equipment. This is limiting because many cases present in underserved areas that lack the facilities for proper, real-time analysis. Antigen and antibody-based tests can be used, but cross-reactivity of other orthopoxviridae limits confirmation of mpox infection. Vaccination status, history and location must be considered.

Vaccination is the chief form of prevention for mpox, although it is not considered entirely protective. Smallpox vaccination provides protection, but widespread administration of the vaccine is no longer practiced, and an estimated 70% of the global population is no longer vaccinated. Vaccination is recommended for anyone at risk of exposure, but as this is a live, attenuated vaccine, the immune status of the patient is important to keep in mind. Tecovirimat and other antiviral medications including cidofovir and brincidofovir may be considered in severe cases.

This case is unique as our patient, who had no known risk factors for mpox, presented with mpox and VZV, simultaneously. Although clinical presentation and epidemiological patterns between these diseases differ, there have been a limited number of cases of coinfection reported in the literature, mainly in the DRC where mpox is endemic. Diagnosis must be made by separate laboratory tests and there are differences in presentation between independent and coinfection for these viruses. Notably, patients with mpox/VZV coinfection may be less likely to present with lesions on the face, thorax, arms, palms, and soles than those with only mpox but experience a higher lesion burden than those afflicted by only VZV. Coinfection may be related to reactivation of dormant VZV, or increased susceptibility to secondary infection when infected with one virus.

This case and photo were submitted by Lucas Shapiro, BS, of the Dr. Kiran C. Patel College of Osteopathic Medicine at Nova Southeastern University, Fort Lauderdale, Fla., and Donna Bilu Martin, MD.

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

References

1. Macneil A et al. Clin Infect Dis. 2009 Jan 1;48(1):e6-8.

2. Di Gennaro F et al. Microorganisms. 2022 Aug 12;10(8):1633.

3. Hughes CM et al. Am J Trop Med Hyg. 2020 Dec 7;104(2):604-11.

In this patient, bacterial and viral cultures were taken and varicella zoster virus (VZV) was isolated. Additionally, Orthopox DNA by PCR and Monkeypox (mpox) virus DNA by PCR were detected. Herpes simplex virus and bacterial viral cultures were negative. Valacyclovir was started at the time of presentation and the patient’s lesions resolved without sequelae.

Mpox is a zoonotic double-stranded DNA virus that is part of the Orthopoxvirus family, including the West African and Central African variants. This disease presents similarly to smallpox, so most mpox research was conducted around the time smallpox was eradicated. It was not until 1970, when the disease was isolated from a patient with suspected smallpox in the Democratic Republic of the Congo (DRC), that human mpox was considered a distinct disease. An epidemic outbreak in the United States occurred in 2003 related to infected prairie dogs, and travel-related outbreaks have been more recently reported up until May 2022, in which mpox was reported in nonendemic areas including North America, Europe, and Australia. Most cases in this outbreak occurred in men who have sex with men (MSM), but this is not always the case, and mpox is not necessarily considered a sexually transmitted infection. Mpox presents similarly to smallpox and VZV, so using laboratory tests is important in diagnosing and tracking this disease.

Although it is not easily transmitted, the disease can spread through bodily secretions both directly and indirectly. Mpox typically begins with a prodrome that includes fever, headache, myalgia, and fatigue. This is followed by lymphadenopathy that precedes and coincides with rash development. The lymph nodes are firm, tender, may be painful, and are a defining factor in presentation that differs from smallpox and varicella. The rash typically starts on the face, then presents on the body in a centrifugal distribution. However, cases related to sexual transmission present with anogenital lesions. The lesions are characterized by a progression from maculopapular to vesiculopustular, and can vary widely in quantity.

Notably, individuals are contagious from the onset of the prodrome until the lesions have scabbed over and fallen off. The eruptive nature of the later lesions poses a threat of secondary infection, and is often accompanied by a second febrile period that signifies deterioration of the patient’s condition. Other signs of secondary infection are variable and include pulmonary symptoms, vomiting, diarrhea, ocular infections, and in rare cases, encephalitis. These sequelae are more common in unvaccinated and immunocompromised individuals. Long-term complications of mpox include pitted scarring from cutaneous lesions with children being more susceptible to severe disease. The mortality rate for the disease is very low. (As of May 10, 2023, there have been 30,395 mpox cases reported in the United States, and 42 deaths, according to the Centers for Disease Control and Prevention.)

There are a variety of diagnostic tests that can aid in mpox identification, but they are most strongly supported when combined with clinical and epidemiological data. The best, least invasive method includes collection of lesion exudate or crust on a swab, and viral DNA is best preserved by keeping the specimen in a cool, dry, and dark environment. PCR is considered the standard, and electron microscopy and immunohistochemistry are valid tests, but all modalities require sophisticated technicians with the proper laboratory equipment. This is limiting because many cases present in underserved areas that lack the facilities for proper, real-time analysis. Antigen and antibody-based tests can be used, but cross-reactivity of other orthopoxviridae limits confirmation of mpox infection. Vaccination status, history and location must be considered.

Vaccination is the chief form of prevention for mpox, although it is not considered entirely protective. Smallpox vaccination provides protection, but widespread administration of the vaccine is no longer practiced, and an estimated 70% of the global population is no longer vaccinated. Vaccination is recommended for anyone at risk of exposure, but as this is a live, attenuated vaccine, the immune status of the patient is important to keep in mind. Tecovirimat and other antiviral medications including cidofovir and brincidofovir may be considered in severe cases.

This case is unique as our patient, who had no known risk factors for mpox, presented with mpox and VZV, simultaneously. Although clinical presentation and epidemiological patterns between these diseases differ, there have been a limited number of cases of coinfection reported in the literature, mainly in the DRC where mpox is endemic. Diagnosis must be made by separate laboratory tests and there are differences in presentation between independent and coinfection for these viruses. Notably, patients with mpox/VZV coinfection may be less likely to present with lesions on the face, thorax, arms, palms, and soles than those with only mpox but experience a higher lesion burden than those afflicted by only VZV. Coinfection may be related to reactivation of dormant VZV, or increased susceptibility to secondary infection when infected with one virus.

This case and photo were submitted by Lucas Shapiro, BS, of the Dr. Kiran C. Patel College of Osteopathic Medicine at Nova Southeastern University, Fort Lauderdale, Fla., and Donna Bilu Martin, MD.

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

References

1. Macneil A et al. Clin Infect Dis. 2009 Jan 1;48(1):e6-8.

2. Di Gennaro F et al. Microorganisms. 2022 Aug 12;10(8):1633.

3. Hughes CM et al. Am J Trop Med Hyg. 2020 Dec 7;104(2):604-11.

The media is filled with stories about the opioid crisis. We have all heard the horror stories of addiction and overdose, as well as “pill mill” doctors. In fact, more than 932,000 people have died of drug overdose since 1999 and, in recent years, approximately 75% of drug overdoses involved opioids.

Yet, they still have their place in the treatment of pain. It has been estimated that approximately 37% of all opioid prescriptions are written by primary care doctors, so it is essential that we doctors know appropriate prescribing guidelines.

The CDC updated the 2016 guidelines for prescribing opioids for pain in 2022. They cover when to initiate prescribing of opioids, selecting appropriate opioids and doses, and deciding the duration of therapy. The guidelines do a great job providing evidence-based recommendations while at the same time keeping the problems with opioids in the picture.

For primary care doctors, pain is one of the most common complaints we see – from broken bones to low back pain to cancer pain. It is important to note that the current guidelines exclude pain from sickle cell disease, cancer-related pain, palliative care, and end-of-life care. The guidelines apply to acute, subacute, and chronic pain. Pain is a complex symptom and often needs a multipronged approach. We make a mistake if we just prescribe a pain medication without understanding the root cause of the pain.

The guidelines suggest starting with nonopioid medications and incorporating nonmedicinal modes of treatments, such as physical therapy, as well. Opioids should be started at the lowest dose and for the shortest duration. Immediate-release medications are preferred over long-acting or extended-release ones. The patient should always be informed of the risks and benefits.

While the guidelines do a great job recommending how to prescribe opioids, they do not go into any depth discussing other treatment options. Perhaps knowledge of other treatment modalities would help primary care physicians avoid opioid prescribing. When treating our patients, it is important to educate them on how to manage their own symptoms.

The guidelines also advise tapering patients who may have been on high-dose opioids for long periods of time. Doctors know this is a very difficult task. However, resources to help with this are often lacking. For example, rehab may not be covered under a patient’s insurance, or it may be cheaper to take an opioid than to go to physical therapy. Although the recommendation is to taper, community assets may not support this. Guidelines are one thing, but the rest of the health care system needs to catch up to them and make them practical.

Primary care doctors often utilize our physical medicine, rehabilitation, and pain management specialists to assist in managing our patients’ pain. Here too, access to this resource is often difficult to come by. Depending on a patient’s insurance, it can take months to get an appointment.

In general, the current guidelines offer 12 key recommendations when prescribing opioids. They are a great reference; however, we need more real-life tools. For many of us in primary care, these guidelines support what we’ve been doing all along.

Primary care doctors will surely play a huge role in addressing the opioid crisis. We can prescribe opioids appropriately, but it doesn’t erase the problems of those patients who were overprescribed in the past. Many still seek out these medications whether for monetary reasons or just for the high. It is often easy to blame the patient but the one in control is the one with the prescription pad. Yet, it is important to remember that many of these patients are in real pain and need help.

Often, it is simpler to just prescribe a pain medication than it is to explain why one is not appropriate. As primary care doctors, we need to be effective ambassadors of appropriate opioid prescribing and often that means doing the hard thing and saying no to a patient.

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J.

[email protected]

The media is filled with stories about the opioid crisis. We have all heard the horror stories of addiction and overdose, as well as “pill mill” doctors. In fact, more than 932,000 people have died of drug overdose since 1999 and, in recent years, approximately 75% of drug overdoses involved opioids.

Yet, they still have their place in the treatment of pain. It has been estimated that approximately 37% of all opioid prescriptions are written by primary care doctors, so it is essential that we doctors know appropriate prescribing guidelines.

The CDC updated the 2016 guidelines for prescribing opioids for pain in 2022. They cover when to initiate prescribing of opioids, selecting appropriate opioids and doses, and deciding the duration of therapy. The guidelines do a great job providing evidence-based recommendations while at the same time keeping the problems with opioids in the picture.

For primary care doctors, pain is one of the most common complaints we see – from broken bones to low back pain to cancer pain. It is important to note that the current guidelines exclude pain from sickle cell disease, cancer-related pain, palliative care, and end-of-life care. The guidelines apply to acute, subacute, and chronic pain. Pain is a complex symptom and often needs a multipronged approach. We make a mistake if we just prescribe a pain medication without understanding the root cause of the pain.

The guidelines suggest starting with nonopioid medications and incorporating nonmedicinal modes of treatments, such as physical therapy, as well. Opioids should be started at the lowest dose and for the shortest duration. Immediate-release medications are preferred over long-acting or extended-release ones. The patient should always be informed of the risks and benefits.

While the guidelines do a great job recommending how to prescribe opioids, they do not go into any depth discussing other treatment options. Perhaps knowledge of other treatment modalities would help primary care physicians avoid opioid prescribing. When treating our patients, it is important to educate them on how to manage their own symptoms.

The guidelines also advise tapering patients who may have been on high-dose opioids for long periods of time. Doctors know this is a very difficult task. However, resources to help with this are often lacking. For example, rehab may not be covered under a patient’s insurance, or it may be cheaper to take an opioid than to go to physical therapy. Although the recommendation is to taper, community assets may not support this. Guidelines are one thing, but the rest of the health care system needs to catch up to them and make them practical.

Primary care doctors often utilize our physical medicine, rehabilitation, and pain management specialists to assist in managing our patients’ pain. Here too, access to this resource is often difficult to come by. Depending on a patient’s insurance, it can take months to get an appointment.

In general, the current guidelines offer 12 key recommendations when prescribing opioids. They are a great reference; however, we need more real-life tools. For many of us in primary care, these guidelines support what we’ve been doing all along.

Primary care doctors will surely play a huge role in addressing the opioid crisis. We can prescribe opioids appropriately, but it doesn’t erase the problems of those patients who were overprescribed in the past. Many still seek out these medications whether for monetary reasons or just for the high. It is often easy to blame the patient but the one in control is the one with the prescription pad. Yet, it is important to remember that many of these patients are in real pain and need help.

Often, it is simpler to just prescribe a pain medication than it is to explain why one is not appropriate. As primary care doctors, we need to be effective ambassadors of appropriate opioid prescribing and often that means doing the hard thing and saying no to a patient.

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J.

[email protected]

The media is filled with stories about the opioid crisis. We have all heard the horror stories of addiction and overdose, as well as “pill mill” doctors. In fact, more than 932,000 people have died of drug overdose since 1999 and, in recent years, approximately 75% of drug overdoses involved opioids.

Yet, they still have their place in the treatment of pain. It has been estimated that approximately 37% of all opioid prescriptions are written by primary care doctors, so it is essential that we doctors know appropriate prescribing guidelines.

The CDC updated the 2016 guidelines for prescribing opioids for pain in 2022. They cover when to initiate prescribing of opioids, selecting appropriate opioids and doses, and deciding the duration of therapy. The guidelines do a great job providing evidence-based recommendations while at the same time keeping the problems with opioids in the picture.

For primary care doctors, pain is one of the most common complaints we see – from broken bones to low back pain to cancer pain. It is important to note that the current guidelines exclude pain from sickle cell disease, cancer-related pain, palliative care, and end-of-life care. The guidelines apply to acute, subacute, and chronic pain. Pain is a complex symptom and often needs a multipronged approach. We make a mistake if we just prescribe a pain medication without understanding the root cause of the pain.

The guidelines suggest starting with nonopioid medications and incorporating nonmedicinal modes of treatments, such as physical therapy, as well. Opioids should be started at the lowest dose and for the shortest duration. Immediate-release medications are preferred over long-acting or extended-release ones. The patient should always be informed of the risks and benefits.

While the guidelines do a great job recommending how to prescribe opioids, they do not go into any depth discussing other treatment options. Perhaps knowledge of other treatment modalities would help primary care physicians avoid opioid prescribing. When treating our patients, it is important to educate them on how to manage their own symptoms.

The guidelines also advise tapering patients who may have been on high-dose opioids for long periods of time. Doctors know this is a very difficult task. However, resources to help with this are often lacking. For example, rehab may not be covered under a patient’s insurance, or it may be cheaper to take an opioid than to go to physical therapy. Although the recommendation is to taper, community assets may not support this. Guidelines are one thing, but the rest of the health care system needs to catch up to them and make them practical.

Primary care doctors often utilize our physical medicine, rehabilitation, and pain management specialists to assist in managing our patients’ pain. Here too, access to this resource is often difficult to come by. Depending on a patient’s insurance, it can take months to get an appointment.

In general, the current guidelines offer 12 key recommendations when prescribing opioids. They are a great reference; however, we need more real-life tools. For many of us in primary care, these guidelines support what we’ve been doing all along.

Primary care doctors will surely play a huge role in addressing the opioid crisis. We can prescribe opioids appropriately, but it doesn’t erase the problems of those patients who were overprescribed in the past. Many still seek out these medications whether for monetary reasons or just for the high. It is often easy to blame the patient but the one in control is the one with the prescription pad. Yet, it is important to remember that many of these patients are in real pain and need help.

Often, it is simpler to just prescribe a pain medication than it is to explain why one is not appropriate. As primary care doctors, we need to be effective ambassadors of appropriate opioid prescribing and often that means doing the hard thing and saying no to a patient.

Dr. Girgis practices family medicine in South River, N.J., and is a clinical assistant professor of family medicine at Robert Wood Johnson Medical School, New Brunswick, N.J.

[email protected]

If you’re looking for it, you’ll find fatigue almost everywhere. It’s so common that it hides in plain sight, never dealt with because it’s present for good reason: the inevitable consequence of age, whatever disease you’re treating, poor lifestyle choices, and the daily grind of twenty-first–century life. Its impact is so ubiquitous and pernicious that it’s considered acceptable.

Is it though? After all, fatigue can be debilitating. Not every symptom is worthy of a chronic syndrome bearing its name. Furthermore, what if its relationship to the disease you’re treating is bidirectional? What if we actually paid attention, asked about it, and expended energy trying to relieve it? Could we improve quality of life and other outcomes too?

Outside of sleep medicine, I see little focus on fatigue among pulmonologists. This despite the existing data on fatigue related to sarcoidosis, chronic obstructive pulmonary disease (COPD), and interstitial lung disease. Even when we do pay it lip service, “addressing” fatigue or sleep is essentially a euphemism for ordering a sleep study.

As with fatigue, if you look for obstructive sleep apnea, it’ll be there, although with OSA, it’s related to the incredibly low, nonevidence-based threshold the American Academy of Sleep Medicine has established for making the diagnosis. With continuous positive airway pressure (CPAP) in hand, the patient has a new disease to worry about and a difficult behavioral change (wearing, cleaning, and resupplying their CPAP equipment) to make. Too often, the CPAP isn’t used – or is – and the fatigue persists. But it’s okay, because we followed somebody’s guideline.

The American Thoracic Society just published a research statement on cancer-related fatigue. It is comprehensive and highlights the high prevalence and poor recognition of cancer-related fatigue. The authors note that among cancers, those of the lung are associated with a higher comorbid disease burden, older age, and cigarette smoking. All these factors make patients with lung cancer particularly prone to fatigue. Interactions between these factors, lung cancer histology, and specific chemotherapy regimens are poorly understood. True to its title, the “research statement” serves more as a call to action than an evidence-based blueprint for diagnosis and management.

The cancer-related fatigue data that does exist suggests treatment starts with recognition followed by a focus on sleep, exercise, and nutrition. This should surprise no one. The data on fatigue in general (not specific to cancer-related fatigue) shows that although fatigue is not synonymous with poor quality or insufficient sleep, sleep is usually a major factor. The cancer-related conditions affecting sleep include anxiety, depression, insufficient sleep, insomnia, medication side effects, and OSA. The intersecting web is complex, but across underlying conditions (cancer or otherwise), the quickest most efficient method for mitigating fatigue is optimizing sleep.

Exercise and nutrition are also important. Again, across disease processes (interstitial lung disease, COPD, lung cancer, and so on), no drug comes close to aerobic exercise for reducing symptoms, including fatigue. If an exercise prescription could be delivered in pill-form, it’d be a blockbuster. But it can’t be, and the ATS lung cancer–related fatigue research statement nicely outlines the evidence for increased activity levels and the barriers to obtaining support and compliance. As is the case with exercise, support for improving nutrition is limited by cost, access, and patient education.

Perhaps most importantly, sleep, exercise, and nutrition require time for counseling and a behavior change for the physician and patient. Both are in short supply, and commitment is always ephemeral. Incentivization could perhaps be re-structured, but the ATS document notes this will be challenging. With respect to pulmonary rehabilitation (about 50% of patients with lung cancer have comorbid COPD), for example, reimbursement is poor, which serves as a disincentive. Their suggestions? Early integration and repeated introduction to rehabilitation and exercise concepts. Sounds great.

In summary, in my opinion, fatigue doesn’t receive the attention level commensurate with its impact. It’s easy to understand why, but I’m glad the ATS is highlighting the problem. Unbeknownst to me, multiple cancer guidelines already recommend screening for fatigue. The recent sarcoidosis treatment guideline published by the European Respiratory Society dedicated a PICO (Patients, Intervention, Comparison, Outcomes) to the topic and recommended exercise (pulmonary rehabilitation). That said, consensus statements on COPD mention it only in passing in relation to severe disease and end-of-life care, and idiopathic pulmonary fibrosis guidelines ignore it entirely. So, recognition is improving, but we’ve got ways to go.

Dr. Holley is professor of medicine at Uniformed Services University, Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He disclosed ties with Metapharm, CHEST College, and WebMD.

A version of this article originally appeared on Medscape.com.

If you’re looking for it, you’ll find fatigue almost everywhere. It’s so common that it hides in plain sight, never dealt with because it’s present for good reason: the inevitable consequence of age, whatever disease you’re treating, poor lifestyle choices, and the daily grind of twenty-first–century life. Its impact is so ubiquitous and pernicious that it’s considered acceptable.

Is it though? After all, fatigue can be debilitating. Not every symptom is worthy of a chronic syndrome bearing its name. Furthermore, what if its relationship to the disease you’re treating is bidirectional? What if we actually paid attention, asked about it, and expended energy trying to relieve it? Could we improve quality of life and other outcomes too?

Outside of sleep medicine, I see little focus on fatigue among pulmonologists. This despite the existing data on fatigue related to sarcoidosis, chronic obstructive pulmonary disease (COPD), and interstitial lung disease. Even when we do pay it lip service, “addressing” fatigue or sleep is essentially a euphemism for ordering a sleep study.

As with fatigue, if you look for obstructive sleep apnea, it’ll be there, although with OSA, it’s related to the incredibly low, nonevidence-based threshold the American Academy of Sleep Medicine has established for making the diagnosis. With continuous positive airway pressure (CPAP) in hand, the patient has a new disease to worry about and a difficult behavioral change (wearing, cleaning, and resupplying their CPAP equipment) to make. Too often, the CPAP isn’t used – or is – and the fatigue persists. But it’s okay, because we followed somebody’s guideline.

The American Thoracic Society just published a research statement on cancer-related fatigue. It is comprehensive and highlights the high prevalence and poor recognition of cancer-related fatigue. The authors note that among cancers, those of the lung are associated with a higher comorbid disease burden, older age, and cigarette smoking. All these factors make patients with lung cancer particularly prone to fatigue. Interactions between these factors, lung cancer histology, and specific chemotherapy regimens are poorly understood. True to its title, the “research statement” serves more as a call to action than an evidence-based blueprint for diagnosis and management.

The cancer-related fatigue data that does exist suggests treatment starts with recognition followed by a focus on sleep, exercise, and nutrition. This should surprise no one. The data on fatigue in general (not specific to cancer-related fatigue) shows that although fatigue is not synonymous with poor quality or insufficient sleep, sleep is usually a major factor. The cancer-related conditions affecting sleep include anxiety, depression, insufficient sleep, insomnia, medication side effects, and OSA. The intersecting web is complex, but across underlying conditions (cancer or otherwise), the quickest most efficient method for mitigating fatigue is optimizing sleep.

Exercise and nutrition are also important. Again, across disease processes (interstitial lung disease, COPD, lung cancer, and so on), no drug comes close to aerobic exercise for reducing symptoms, including fatigue. If an exercise prescription could be delivered in pill-form, it’d be a blockbuster. But it can’t be, and the ATS lung cancer–related fatigue research statement nicely outlines the evidence for increased activity levels and the barriers to obtaining support and compliance. As is the case with exercise, support for improving nutrition is limited by cost, access, and patient education.

Perhaps most importantly, sleep, exercise, and nutrition require time for counseling and a behavior change for the physician and patient. Both are in short supply, and commitment is always ephemeral. Incentivization could perhaps be re-structured, but the ATS document notes this will be challenging. With respect to pulmonary rehabilitation (about 50% of patients with lung cancer have comorbid COPD), for example, reimbursement is poor, which serves as a disincentive. Their suggestions? Early integration and repeated introduction to rehabilitation and exercise concepts. Sounds great.

In summary, in my opinion, fatigue doesn’t receive the attention level commensurate with its impact. It’s easy to understand why, but I’m glad the ATS is highlighting the problem. Unbeknownst to me, multiple cancer guidelines already recommend screening for fatigue. The recent sarcoidosis treatment guideline published by the European Respiratory Society dedicated a PICO (Patients, Intervention, Comparison, Outcomes) to the topic and recommended exercise (pulmonary rehabilitation). That said, consensus statements on COPD mention it only in passing in relation to severe disease and end-of-life care, and idiopathic pulmonary fibrosis guidelines ignore it entirely. So, recognition is improving, but we’ve got ways to go.

Dr. Holley is professor of medicine at Uniformed Services University, Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He disclosed ties with Metapharm, CHEST College, and WebMD.

A version of this article originally appeared on Medscape.com.

If you’re looking for it, you’ll find fatigue almost everywhere. It’s so common that it hides in plain sight, never dealt with because it’s present for good reason: the inevitable consequence of age, whatever disease you’re treating, poor lifestyle choices, and the daily grind of twenty-first–century life. Its impact is so ubiquitous and pernicious that it’s considered acceptable.

Is it though? After all, fatigue can be debilitating. Not every symptom is worthy of a chronic syndrome bearing its name. Furthermore, what if its relationship to the disease you’re treating is bidirectional? What if we actually paid attention, asked about it, and expended energy trying to relieve it? Could we improve quality of life and other outcomes too?

Outside of sleep medicine, I see little focus on fatigue among pulmonologists. This despite the existing data on fatigue related to sarcoidosis, chronic obstructive pulmonary disease (COPD), and interstitial lung disease. Even when we do pay it lip service, “addressing” fatigue or sleep is essentially a euphemism for ordering a sleep study.

As with fatigue, if you look for obstructive sleep apnea, it’ll be there, although with OSA, it’s related to the incredibly low, nonevidence-based threshold the American Academy of Sleep Medicine has established for making the diagnosis. With continuous positive airway pressure (CPAP) in hand, the patient has a new disease to worry about and a difficult behavioral change (wearing, cleaning, and resupplying their CPAP equipment) to make. Too often, the CPAP isn’t used – or is – and the fatigue persists. But it’s okay, because we followed somebody’s guideline.

The American Thoracic Society just published a research statement on cancer-related fatigue. It is comprehensive and highlights the high prevalence and poor recognition of cancer-related fatigue. The authors note that among cancers, those of the lung are associated with a higher comorbid disease burden, older age, and cigarette smoking. All these factors make patients with lung cancer particularly prone to fatigue. Interactions between these factors, lung cancer histology, and specific chemotherapy regimens are poorly understood. True to its title, the “research statement” serves more as a call to action than an evidence-based blueprint for diagnosis and management.

The cancer-related fatigue data that does exist suggests treatment starts with recognition followed by a focus on sleep, exercise, and nutrition. This should surprise no one. The data on fatigue in general (not specific to cancer-related fatigue) shows that although fatigue is not synonymous with poor quality or insufficient sleep, sleep is usually a major factor. The cancer-related conditions affecting sleep include anxiety, depression, insufficient sleep, insomnia, medication side effects, and OSA. The intersecting web is complex, but across underlying conditions (cancer or otherwise), the quickest most efficient method for mitigating fatigue is optimizing sleep.

Exercise and nutrition are also important. Again, across disease processes (interstitial lung disease, COPD, lung cancer, and so on), no drug comes close to aerobic exercise for reducing symptoms, including fatigue. If an exercise prescription could be delivered in pill-form, it’d be a blockbuster. But it can’t be, and the ATS lung cancer–related fatigue research statement nicely outlines the evidence for increased activity levels and the barriers to obtaining support and compliance. As is the case with exercise, support for improving nutrition is limited by cost, access, and patient education.

Perhaps most importantly, sleep, exercise, and nutrition require time for counseling and a behavior change for the physician and patient. Both are in short supply, and commitment is always ephemeral. Incentivization could perhaps be re-structured, but the ATS document notes this will be challenging. With respect to pulmonary rehabilitation (about 50% of patients with lung cancer have comorbid COPD), for example, reimbursement is poor, which serves as a disincentive. Their suggestions? Early integration and repeated introduction to rehabilitation and exercise concepts. Sounds great.

In summary, in my opinion, fatigue doesn’t receive the attention level commensurate with its impact. It’s easy to understand why, but I’m glad the ATS is highlighting the problem. Unbeknownst to me, multiple cancer guidelines already recommend screening for fatigue. The recent sarcoidosis treatment guideline published by the European Respiratory Society dedicated a PICO (Patients, Intervention, Comparison, Outcomes) to the topic and recommended exercise (pulmonary rehabilitation). That said, consensus statements on COPD mention it only in passing in relation to severe disease and end-of-life care, and idiopathic pulmonary fibrosis guidelines ignore it entirely. So, recognition is improving, but we’ve got ways to go.

Dr. Holley is professor of medicine at Uniformed Services University, Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He disclosed ties with Metapharm, CHEST College, and WebMD.

A version of this article originally appeared on Medscape.com.

The Centers for Disease Control and Prevention and the U.S. Census Bureau estimate that 6.1% of the U.S. adult population is living with long COVID, with millions more debilitated worldwide. The demand for substantial treatment is enormous, but the urgency to fund and begin the necessary range of clinical trials has not met the severity of the problem.
 

While trials are slowly beginning to happen, the treatment choices and trial design require crucial nuances and understanding of viral-onset illnesses, and few research groups are creating strong trials that fully reflect the complexities of this landscape.

This article aims to share key considerations and best practices that are essential to the success of these trials. These recommendations recognize that roughly half of long COVID patients have new-onset myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and dysautonomia from COVID, which must be at the forefront of how trials are designed and conducted, and are additionally based on the current hypotheses about long COVID’s pathophysiologies. 
 

1: Drugs proposed by experts in postviral fields should be prioritized

Upward of 50 drugs for viral-onset conditions like ME/CFS, dysautonomia, AIDS, and others have been waiting for years to go to trial, but have not had the funding to do so. 

Treatments proposed by experts in viral-onset illnesses (such as ME/CFS and dysautonomia) should be prioritized (PM R. 2022 Oct;14[10]:1270-91), as outside researchers are not familiar with these fields and their potential treatment options.
 

2: Drugs targeting a wide range of mechanisms should be trialed

Treatments that should be trialed include anticoagulants/antiplatelets for clotting and vascular functioning, immunomodulators including JAK-STAT inhibitors, COVID-specific antivirals and antivirals against reactivated herpesviruses (Valcyte, Valacyclovir, EBV vaccine). 

Other options include prescription mast cell stabilizers (ketotifen, cromolyn sodium), drugs that regulate microglial activation (low-dose naltrexone, low-dose aripiprazole), anti-CGRP medications, beta-blockers, and intravenous immunoglobulin.

Others include medications that target mitochondrial dysfunction; ivabradine; pyridostigmine;, DRP1 inhibitors; supplements showing success in patient communities including lactoferrin, ubiquinone, and nattokinase; and therapies targeting glymphatic/lymphatic dysfunction, microbiome therapies, and therapeutic peptides. 
 

3: Use appropriate long COVID subtypes 

Long COVID is an umbrella term that encompasses multiple new-onset and worsened conditions and symptoms after COVID. Roughly half of long COVID patients likely meet the criteria for ME/CFS and/or dysautonomia. Others may have new-onset diabetes, major clotting events, lung damage, neurological disorders, loss of smell or taste, and other manifestations. 

Patients in different categories likely have different responses to treatments. It’s critical to identify appropriate subtypes for each trial, ideally performing detailed analyses to identify the treatments that work best, and don’t, for each subtype. 
 

4: Behavioral treatments, especially those that have harmed similar populations, should not be trialed

Behavioral treatments including exercise, graded exercise therapy (GET), and cognitive-behavioral therapy (CBT) should not be trialed, let alone prioritized, for long COVID. 

In patients with postexertional malaise (PEM), one of the most common long COVID symptoms, exercise is actively harmful and causes dysfunctional metabolic patterns, cardiac preload failure, impaired systemic oxygen extraction, and more. GET and CBT have failed similar populations , and exercise is explicitly contraindicated by the World Health Organization, the British National Institute for Health and Care Excellence, the CDC, and other organizations. 

Resources should instead be put toward the wide range of medications that have not yet adequately undergone clinical trials.  
 

5: PCR and antibody tests should not be used as inclusion criteria for trial participants

Only an estimated 1%-3% of cases in the first wave of COVID were documented, and the CDC estimates that only 25% of cases through September 2021 were documented. Similarly, antibody tests are unreliable to determine past infection, as roughly a third of patients don’t seroconvert, and a similar proportion serorevert within a few months. Using polymerase chain reaction (PCR) and antibody testing to determine who should be included in clinical trials limits who is eligible to participate in research, particularly those who have been ill for longer. Additionally, the majority of those who serorevert are women, so using antibody tests for inclusion introduces a selection bias and may miss mechanisms of immune system functioning that are part of long COVID.

PCR tests also have high false-negative rates and requiring them in research excludes people with lower viral loads with long COVID, which would confound findings. 

These issues with testing also lead to COVID-infected people accidentally being included in control groups, which ruins the credibility of the research findings completely.
 

6: Include comparator groups

There are several common diagnoses that occur in people with long COVID, including ME/CFS, postural orthostatic tachycardia syndrome, small-fiber neuropathy, mast cell activation syndrome, and Ehlers-Danlos syndrome.

Identifying people with these conditions within the trial cohort improves research across all fields, benefiting all groups, and helps clarify what types of patients benefit most from certain medications. 
 

7: Identify the right endpoints; avoid the wrong ones

Even though our understanding of the pathophysiology of long COVID is still evolving, it’s still possible to do clinical trials by identifying strong endpoints and outcome measures. 

Several tools have been designed for viral-onset conditions and should be used alongside other endpoints. Postexertional malaise and autonomic symptoms, which are some of the most common symptoms of long COVID, can be measured with the validated DSQ-PEM and COMPASS-31, respectively. Tools for cognitive dysfunction trials should capture specific and common types of impairment, like processing speed. 

Endpoints should be high-impact and aim for large improvements that have clinical significance over small improvements that do not have clinical significance. 

Objective tests should be incorporated where possible; some to consider include natural killer cell functioning, cerebral blood flow, T-cell functioning, levels of reactivated herpesviruses, blood lactate levels, and microclots, as testing becomes available. 

Mental health outcomes shouldn’t be primary endpoints, except where a trial is targeting a specific mental health condition because of COVID (for example, premenstrual dysphoric disorder). 

If mental health conditions are tracked secondarily, it’s vital not to use questionnaires that include physical symptoms like fatigue, difficulty concentrating, difficulty sleeping, or palpitations, as these artificially increase depression and anxiety scores in chronically ill respondents. Tools that include physical symptoms (Patient Health Questionnaire–9, Beck Anxiety Inventory, Beck Depression Inventory) can be replaced with scales like the PHQ-2, General Anxiety Disorder–7, Hospital Anxiety and Depression Scale, or PROMIS-29 subscales.

Because certain cytokines and other inflammatory markers may naturally decrease over time without corresponding improvement in the ME/CFS subtype, caution should be taken when using cytokines as endpoints.
 

8: Consider enrollment and objectives carefully

A proportion of people with long COVID will recover in the early months after infection. Ideally, clinical trials will primarily study treatments in patients who have been ill 6 months or longer, as some natural recovery will happen before that can bias studies.

But where resources are abundant, it is ideal for trials to additionally look at whether the treatments can help patients in the early months recover and prevent progression to the later stage.
 

9: Tracking illness duration is crucial

Research from ME/CFS shows that there may be an immune change in the first few years of the illness, where cytokines decrease without any corresponding change in symptom improvement. 

Because of this and the possibility that other markers follow the same pattern, disease duration should be a core feature of all analyses and trial designs. Trial outcomes should be designed to answer the question of whether the medication helps patients at different durations of illness. 
 

10: Prioritize patient populations less likely to recover without intervention

Some long COVID phenotypes seem less likely to recover without intervention. Trials should take care to focus on these patient populations, which include those with neurologic symptoms and those meeting ME/CFS criteria.

 

11: Account for the relapsing/remitting nature

Outcome measures need to be assessed in a way that can distinguish a temporary remission, which is part of the natural course of the disease, from a permanent cure. 

Factors that can contribute to the relapsing/remitting nature include physical and cognitive postexertional malaise, menstrual cycle changes, and seasonal changes.
 

12: Trial participants should reflect the diversity of the long COVID population

Certain demographics are more likely to be affected by acute and long COVID and need to be appropriately recruited and reflected in research, including in patient engagement. 

Trials must include high numbers of Hispanic/Latinx, Black, and indigenous communities, queer and transgender populations, and women. Trial materials and design need to incorporate linguistic diversity in addition to racial/ethnic diversity.

Upward of 75% of long COVID cases happen after mild acute cases; clinical researchers should ensure that nonhospitalized patients make up the bulk of trial participants. 
 

13: Utilize meaningful engagement of patients, especially in treatment selection and study design

Meaningful patient engagement means engaging multiple patients at every step of the trial process, from treatment selection to study design to analysis to communication of the results. 

Patient experiences are extremely valuable and contain information that researchers may not be familiar with, including the nature and patterns of the illness, insights into possible treatments, and barriers to documentation and care that may also impact research. Tapping into those patient experiences will make trials stronger.

Overall, the landscape of long COVID clinical trials is ripe for discovery, and researchers choosing to go down this path will be deeply appreciated by the patient community. 

Hannah Davis is a long COVID patient-researcher and cofounder of the Patient-Led Research Collaborative, an organization studying the long-term effects of COVID.

A version of this article first appeared on Medscape.com.

The Centers for Disease Control and Prevention and the U.S. Census Bureau estimate that 6.1% of the U.S. adult population is living with long COVID, with millions more debilitated worldwide. The demand for substantial treatment is enormous, but the urgency to fund and begin the necessary range of clinical trials has not met the severity of the problem.
 

While trials are slowly beginning to happen, the treatment choices and trial design require crucial nuances and understanding of viral-onset illnesses, and few research groups are creating strong trials that fully reflect the complexities of this landscape.

This article aims to share key considerations and best practices that are essential to the success of these trials. These recommendations recognize that roughly half of long COVID patients have new-onset myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and dysautonomia from COVID, which must be at the forefront of how trials are designed and conducted, and are additionally based on the current hypotheses about long COVID’s pathophysiologies. 
 

1: Drugs proposed by experts in postviral fields should be prioritized

Upward of 50 drugs for viral-onset conditions like ME/CFS, dysautonomia, AIDS, and others have been waiting for years to go to trial, but have not had the funding to do so. 

Treatments proposed by experts in viral-onset illnesses (such as ME/CFS and dysautonomia) should be prioritized (PM R. 2022 Oct;14[10]:1270-91), as outside researchers are not familiar with these fields and their potential treatment options.
 

2: Drugs targeting a wide range of mechanisms should be trialed

Treatments that should be trialed include anticoagulants/antiplatelets for clotting and vascular functioning, immunomodulators including JAK-STAT inhibitors, COVID-specific antivirals and antivirals against reactivated herpesviruses (Valcyte, Valacyclovir, EBV vaccine). 

Other options include prescription mast cell stabilizers (ketotifen, cromolyn sodium), drugs that regulate microglial activation (low-dose naltrexone, low-dose aripiprazole), anti-CGRP medications, beta-blockers, and intravenous immunoglobulin.

Others include medications that target mitochondrial dysfunction; ivabradine; pyridostigmine;, DRP1 inhibitors; supplements showing success in patient communities including lactoferrin, ubiquinone, and nattokinase; and therapies targeting glymphatic/lymphatic dysfunction, microbiome therapies, and therapeutic peptides. 
 

3: Use appropriate long COVID subtypes 

Long COVID is an umbrella term that encompasses multiple new-onset and worsened conditions and symptoms after COVID. Roughly half of long COVID patients likely meet the criteria for ME/CFS and/or dysautonomia. Others may have new-onset diabetes, major clotting events, lung damage, neurological disorders, loss of smell or taste, and other manifestations. 

Patients in different categories likely have different responses to treatments. It’s critical to identify appropriate subtypes for each trial, ideally performing detailed analyses to identify the treatments that work best, and don’t, for each subtype. 
 

4: Behavioral treatments, especially those that have harmed similar populations, should not be trialed

Behavioral treatments including exercise, graded exercise therapy (GET), and cognitive-behavioral therapy (CBT) should not be trialed, let alone prioritized, for long COVID. 

In patients with postexertional malaise (PEM), one of the most common long COVID symptoms, exercise is actively harmful and causes dysfunctional metabolic patterns, cardiac preload failure, impaired systemic oxygen extraction, and more. GET and CBT have failed similar populations , and exercise is explicitly contraindicated by the World Health Organization, the British National Institute for Health and Care Excellence, the CDC, and other organizations. 

Resources should instead be put toward the wide range of medications that have not yet adequately undergone clinical trials.  
 

5: PCR and antibody tests should not be used as inclusion criteria for trial participants

Only an estimated 1%-3% of cases in the first wave of COVID were documented, and the CDC estimates that only 25% of cases through September 2021 were documented. Similarly, antibody tests are unreliable to determine past infection, as roughly a third of patients don’t seroconvert, and a similar proportion serorevert within a few months. Using polymerase chain reaction (PCR) and antibody testing to determine who should be included in clinical trials limits who is eligible to participate in research, particularly those who have been ill for longer. Additionally, the majority of those who serorevert are women, so using antibody tests for inclusion introduces a selection bias and may miss mechanisms of immune system functioning that are part of long COVID.

PCR tests also have high false-negative rates and requiring them in research excludes people with lower viral loads with long COVID, which would confound findings. 

These issues with testing also lead to COVID-infected people accidentally being included in control groups, which ruins the credibility of the research findings completely.
 

6: Include comparator groups

There are several common diagnoses that occur in people with long COVID, including ME/CFS, postural orthostatic tachycardia syndrome, small-fiber neuropathy, mast cell activation syndrome, and Ehlers-Danlos syndrome.

Identifying people with these conditions within the trial cohort improves research across all fields, benefiting all groups, and helps clarify what types of patients benefit most from certain medications. 
 

7: Identify the right endpoints; avoid the wrong ones

Even though our understanding of the pathophysiology of long COVID is still evolving, it’s still possible to do clinical trials by identifying strong endpoints and outcome measures. 

Several tools have been designed for viral-onset conditions and should be used alongside other endpoints. Postexertional malaise and autonomic symptoms, which are some of the most common symptoms of long COVID, can be measured with the validated DSQ-PEM and COMPASS-31, respectively. Tools for cognitive dysfunction trials should capture specific and common types of impairment, like processing speed. 

Endpoints should be high-impact and aim for large improvements that have clinical significance over small improvements that do not have clinical significance. 

Objective tests should be incorporated where possible; some to consider include natural killer cell functioning, cerebral blood flow, T-cell functioning, levels of reactivated herpesviruses, blood lactate levels, and microclots, as testing becomes available. 

Mental health outcomes shouldn’t be primary endpoints, except where a trial is targeting a specific mental health condition because of COVID (for example, premenstrual dysphoric disorder). 

If mental health conditions are tracked secondarily, it’s vital not to use questionnaires that include physical symptoms like fatigue, difficulty concentrating, difficulty sleeping, or palpitations, as these artificially increase depression and anxiety scores in chronically ill respondents. Tools that include physical symptoms (Patient Health Questionnaire–9, Beck Anxiety Inventory, Beck Depression Inventory) can be replaced with scales like the PHQ-2, General Anxiety Disorder–7, Hospital Anxiety and Depression Scale, or PROMIS-29 subscales.

Because certain cytokines and other inflammatory markers may naturally decrease over time without corresponding improvement in the ME/CFS subtype, caution should be taken when using cytokines as endpoints.
 

8: Consider enrollment and objectives carefully

A proportion of people with long COVID will recover in the early months after infection. Ideally, clinical trials will primarily study treatments in patients who have been ill 6 months or longer, as some natural recovery will happen before that can bias studies.

But where resources are abundant, it is ideal for trials to additionally look at whether the treatments can help patients in the early months recover and prevent progression to the later stage.
 

9: Tracking illness duration is crucial

Research from ME/CFS shows that there may be an immune change in the first few years of the illness, where cytokines decrease without any corresponding change in symptom improvement. 

Because of this and the possibility that other markers follow the same pattern, disease duration should be a core feature of all analyses and trial designs. Trial outcomes should be designed to answer the question of whether the medication helps patients at different durations of illness. 
 

10: Prioritize patient populations less likely to recover without intervention

Some long COVID phenotypes seem less likely to recover without intervention. Trials should take care to focus on these patient populations, which include those with neurologic symptoms and those meeting ME/CFS criteria.

 

11: Account for the relapsing/remitting nature

Outcome measures need to be assessed in a way that can distinguish a temporary remission, which is part of the natural course of the disease, from a permanent cure. 

Factors that can contribute to the relapsing/remitting nature include physical and cognitive postexertional malaise, menstrual cycle changes, and seasonal changes.
 

12: Trial participants should reflect the diversity of the long COVID population

Certain demographics are more likely to be affected by acute and long COVID and need to be appropriately recruited and reflected in research, including in patient engagement. 

Trials must include high numbers of Hispanic/Latinx, Black, and indigenous communities, queer and transgender populations, and women. Trial materials and design need to incorporate linguistic diversity in addition to racial/ethnic diversity.

Upward of 75% of long COVID cases happen after mild acute cases; clinical researchers should ensure that nonhospitalized patients make up the bulk of trial participants. 
 

13: Utilize meaningful engagement of patients, especially in treatment selection and study design

Meaningful patient engagement means engaging multiple patients at every step of the trial process, from treatment selection to study design to analysis to communication of the results. 

Patient experiences are extremely valuable and contain information that researchers may not be familiar with, including the nature and patterns of the illness, insights into possible treatments, and barriers to documentation and care that may also impact research. Tapping into those patient experiences will make trials stronger.

Overall, the landscape of long COVID clinical trials is ripe for discovery, and researchers choosing to go down this path will be deeply appreciated by the patient community. 

Hannah Davis is a long COVID patient-researcher and cofounder of the Patient-Led Research Collaborative, an organization studying the long-term effects of COVID.

A version of this article first appeared on Medscape.com.

The Centers for Disease Control and Prevention and the U.S. Census Bureau estimate that 6.1% of the U.S. adult population is living with long COVID, with millions more debilitated worldwide. The demand for substantial treatment is enormous, but the urgency to fund and begin the necessary range of clinical trials has not met the severity of the problem.
 

While trials are slowly beginning to happen, the treatment choices and trial design require crucial nuances and understanding of viral-onset illnesses, and few research groups are creating strong trials that fully reflect the complexities of this landscape.

This article aims to share key considerations and best practices that are essential to the success of these trials. These recommendations recognize that roughly half of long COVID patients have new-onset myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and dysautonomia from COVID, which must be at the forefront of how trials are designed and conducted, and are additionally based on the current hypotheses about long COVID’s pathophysiologies. 
 

1: Drugs proposed by experts in postviral fields should be prioritized

Upward of 50 drugs for viral-onset conditions like ME/CFS, dysautonomia, AIDS, and others have been waiting for years to go to trial, but have not had the funding to do so. 

Treatments proposed by experts in viral-onset illnesses (such as ME/CFS and dysautonomia) should be prioritized (PM R. 2022 Oct;14[10]:1270-91), as outside researchers are not familiar with these fields and their potential treatment options.
 

2: Drugs targeting a wide range of mechanisms should be trialed

Treatments that should be trialed include anticoagulants/antiplatelets for clotting and vascular functioning, immunomodulators including JAK-STAT inhibitors, COVID-specific antivirals and antivirals against reactivated herpesviruses (Valcyte, Valacyclovir, EBV vaccine). 

Other options include prescription mast cell stabilizers (ketotifen, cromolyn sodium), drugs that regulate microglial activation (low-dose naltrexone, low-dose aripiprazole), anti-CGRP medications, beta-blockers, and intravenous immunoglobulin.

Others include medications that target mitochondrial dysfunction; ivabradine; pyridostigmine;, DRP1 inhibitors; supplements showing success in patient communities including lactoferrin, ubiquinone, and nattokinase; and therapies targeting glymphatic/lymphatic dysfunction, microbiome therapies, and therapeutic peptides. 
 

3: Use appropriate long COVID subtypes 

Long COVID is an umbrella term that encompasses multiple new-onset and worsened conditions and symptoms after COVID. Roughly half of long COVID patients likely meet the criteria for ME/CFS and/or dysautonomia. Others may have new-onset diabetes, major clotting events, lung damage, neurological disorders, loss of smell or taste, and other manifestations. 

Patients in different categories likely have different responses to treatments. It’s critical to identify appropriate subtypes for each trial, ideally performing detailed analyses to identify the treatments that work best, and don’t, for each subtype. 
 

4: Behavioral treatments, especially those that have harmed similar populations, should not be trialed

Behavioral treatments including exercise, graded exercise therapy (GET), and cognitive-behavioral therapy (CBT) should not be trialed, let alone prioritized, for long COVID. 

In patients with postexertional malaise (PEM), one of the most common long COVID symptoms, exercise is actively harmful and causes dysfunctional metabolic patterns, cardiac preload failure, impaired systemic oxygen extraction, and more. GET and CBT have failed similar populations , and exercise is explicitly contraindicated by the World Health Organization, the British National Institute for Health and Care Excellence, the CDC, and other organizations. 

Resources should instead be put toward the wide range of medications that have not yet adequately undergone clinical trials.  
 

5: PCR and antibody tests should not be used as inclusion criteria for trial participants

Only an estimated 1%-3% of cases in the first wave of COVID were documented, and the CDC estimates that only 25% of cases through September 2021 were documented. Similarly, antibody tests are unreliable to determine past infection, as roughly a third of patients don’t seroconvert, and a similar proportion serorevert within a few months. Using polymerase chain reaction (PCR) and antibody testing to determine who should be included in clinical trials limits who is eligible to participate in research, particularly those who have been ill for longer. Additionally, the majority of those who serorevert are women, so using antibody tests for inclusion introduces a selection bias and may miss mechanisms of immune system functioning that are part of long COVID.

PCR tests also have high false-negative rates and requiring them in research excludes people with lower viral loads with long COVID, which would confound findings. 

These issues with testing also lead to COVID-infected people accidentally being included in control groups, which ruins the credibility of the research findings completely.
 

6: Include comparator groups

There are several common diagnoses that occur in people with long COVID, including ME/CFS, postural orthostatic tachycardia syndrome, small-fiber neuropathy, mast cell activation syndrome, and Ehlers-Danlos syndrome.

Identifying people with these conditions within the trial cohort improves research across all fields, benefiting all groups, and helps clarify what types of patients benefit most from certain medications. 
 

7: Identify the right endpoints; avoid the wrong ones

Even though our understanding of the pathophysiology of long COVID is still evolving, it’s still possible to do clinical trials by identifying strong endpoints and outcome measures. 

Several tools have been designed for viral-onset conditions and should be used alongside other endpoints. Postexertional malaise and autonomic symptoms, which are some of the most common symptoms of long COVID, can be measured with the validated DSQ-PEM and COMPASS-31, respectively. Tools for cognitive dysfunction trials should capture specific and common types of impairment, like processing speed. 

Endpoints should be high-impact and aim for large improvements that have clinical significance over small improvements that do not have clinical significance. 

Objective tests should be incorporated where possible; some to consider include natural killer cell functioning, cerebral blood flow, T-cell functioning, levels of reactivated herpesviruses, blood lactate levels, and microclots, as testing becomes available. 

Mental health outcomes shouldn’t be primary endpoints, except where a trial is targeting a specific mental health condition because of COVID (for example, premenstrual dysphoric disorder). 

If mental health conditions are tracked secondarily, it’s vital not to use questionnaires that include physical symptoms like fatigue, difficulty concentrating, difficulty sleeping, or palpitations, as these artificially increase depression and anxiety scores in chronically ill respondents. Tools that include physical symptoms (Patient Health Questionnaire–9, Beck Anxiety Inventory, Beck Depression Inventory) can be replaced with scales like the PHQ-2, General Anxiety Disorder–7, Hospital Anxiety and Depression Scale, or PROMIS-29 subscales.

Because certain cytokines and other inflammatory markers may naturally decrease over time without corresponding improvement in the ME/CFS subtype, caution should be taken when using cytokines as endpoints.
 

8: Consider enrollment and objectives carefully

A proportion of people with long COVID will recover in the early months after infection. Ideally, clinical trials will primarily study treatments in patients who have been ill 6 months or longer, as some natural recovery will happen before that can bias studies.

But where resources are abundant, it is ideal for trials to additionally look at whether the treatments can help patients in the early months recover and prevent progression to the later stage.
 

9: Tracking illness duration is crucial

Research from ME/CFS shows that there may be an immune change in the first few years of the illness, where cytokines decrease without any corresponding change in symptom improvement. 

Because of this and the possibility that other markers follow the same pattern, disease duration should be a core feature of all analyses and trial designs. Trial outcomes should be designed to answer the question of whether the medication helps patients at different durations of illness. 
 

10: Prioritize patient populations less likely to recover without intervention

Some long COVID phenotypes seem less likely to recover without intervention. Trials should take care to focus on these patient populations, which include those with neurologic symptoms and those meeting ME/CFS criteria.

 

11: Account for the relapsing/remitting nature

Outcome measures need to be assessed in a way that can distinguish a temporary remission, which is part of the natural course of the disease, from a permanent cure. 

Factors that can contribute to the relapsing/remitting nature include physical and cognitive postexertional malaise, menstrual cycle changes, and seasonal changes.
 

12: Trial participants should reflect the diversity of the long COVID population

Certain demographics are more likely to be affected by acute and long COVID and need to be appropriately recruited and reflected in research, including in patient engagement. 

Trials must include high numbers of Hispanic/Latinx, Black, and indigenous communities, queer and transgender populations, and women. Trial materials and design need to incorporate linguistic diversity in addition to racial/ethnic diversity.

Upward of 75% of long COVID cases happen after mild acute cases; clinical researchers should ensure that nonhospitalized patients make up the bulk of trial participants. 
 

13: Utilize meaningful engagement of patients, especially in treatment selection and study design

Meaningful patient engagement means engaging multiple patients at every step of the trial process, from treatment selection to study design to analysis to communication of the results. 

Patient experiences are extremely valuable and contain information that researchers may not be familiar with, including the nature and patterns of the illness, insights into possible treatments, and barriers to documentation and care that may also impact research. Tapping into those patient experiences will make trials stronger.

Overall, the landscape of long COVID clinical trials is ripe for discovery, and researchers choosing to go down this path will be deeply appreciated by the patient community. 

Hannah Davis is a long COVID patient-researcher and cofounder of the Patient-Led Research Collaborative, an organization studying the long-term effects of COVID.

A version of this article first appeared on Medscape.com.

Try practicing inpatient medicine without nurses.

You can’t.

In a world where doctors get top billing, nurses are the unsung heroes that really make it all happen. We blow in and out of the rooms, write notes, check results and vitals, then move on to the next person.

But the nurses are the ones who actually make this all happen. And, amazingly, can do all that work with a smile.

But in our current postpandemic world, we’re facing a serious shortage. A recent survey of registered nurses found that only 15% of hospital nurses were planning on being there in 1 year. Thirty percent said they were planning on changing careers entirely in the aftermath of the pandemic. Their job satisfaction scores have dropped 15% from 2019 to 2023. Their stress scores, and concerns that the job is affecting their health, have increased 15%-20%.

The problem reflects a combination of things intersecting at a bad time: Staffing shortages resulting in more patients per nurse, hospital administrators cutting corners on staffing and pay, and the ongoing state of incivility.

The last one is a particularly new issue. Difficult patients and their families are nothing new. We all encounter them, and learn to deal with them in our own way. It’s part of the territory.

But since 2020 it’s climbed to a new-level of in-your-face confrontation, rudeness, and aggression, sometimes leading to violence. Physical attacks on people in all jobs have increased, but health care workers are five times more likely to encounter workplace violence than any other field.

Underpaid, overworked, and a sitting duck for violence. Can you blame people for looking elsewhere?

All of this is coming at a time when a whole generation of nurses is retiring, another generation is starting to reach an age of needing more health care, and nursing schools are short on teaching staff, limiting the number of new people that can be trained. Nursing education, like medical school, isn’t a place to cut corners (neither is care, obviously).

These days we toss the word “burnout” around to the point that it’s become almost meaningless, but to those affected by it, the consequences are quite real. And when it causes a loss of staff and impairs the ability of all to provide quality medical care, it quickly becomes everyone’s problem.

Finding solutions for such things isn’t a can you just kick down the road, as governmental agencies have always been so good at doing. These are things that have real-world consequences for all involved, and solutions need to involve private, public, and educational sectors working together.

I don’t have any ideas, but I hope the people who can change this will sit down and work some out.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Try practicing inpatient medicine without nurses.

You can’t.

In a world where doctors get top billing, nurses are the unsung heroes that really make it all happen. We blow in and out of the rooms, write notes, check results and vitals, then move on to the next person.

But the nurses are the ones who actually make this all happen. And, amazingly, can do all that work with a smile.

But in our current postpandemic world, we’re facing a serious shortage. A recent survey of registered nurses found that only 15% of hospital nurses were planning on being there in 1 year. Thirty percent said they were planning on changing careers entirely in the aftermath of the pandemic. Their job satisfaction scores have dropped 15% from 2019 to 2023. Their stress scores, and concerns that the job is affecting their health, have increased 15%-20%.

The problem reflects a combination of things intersecting at a bad time: Staffing shortages resulting in more patients per nurse, hospital administrators cutting corners on staffing and pay, and the ongoing state of incivility.

The last one is a particularly new issue. Difficult patients and their families are nothing new. We all encounter them, and learn to deal with them in our own way. It’s part of the territory.

But since 2020 it’s climbed to a new-level of in-your-face confrontation, rudeness, and aggression, sometimes leading to violence. Physical attacks on people in all jobs have increased, but health care workers are five times more likely to encounter workplace violence than any other field.

Underpaid, overworked, and a sitting duck for violence. Can you blame people for looking elsewhere?

All of this is coming at a time when a whole generation of nurses is retiring, another generation is starting to reach an age of needing more health care, and nursing schools are short on teaching staff, limiting the number of new people that can be trained. Nursing education, like medical school, isn’t a place to cut corners (neither is care, obviously).

These days we toss the word “burnout” around to the point that it’s become almost meaningless, but to those affected by it, the consequences are quite real. And when it causes a loss of staff and impairs the ability of all to provide quality medical care, it quickly becomes everyone’s problem.

Finding solutions for such things isn’t a can you just kick down the road, as governmental agencies have always been so good at doing. These are things that have real-world consequences for all involved, and solutions need to involve private, public, and educational sectors working together.

I don’t have any ideas, but I hope the people who can change this will sit down and work some out.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Try practicing inpatient medicine without nurses.

You can’t.

In a world where doctors get top billing, nurses are the unsung heroes that really make it all happen. We blow in and out of the rooms, write notes, check results and vitals, then move on to the next person.

But the nurses are the ones who actually make this all happen. And, amazingly, can do all that work with a smile.

But in our current postpandemic world, we’re facing a serious shortage. A recent survey of registered nurses found that only 15% of hospital nurses were planning on being there in 1 year. Thirty percent said they were planning on changing careers entirely in the aftermath of the pandemic. Their job satisfaction scores have dropped 15% from 2019 to 2023. Their stress scores, and concerns that the job is affecting their health, have increased 15%-20%.

The problem reflects a combination of things intersecting at a bad time: Staffing shortages resulting in more patients per nurse, hospital administrators cutting corners on staffing and pay, and the ongoing state of incivility.

The last one is a particularly new issue. Difficult patients and their families are nothing new. We all encounter them, and learn to deal with them in our own way. It’s part of the territory.

But since 2020 it’s climbed to a new-level of in-your-face confrontation, rudeness, and aggression, sometimes leading to violence. Physical attacks on people in all jobs have increased, but health care workers are five times more likely to encounter workplace violence than any other field.

Underpaid, overworked, and a sitting duck for violence. Can you blame people for looking elsewhere?

All of this is coming at a time when a whole generation of nurses is retiring, another generation is starting to reach an age of needing more health care, and nursing schools are short on teaching staff, limiting the number of new people that can be trained. Nursing education, like medical school, isn’t a place to cut corners (neither is care, obviously).

These days we toss the word “burnout” around to the point that it’s become almost meaningless, but to those affected by it, the consequences are quite real. And when it causes a loss of staff and impairs the ability of all to provide quality medical care, it quickly becomes everyone’s problem.

Finding solutions for such things isn’t a can you just kick down the road, as governmental agencies have always been so good at doing. These are things that have real-world consequences for all involved, and solutions need to involve private, public, and educational sectors working together.

I don’t have any ideas, but I hope the people who can change this will sit down and work some out.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I’m Dr F. Perry Wilson of the Yale School of Medicine.

Milestone birthdays are always memorable – those ages when your life seems to fundamentally change somehow. Age 16: A license to drive. Age 18: You can vote to determine your own future and serve in the military. At 21, 3 years after adulthood, you are finally allowed to drink alcohol, for some reason. And then ... nothing much happens. At least until you turn 65 and become eligible for Medicare.

But imagine a future when turning 30 might be the biggest milestone birthday of all. Imagine a future when, at 30, you get your genome sequenced and doctors tell you what needs to be done to save your life.

That future may not be far off, as a new study shows us that screening every single 30-year-old in the United States for three particular genetic conditions may not only save lives but be reasonably cost-effective.

Getting your genome sequenced is a double-edged sword. Of course, there is the potential for substantial benefit; finding certain mutations allows for definitive therapy before it’s too late. That said, there are genetic diseases without a cure and without a treatment. Knowing about that destiny may do more harm than good.

Three conditions are described by the CDC as “Tier 1” conditions, genetic syndromes with a significant impact on life expectancy that also have definitive, effective therapies.

Dr. F. Perry Wilson

Dr. Wilson is an associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator in New Haven, Conn. He disclosed no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I’m Dr F. Perry Wilson of the Yale School of Medicine.

Milestone birthdays are always memorable – those ages when your life seems to fundamentally change somehow. Age 16: A license to drive. Age 18: You can vote to determine your own future and serve in the military. At 21, 3 years after adulthood, you are finally allowed to drink alcohol, for some reason. And then ... nothing much happens. At least until you turn 65 and become eligible for Medicare.

But imagine a future when turning 30 might be the biggest milestone birthday of all. Imagine a future when, at 30, you get your genome sequenced and doctors tell you what needs to be done to save your life.

That future may not be far off, as a new study shows us that screening every single 30-year-old in the United States for three particular genetic conditions may not only save lives but be reasonably cost-effective.

Getting your genome sequenced is a double-edged sword. Of course, there is the potential for substantial benefit; finding certain mutations allows for definitive therapy before it’s too late. That said, there are genetic diseases without a cure and without a treatment. Knowing about that destiny may do more harm than good.

Three conditions are described by the CDC as “Tier 1” conditions, genetic syndromes with a significant impact on life expectancy that also have definitive, effective therapies.

Dr. F. Perry Wilson

Dr. Wilson is an associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator in New Haven, Conn. He disclosed no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I’m Dr F. Perry Wilson of the Yale School of Medicine.

Milestone birthdays are always memorable – those ages when your life seems to fundamentally change somehow. Age 16: A license to drive. Age 18: You can vote to determine your own future and serve in the military. At 21, 3 years after adulthood, you are finally allowed to drink alcohol, for some reason. And then ... nothing much happens. At least until you turn 65 and become eligible for Medicare.

But imagine a future when turning 30 might be the biggest milestone birthday of all. Imagine a future when, at 30, you get your genome sequenced and doctors tell you what needs to be done to save your life.

That future may not be far off, as a new study shows us that screening every single 30-year-old in the United States for three particular genetic conditions may not only save lives but be reasonably cost-effective.

Getting your genome sequenced is a double-edged sword. Of course, there is the potential for substantial benefit; finding certain mutations allows for definitive therapy before it’s too late. That said, there are genetic diseases without a cure and without a treatment. Knowing about that destiny may do more harm than good.

Three conditions are described by the CDC as “Tier 1” conditions, genetic syndromes with a significant impact on life expectancy that also have definitive, effective therapies.

Dr. F. Perry Wilson

Dr. Wilson is an associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator in New Haven, Conn. He disclosed no relevant conflicts of interest.

A version of this article first appeared on Medscape.com.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.

An 85-year-old woman is brought to the emergency department after a syncopal episode. Her caregivers report a similar episode 2 weeks ago, but she recovered so quickly they did not seek evaluation for her.

Medications: Omeprazole 20 mg, pravastatin 40 mg, citalopram 10 mg, albuterol, donepezil 10 mg, isosorbide mononitrate 60 mg, and calcium. On exam, blood pressure is 100/60 mm Hg, pulse 55. ECG indicates bradycardia with normal intervals. What drug most likely caused her syncope?

A. Citalopram

B. Pravastatin

C. Donepezil

D. Isosorbide

E. Calcium

This woman’s syncope is likely caused by donepezil. Citalopram can lengthen the QT interval, especially in elderly patients, but the normal intervals on ECG eliminate this possibility. Donepezil can cause bradycardia, which can contribute to syncope.

Hernandez and colleagues evaluated a cohort of veterans with dementia over an 8-year period.¹ They found that there was a 1.4-fold increased risk of bradycardia in patients with dementia treated with an acetylcholine inhibitor (compared with that in patients who were not taking these medications) and that there was a dose-dependent increase in risk for patients on donepezil.

Park-Wyllie et al. found in a study of 1.4 million older adults a greater than twofold risk of hospitalization for bradycardia in patients treated with a cholinesterase inhibitor.² Gill and colleagues performed a population-based cohort study of 19,803 elderly patients with dementia who were prescribed cholinesterase inhibitors, and compared them to age-matched controls.³ They found increased hospital visits for syncope in people receiving cholinesterase inhibitors (hazard ratio, 1.76; 95% confidence interval, 1.57-1.98). Other syncope-related events were also more common in people receiving cholinesterase inhibitors, compared with controls: hospital visits for bradycardia (HR, 1.69; 95% CI, 1.32-2.15), permanent pacemaker insertion (HR, 1.49; 95% CI, 1.12-2.00), and hip fracture (HR, 1.18; (95% CI, 1.04-1.34).

Nausea, vomiting, and weight loss are much more common than the rarer side effects of bradycardia and syncope. The frequency of gastroenterological side effects is up to 25%. Cholinesterase inhibitors have modest effects on cognitive function with a high number needed to treat (NNT) of 10, and an NNT as high as 100 for global function. The number needed to harm (NNH) is 4, when gastrointestinal symptoms are added in.⁴ Another important, problematic side effect of cholinesterase inhibitors is urinary incontinence. This often leads to patients receiving medications, to combat this side effect, that may worsen cognitive function.

Another commonly used medication that scares me in certain circumstances is trimethoprim-sulfamethoxazole. My main concern is when it is used in patients who are elderly, have chronic kidney disease, or are taking other medications that can cause hyperkalemia (ACEIs, ARBs, potassium-sparing diuretics including spironolactone). Hyperkalemia is a real concern in these patient populations. Trimethoprim reduces renal potassium excretion through the competitive inhibition of sodium channels in the distal nephron, in a manner similar to the potassium-sparing diuretic amiloride. Hospitalizations for hyperkalemia are more common in patients who take ACEIs and ARBs and are prescribed trimethoprim-sulfamethoxazole, compared with other antibiotics.⁵

Sudden cardiac death is also more common in patients who are taking ACEIs or ARBs and receive trimethoprim-sulfamethoxazole.⁶ Trimethoprim-sulfamethoxazole also has a powerful interaction with warfarin, both displacing warfarin from albumin and inhibiting its metabolism. It raises the INR (international normalized ratio) in warfarin-treated patients much greater than do other antibiotics.⁷
 

Pearls

• Think carefully about the use of cholinesterase inhibitors because of the unfavorable NNH vs. NNT.
• Use caution prescribing trimethoprim for patients who are elderly, especially if they are on an ACEI, an ARB, or spironolactone, and in patients with chronic kidney disease.

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at [email protected].

References

1. Hernandez RK et al. J Am Geriatr Soc. 2009;57:1997-2003.

2. Park-Wyllie LY et al. PLoS Med. 2009;6:e1000157.

3. Gill SS et al. Arch Intern Med 2009;169:867-73.

4. Peters KR. J Am Geriatr Soc. 2013 Jul;61(7):1170-4.

5. Antoniou TN et al. Arch Intern Med. 2010;170(12):1045-9.

6. Fralick M et al. BMJ. 2014 Oct 30;349:g6196.

7. Glasheen JJ et al. J Gen Intern Med. 2005 Jul;20(7):653-6.