Opinion

Emergencies happen anywhere, anytime, and sometimes medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

In December 2017, I was a second-year urology resident at Cleveland Clinic. I’d gone to New Delhi to attend my best friend’s wedding. My flight back was New Delhi to Paris to JFK via Air France. I didn’t sleep on the first flight. So, on the second, I wanted to get some rest, because I had to go back to work the next day. I put on a movie and tried to snooze. As the saying goes in residency, you sleep when you can.

About 3 hours later, a flight attendant made an announcement in French, but I didn’t really hear it. Then they announced in English that they needed a physician. I noticed some flight attendants walking frantically around the economy cabin asking, “Is there a doctor on the plane?” Turns out there were two – the woman sitting next to me happened to be a pediatrician with Doctors Without Borders. I volunteered.

The flight attendant told me a woman was having abdominal pain. I thought it would be something straightforward. Usually, medical emergencies on planes involve chest pain or a panic attack or a vasovagal syncopal episode. Well, I was in for a ride that day.

The woman in pain was traveling from Nigeria. She told me about the abdominal pain. Then she lifted her blanket – she was pregnant. She said she was 37 or 38 weeks in. I said, “Okay, if you’re having this significant abdominal pain, then I need to examine you.” So we decided to move her to the first-class cabin, which was empty (I never did ask why – but it was good we had room to work).

Next step, I went back to my seat and asked the pediatrician if she could assist. My plan was to simply get the passenger through the flight, and as soon as we landed, she would go to the hospital.

There was room to lie down in first class. The pediatrician and I examined her, and she appeared fine. She was traveling with her 4-year-old daughter, and the flight attendants were taking care of her. Everything was okay.

The pilot came back and asked if we would need an emergency landing. I asked him how far it was to JFK – 4 hours. He said the closest place to land would be the Azores Islands, which is Portuguese territory, 2 hours away.

The problem: Even if we made it to the Azores, the hospital there was a very basic facility with no obstetric care available. And by the time the ambulance picked her up and got her there, it would still be 2 or 3 hours total. I said, “No, let’s just observe and continue our course.” Inside my head, I was hoping and praying to God that was the right decision.

Within an hour, everything changed.

The woman’s pain got worse, and she started having contractions. Then her water broke.

Things progressed quickly from there. The contractions progressively got worse and worse. The interval between them got smaller and smaller. The next time we examined her, we could see the baby’s head beginning to crown.

At that point, we had to decide – are we going to deliver? We were in the middle of the North Atlantic Ocean. There was nothing around us. We were 35,000 feet in the air, surrounded by blue.

The crew wanted us to sign a Good Samaritan agreement. So, we did that. And then I said, “Okay, let’s just go for it.”

We got the plane’s medical kit. They had IV fluids, so I started an IV. I was able to monitor the woman’s blood pressure. They had the usual drugs for doing ACLS [advanced cardiac life support], running the code, and things like that. But they didn’t have a suturing kit or a laceration kit. They didn’t have a scalpel. There was nothing else.

Honestly, there was a lot of panic going through my head. I started thinking about what could go wrong. I’d done an ob.gyn. rotation in medical school and delivered seven babies before it was over. But a plane – even the first-class cabin – is in no way, shape, or form like a delivery room. I was really scared she would hemorrhage out or something.

So, internally, I was having a meltdown. Sij, you have to keep it together right now, because there’s no one else that’s going to do this. Just give it your best shot. And that’s what I did.

I asked the pilot to go to an altitude that would minimize any turbulence, and we were very lucky that the notorious North Atlantic air wasn’t choppy.

More luck: This was the passenger’s second baby, and I was counting on second deliveries being easier. The pediatrician, the flight attendants, and I came together as a team. Two flight attendants had given birth before, so they held the patient’s hand and guided her to push. I was “downstairs” waiting to catch.

She was in some pain. At this point, usually people get an epidural. I kept thinking about what drugs were safe in pregnancy, but I wasn’t sure. I don’t know if they even had morphine or anything on the plane. We gave her some Tylenol.

It didn’t take long. After about 30 minutes, the baby’s head emerged. I was able to navigate it out, avoiding any shoulder dystocia. There’s a certain technique that you learn in medical school, which thankfully came back to me. I caught it – it was a boy born right there in a first-class seat.

I gave him to the pediatrician, and she did the Apgar score, calculating his breathing and appearance. Then my job was to make sure there were no postpartum complications.

I ended up using a piece of string in the kit to tie around the umbilical cord, and then I cut it with scissors. After that, the woman was able to deliver the placenta. She did have some vaginal bleeding, but that resolved by just holding pressure.

The baby was fine. Mom was doing great. No complications. It was a miracle. I was the right person at the right place at the right time. I just think it was something from God.

The pilot made an announcement, “We’re en route to JFK, and there’s an additional passenger on this plane now.”

When we landed, I had very little time because I had to catch my flight to Cleveland. I didn’t even process what had happened.

A few days later, I got this package from Air France with a very expensive bottle of champagne along with a travel voucher. I heard from the mom by email – she and baby were doing fine.

Eventually, the media relations people at Cleveland Clinic heard about the incident, and it became a story that went viral. That was very weird, because I’m usually someone who’s private. All through my residency, people would introduce me with, “Remember that guy who delivered a baby on a plane? That’s him.”

I’m so thankful for everyone who was on that team. It was very beautiful because it was people from different cultures, backgrounds, and faiths who came together to achieve something so miraculous. The patient was Nigerian. The flight attendants were French. The pediatrician and I were American.

That just shows you the power of teamwork and how humanity can come together. Medicine, surgery – everything, in fact – is a team sport.

Sij Hemal, MD, graduated from urology residency at the Cleveland Clinic and is currently a robotic urologic oncology and minimally invasive surgery fellow at the University of Southern California, Los Angeles.

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

Emergencies happen anywhere, anytime, and sometimes medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

In December 2017, I was a second-year urology resident at Cleveland Clinic. I’d gone to New Delhi to attend my best friend’s wedding. My flight back was New Delhi to Paris to JFK via Air France. I didn’t sleep on the first flight. So, on the second, I wanted to get some rest, because I had to go back to work the next day. I put on a movie and tried to snooze. As the saying goes in residency, you sleep when you can.

About 3 hours later, a flight attendant made an announcement in French, but I didn’t really hear it. Then they announced in English that they needed a physician. I noticed some flight attendants walking frantically around the economy cabin asking, “Is there a doctor on the plane?” Turns out there were two – the woman sitting next to me happened to be a pediatrician with Doctors Without Borders. I volunteered.

The flight attendant told me a woman was having abdominal pain. I thought it would be something straightforward. Usually, medical emergencies on planes involve chest pain or a panic attack or a vasovagal syncopal episode. Well, I was in for a ride that day.

The woman in pain was traveling from Nigeria. She told me about the abdominal pain. Then she lifted her blanket – she was pregnant. She said she was 37 or 38 weeks in. I said, “Okay, if you’re having this significant abdominal pain, then I need to examine you.” So we decided to move her to the first-class cabin, which was empty (I never did ask why – but it was good we had room to work).

Next step, I went back to my seat and asked the pediatrician if she could assist. My plan was to simply get the passenger through the flight, and as soon as we landed, she would go to the hospital.

There was room to lie down in first class. The pediatrician and I examined her, and she appeared fine. She was traveling with her 4-year-old daughter, and the flight attendants were taking care of her. Everything was okay.

The pilot came back and asked if we would need an emergency landing. I asked him how far it was to JFK – 4 hours. He said the closest place to land would be the Azores Islands, which is Portuguese territory, 2 hours away.

The problem: Even if we made it to the Azores, the hospital there was a very basic facility with no obstetric care available. And by the time the ambulance picked her up and got her there, it would still be 2 or 3 hours total. I said, “No, let’s just observe and continue our course.” Inside my head, I was hoping and praying to God that was the right decision.

Within an hour, everything changed.

The woman’s pain got worse, and she started having contractions. Then her water broke.

Things progressed quickly from there. The contractions progressively got worse and worse. The interval between them got smaller and smaller. The next time we examined her, we could see the baby’s head beginning to crown.

At that point, we had to decide – are we going to deliver? We were in the middle of the North Atlantic Ocean. There was nothing around us. We were 35,000 feet in the air, surrounded by blue.

The crew wanted us to sign a Good Samaritan agreement. So, we did that. And then I said, “Okay, let’s just go for it.”

We got the plane’s medical kit. They had IV fluids, so I started an IV. I was able to monitor the woman’s blood pressure. They had the usual drugs for doing ACLS [advanced cardiac life support], running the code, and things like that. But they didn’t have a suturing kit or a laceration kit. They didn’t have a scalpel. There was nothing else.

Honestly, there was a lot of panic going through my head. I started thinking about what could go wrong. I’d done an ob.gyn. rotation in medical school and delivered seven babies before it was over. But a plane – even the first-class cabin – is in no way, shape, or form like a delivery room. I was really scared she would hemorrhage out or something.

So, internally, I was having a meltdown. Sij, you have to keep it together right now, because there’s no one else that’s going to do this. Just give it your best shot. And that’s what I did.

I asked the pilot to go to an altitude that would minimize any turbulence, and we were very lucky that the notorious North Atlantic air wasn’t choppy.

More luck: This was the passenger’s second baby, and I was counting on second deliveries being easier. The pediatrician, the flight attendants, and I came together as a team. Two flight attendants had given birth before, so they held the patient’s hand and guided her to push. I was “downstairs” waiting to catch.

She was in some pain. At this point, usually people get an epidural. I kept thinking about what drugs were safe in pregnancy, but I wasn’t sure. I don’t know if they even had morphine or anything on the plane. We gave her some Tylenol.

It didn’t take long. After about 30 minutes, the baby’s head emerged. I was able to navigate it out, avoiding any shoulder dystocia. There’s a certain technique that you learn in medical school, which thankfully came back to me. I caught it – it was a boy born right there in a first-class seat.

I gave him to the pediatrician, and she did the Apgar score, calculating his breathing and appearance. Then my job was to make sure there were no postpartum complications.

I ended up using a piece of string in the kit to tie around the umbilical cord, and then I cut it with scissors. After that, the woman was able to deliver the placenta. She did have some vaginal bleeding, but that resolved by just holding pressure.

The baby was fine. Mom was doing great. No complications. It was a miracle. I was the right person at the right place at the right time. I just think it was something from God.

The pilot made an announcement, “We’re en route to JFK, and there’s an additional passenger on this plane now.”

When we landed, I had very little time because I had to catch my flight to Cleveland. I didn’t even process what had happened.

A few days later, I got this package from Air France with a very expensive bottle of champagne along with a travel voucher. I heard from the mom by email – she and baby were doing fine.

Eventually, the media relations people at Cleveland Clinic heard about the incident, and it became a story that went viral. That was very weird, because I’m usually someone who’s private. All through my residency, people would introduce me with, “Remember that guy who delivered a baby on a plane? That’s him.”

I’m so thankful for everyone who was on that team. It was very beautiful because it was people from different cultures, backgrounds, and faiths who came together to achieve something so miraculous. The patient was Nigerian. The flight attendants were French. The pediatrician and I were American.

That just shows you the power of teamwork and how humanity can come together. Medicine, surgery – everything, in fact – is a team sport.

Sij Hemal, MD, graduated from urology residency at the Cleveland Clinic and is currently a robotic urologic oncology and minimally invasive surgery fellow at the University of Southern California, Los Angeles.

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

Emergencies happen anywhere, anytime, and sometimes medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series telling these stories.

In December 2017, I was a second-year urology resident at Cleveland Clinic. I’d gone to New Delhi to attend my best friend’s wedding. My flight back was New Delhi to Paris to JFK via Air France. I didn’t sleep on the first flight. So, on the second, I wanted to get some rest, because I had to go back to work the next day. I put on a movie and tried to snooze. As the saying goes in residency, you sleep when you can.

About 3 hours later, a flight attendant made an announcement in French, but I didn’t really hear it. Then they announced in English that they needed a physician. I noticed some flight attendants walking frantically around the economy cabin asking, “Is there a doctor on the plane?” Turns out there were two – the woman sitting next to me happened to be a pediatrician with Doctors Without Borders. I volunteered.

The flight attendant told me a woman was having abdominal pain. I thought it would be something straightforward. Usually, medical emergencies on planes involve chest pain or a panic attack or a vasovagal syncopal episode. Well, I was in for a ride that day.

The woman in pain was traveling from Nigeria. She told me about the abdominal pain. Then she lifted her blanket – she was pregnant. She said she was 37 or 38 weeks in. I said, “Okay, if you’re having this significant abdominal pain, then I need to examine you.” So we decided to move her to the first-class cabin, which was empty (I never did ask why – but it was good we had room to work).

Next step, I went back to my seat and asked the pediatrician if she could assist. My plan was to simply get the passenger through the flight, and as soon as we landed, she would go to the hospital.

There was room to lie down in first class. The pediatrician and I examined her, and she appeared fine. She was traveling with her 4-year-old daughter, and the flight attendants were taking care of her. Everything was okay.

The pilot came back and asked if we would need an emergency landing. I asked him how far it was to JFK – 4 hours. He said the closest place to land would be the Azores Islands, which is Portuguese territory, 2 hours away.

The problem: Even if we made it to the Azores, the hospital there was a very basic facility with no obstetric care available. And by the time the ambulance picked her up and got her there, it would still be 2 or 3 hours total. I said, “No, let’s just observe and continue our course.” Inside my head, I was hoping and praying to God that was the right decision.

Within an hour, everything changed.

The woman’s pain got worse, and she started having contractions. Then her water broke.

Things progressed quickly from there. The contractions progressively got worse and worse. The interval between them got smaller and smaller. The next time we examined her, we could see the baby’s head beginning to crown.

At that point, we had to decide – are we going to deliver? We were in the middle of the North Atlantic Ocean. There was nothing around us. We were 35,000 feet in the air, surrounded by blue.

The crew wanted us to sign a Good Samaritan agreement. So, we did that. And then I said, “Okay, let’s just go for it.”

We got the plane’s medical kit. They had IV fluids, so I started an IV. I was able to monitor the woman’s blood pressure. They had the usual drugs for doing ACLS [advanced cardiac life support], running the code, and things like that. But they didn’t have a suturing kit or a laceration kit. They didn’t have a scalpel. There was nothing else.

Honestly, there was a lot of panic going through my head. I started thinking about what could go wrong. I’d done an ob.gyn. rotation in medical school and delivered seven babies before it was over. But a plane – even the first-class cabin – is in no way, shape, or form like a delivery room. I was really scared she would hemorrhage out or something.

So, internally, I was having a meltdown. Sij, you have to keep it together right now, because there’s no one else that’s going to do this. Just give it your best shot. And that’s what I did.

I asked the pilot to go to an altitude that would minimize any turbulence, and we were very lucky that the notorious North Atlantic air wasn’t choppy.

More luck: This was the passenger’s second baby, and I was counting on second deliveries being easier. The pediatrician, the flight attendants, and I came together as a team. Two flight attendants had given birth before, so they held the patient’s hand and guided her to push. I was “downstairs” waiting to catch.

She was in some pain. At this point, usually people get an epidural. I kept thinking about what drugs were safe in pregnancy, but I wasn’t sure. I don’t know if they even had morphine or anything on the plane. We gave her some Tylenol.

It didn’t take long. After about 30 minutes, the baby’s head emerged. I was able to navigate it out, avoiding any shoulder dystocia. There’s a certain technique that you learn in medical school, which thankfully came back to me. I caught it – it was a boy born right there in a first-class seat.

I gave him to the pediatrician, and she did the Apgar score, calculating his breathing and appearance. Then my job was to make sure there were no postpartum complications.

I ended up using a piece of string in the kit to tie around the umbilical cord, and then I cut it with scissors. After that, the woman was able to deliver the placenta. She did have some vaginal bleeding, but that resolved by just holding pressure.

The baby was fine. Mom was doing great. No complications. It was a miracle. I was the right person at the right place at the right time. I just think it was something from God.

The pilot made an announcement, “We’re en route to JFK, and there’s an additional passenger on this plane now.”

When we landed, I had very little time because I had to catch my flight to Cleveland. I didn’t even process what had happened.

A few days later, I got this package from Air France with a very expensive bottle of champagne along with a travel voucher. I heard from the mom by email – she and baby were doing fine.

Eventually, the media relations people at Cleveland Clinic heard about the incident, and it became a story that went viral. That was very weird, because I’m usually someone who’s private. All through my residency, people would introduce me with, “Remember that guy who delivered a baby on a plane? That’s him.”

I’m so thankful for everyone who was on that team. It was very beautiful because it was people from different cultures, backgrounds, and faiths who came together to achieve something so miraculous. The patient was Nigerian. The flight attendants were French. The pediatrician and I were American.

That just shows you the power of teamwork and how humanity can come together. Medicine, surgery – everything, in fact – is a team sport.

Sij Hemal, MD, graduated from urology residency at the Cleveland Clinic and is currently a robotic urologic oncology and minimally invasive surgery fellow at the University of Southern California, Los Angeles.

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

This transcript has been edited for clarity.

Matthew F. Watto, MD: Welcome back to The Curbsiders. On tonight’s episode, we are going to be talking about back pain. This is based on an interview, Back Pain Update with Dr. Austin Baraki. He gave us some great pearls about how to manage back pain, which we see so much of in primary care. I’ll use one of my famous teaching techniques: If the patient has any kind of back pain, they should just not move. Right?

Paul N. Williams, MD: That’s right, Matt – we should recommend bedrest until they get better for anyone who has any back pain? No. For back pain, early activity and exercise are great. Patients are often concerned that physical therapy will make their pain worse, so they don’t exercise. This misunderstanding is not surprising. They believe that if they are experiencing pain, it’s facilitating more damage, which is not necessarily the case. It will get better, and a little bit of anticipatory guidance goes a long way in terms of managing patient expectations related to early mobilization, early exercise, and physical therapy.

Dr. Watto: Absolutely. One of the goals of treatment is symptom relief to the extent that we’re able to achieve. We’re not expecting the pain to go to zero. That just doesn’t happen, especially if someone’s on a medication long term. Another goal is return to function. We want them sleeping. We want them to be able to tolerate movement.

We have medications – NSAIDs and muscle relaxants, which are actually tranquilizers. But most therapy for back pain doesn’t involve medications. It involves active movement, so we have to find movement that the patient enjoys doing. Passive treatments, things being done to patients, just don’t work as well.
 

Dr. Williams: We should be clear – we’re talking primarily about chronic back pain here. For acute back pain, we actually have some decent medications, but acute back pain tends to improve no matter what you do. We don’t have much to offer pharmacologically for chronic low back pain. The best modalities usually involve physical activity of some kind.

Dr. Watto: Let’s discuss the evaluation of back pain. Something that always comes up: Should we order imaging, and is there a right time to get it? Dr. Baraki was very clear about when to do imaging. Two big buckets of patients might need imaging.

First, a patient who has a serious underlying condition and you’re using imaging to try to diagnose it; or in a chronic setting, a patient who needs surgery, and imaging is part of the presurgical evaluation. We talked about red flags.

The red flags are major trauma, where we have reason to believe there might be something going on – if we strongly suspect infection, or the patient is injecting drugs. If the patient has a history of cancer, we would be worried that they might have a recurrence. Those are some of the main red flags. With a patient who has osteoporosis or is on chronic steroids, you might even be able to get by with plain films instead of an MRI to look for fracture.

The other thing I wanted to ask you about is, when should we get imaging? Are there any pitfalls we need to worry about?
 

Dr. Williams: I always like podcasts I’m not on because I enjoy listening to them much more. Dr. Baraki talked about the very specific language that is used in radiology reports, such as spondylitis, spondylolysis, and multilevel degenerative disease. They sound bad, but if they are just reframed as age-related degenerative changes, that sounds so much more benign. When discussing with patients, we should avoid medical jargon and say that we saw some changes that we would expect for someone of your age. That sounds so much better than saying we saw multilevel degenerative disease, which sounds like an alarming pathology if you’re not a physician. Without being inaccurate, we should frame the discussion such that we aren’t providing a very specific diagnosis, because that is rarely the case with chronic low back pain. Typically, many things are going on and you may never identify a single unifying diagnosis, which doesn’t tend to help anyway.

Dr. Watto: There’s evidence showing that if the radiology report uses clinical terminology that both clinician and patient think of as less serious, they are less likely to proceed to more invasive treatments. Calling an episode of back pain a “lumbar strain” helps the patient understand that this is a pretty common thing. Almost everyone is going to have an episode of back pain at some point in their life, and almost all of them will get better. Most of the time there’s no serious underlying condition.

This was a great discussion with Dr. Baraki. Click on Back Pain Update with Dr Austin Baraki to hear the full discussion. Until next time, I’ve been Dr. Matthew Frank Watto.
 

Dr. Williams: And I’m Dr. Paul Nelson Williams.

Dr. Watto is Clinical Assistant Professor, Department of Medicine, University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, Temple University, Philadelphia. Neither reported any conflicts of interest.

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

This transcript has been edited for clarity.

Matthew F. Watto, MD: Welcome back to The Curbsiders. On tonight’s episode, we are going to be talking about back pain. This is based on an interview, Back Pain Update with Dr. Austin Baraki. He gave us some great pearls about how to manage back pain, which we see so much of in primary care. I’ll use one of my famous teaching techniques: If the patient has any kind of back pain, they should just not move. Right?

Paul N. Williams, MD: That’s right, Matt – we should recommend bedrest until they get better for anyone who has any back pain? No. For back pain, early activity and exercise are great. Patients are often concerned that physical therapy will make their pain worse, so they don’t exercise. This misunderstanding is not surprising. They believe that if they are experiencing pain, it’s facilitating more damage, which is not necessarily the case. It will get better, and a little bit of anticipatory guidance goes a long way in terms of managing patient expectations related to early mobilization, early exercise, and physical therapy.

Dr. Watto: Absolutely. One of the goals of treatment is symptom relief to the extent that we’re able to achieve. We’re not expecting the pain to go to zero. That just doesn’t happen, especially if someone’s on a medication long term. Another goal is return to function. We want them sleeping. We want them to be able to tolerate movement.

We have medications – NSAIDs and muscle relaxants, which are actually tranquilizers. But most therapy for back pain doesn’t involve medications. It involves active movement, so we have to find movement that the patient enjoys doing. Passive treatments, things being done to patients, just don’t work as well.
 

Dr. Williams: We should be clear – we’re talking primarily about chronic back pain here. For acute back pain, we actually have some decent medications, but acute back pain tends to improve no matter what you do. We don’t have much to offer pharmacologically for chronic low back pain. The best modalities usually involve physical activity of some kind.

Dr. Watto: Let’s discuss the evaluation of back pain. Something that always comes up: Should we order imaging, and is there a right time to get it? Dr. Baraki was very clear about when to do imaging. Two big buckets of patients might need imaging.

First, a patient who has a serious underlying condition and you’re using imaging to try to diagnose it; or in a chronic setting, a patient who needs surgery, and imaging is part of the presurgical evaluation. We talked about red flags.

The red flags are major trauma, where we have reason to believe there might be something going on – if we strongly suspect infection, or the patient is injecting drugs. If the patient has a history of cancer, we would be worried that they might have a recurrence. Those are some of the main red flags. With a patient who has osteoporosis or is on chronic steroids, you might even be able to get by with plain films instead of an MRI to look for fracture.

The other thing I wanted to ask you about is, when should we get imaging? Are there any pitfalls we need to worry about?
 

Dr. Williams: I always like podcasts I’m not on because I enjoy listening to them much more. Dr. Baraki talked about the very specific language that is used in radiology reports, such as spondylitis, spondylolysis, and multilevel degenerative disease. They sound bad, but if they are just reframed as age-related degenerative changes, that sounds so much more benign. When discussing with patients, we should avoid medical jargon and say that we saw some changes that we would expect for someone of your age. That sounds so much better than saying we saw multilevel degenerative disease, which sounds like an alarming pathology if you’re not a physician. Without being inaccurate, we should frame the discussion such that we aren’t providing a very specific diagnosis, because that is rarely the case with chronic low back pain. Typically, many things are going on and you may never identify a single unifying diagnosis, which doesn’t tend to help anyway.

Dr. Watto: There’s evidence showing that if the radiology report uses clinical terminology that both clinician and patient think of as less serious, they are less likely to proceed to more invasive treatments. Calling an episode of back pain a “lumbar strain” helps the patient understand that this is a pretty common thing. Almost everyone is going to have an episode of back pain at some point in their life, and almost all of them will get better. Most of the time there’s no serious underlying condition.

This was a great discussion with Dr. Baraki. Click on Back Pain Update with Dr Austin Baraki to hear the full discussion. Until next time, I’ve been Dr. Matthew Frank Watto.
 

Dr. Williams: And I’m Dr. Paul Nelson Williams.

Dr. Watto is Clinical Assistant Professor, Department of Medicine, University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, Temple University, Philadelphia. Neither reported any conflicts of interest.

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

This transcript has been edited for clarity.

Matthew F. Watto, MD: Welcome back to The Curbsiders. On tonight’s episode, we are going to be talking about back pain. This is based on an interview, Back Pain Update with Dr. Austin Baraki. He gave us some great pearls about how to manage back pain, which we see so much of in primary care. I’ll use one of my famous teaching techniques: If the patient has any kind of back pain, they should just not move. Right?

Paul N. Williams, MD: That’s right, Matt – we should recommend bedrest until they get better for anyone who has any back pain? No. For back pain, early activity and exercise are great. Patients are often concerned that physical therapy will make their pain worse, so they don’t exercise. This misunderstanding is not surprising. They believe that if they are experiencing pain, it’s facilitating more damage, which is not necessarily the case. It will get better, and a little bit of anticipatory guidance goes a long way in terms of managing patient expectations related to early mobilization, early exercise, and physical therapy.

Dr. Watto: Absolutely. One of the goals of treatment is symptom relief to the extent that we’re able to achieve. We’re not expecting the pain to go to zero. That just doesn’t happen, especially if someone’s on a medication long term. Another goal is return to function. We want them sleeping. We want them to be able to tolerate movement.

We have medications – NSAIDs and muscle relaxants, which are actually tranquilizers. But most therapy for back pain doesn’t involve medications. It involves active movement, so we have to find movement that the patient enjoys doing. Passive treatments, things being done to patients, just don’t work as well.
 

Dr. Williams: We should be clear – we’re talking primarily about chronic back pain here. For acute back pain, we actually have some decent medications, but acute back pain tends to improve no matter what you do. We don’t have much to offer pharmacologically for chronic low back pain. The best modalities usually involve physical activity of some kind.

Dr. Watto: Let’s discuss the evaluation of back pain. Something that always comes up: Should we order imaging, and is there a right time to get it? Dr. Baraki was very clear about when to do imaging. Two big buckets of patients might need imaging.

First, a patient who has a serious underlying condition and you’re using imaging to try to diagnose it; or in a chronic setting, a patient who needs surgery, and imaging is part of the presurgical evaluation. We talked about red flags.

The red flags are major trauma, where we have reason to believe there might be something going on – if we strongly suspect infection, or the patient is injecting drugs. If the patient has a history of cancer, we would be worried that they might have a recurrence. Those are some of the main red flags. With a patient who has osteoporosis or is on chronic steroids, you might even be able to get by with plain films instead of an MRI to look for fracture.

The other thing I wanted to ask you about is, when should we get imaging? Are there any pitfalls we need to worry about?
 

Dr. Williams: I always like podcasts I’m not on because I enjoy listening to them much more. Dr. Baraki talked about the very specific language that is used in radiology reports, such as spondylitis, spondylolysis, and multilevel degenerative disease. They sound bad, but if they are just reframed as age-related degenerative changes, that sounds so much more benign. When discussing with patients, we should avoid medical jargon and say that we saw some changes that we would expect for someone of your age. That sounds so much better than saying we saw multilevel degenerative disease, which sounds like an alarming pathology if you’re not a physician. Without being inaccurate, we should frame the discussion such that we aren’t providing a very specific diagnosis, because that is rarely the case with chronic low back pain. Typically, many things are going on and you may never identify a single unifying diagnosis, which doesn’t tend to help anyway.

Dr. Watto: There’s evidence showing that if the radiology report uses clinical terminology that both clinician and patient think of as less serious, they are less likely to proceed to more invasive treatments. Calling an episode of back pain a “lumbar strain” helps the patient understand that this is a pretty common thing. Almost everyone is going to have an episode of back pain at some point in their life, and almost all of them will get better. Most of the time there’s no serious underlying condition.

This was a great discussion with Dr. Baraki. Click on Back Pain Update with Dr Austin Baraki to hear the full discussion. Until next time, I’ve been Dr. Matthew Frank Watto.
 

Dr. Williams: And I’m Dr. Paul Nelson Williams.

Dr. Watto is Clinical Assistant Professor, Department of Medicine, University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, Temple University, Philadelphia. Neither reported any conflicts of interest.

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

This transcript has been edited for clarity.

I’m David Kerr, professor of cancer medicine at the University of Oxford. I’d like to talk to you today about something specific and generic around guidelines.

Annals of Oncology, my old journal, has just published an outstanding set of guidelines delivered by the ESMO (European Society for Medical Oncology) guidelines group. It’s around the management of toxicities from immunotherapy, and it’s the ESMO Clinical Practice Guideline for diagnosis, treatment, and follow-up, delivered by Dr. Haanen and, of course, a number of colleagues on behalf of the wider committee.

Have a look at it. I’m not going to talk about the details of it. It’s very well written. It’s very clear and evidence based, of course. There are many helpful hints and a very clear blueprint as to how we should better manage the myriad of potential side effects from immunotherapy.

It tells us a little about the basis of the science, some of the mechanistic work that’s going on in allowing us to understand why some people react in such different ways, almost as if the immune systems are primed to overreact. It gives a very helpful, stepwise look at how we best diagnose, manage, and, in the longer term, follow up patients who have problems with these very important drugs.

All of us recognize the extraordinary impact they’ve made across a wide range of different tumor types, and therefore, as practicing oncologists and health care professionals in the field, all of us need to understand better the details as to how we better care for our patients on these drugs.

Have a look at it. It’s well written and useful, and I think it’s a document that I’ll turn to when I’m looking for a refresher or advice in the future.

The generic focus is about guidelines. Many years ago, I was one of the architects of the British National Cancer Plan, and for me, there were four simple principles at that stage in our development of how we would improve the delivery of cancer control in the United Kingdom. It was around site specialization, particularly of our surgical colleagues who embraced this with vigor. God bless them.

It was using guidelines to help level up the quality of treatment that we were giving, of course underpinned by research, and using – one would hope – modern IT and telecommunications to improve the networking that we use to deliver multidisciplinary cancer care, one of the key elements. Guidelines were embedded in that.

A couple of years ago, we did a survey of cancer physicians around the world. Almost 30 different countries were represented, and we asked which guidelines were most used. It was a very interesting set of responses. The three dominant guidelines – this will surprise no one – are the NCCN (National Comprehensive Cancer Network) guidelines, the ESMO guidelines, and the ASCO (American Society of Clinical Oncology) guidelines.

Rather than selecting one and one being completely dominant, what seemed to be the case is that our colleagues around the world dipped in and used all three. They may prefer NCCN for some particular tumor type or some particular aspect of how they’re structured, but at the same time, we would dip into the ESMO guidelines for specific bits of help, as well as the ASCO guidelines.

I find this fascinating. I assume that in different regions, depending on how they were affiliated in terms of additional training or links to Europe or links to the United States, that one or other of these guideline groups would predominate, but no. In each country, in each region, given the large data bank that we have of guidelines now, it’s a sort of pick-and-mix situation.

I was initially surprised but then took comfort from it. There’s nothing I hate more than the wasted energy of reduplication and saying, well come on, if there is one guideline set that does truly command the attention of the world, then the other should stop. It’s wasted energy, which is something that none of us can afford.

The fact that each of these trusted, evidence-based, beautifully presented guidelines is used in different ways was important. A message to the guideline groups from me is: “Thank you for your professionalism, for the hard work of hundreds of cancer specialists from all different specialties, and for their contribution to developing these guidelines.”

It’s worth it, it’s working, people are using them, and they’re making a difference. It’s all about leveling up the quality of cancer care that we deliver.

Specifically, have a look at the ESMO immune guidelines. They are great. I hope you find them helpful. Generically, thanks to all of you who are contributing and working so hard to make these data available to improve the quality of cancer care around the world.

Thanks for listening, as always. I’m interested in any comments that you might have, but for the time being, Medscapers, ahoy.

David J. Kerr, CBE, MD, DSc, is a professor of cancer medicine at the University of Oxford. He reported conflicts of interest with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, and Merck Serono.

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

This transcript has been edited for clarity.

I’m David Kerr, professor of cancer medicine at the University of Oxford. I’d like to talk to you today about something specific and generic around guidelines.

Annals of Oncology, my old journal, has just published an outstanding set of guidelines delivered by the ESMO (European Society for Medical Oncology) guidelines group. It’s around the management of toxicities from immunotherapy, and it’s the ESMO Clinical Practice Guideline for diagnosis, treatment, and follow-up, delivered by Dr. Haanen and, of course, a number of colleagues on behalf of the wider committee.

Have a look at it. I’m not going to talk about the details of it. It’s very well written. It’s very clear and evidence based, of course. There are many helpful hints and a very clear blueprint as to how we should better manage the myriad of potential side effects from immunotherapy.

It tells us a little about the basis of the science, some of the mechanistic work that’s going on in allowing us to understand why some people react in such different ways, almost as if the immune systems are primed to overreact. It gives a very helpful, stepwise look at how we best diagnose, manage, and, in the longer term, follow up patients who have problems with these very important drugs.

All of us recognize the extraordinary impact they’ve made across a wide range of different tumor types, and therefore, as practicing oncologists and health care professionals in the field, all of us need to understand better the details as to how we better care for our patients on these drugs.

Have a look at it. It’s well written and useful, and I think it’s a document that I’ll turn to when I’m looking for a refresher or advice in the future.

The generic focus is about guidelines. Many years ago, I was one of the architects of the British National Cancer Plan, and for me, there were four simple principles at that stage in our development of how we would improve the delivery of cancer control in the United Kingdom. It was around site specialization, particularly of our surgical colleagues who embraced this with vigor. God bless them.

It was using guidelines to help level up the quality of treatment that we were giving, of course underpinned by research, and using – one would hope – modern IT and telecommunications to improve the networking that we use to deliver multidisciplinary cancer care, one of the key elements. Guidelines were embedded in that.

A couple of years ago, we did a survey of cancer physicians around the world. Almost 30 different countries were represented, and we asked which guidelines were most used. It was a very interesting set of responses. The three dominant guidelines – this will surprise no one – are the NCCN (National Comprehensive Cancer Network) guidelines, the ESMO guidelines, and the ASCO (American Society of Clinical Oncology) guidelines.

Rather than selecting one and one being completely dominant, what seemed to be the case is that our colleagues around the world dipped in and used all three. They may prefer NCCN for some particular tumor type or some particular aspect of how they’re structured, but at the same time, we would dip into the ESMO guidelines for specific bits of help, as well as the ASCO guidelines.

I find this fascinating. I assume that in different regions, depending on how they were affiliated in terms of additional training or links to Europe or links to the United States, that one or other of these guideline groups would predominate, but no. In each country, in each region, given the large data bank that we have of guidelines now, it’s a sort of pick-and-mix situation.

I was initially surprised but then took comfort from it. There’s nothing I hate more than the wasted energy of reduplication and saying, well come on, if there is one guideline set that does truly command the attention of the world, then the other should stop. It’s wasted energy, which is something that none of us can afford.

The fact that each of these trusted, evidence-based, beautifully presented guidelines is used in different ways was important. A message to the guideline groups from me is: “Thank you for your professionalism, for the hard work of hundreds of cancer specialists from all different specialties, and for their contribution to developing these guidelines.”

It’s worth it, it’s working, people are using them, and they’re making a difference. It’s all about leveling up the quality of cancer care that we deliver.

Specifically, have a look at the ESMO immune guidelines. They are great. I hope you find them helpful. Generically, thanks to all of you who are contributing and working so hard to make these data available to improve the quality of cancer care around the world.

Thanks for listening, as always. I’m interested in any comments that you might have, but for the time being, Medscapers, ahoy.

David J. Kerr, CBE, MD, DSc, is a professor of cancer medicine at the University of Oxford. He reported conflicts of interest with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, and Merck Serono.

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

This transcript has been edited for clarity.

I’m David Kerr, professor of cancer medicine at the University of Oxford. I’d like to talk to you today about something specific and generic around guidelines.

Annals of Oncology, my old journal, has just published an outstanding set of guidelines delivered by the ESMO (European Society for Medical Oncology) guidelines group. It’s around the management of toxicities from immunotherapy, and it’s the ESMO Clinical Practice Guideline for diagnosis, treatment, and follow-up, delivered by Dr. Haanen and, of course, a number of colleagues on behalf of the wider committee.

Have a look at it. I’m not going to talk about the details of it. It’s very well written. It’s very clear and evidence based, of course. There are many helpful hints and a very clear blueprint as to how we should better manage the myriad of potential side effects from immunotherapy.

It tells us a little about the basis of the science, some of the mechanistic work that’s going on in allowing us to understand why some people react in such different ways, almost as if the immune systems are primed to overreact. It gives a very helpful, stepwise look at how we best diagnose, manage, and, in the longer term, follow up patients who have problems with these very important drugs.

All of us recognize the extraordinary impact they’ve made across a wide range of different tumor types, and therefore, as practicing oncologists and health care professionals in the field, all of us need to understand better the details as to how we better care for our patients on these drugs.

Have a look at it. It’s well written and useful, and I think it’s a document that I’ll turn to when I’m looking for a refresher or advice in the future.

The generic focus is about guidelines. Many years ago, I was one of the architects of the British National Cancer Plan, and for me, there were four simple principles at that stage in our development of how we would improve the delivery of cancer control in the United Kingdom. It was around site specialization, particularly of our surgical colleagues who embraced this with vigor. God bless them.

It was using guidelines to help level up the quality of treatment that we were giving, of course underpinned by research, and using – one would hope – modern IT and telecommunications to improve the networking that we use to deliver multidisciplinary cancer care, one of the key elements. Guidelines were embedded in that.

A couple of years ago, we did a survey of cancer physicians around the world. Almost 30 different countries were represented, and we asked which guidelines were most used. It was a very interesting set of responses. The three dominant guidelines – this will surprise no one – are the NCCN (National Comprehensive Cancer Network) guidelines, the ESMO guidelines, and the ASCO (American Society of Clinical Oncology) guidelines.

Rather than selecting one and one being completely dominant, what seemed to be the case is that our colleagues around the world dipped in and used all three. They may prefer NCCN for some particular tumor type or some particular aspect of how they’re structured, but at the same time, we would dip into the ESMO guidelines for specific bits of help, as well as the ASCO guidelines.

I find this fascinating. I assume that in different regions, depending on how they were affiliated in terms of additional training or links to Europe or links to the United States, that one or other of these guideline groups would predominate, but no. In each country, in each region, given the large data bank that we have of guidelines now, it’s a sort of pick-and-mix situation.

I was initially surprised but then took comfort from it. There’s nothing I hate more than the wasted energy of reduplication and saying, well come on, if there is one guideline set that does truly command the attention of the world, then the other should stop. It’s wasted energy, which is something that none of us can afford.

The fact that each of these trusted, evidence-based, beautifully presented guidelines is used in different ways was important. A message to the guideline groups from me is: “Thank you for your professionalism, for the hard work of hundreds of cancer specialists from all different specialties, and for their contribution to developing these guidelines.”

It’s worth it, it’s working, people are using them, and they’re making a difference. It’s all about leveling up the quality of cancer care that we deliver.

Specifically, have a look at the ESMO immune guidelines. They are great. I hope you find them helpful. Generically, thanks to all of you who are contributing and working so hard to make these data available to improve the quality of cancer care around the world.

Thanks for listening, as always. I’m interested in any comments that you might have, but for the time being, Medscapers, ahoy.

David J. Kerr, CBE, MD, DSc, is a professor of cancer medicine at the University of Oxford. He reported conflicts of interest with Celleron Therapeutics, Oxford Cancer Biomarkers, Afrox, GlaxoSmithKline, Bayer, Genomic Health, and Merck Serono.

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

Dear colleagues,

We continue our theme of highlighting innovations in gastroenterology by exploring how endoscopy continues to blur the lines with surgery. In this issue of Perspectives, Dr. RJ Sealock, assistant professor of medicine at the Baylor College of Medicine, and Dr. Thiru Muniraj, associate professor of medicine at the Yale School of Medicine share their experiences performing minimally invasive alternatives to surgery, discussing both sides of gastrointestinal perforations – treating and creating. Dr. Sealock describes how we can “MacGyver” traditional surgical wound vacs to treat Boerhaave's, while Dr. Muniraj shows how lumen-apposing metal stents allow us to treat acute cholecystitis in poor surgical candidates. 

Gyanprakash A. Ketwaroo, MD, MSc, is associate professor of medicine, Yale University, New Haven, Conn., and chief of endoscopy at West Haven (Conn.) VA Medical Center. He is an associate editor for GI & Hepatology News.
 

Endoscopic vacuum therapy for GI perforation

BY ROBERT JAY SEALOCK, MD

Gastrointestinal endoscopy has evolved from a diagnostic modality into a therapeutic tool used to treat a wide variety of luminal pathology. Endoscopic closure of full thickness injuries is a field that has rapidly expanded because of advanced endoscopic tissue resection and the need for subsequent defect closure as well as technological advances in closure devices such an endoscopic suturing platforms and large over-the-scope clips.

Prior to the advent of closure devices, endoscopic means of treating full thickness defects included through-the-scope (TTS) clips and fully covered metal stents. Given the small size, TTS clips are useful for mucosal closure but are limited in their ability to achieve full thickness closure. Fully covered metal stents utilized particularly for upper GI tract perforations and leaks are intended to divert gastrointestinal content away from the site of injury, thereby allowing secondary intention healing. Stents have several limitations, including frequent downstream migration and an inability to create a “watertight” seal in minimizing wound contamination. For decades, our surgical colleagues have utilized negative pressure wound therapy or vacuum therapy to expedite large wound closure. Given their familiarity with the technique, surgeons began adapting vacuum therapy for the treatment of postsurgical anastomotic leaks and fistulas particularly within the rectum.¹ Eventually, the same technique was applied to the treatment of upper GI tract anastomotic leaks.² Endoscopic vacuum therapy (EVT) overcomes many of the limitations of traditional endoscopic closure or diversion using covered stents through the use of suction to promote granulation tissue and aspirate infected wound contents.³

The approach to full thickness luminal injury must be individualized, but for a majority of indications EVT can be considered as a first-line approach. In our own experience, EVT closure can be achieved in more than 80% of patients with a variety of injuries such as iatrogenic endoscopic perforations (e.g., esophageal perforation during Savary dilation), surgical defects (sleeve gastrectomy leaks), and spontaneous perforations (e.g., Boerhaave syndrome). The initial step is endoscopic assessment of the luminal injury as well as the extraluminal cavity. In some situations, it is necessary to manually clean the defect cavity of necrotic material and food.

Once the cavity is cleaned and the size of the defect is assessed, the EVT device is manufactured at the bedside using commonly available materials and tools. A wound vacuum polyurethane sponge is affixed to a nasogastric tube, trimmed to the desired shape and size, and placed either within the defect cavity or within the GI lumen next to the defect opening.⁴ The EVT device is exchanged at an interval of 3-5 days, which allows the promotion of granulation tissue and subsequent downsizing as the cavity shrinks. In our series, an average number of five exchanges was necessary to achieve closure, with an average time to closure of 25 days.

Most experts would recommend initially placing the EVT device within the defect cavity. Once the cavity size can no longer accommodate the device, complete closure is achieved via intraluminal placement. The use of constant negative pressure (typically 150 mm to 175 mm Hg) prevents migration or dislodgement of the device.

For those who use EVT, there is some satisfaction from assembling and tailoring your own device, much like the protagonist in the 1980s television series “MacGyver,” who would manufacture devices out of readily available materials to address difficult and life-threatening situations. This need for self-assembly also has fostered ingenuity and creativity in the field, which can be found in social media and peer-reviewed sources.⁵ For some, however, the need to assemble your own device may be a deterrent. There is certainly an opportunity for commercialization and innovation, thereby putting Food and Drug Administration–approved devices into the hands of endoscopists. EVT is also a time- and labor-intensive therapy without specific reimbursement codes. Despite these limitations we continue to use and advocate for EVT given its clinical success in a population of patients with complex luminal injuries.


Dr. Sealock is assistant professor of medicine, department of gastroenterology and hepatology, Baylor College of Medicine, Houston. He receives research funding from AbbVie and is a consultant to ConMed and Ambu.
 

References

1. Weidenhagen R et al. Endoscopic vacuum-assisted closure of anastomotic leakage following anterior resection of the rectum: A new method. Surg Endosc Other Interv Tech. 2008;22(8):1818-25. doi: 10.1007/s00464-007-9706-x.

2. Wedemeyer J et al. Endoscopic vacuum-assisted closure of upper intestinal anastomotic leaks. Gastrointest Endosc. 2008;67(4):708-11. doi: 10.1016/j.gie.2007.10.064.

3. Mennigen R et al. Comparison of endoscopic vacuum therapy versus stent for anastomotic leak after esophagectomy. J Gastrointest Surg. 2015;19(7):1229-35.

4. Abdulsada M et al. Endoluminal vacuum therapy of esophageal perforations. VideoGIE. 2020;5(1):8-10. doi: 10.1016/j.vgie.2019.10.004

5. de Moura DTH et al. Cost-effective modified endoscopic vacuum therapy for the treatment of gastrointestinal transmural defects: Step-by-step process of manufacturing and its advantages. VideoGIE. 2021 Sep 4;6(12):523-8. doi: 10.1016/j.vgie.2021.08.002.

LAMS for gallbladder drainage

BY THIRU MUNIRAJ, MD, PHD, FACG, FRCP

Surgical cholecystectomy is the gold standard of treatment for acute cholecystitis (AC).¹ The morbidity and mortality rates remain high in high-risk surgical patients, such as those with cirrhosis, coagulopathy, advanced malignancy, severe cardiopulmonary conditions, or poor performance status. Percutaneous gallbladder drainage (PT-GBD) typically has been performed as an alternative in these cases. Endoscopic ultrasound-guided gallbladder drainage (EUS-GBD) is rapidly becoming a preferred alternative treatment to surgery in the case of AC at expert centers.

Since Baron and Topazian introduced EUS-GBD using a double pigtail stent in 2007, the procedure has evolved with the introduction of dedicated newly developed short, bi-flanged, covered lumen-apposing metal stents (LAMS) that have revolutionized this procedure as a single-step technique with excellent efficacy and safety outcomes. Although EUS-GBD is widely adopted among endosonographers, several skilled ERCP [endoscopic retrograde cholangiopancreatography] endoscopists still perform endoscopic transpapillary gallbladder drainage (ET-GBD) with ERCP as an alternative for high-risk surgical patients with AC. However, three-way comparative studies and randomized trials between PT-GBD, ETGBD, and EUS-GBD have clearly shown that EUS-GBD with LAMS is the most effective and safer alternative with the lowest rate of recurrent cholecystitis.^2,3 The recent Tokyo Guidelines 2018 now suggest EUS-GBD as one of the viable options for AC treatment.⁴

In my institution, we offer EUS-GBD for nonsurgical candidates with AC with and without gallstones. In addition to its excellent benefits on quality of life through avoidance of an external percutaneous drain, EUS-GBD offers the ability to remove gallstones endoscopically using irrigation, suction, basket, and direct electrohydraulic lithotripsy. Moreover, EUS-GBD allows direct visualization and mucosal evaluation of the gallbladder when dysplasia or malignancy is suspected. The other indications where I perform EUS-GBD drainage are conversion of PT-GBD to EUS-GBD and as a backdoor alternate to failed ERCP where the cystic duct is patent and EUS-bile duct drainage is not amenable. In nonoperative malignant biliary stricture patients with indwelling metal biliary stents covering the cystic duct, I have a low threshold to perform a prophylactic EUS-GBD if the gallbladder is distended.

I perform EUS-GBD procedures under propofol intravenous anesthesia with the patient in the left lateral position on the fluoroscopy table. I choose the site to create the fistula for EUS-GBD either in the duodenal bulb or gastric antrum, whichever seems safer and easier to deploy the LAMS stent without torquing the endoscope much. In case of inadvertent complications such as stent maldeployment, the gastric site is often very forgiving. My preferred stent for EUS-GBD is 10 mm x 10 mm LAMS with hot cautery, as this seems to be the ideal size. We can choose a 10 mm x 15 mm stent if a larger stone removal is expected. I never choose smaller LAMS stents (6 mm and 8 mm), as the saddle length is not enough to bridge the thickened gallbladder wall and the thick gastric antral wall. In patients with calculous cholecystitis, I prefer to place a 7Fr 4cm pigtail plastic stent within the lumen of LAMS to ensure patency, especially if it is a gastric site, as food occlusion is more common. Unlike with pseudocyst drainage, these LAMS for EUS-GBD can be left indefinitely without removal. I avoid EUS-GBD in patients who have large-volume ascites or are too sick to tolerate anesthesia. Although a subsequent cholecystectomy post EUS-GBD is doable, I have a clear discussion with the surgeon before choosing this approach over ERCP ET-GBD in case future surgery is still an option. This is more important in patients who are awaiting liver transplantation.

The first step in establishing a program for EUS-GBD is to establish strong collaboration with your surgeons. In our institution, once our surgeons determine that patients with AC are high risk for surgery, they initiate a multidisciplinary discussion and reach out to advanced endoscopists at the same time or before consulting interventional radiology. The key to establishing a successful EUS-GBD program is to get “buy-in” from the surgeons and create a “signature” pathway for AC in your own institution.

EUS-GBD to drain the gallbladder in nonsurgical patients is one of my favorite procedures. Until the currently available LAMS secures an on-label indication for AC, we must wait and watch to see if there are enough advanced endoscopists ready to take over the challenge of all nonsurgical cholecystitis gallbladders – especially during late-night calls – rather than requesting PT-GBD. Soon, EUS-GBD will consign PT-GBD to centers without access to advanced endoscopists who perform EUS-guided interventions and limit ERCP transpapillary ET-GBD to patients with coagulopathy or large ascites.

Dr. Muniraj is associate professor of medicine, Yale School of Medicine, New Haven, Conn., and a consultant to Boston Scientific.
 

References

1. Endo I et al. Optimal treatment strategy for acute cholecystitis based on predictive factors: Japan-Taiwan multicenter cohort study. J Hepatobiliary Pancreat Sci. 2017. 24(6):346-61.

2. Siddiqui A et al. Three-way comparative study of endoscopic ultrasound-guided transmural gallbladder drainage using lumen-apposing metal stents versus endoscopic transpapillary drainage versus percutaneous cholecystostomy for gallbladder drainage in high-risk surgical patients with acute cholecystitis: clinical outcomes and success in an international, multicenter study. Surg Endosc. 2019;33(4):1260-70.

3. Teoh AYB et al. Endosonography-guided gallbladder drainage versus percutaneous cholecystostomy in very high-risk surgical patients with acute cholecystitis: An international randomised multicentre controlled superiority trial (DRAC 1). Gut. 2020;69(6):1085-91.

4. Mori Y et al. Tokyo Guidelines 2018: Management strategies for gallbladder drainage in patients with acute cholecystitis (with videos). J Hepatobiliary Pancreat Sci. 2018;25(1):87-95.

Dear colleagues,

We continue our theme of highlighting innovations in gastroenterology by exploring how endoscopy continues to blur the lines with surgery. In this issue of Perspectives, Dr. RJ Sealock, assistant professor of medicine at the Baylor College of Medicine, and Dr. Thiru Muniraj, associate professor of medicine at the Yale School of Medicine share their experiences performing minimally invasive alternatives to surgery, discussing both sides of gastrointestinal perforations – treating and creating. Dr. Sealock describes how we can “MacGyver” traditional surgical wound vacs to treat Boerhaave's, while Dr. Muniraj shows how lumen-apposing metal stents allow us to treat acute cholecystitis in poor surgical candidates. 

Gyanprakash A. Ketwaroo, MD, MSc, is associate professor of medicine, Yale University, New Haven, Conn., and chief of endoscopy at West Haven (Conn.) VA Medical Center. He is an associate editor for GI & Hepatology News.
 

Endoscopic vacuum therapy for GI perforation

BY ROBERT JAY SEALOCK, MD

Gastrointestinal endoscopy has evolved from a diagnostic modality into a therapeutic tool used to treat a wide variety of luminal pathology. Endoscopic closure of full thickness injuries is a field that has rapidly expanded because of advanced endoscopic tissue resection and the need for subsequent defect closure as well as technological advances in closure devices such an endoscopic suturing platforms and large over-the-scope clips.

Prior to the advent of closure devices, endoscopic means of treating full thickness defects included through-the-scope (TTS) clips and fully covered metal stents. Given the small size, TTS clips are useful for mucosal closure but are limited in their ability to achieve full thickness closure. Fully covered metal stents utilized particularly for upper GI tract perforations and leaks are intended to divert gastrointestinal content away from the site of injury, thereby allowing secondary intention healing. Stents have several limitations, including frequent downstream migration and an inability to create a “watertight” seal in minimizing wound contamination. For decades, our surgical colleagues have utilized negative pressure wound therapy or vacuum therapy to expedite large wound closure. Given their familiarity with the technique, surgeons began adapting vacuum therapy for the treatment of postsurgical anastomotic leaks and fistulas particularly within the rectum.¹ Eventually, the same technique was applied to the treatment of upper GI tract anastomotic leaks.² Endoscopic vacuum therapy (EVT) overcomes many of the limitations of traditional endoscopic closure or diversion using covered stents through the use of suction to promote granulation tissue and aspirate infected wound contents.³

The approach to full thickness luminal injury must be individualized, but for a majority of indications EVT can be considered as a first-line approach. In our own experience, EVT closure can be achieved in more than 80% of patients with a variety of injuries such as iatrogenic endoscopic perforations (e.g., esophageal perforation during Savary dilation), surgical defects (sleeve gastrectomy leaks), and spontaneous perforations (e.g., Boerhaave syndrome). The initial step is endoscopic assessment of the luminal injury as well as the extraluminal cavity. In some situations, it is necessary to manually clean the defect cavity of necrotic material and food.

Once the cavity is cleaned and the size of the defect is assessed, the EVT device is manufactured at the bedside using commonly available materials and tools. A wound vacuum polyurethane sponge is affixed to a nasogastric tube, trimmed to the desired shape and size, and placed either within the defect cavity or within the GI lumen next to the defect opening.⁴ The EVT device is exchanged at an interval of 3-5 days, which allows the promotion of granulation tissue and subsequent downsizing as the cavity shrinks. In our series, an average number of five exchanges was necessary to achieve closure, with an average time to closure of 25 days.

Most experts would recommend initially placing the EVT device within the defect cavity. Once the cavity size can no longer accommodate the device, complete closure is achieved via intraluminal placement. The use of constant negative pressure (typically 150 mm to 175 mm Hg) prevents migration or dislodgement of the device.

For those who use EVT, there is some satisfaction from assembling and tailoring your own device, much like the protagonist in the 1980s television series “MacGyver,” who would manufacture devices out of readily available materials to address difficult and life-threatening situations. This need for self-assembly also has fostered ingenuity and creativity in the field, which can be found in social media and peer-reviewed sources.⁵ For some, however, the need to assemble your own device may be a deterrent. There is certainly an opportunity for commercialization and innovation, thereby putting Food and Drug Administration–approved devices into the hands of endoscopists. EVT is also a time- and labor-intensive therapy without specific reimbursement codes. Despite these limitations we continue to use and advocate for EVT given its clinical success in a population of patients with complex luminal injuries.


Dr. Sealock is assistant professor of medicine, department of gastroenterology and hepatology, Baylor College of Medicine, Houston. He receives research funding from AbbVie and is a consultant to ConMed and Ambu.
 

References

1. Weidenhagen R et al. Endoscopic vacuum-assisted closure of anastomotic leakage following anterior resection of the rectum: A new method. Surg Endosc Other Interv Tech. 2008;22(8):1818-25. doi: 10.1007/s00464-007-9706-x.

2. Wedemeyer J et al. Endoscopic vacuum-assisted closure of upper intestinal anastomotic leaks. Gastrointest Endosc. 2008;67(4):708-11. doi: 10.1016/j.gie.2007.10.064.

3. Mennigen R et al. Comparison of endoscopic vacuum therapy versus stent for anastomotic leak after esophagectomy. J Gastrointest Surg. 2015;19(7):1229-35.

4. Abdulsada M et al. Endoluminal vacuum therapy of esophageal perforations. VideoGIE. 2020;5(1):8-10. doi: 10.1016/j.vgie.2019.10.004

5. de Moura DTH et al. Cost-effective modified endoscopic vacuum therapy for the treatment of gastrointestinal transmural defects: Step-by-step process of manufacturing and its advantages. VideoGIE. 2021 Sep 4;6(12):523-8. doi: 10.1016/j.vgie.2021.08.002.

LAMS for gallbladder drainage

BY THIRU MUNIRAJ, MD, PHD, FACG, FRCP

Surgical cholecystectomy is the gold standard of treatment for acute cholecystitis (AC).¹ The morbidity and mortality rates remain high in high-risk surgical patients, such as those with cirrhosis, coagulopathy, advanced malignancy, severe cardiopulmonary conditions, or poor performance status. Percutaneous gallbladder drainage (PT-GBD) typically has been performed as an alternative in these cases. Endoscopic ultrasound-guided gallbladder drainage (EUS-GBD) is rapidly becoming a preferred alternative treatment to surgery in the case of AC at expert centers.

Since Baron and Topazian introduced EUS-GBD using a double pigtail stent in 2007, the procedure has evolved with the introduction of dedicated newly developed short, bi-flanged, covered lumen-apposing metal stents (LAMS) that have revolutionized this procedure as a single-step technique with excellent efficacy and safety outcomes. Although EUS-GBD is widely adopted among endosonographers, several skilled ERCP [endoscopic retrograde cholangiopancreatography] endoscopists still perform endoscopic transpapillary gallbladder drainage (ET-GBD) with ERCP as an alternative for high-risk surgical patients with AC. However, three-way comparative studies and randomized trials between PT-GBD, ETGBD, and EUS-GBD have clearly shown that EUS-GBD with LAMS is the most effective and safer alternative with the lowest rate of recurrent cholecystitis.^2,3 The recent Tokyo Guidelines 2018 now suggest EUS-GBD as one of the viable options for AC treatment.⁴

In my institution, we offer EUS-GBD for nonsurgical candidates with AC with and without gallstones. In addition to its excellent benefits on quality of life through avoidance of an external percutaneous drain, EUS-GBD offers the ability to remove gallstones endoscopically using irrigation, suction, basket, and direct electrohydraulic lithotripsy. Moreover, EUS-GBD allows direct visualization and mucosal evaluation of the gallbladder when dysplasia or malignancy is suspected. The other indications where I perform EUS-GBD drainage are conversion of PT-GBD to EUS-GBD and as a backdoor alternate to failed ERCP where the cystic duct is patent and EUS-bile duct drainage is not amenable. In nonoperative malignant biliary stricture patients with indwelling metal biliary stents covering the cystic duct, I have a low threshold to perform a prophylactic EUS-GBD if the gallbladder is distended.

I perform EUS-GBD procedures under propofol intravenous anesthesia with the patient in the left lateral position on the fluoroscopy table. I choose the site to create the fistula for EUS-GBD either in the duodenal bulb or gastric antrum, whichever seems safer and easier to deploy the LAMS stent without torquing the endoscope much. In case of inadvertent complications such as stent maldeployment, the gastric site is often very forgiving. My preferred stent for EUS-GBD is 10 mm x 10 mm LAMS with hot cautery, as this seems to be the ideal size. We can choose a 10 mm x 15 mm stent if a larger stone removal is expected. I never choose smaller LAMS stents (6 mm and 8 mm), as the saddle length is not enough to bridge the thickened gallbladder wall and the thick gastric antral wall. In patients with calculous cholecystitis, I prefer to place a 7Fr 4cm pigtail plastic stent within the lumen of LAMS to ensure patency, especially if it is a gastric site, as food occlusion is more common. Unlike with pseudocyst drainage, these LAMS for EUS-GBD can be left indefinitely without removal. I avoid EUS-GBD in patients who have large-volume ascites or are too sick to tolerate anesthesia. Although a subsequent cholecystectomy post EUS-GBD is doable, I have a clear discussion with the surgeon before choosing this approach over ERCP ET-GBD in case future surgery is still an option. This is more important in patients who are awaiting liver transplantation.

The first step in establishing a program for EUS-GBD is to establish strong collaboration with your surgeons. In our institution, once our surgeons determine that patients with AC are high risk for surgery, they initiate a multidisciplinary discussion and reach out to advanced endoscopists at the same time or before consulting interventional radiology. The key to establishing a successful EUS-GBD program is to get “buy-in” from the surgeons and create a “signature” pathway for AC in your own institution.

EUS-GBD to drain the gallbladder in nonsurgical patients is one of my favorite procedures. Until the currently available LAMS secures an on-label indication for AC, we must wait and watch to see if there are enough advanced endoscopists ready to take over the challenge of all nonsurgical cholecystitis gallbladders – especially during late-night calls – rather than requesting PT-GBD. Soon, EUS-GBD will consign PT-GBD to centers without access to advanced endoscopists who perform EUS-guided interventions and limit ERCP transpapillary ET-GBD to patients with coagulopathy or large ascites.

Dr. Muniraj is associate professor of medicine, Yale School of Medicine, New Haven, Conn., and a consultant to Boston Scientific.
 

References

1. Endo I et al. Optimal treatment strategy for acute cholecystitis based on predictive factors: Japan-Taiwan multicenter cohort study. J Hepatobiliary Pancreat Sci. 2017. 24(6):346-61.

2. Siddiqui A et al. Three-way comparative study of endoscopic ultrasound-guided transmural gallbladder drainage using lumen-apposing metal stents versus endoscopic transpapillary drainage versus percutaneous cholecystostomy for gallbladder drainage in high-risk surgical patients with acute cholecystitis: clinical outcomes and success in an international, multicenter study. Surg Endosc. 2019;33(4):1260-70.

3. Teoh AYB et al. Endosonography-guided gallbladder drainage versus percutaneous cholecystostomy in very high-risk surgical patients with acute cholecystitis: An international randomised multicentre controlled superiority trial (DRAC 1). Gut. 2020;69(6):1085-91.

4. Mori Y et al. Tokyo Guidelines 2018: Management strategies for gallbladder drainage in patients with acute cholecystitis (with videos). J Hepatobiliary Pancreat Sci. 2018;25(1):87-95.

Dear colleagues,

We continue our theme of highlighting innovations in gastroenterology by exploring how endoscopy continues to blur the lines with surgery. In this issue of Perspectives, Dr. RJ Sealock, assistant professor of medicine at the Baylor College of Medicine, and Dr. Thiru Muniraj, associate professor of medicine at the Yale School of Medicine share their experiences performing minimally invasive alternatives to surgery, discussing both sides of gastrointestinal perforations – treating and creating. Dr. Sealock describes how we can “MacGyver” traditional surgical wound vacs to treat Boerhaave's, while Dr. Muniraj shows how lumen-apposing metal stents allow us to treat acute cholecystitis in poor surgical candidates. 

Gyanprakash A. Ketwaroo, MD, MSc, is associate professor of medicine, Yale University, New Haven, Conn., and chief of endoscopy at West Haven (Conn.) VA Medical Center. He is an associate editor for GI & Hepatology News.
 

Endoscopic vacuum therapy for GI perforation

BY ROBERT JAY SEALOCK, MD

Gastrointestinal endoscopy has evolved from a diagnostic modality into a therapeutic tool used to treat a wide variety of luminal pathology. Endoscopic closure of full thickness injuries is a field that has rapidly expanded because of advanced endoscopic tissue resection and the need for subsequent defect closure as well as technological advances in closure devices such an endoscopic suturing platforms and large over-the-scope clips.

Prior to the advent of closure devices, endoscopic means of treating full thickness defects included through-the-scope (TTS) clips and fully covered metal stents. Given the small size, TTS clips are useful for mucosal closure but are limited in their ability to achieve full thickness closure. Fully covered metal stents utilized particularly for upper GI tract perforations and leaks are intended to divert gastrointestinal content away from the site of injury, thereby allowing secondary intention healing. Stents have several limitations, including frequent downstream migration and an inability to create a “watertight” seal in minimizing wound contamination. For decades, our surgical colleagues have utilized negative pressure wound therapy or vacuum therapy to expedite large wound closure. Given their familiarity with the technique, surgeons began adapting vacuum therapy for the treatment of postsurgical anastomotic leaks and fistulas particularly within the rectum.¹ Eventually, the same technique was applied to the treatment of upper GI tract anastomotic leaks.² Endoscopic vacuum therapy (EVT) overcomes many of the limitations of traditional endoscopic closure or diversion using covered stents through the use of suction to promote granulation tissue and aspirate infected wound contents.³

The approach to full thickness luminal injury must be individualized, but for a majority of indications EVT can be considered as a first-line approach. In our own experience, EVT closure can be achieved in more than 80% of patients with a variety of injuries such as iatrogenic endoscopic perforations (e.g., esophageal perforation during Savary dilation), surgical defects (sleeve gastrectomy leaks), and spontaneous perforations (e.g., Boerhaave syndrome). The initial step is endoscopic assessment of the luminal injury as well as the extraluminal cavity. In some situations, it is necessary to manually clean the defect cavity of necrotic material and food.

Once the cavity is cleaned and the size of the defect is assessed, the EVT device is manufactured at the bedside using commonly available materials and tools. A wound vacuum polyurethane sponge is affixed to a nasogastric tube, trimmed to the desired shape and size, and placed either within the defect cavity or within the GI lumen next to the defect opening.⁴ The EVT device is exchanged at an interval of 3-5 days, which allows the promotion of granulation tissue and subsequent downsizing as the cavity shrinks. In our series, an average number of five exchanges was necessary to achieve closure, with an average time to closure of 25 days.

Most experts would recommend initially placing the EVT device within the defect cavity. Once the cavity size can no longer accommodate the device, complete closure is achieved via intraluminal placement. The use of constant negative pressure (typically 150 mm to 175 mm Hg) prevents migration or dislodgement of the device.

For those who use EVT, there is some satisfaction from assembling and tailoring your own device, much like the protagonist in the 1980s television series “MacGyver,” who would manufacture devices out of readily available materials to address difficult and life-threatening situations. This need for self-assembly also has fostered ingenuity and creativity in the field, which can be found in social media and peer-reviewed sources.⁵ For some, however, the need to assemble your own device may be a deterrent. There is certainly an opportunity for commercialization and innovation, thereby putting Food and Drug Administration–approved devices into the hands of endoscopists. EVT is also a time- and labor-intensive therapy without specific reimbursement codes. Despite these limitations we continue to use and advocate for EVT given its clinical success in a population of patients with complex luminal injuries.


Dr. Sealock is assistant professor of medicine, department of gastroenterology and hepatology, Baylor College of Medicine, Houston. He receives research funding from AbbVie and is a consultant to ConMed and Ambu.
 

References

1. Weidenhagen R et al. Endoscopic vacuum-assisted closure of anastomotic leakage following anterior resection of the rectum: A new method. Surg Endosc Other Interv Tech. 2008;22(8):1818-25. doi: 10.1007/s00464-007-9706-x.

2. Wedemeyer J et al. Endoscopic vacuum-assisted closure of upper intestinal anastomotic leaks. Gastrointest Endosc. 2008;67(4):708-11. doi: 10.1016/j.gie.2007.10.064.

3. Mennigen R et al. Comparison of endoscopic vacuum therapy versus stent for anastomotic leak after esophagectomy. J Gastrointest Surg. 2015;19(7):1229-35.

4. Abdulsada M et al. Endoluminal vacuum therapy of esophageal perforations. VideoGIE. 2020;5(1):8-10. doi: 10.1016/j.vgie.2019.10.004

5. de Moura DTH et al. Cost-effective modified endoscopic vacuum therapy for the treatment of gastrointestinal transmural defects: Step-by-step process of manufacturing and its advantages. VideoGIE. 2021 Sep 4;6(12):523-8. doi: 10.1016/j.vgie.2021.08.002.

LAMS for gallbladder drainage

BY THIRU MUNIRAJ, MD, PHD, FACG, FRCP

Surgical cholecystectomy is the gold standard of treatment for acute cholecystitis (AC).¹ The morbidity and mortality rates remain high in high-risk surgical patients, such as those with cirrhosis, coagulopathy, advanced malignancy, severe cardiopulmonary conditions, or poor performance status. Percutaneous gallbladder drainage (PT-GBD) typically has been performed as an alternative in these cases. Endoscopic ultrasound-guided gallbladder drainage (EUS-GBD) is rapidly becoming a preferred alternative treatment to surgery in the case of AC at expert centers.

Since Baron and Topazian introduced EUS-GBD using a double pigtail stent in 2007, the procedure has evolved with the introduction of dedicated newly developed short, bi-flanged, covered lumen-apposing metal stents (LAMS) that have revolutionized this procedure as a single-step technique with excellent efficacy and safety outcomes. Although EUS-GBD is widely adopted among endosonographers, several skilled ERCP [endoscopic retrograde cholangiopancreatography] endoscopists still perform endoscopic transpapillary gallbladder drainage (ET-GBD) with ERCP as an alternative for high-risk surgical patients with AC. However, three-way comparative studies and randomized trials between PT-GBD, ETGBD, and EUS-GBD have clearly shown that EUS-GBD with LAMS is the most effective and safer alternative with the lowest rate of recurrent cholecystitis.^2,3 The recent Tokyo Guidelines 2018 now suggest EUS-GBD as one of the viable options for AC treatment.⁴

In my institution, we offer EUS-GBD for nonsurgical candidates with AC with and without gallstones. In addition to its excellent benefits on quality of life through avoidance of an external percutaneous drain, EUS-GBD offers the ability to remove gallstones endoscopically using irrigation, suction, basket, and direct electrohydraulic lithotripsy. Moreover, EUS-GBD allows direct visualization and mucosal evaluation of the gallbladder when dysplasia or malignancy is suspected. The other indications where I perform EUS-GBD drainage are conversion of PT-GBD to EUS-GBD and as a backdoor alternate to failed ERCP where the cystic duct is patent and EUS-bile duct drainage is not amenable. In nonoperative malignant biliary stricture patients with indwelling metal biliary stents covering the cystic duct, I have a low threshold to perform a prophylactic EUS-GBD if the gallbladder is distended.

I perform EUS-GBD procedures under propofol intravenous anesthesia with the patient in the left lateral position on the fluoroscopy table. I choose the site to create the fistula for EUS-GBD either in the duodenal bulb or gastric antrum, whichever seems safer and easier to deploy the LAMS stent without torquing the endoscope much. In case of inadvertent complications such as stent maldeployment, the gastric site is often very forgiving. My preferred stent for EUS-GBD is 10 mm x 10 mm LAMS with hot cautery, as this seems to be the ideal size. We can choose a 10 mm x 15 mm stent if a larger stone removal is expected. I never choose smaller LAMS stents (6 mm and 8 mm), as the saddle length is not enough to bridge the thickened gallbladder wall and the thick gastric antral wall. In patients with calculous cholecystitis, I prefer to place a 7Fr 4cm pigtail plastic stent within the lumen of LAMS to ensure patency, especially if it is a gastric site, as food occlusion is more common. Unlike with pseudocyst drainage, these LAMS for EUS-GBD can be left indefinitely without removal. I avoid EUS-GBD in patients who have large-volume ascites or are too sick to tolerate anesthesia. Although a subsequent cholecystectomy post EUS-GBD is doable, I have a clear discussion with the surgeon before choosing this approach over ERCP ET-GBD in case future surgery is still an option. This is more important in patients who are awaiting liver transplantation.

The first step in establishing a program for EUS-GBD is to establish strong collaboration with your surgeons. In our institution, once our surgeons determine that patients with AC are high risk for surgery, they initiate a multidisciplinary discussion and reach out to advanced endoscopists at the same time or before consulting interventional radiology. The key to establishing a successful EUS-GBD program is to get “buy-in” from the surgeons and create a “signature” pathway for AC in your own institution.

EUS-GBD to drain the gallbladder in nonsurgical patients is one of my favorite procedures. Until the currently available LAMS secures an on-label indication for AC, we must wait and watch to see if there are enough advanced endoscopists ready to take over the challenge of all nonsurgical cholecystitis gallbladders – especially during late-night calls – rather than requesting PT-GBD. Soon, EUS-GBD will consign PT-GBD to centers without access to advanced endoscopists who perform EUS-guided interventions and limit ERCP transpapillary ET-GBD to patients with coagulopathy or large ascites.

Dr. Muniraj is associate professor of medicine, Yale School of Medicine, New Haven, Conn., and a consultant to Boston Scientific.
 

References

1. Endo I et al. Optimal treatment strategy for acute cholecystitis based on predictive factors: Japan-Taiwan multicenter cohort study. J Hepatobiliary Pancreat Sci. 2017. 24(6):346-61.

2. Siddiqui A et al. Three-way comparative study of endoscopic ultrasound-guided transmural gallbladder drainage using lumen-apposing metal stents versus endoscopic transpapillary drainage versus percutaneous cholecystostomy for gallbladder drainage in high-risk surgical patients with acute cholecystitis: clinical outcomes and success in an international, multicenter study. Surg Endosc. 2019;33(4):1260-70.

3. Teoh AYB et al. Endosonography-guided gallbladder drainage versus percutaneous cholecystostomy in very high-risk surgical patients with acute cholecystitis: An international randomised multicentre controlled superiority trial (DRAC 1). Gut. 2020;69(6):1085-91.

4. Mori Y et al. Tokyo Guidelines 2018: Management strategies for gallbladder drainage in patients with acute cholecystitis (with videos). J Hepatobiliary Pancreat Sci. 2018;25(1):87-95.

Each March, we celebrate National Colorectal Cancer Awareness Month to raise awareness of this common, deadly, and preventable form of cancer and advocate for increased screening uptake and investment in related research. Enhancing awareness is particularly important for those estimated 20 million average-risk individuals between the ages of 45 and 49 who became newly eligible for screening under the revised 2021 U.S. Preventive Services Task Force CRC screening guidelines, given alarming increases in early-onset CRC incidence. But as we know, awareness of CRC and screening eligibility alone is not enough to improve outcomes without addressing the many other patient, provider, and system-level barriers to screening uptake. Indeed, even before health care delivery disruptions related to the COVID-19 pandemic, CRC screening was underutilized, and inequities in screening uptake and downstream outcomes existed.

While there is not space here for a full discussion of these important topics, I refer you to our Gastroenterology Data Trends 2022 supplement (https://cdn.mdedge.com/files/s3fs-public/aga_data_trends_2022_web.pdf), which includes two excellent articles by Dr. Rachel Issaka of the University of Washington (“The Impact of COVID-19 on Colorectal Cancer Screening Programs”) and Dr. Aasma Shaukat of NYU (“Early Onset Colorectal Cancer: Trends in Incidence and Screening”).

In our March issue, we highlight the AGA’s decade-long advocacy efforts to close the “colonoscopy loophole” and reduce financial barriers to colorectal cancer screening. From AGA’s flagship journals, we report on the first Delphi-based consensus recommendations on early-onset colorectal cancer and highlight a study out of Italy comparing two computer-aided optical diagnosis systems for detection of small, leave-in-situ colon polyps. In our March Member Spotlight, we introduce you to gastroenterologist Christina Tennyson, MD, who shares the rewards and challenges of practicing gastroenterology in a rural area and explains how she incorporates “lifestyle medicine” into her clinical practice. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column on endoscopic innovation in management of GI perforation and acute cholecystitis.

We hope you enjoy these stories and all the exciting content featured in our March issue!

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Each March, we celebrate National Colorectal Cancer Awareness Month to raise awareness of this common, deadly, and preventable form of cancer and advocate for increased screening uptake and investment in related research. Enhancing awareness is particularly important for those estimated 20 million average-risk individuals between the ages of 45 and 49 who became newly eligible for screening under the revised 2021 U.S. Preventive Services Task Force CRC screening guidelines, given alarming increases in early-onset CRC incidence. But as we know, awareness of CRC and screening eligibility alone is not enough to improve outcomes without addressing the many other patient, provider, and system-level barriers to screening uptake. Indeed, even before health care delivery disruptions related to the COVID-19 pandemic, CRC screening was underutilized, and inequities in screening uptake and downstream outcomes existed.

While there is not space here for a full discussion of these important topics, I refer you to our Gastroenterology Data Trends 2022 supplement (https://cdn.mdedge.com/files/s3fs-public/aga_data_trends_2022_web.pdf), which includes two excellent articles by Dr. Rachel Issaka of the University of Washington (“The Impact of COVID-19 on Colorectal Cancer Screening Programs”) and Dr. Aasma Shaukat of NYU (“Early Onset Colorectal Cancer: Trends in Incidence and Screening”).

In our March issue, we highlight the AGA’s decade-long advocacy efforts to close the “colonoscopy loophole” and reduce financial barriers to colorectal cancer screening. From AGA’s flagship journals, we report on the first Delphi-based consensus recommendations on early-onset colorectal cancer and highlight a study out of Italy comparing two computer-aided optical diagnosis systems for detection of small, leave-in-situ colon polyps. In our March Member Spotlight, we introduce you to gastroenterologist Christina Tennyson, MD, who shares the rewards and challenges of practicing gastroenterology in a rural area and explains how she incorporates “lifestyle medicine” into her clinical practice. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column on endoscopic innovation in management of GI perforation and acute cholecystitis.

We hope you enjoy these stories and all the exciting content featured in our March issue!

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Each March, we celebrate National Colorectal Cancer Awareness Month to raise awareness of this common, deadly, and preventable form of cancer and advocate for increased screening uptake and investment in related research. Enhancing awareness is particularly important for those estimated 20 million average-risk individuals between the ages of 45 and 49 who became newly eligible for screening under the revised 2021 U.S. Preventive Services Task Force CRC screening guidelines, given alarming increases in early-onset CRC incidence. But as we know, awareness of CRC and screening eligibility alone is not enough to improve outcomes without addressing the many other patient, provider, and system-level barriers to screening uptake. Indeed, even before health care delivery disruptions related to the COVID-19 pandemic, CRC screening was underutilized, and inequities in screening uptake and downstream outcomes existed.

While there is not space here for a full discussion of these important topics, I refer you to our Gastroenterology Data Trends 2022 supplement (https://cdn.mdedge.com/files/s3fs-public/aga_data_trends_2022_web.pdf), which includes two excellent articles by Dr. Rachel Issaka of the University of Washington (“The Impact of COVID-19 on Colorectal Cancer Screening Programs”) and Dr. Aasma Shaukat of NYU (“Early Onset Colorectal Cancer: Trends in Incidence and Screening”).

In our March issue, we highlight the AGA’s decade-long advocacy efforts to close the “colonoscopy loophole” and reduce financial barriers to colorectal cancer screening. From AGA’s flagship journals, we report on the first Delphi-based consensus recommendations on early-onset colorectal cancer and highlight a study out of Italy comparing two computer-aided optical diagnosis systems for detection of small, leave-in-situ colon polyps. In our March Member Spotlight, we introduce you to gastroenterologist Christina Tennyson, MD, who shares the rewards and challenges of practicing gastroenterology in a rural area and explains how she incorporates “lifestyle medicine” into her clinical practice. Finally, GIHN Associate Editor Dr. Avi Ketwaroo introduces our quarterly Perspectives column on endoscopic innovation in management of GI perforation and acute cholecystitis.

We hope you enjoy these stories and all the exciting content featured in our March issue!

Megan A. Adams, MD, JD, MSc

Editor-in-Chief

Introduction: The preoperative evaluation for endometriosis – more than meets the eye

It is well known that it often takes 6-10 years for endometriosis to be diagnosed in patients who have the disease, depending on where the patient lives. I certainly am not surprised. During my residency at Parkland Memorial Hospital, if a patient had chronic pelvic pain and no fibroids, her diagnosis was usually pelvic inflammatory disease. Later, during my fellowship in reproductive endocrinology at the University of Pennsylvania, the diagnosis became endometriosis.

As I gained more interest and expertise in the treatment of endometriosis, I became aware of several articles concluding that if a woman sought treatment for chronic pelvic pain with an internist, the diagnosis would be irritable bowel syndrome (IBS); with a urologist, it would be interstitial cystitis; and with a gynecologist, endometriosis. Moreover, there is an increased propensity for IBS and IC in patients with endometriosis. There also is an increased risk of small intestine bacterial overgrowth (SIBO), as noted by our guest author for this latest installment of the Master Class in Gynecologic Surgery, Iris Orbuch, MD.

Like our guest author, I have also noted increased risk of pelvic floor myalgia. Dr. Orbuch clearly outlines why this occurs. In fact, we can now understand why many patients have multiple pelvic pain–inducing issues compounding their pain secondary to endometriosis and leading to remodeling of the central nervous system. Therefore, it certainly makes sense to follow Dr. Orbuch’s recommendation for a multidisciplinary pre- and postsurgical approach “to downregulate the pain generators.”

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in the treatment of patients diagnosed with endometriosis. Dr. Orbuch serves on the Board of Directors of the Foundation of the American Association of Gynecologic Laparoscopists and has served as the chair of the AAGL’s Special Interest Group on Endometriosis and Reproductive Surgery. She is the coauthor of the book “Beating Endo – How to Reclaim Your Life From Endometriosis” (New York: HarperCollins; 2019). The book is written for patients but addresses many issues discussed in this installment of the Master Class in Gynecologic Surgery.

Dr. Miller, MD, FACOG, is professor of obstetrics and gynecology, department of clinical sciences, Rosalind Franklin University of Medicine and Science, North Chicago. He has no conflicts of interest to report.

For optimal surgical outcomes, and to help our patients recover from years of this inflammatory, systemic disease, we must treat our patients holistically and work to downregulate their pain as much as possible before excision surgery. I work with patients a few months prior to surgery, often for 4-5 months, during which time they not only see me for informative follow-ups, but also pelvic floor physical therapists, gastroenterologists, mental health professionals, integrative nutritionists, and physiatrists or pain specialists, depending on their needs.¹

By identifying coexisting conditions in an initial consult and employing a presurgical multidisciplinary approach to downregulate the pain generators, my patients recover well from excision surgery, with greater and faster relief from pain, compared with those using standard approaches, and with little to no use of opioids.

At a minimum, given the unfortunate time constraints and productivity demands of working within health systems – and considering that surgeries are often scheduled a couple of months out – the surgeon could ensure that patients are engaged in at least 6-8 weeks of pelvic floor physical therapy before surgery to sufficiently lengthen the pelvic muscles and loosen surrounding fascia.

Short, tight pelvic floor muscles are almost universal in patients with delayed diagnosis of endometriosis and are significant generators of pain.
 

Appreciating sequelae of diagnostic delay

After my fellowship in advanced laparoscopic and pelvic surgery with Harry Reich, MD, and C. Y. Liu, MD, pioneers of endometriosis excision surgery, and as I did my residency in the early 2000s, I noticed puzzlement in the literature about why some patients still had lasting pain after thorough excision.

I didn’t doubt the efficacy of excision. It is the cornerstone of treatment, and at least one randomized double-blind trial² and a systematic review and meta-analysis³ have demonstrated its superior efficacy over ablation in symptom reduction. What I did doubt was any presumption that surgery alone was enough. I knew there was more to healing when a disease process wreaks havoc on the body for more than a decade and that there were other generators of pain in addition to the endometriosis implants themselves.

As I began to focus on endometriosis in my own surgical practice, I strove to detect and treat endometriosis in teens. But in those patients with longstanding disease, I recognized patterns and began to more fully appreciate the systemic sequelae of endometriosis.

To cope with dysmenorrhea, patients curl up and assume a fetal position, tensing the abdominal muscles, inner thigh muscles, and pelvic floor muscles. Over time, these muscles come to maintain a short, tight, and painful state. (Hence the need for physical therapy to undo this decade-long pattern.)

Endometriosis implants on or near the gastrointestinal tract tug on fascia and muscles and commonly cause constipation, leading women to further overwork the pelvic floor muscles. In the case of diarrhea-predominant dysfunction, our patients squeeze pelvic floor muscles to prevent leakage. And in the case of urinary urgency, they squeeze muscles to release urine that isn’t really there.

As the chronic inflammation of the disease grows, and as pain worsens, the patient is increasingly in sympathetic overdrive (also known as ”fight or flight”), as opposed to a parasympathetic state (also known as “rest and digest”). The bowel’s motility slows, allowing the bacteria of the small intestine to grow beyond what is normal, leading to SIBO, a condition increasingly recognized by gastroenterologists and others that can impede nutrient absorption and cause bloat and pain and exacerbate constipation and diarrhea.

Key to my conceptualization of pain was a review published in 2011 by Pam Stratton, MD, of the National Institutes of Health, and Karen J. Berkley, PhD, then of Florida State University, on chronic pain and endometriosis.⁴ They detailed how endometriotic lesions can develop their own nerve supply that interacts directly and in a two-way fashion with the CNS – and how the lesions can engage the nervous system in ways that create comorbid conditions and pain that becomes “independent of the disease itself.”

Sensitized peripheral nerve fibers innervating a deeply infiltrating lesion on the left uterosacral ligament, for instance, can sensitize neurons in the spinal sacral segment. Branches of these nerve fibers can extend to other segments of the spinal cord, and, once sensitized themselves, turn on neurons in these other segments. There is a resultant remodeling of the central nervous system, in essence, and what is called “remote central sensitization.” The CNS becomes independent from peripheral neural processes.

I now explain to both patients and physicians that those who have had endometriosis for years have had an enduring “hand on the stove,” with a persistent signal to the CNS. Tight muscles are a hand on the stove, painful bladder syndrome is another hand on the stove, and SIBO is yet another. So are anxiety and depression.

The CNS becomes so upregulated and overloaded that messages branch out through the spinal cord to other available pathways and to other organs, muscles, and nerves. The CNS also starts firing on its own – and once it becomes its own pain generator, taking one hand off the stove (for instance, excising implants) while leaving multiple other hands on the hot stove won’t remove all pain. We must downregulate the CNS more broadly.

As I began addressing pain generators and instigators of CNS sensitization – and waiting for excision surgery until the CNS had sufficiently cooled – I saw that my patients had a better chance of more significant and lasting pain relief.
 

Pearls for a multimodal approach

My initial physical exam includes an assessment of the pelvic floor for overly tight musculature. An abdominal exam will usually reveal whether there is asymmetry of the abdominal wall muscles, which typically informs me of the likelihood of tightness and pulling on either side of the pelvic anatomy. On the internal exam, then, the pelvic floor muscles can be palpated and assessed. These findings will guide my referrals and my discussions with patients about the value of pelvic floor physical therapy. The cervix should be in the midline of the vagina – equidistant from the left and right vaginal fornices. If the cervix is pulled away from this midline, and a palpation of a thickened uterosacral ligament reproduces pain, endometriosis is 90% likely.

Patients who report significant “burning” pain that’s suggestive of neuropathic pain should be referred to a physical medicine rehabilitation physician or a pain specialist who can help downregulate their CNS. And patients who have symptoms of depression, anxiety disorders (including obsessive-compulsive disorder), or posttraumatic stress disorder should be referred to pain therapists, psychologists, or other mental health professionals, preferably well before surgery. I will also often discuss mindfulness practices and give my patients “meditation challenges” to achieve during the presurgical phase.

Additional points of emphasis about a multidisciplinary, multimodal approach include:

Advanced pelvic floor therapy: Therapists with specialized training in pelvic health and manual therapy utilize a range of techniques and modalities to release tension in affected muscles, fascia, nerves, and bone, and in doing so, they help to downregulate the CNS. Myofascial release, myofascial trigger point release, neural mobilization, and visceral mobilization are among these techniques. In addition to using manual therapy, many of these therapists may also employ neuromuscular reeducation and other techniques that will be helpful for the longer term.

It is important to identify physical therapists who have training in this approach; women with endometriosis often have a history of treatment by physical therapists whose focus is on incontinence and muscle strengthening (that is, Kegel exercises), which is the opposite of what endometriosis patients need.

Treating SIBO: Symptoms commonly associated with SIBO often overlap with symptoms of irritable bowel syndrome (IBS) – namely constipation, diarrhea (or both), and bloating. Indeed, many patients with undiagnosed endometriosis have been diagnosed with IBS. I send every patient who has one of these symptoms for SIBO breath testing, which utilizes carbohydrate substrates (glucose or lactulose) and measures hydrogen and/or methane in the breath.

SIBO is typically treated with rifampin, which stays in the small bowel and will not negatively affect beneficial bacteria, with or without neomycin. Gastroenterologists with more integrative practices also consider the use of herbals in addition to – or instead of – antibiotics. It can sometimes take months or a couple of years to correct SIBO, depending on how long the patient has been affected, but with presurgical diagnosis and a start on treatment, we can remove or at least tone down another instigator of CNS sensitization.

I estimate that 80% of my patients have tested positive for SIBO. Notably, in a testament to the systemic nature of endometriosis, a study published in 2009 of 355 women undergoing operative laparoscopy for suspected endometriosis found that 90% had gastrointestinal symptoms, but only 7.6% of the vast majority whose endometriosis was confirmed were found to have endometrial implants on the bowel itself.⁵

Addressing bladder issues: I routinely administer the PUF (Pain, Urgency, Frequency) questionnaire as part of my intake package and follow it up with conversation. For just about every patient with painful bladder syndrome, pelvic floor physical therapy in combination with a low-acid, low-potassium diet will work effectively together to reduce symptoms and pain. The IC Network offers a helpful food list, and patients can be counseled to choose foods that are also anti-inflammatory. When referrals to a urologist for bladder instillations are possible, these can be helpful as well.

Our communication with patients

Our patients need to have their symptoms and pain validated and to understand why we’re recommending these measures before surgery. Some education is necessary. Few patients will go to an integrative nutritionist, for example, if we just write a referral without explaining how years of inflammation and disruption in the gut can affect the whole body – including mental health – and that it can be corrected over time.

Also necessary is an appreciation of the fact that patients with delayed diagnoses have lived with gastrointestinal and other symptoms and patterns for so long – and often have mothers whose endometriosis caused similar symptoms – that some of their own experiences can seem almost “normal.” A patient whose mother had bowel movements every 7 days may think that 4-5 day intervals are acceptable, for instance. This means we have to carefully consider how we ask our questions.

I always ask my patients as we’re going into surgery, what percentage better are you? I’ve long aimed for at least 30% improvement, but most of the time, with pelvic floor therapy and as many other pain-generator–focused measures as possible, we’re getting them 70% better.

Excision surgery will remove the inflammation that has helped fuel the SIBO and other coconditions. Then, everything done to prepare the body must continue for some time. Certain practices, such as eating an anti-inflammatory diet, should be lifelong.

One day, it is hoped, a pediatrician or other physician will suspect endometriosis early on. The patient will see the surgeon within several months of the onset of pain, and we won’t need to unravel layers of pain generation and CNS upregulation before operating. But until this happens and we shorten the diagnostic delay, we must consider the benefits of presurgical preparation.
 

References

1. Orbuch I, Stein A. Beating Endo: How to Reclaim Your Life From Endometriosis. (New York: HarperCollins, 2019).

2. Healey M et al. J Minim Invasive Gynecol. 2014;21(6):999-1004.

3. Pundir J et al. J Minim Invasive Gynecol. 2017;24(5):747-56.

4. Stratton P, Berkley KJ. Hum Repro Update. 2011;17(3):327-46.

5. Maroun P et al. Aust N Z J Obstet Gynaecol. 2009;49(4):411-4.

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in endometriosis. She has no conflicts of interest to report.

Introduction: The preoperative evaluation for endometriosis – more than meets the eye

It is well known that it often takes 6-10 years for endometriosis to be diagnosed in patients who have the disease, depending on where the patient lives. I certainly am not surprised. During my residency at Parkland Memorial Hospital, if a patient had chronic pelvic pain and no fibroids, her diagnosis was usually pelvic inflammatory disease. Later, during my fellowship in reproductive endocrinology at the University of Pennsylvania, the diagnosis became endometriosis.

As I gained more interest and expertise in the treatment of endometriosis, I became aware of several articles concluding that if a woman sought treatment for chronic pelvic pain with an internist, the diagnosis would be irritable bowel syndrome (IBS); with a urologist, it would be interstitial cystitis; and with a gynecologist, endometriosis. Moreover, there is an increased propensity for IBS and IC in patients with endometriosis. There also is an increased risk of small intestine bacterial overgrowth (SIBO), as noted by our guest author for this latest installment of the Master Class in Gynecologic Surgery, Iris Orbuch, MD.

Like our guest author, I have also noted increased risk of pelvic floor myalgia. Dr. Orbuch clearly outlines why this occurs. In fact, we can now understand why many patients have multiple pelvic pain–inducing issues compounding their pain secondary to endometriosis and leading to remodeling of the central nervous system. Therefore, it certainly makes sense to follow Dr. Orbuch’s recommendation for a multidisciplinary pre- and postsurgical approach “to downregulate the pain generators.”

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in the treatment of patients diagnosed with endometriosis. Dr. Orbuch serves on the Board of Directors of the Foundation of the American Association of Gynecologic Laparoscopists and has served as the chair of the AAGL’s Special Interest Group on Endometriosis and Reproductive Surgery. She is the coauthor of the book “Beating Endo – How to Reclaim Your Life From Endometriosis” (New York: HarperCollins; 2019). The book is written for patients but addresses many issues discussed in this installment of the Master Class in Gynecologic Surgery.

Dr. Miller, MD, FACOG, is professor of obstetrics and gynecology, department of clinical sciences, Rosalind Franklin University of Medicine and Science, North Chicago. He has no conflicts of interest to report.

For optimal surgical outcomes, and to help our patients recover from years of this inflammatory, systemic disease, we must treat our patients holistically and work to downregulate their pain as much as possible before excision surgery. I work with patients a few months prior to surgery, often for 4-5 months, during which time they not only see me for informative follow-ups, but also pelvic floor physical therapists, gastroenterologists, mental health professionals, integrative nutritionists, and physiatrists or pain specialists, depending on their needs.¹

By identifying coexisting conditions in an initial consult and employing a presurgical multidisciplinary approach to downregulate the pain generators, my patients recover well from excision surgery, with greater and faster relief from pain, compared with those using standard approaches, and with little to no use of opioids.

At a minimum, given the unfortunate time constraints and productivity demands of working within health systems – and considering that surgeries are often scheduled a couple of months out – the surgeon could ensure that patients are engaged in at least 6-8 weeks of pelvic floor physical therapy before surgery to sufficiently lengthen the pelvic muscles and loosen surrounding fascia.

Short, tight pelvic floor muscles are almost universal in patients with delayed diagnosis of endometriosis and are significant generators of pain.
 

Appreciating sequelae of diagnostic delay

After my fellowship in advanced laparoscopic and pelvic surgery with Harry Reich, MD, and C. Y. Liu, MD, pioneers of endometriosis excision surgery, and as I did my residency in the early 2000s, I noticed puzzlement in the literature about why some patients still had lasting pain after thorough excision.

I didn’t doubt the efficacy of excision. It is the cornerstone of treatment, and at least one randomized double-blind trial² and a systematic review and meta-analysis³ have demonstrated its superior efficacy over ablation in symptom reduction. What I did doubt was any presumption that surgery alone was enough. I knew there was more to healing when a disease process wreaks havoc on the body for more than a decade and that there were other generators of pain in addition to the endometriosis implants themselves.

As I began to focus on endometriosis in my own surgical practice, I strove to detect and treat endometriosis in teens. But in those patients with longstanding disease, I recognized patterns and began to more fully appreciate the systemic sequelae of endometriosis.

To cope with dysmenorrhea, patients curl up and assume a fetal position, tensing the abdominal muscles, inner thigh muscles, and pelvic floor muscles. Over time, these muscles come to maintain a short, tight, and painful state. (Hence the need for physical therapy to undo this decade-long pattern.)

Endometriosis implants on or near the gastrointestinal tract tug on fascia and muscles and commonly cause constipation, leading women to further overwork the pelvic floor muscles. In the case of diarrhea-predominant dysfunction, our patients squeeze pelvic floor muscles to prevent leakage. And in the case of urinary urgency, they squeeze muscles to release urine that isn’t really there.

As the chronic inflammation of the disease grows, and as pain worsens, the patient is increasingly in sympathetic overdrive (also known as ”fight or flight”), as opposed to a parasympathetic state (also known as “rest and digest”). The bowel’s motility slows, allowing the bacteria of the small intestine to grow beyond what is normal, leading to SIBO, a condition increasingly recognized by gastroenterologists and others that can impede nutrient absorption and cause bloat and pain and exacerbate constipation and diarrhea.

Key to my conceptualization of pain was a review published in 2011 by Pam Stratton, MD, of the National Institutes of Health, and Karen J. Berkley, PhD, then of Florida State University, on chronic pain and endometriosis.⁴ They detailed how endometriotic lesions can develop their own nerve supply that interacts directly and in a two-way fashion with the CNS – and how the lesions can engage the nervous system in ways that create comorbid conditions and pain that becomes “independent of the disease itself.”

Sensitized peripheral nerve fibers innervating a deeply infiltrating lesion on the left uterosacral ligament, for instance, can sensitize neurons in the spinal sacral segment. Branches of these nerve fibers can extend to other segments of the spinal cord, and, once sensitized themselves, turn on neurons in these other segments. There is a resultant remodeling of the central nervous system, in essence, and what is called “remote central sensitization.” The CNS becomes independent from peripheral neural processes.

I now explain to both patients and physicians that those who have had endometriosis for years have had an enduring “hand on the stove,” with a persistent signal to the CNS. Tight muscles are a hand on the stove, painful bladder syndrome is another hand on the stove, and SIBO is yet another. So are anxiety and depression.

The CNS becomes so upregulated and overloaded that messages branch out through the spinal cord to other available pathways and to other organs, muscles, and nerves. The CNS also starts firing on its own – and once it becomes its own pain generator, taking one hand off the stove (for instance, excising implants) while leaving multiple other hands on the hot stove won’t remove all pain. We must downregulate the CNS more broadly.

As I began addressing pain generators and instigators of CNS sensitization – and waiting for excision surgery until the CNS had sufficiently cooled – I saw that my patients had a better chance of more significant and lasting pain relief.
 

Pearls for a multimodal approach

My initial physical exam includes an assessment of the pelvic floor for overly tight musculature. An abdominal exam will usually reveal whether there is asymmetry of the abdominal wall muscles, which typically informs me of the likelihood of tightness and pulling on either side of the pelvic anatomy. On the internal exam, then, the pelvic floor muscles can be palpated and assessed. These findings will guide my referrals and my discussions with patients about the value of pelvic floor physical therapy. The cervix should be in the midline of the vagina – equidistant from the left and right vaginal fornices. If the cervix is pulled away from this midline, and a palpation of a thickened uterosacral ligament reproduces pain, endometriosis is 90% likely.

Patients who report significant “burning” pain that’s suggestive of neuropathic pain should be referred to a physical medicine rehabilitation physician or a pain specialist who can help downregulate their CNS. And patients who have symptoms of depression, anxiety disorders (including obsessive-compulsive disorder), or posttraumatic stress disorder should be referred to pain therapists, psychologists, or other mental health professionals, preferably well before surgery. I will also often discuss mindfulness practices and give my patients “meditation challenges” to achieve during the presurgical phase.

Additional points of emphasis about a multidisciplinary, multimodal approach include:

Advanced pelvic floor therapy: Therapists with specialized training in pelvic health and manual therapy utilize a range of techniques and modalities to release tension in affected muscles, fascia, nerves, and bone, and in doing so, they help to downregulate the CNS. Myofascial release, myofascial trigger point release, neural mobilization, and visceral mobilization are among these techniques. In addition to using manual therapy, many of these therapists may also employ neuromuscular reeducation and other techniques that will be helpful for the longer term.

It is important to identify physical therapists who have training in this approach; women with endometriosis often have a history of treatment by physical therapists whose focus is on incontinence and muscle strengthening (that is, Kegel exercises), which is the opposite of what endometriosis patients need.

Treating SIBO: Symptoms commonly associated with SIBO often overlap with symptoms of irritable bowel syndrome (IBS) – namely constipation, diarrhea (or both), and bloating. Indeed, many patients with undiagnosed endometriosis have been diagnosed with IBS. I send every patient who has one of these symptoms for SIBO breath testing, which utilizes carbohydrate substrates (glucose or lactulose) and measures hydrogen and/or methane in the breath.

SIBO is typically treated with rifampin, which stays in the small bowel and will not negatively affect beneficial bacteria, with or without neomycin. Gastroenterologists with more integrative practices also consider the use of herbals in addition to – or instead of – antibiotics. It can sometimes take months or a couple of years to correct SIBO, depending on how long the patient has been affected, but with presurgical diagnosis and a start on treatment, we can remove or at least tone down another instigator of CNS sensitization.

I estimate that 80% of my patients have tested positive for SIBO. Notably, in a testament to the systemic nature of endometriosis, a study published in 2009 of 355 women undergoing operative laparoscopy for suspected endometriosis found that 90% had gastrointestinal symptoms, but only 7.6% of the vast majority whose endometriosis was confirmed were found to have endometrial implants on the bowel itself.⁵

Addressing bladder issues: I routinely administer the PUF (Pain, Urgency, Frequency) questionnaire as part of my intake package and follow it up with conversation. For just about every patient with painful bladder syndrome, pelvic floor physical therapy in combination with a low-acid, low-potassium diet will work effectively together to reduce symptoms and pain. The IC Network offers a helpful food list, and patients can be counseled to choose foods that are also anti-inflammatory. When referrals to a urologist for bladder instillations are possible, these can be helpful as well.

Our communication with patients

Our patients need to have their symptoms and pain validated and to understand why we’re recommending these measures before surgery. Some education is necessary. Few patients will go to an integrative nutritionist, for example, if we just write a referral without explaining how years of inflammation and disruption in the gut can affect the whole body – including mental health – and that it can be corrected over time.

Also necessary is an appreciation of the fact that patients with delayed diagnoses have lived with gastrointestinal and other symptoms and patterns for so long – and often have mothers whose endometriosis caused similar symptoms – that some of their own experiences can seem almost “normal.” A patient whose mother had bowel movements every 7 days may think that 4-5 day intervals are acceptable, for instance. This means we have to carefully consider how we ask our questions.

I always ask my patients as we’re going into surgery, what percentage better are you? I’ve long aimed for at least 30% improvement, but most of the time, with pelvic floor therapy and as many other pain-generator–focused measures as possible, we’re getting them 70% better.

Excision surgery will remove the inflammation that has helped fuel the SIBO and other coconditions. Then, everything done to prepare the body must continue for some time. Certain practices, such as eating an anti-inflammatory diet, should be lifelong.

One day, it is hoped, a pediatrician or other physician will suspect endometriosis early on. The patient will see the surgeon within several months of the onset of pain, and we won’t need to unravel layers of pain generation and CNS upregulation before operating. But until this happens and we shorten the diagnostic delay, we must consider the benefits of presurgical preparation.
 

References

1. Orbuch I, Stein A. Beating Endo: How to Reclaim Your Life From Endometriosis. (New York: HarperCollins, 2019).

2. Healey M et al. J Minim Invasive Gynecol. 2014;21(6):999-1004.

3. Pundir J et al. J Minim Invasive Gynecol. 2017;24(5):747-56.

4. Stratton P, Berkley KJ. Hum Repro Update. 2011;17(3):327-46.

5. Maroun P et al. Aust N Z J Obstet Gynaecol. 2009;49(4):411-4.

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in endometriosis. She has no conflicts of interest to report.

Introduction: The preoperative evaluation for endometriosis – more than meets the eye

It is well known that it often takes 6-10 years for endometriosis to be diagnosed in patients who have the disease, depending on where the patient lives. I certainly am not surprised. During my residency at Parkland Memorial Hospital, if a patient had chronic pelvic pain and no fibroids, her diagnosis was usually pelvic inflammatory disease. Later, during my fellowship in reproductive endocrinology at the University of Pennsylvania, the diagnosis became endometriosis.

As I gained more interest and expertise in the treatment of endometriosis, I became aware of several articles concluding that if a woman sought treatment for chronic pelvic pain with an internist, the diagnosis would be irritable bowel syndrome (IBS); with a urologist, it would be interstitial cystitis; and with a gynecologist, endometriosis. Moreover, there is an increased propensity for IBS and IC in patients with endometriosis. There also is an increased risk of small intestine bacterial overgrowth (SIBO), as noted by our guest author for this latest installment of the Master Class in Gynecologic Surgery, Iris Orbuch, MD.

Like our guest author, I have also noted increased risk of pelvic floor myalgia. Dr. Orbuch clearly outlines why this occurs. In fact, we can now understand why many patients have multiple pelvic pain–inducing issues compounding their pain secondary to endometriosis and leading to remodeling of the central nervous system. Therefore, it certainly makes sense to follow Dr. Orbuch’s recommendation for a multidisciplinary pre- and postsurgical approach “to downregulate the pain generators.”

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in the treatment of patients diagnosed with endometriosis. Dr. Orbuch serves on the Board of Directors of the Foundation of the American Association of Gynecologic Laparoscopists and has served as the chair of the AAGL’s Special Interest Group on Endometriosis and Reproductive Surgery. She is the coauthor of the book “Beating Endo – How to Reclaim Your Life From Endometriosis” (New York: HarperCollins; 2019). The book is written for patients but addresses many issues discussed in this installment of the Master Class in Gynecologic Surgery.

Dr. Miller, MD, FACOG, is professor of obstetrics and gynecology, department of clinical sciences, Rosalind Franklin University of Medicine and Science, North Chicago. He has no conflicts of interest to report.

For optimal surgical outcomes, and to help our patients recover from years of this inflammatory, systemic disease, we must treat our patients holistically and work to downregulate their pain as much as possible before excision surgery. I work with patients a few months prior to surgery, often for 4-5 months, during which time they not only see me for informative follow-ups, but also pelvic floor physical therapists, gastroenterologists, mental health professionals, integrative nutritionists, and physiatrists or pain specialists, depending on their needs.¹

By identifying coexisting conditions in an initial consult and employing a presurgical multidisciplinary approach to downregulate the pain generators, my patients recover well from excision surgery, with greater and faster relief from pain, compared with those using standard approaches, and with little to no use of opioids.

At a minimum, given the unfortunate time constraints and productivity demands of working within health systems – and considering that surgeries are often scheduled a couple of months out – the surgeon could ensure that patients are engaged in at least 6-8 weeks of pelvic floor physical therapy before surgery to sufficiently lengthen the pelvic muscles and loosen surrounding fascia.

Short, tight pelvic floor muscles are almost universal in patients with delayed diagnosis of endometriosis and are significant generators of pain.
 

Appreciating sequelae of diagnostic delay

After my fellowship in advanced laparoscopic and pelvic surgery with Harry Reich, MD, and C. Y. Liu, MD, pioneers of endometriosis excision surgery, and as I did my residency in the early 2000s, I noticed puzzlement in the literature about why some patients still had lasting pain after thorough excision.

I didn’t doubt the efficacy of excision. It is the cornerstone of treatment, and at least one randomized double-blind trial² and a systematic review and meta-analysis³ have demonstrated its superior efficacy over ablation in symptom reduction. What I did doubt was any presumption that surgery alone was enough. I knew there was more to healing when a disease process wreaks havoc on the body for more than a decade and that there were other generators of pain in addition to the endometriosis implants themselves.

As I began to focus on endometriosis in my own surgical practice, I strove to detect and treat endometriosis in teens. But in those patients with longstanding disease, I recognized patterns and began to more fully appreciate the systemic sequelae of endometriosis.

To cope with dysmenorrhea, patients curl up and assume a fetal position, tensing the abdominal muscles, inner thigh muscles, and pelvic floor muscles. Over time, these muscles come to maintain a short, tight, and painful state. (Hence the need for physical therapy to undo this decade-long pattern.)

Endometriosis implants on or near the gastrointestinal tract tug on fascia and muscles and commonly cause constipation, leading women to further overwork the pelvic floor muscles. In the case of diarrhea-predominant dysfunction, our patients squeeze pelvic floor muscles to prevent leakage. And in the case of urinary urgency, they squeeze muscles to release urine that isn’t really there.

As the chronic inflammation of the disease grows, and as pain worsens, the patient is increasingly in sympathetic overdrive (also known as ”fight or flight”), as opposed to a parasympathetic state (also known as “rest and digest”). The bowel’s motility slows, allowing the bacteria of the small intestine to grow beyond what is normal, leading to SIBO, a condition increasingly recognized by gastroenterologists and others that can impede nutrient absorption and cause bloat and pain and exacerbate constipation and diarrhea.

Key to my conceptualization of pain was a review published in 2011 by Pam Stratton, MD, of the National Institutes of Health, and Karen J. Berkley, PhD, then of Florida State University, on chronic pain and endometriosis.⁴ They detailed how endometriotic lesions can develop their own nerve supply that interacts directly and in a two-way fashion with the CNS – and how the lesions can engage the nervous system in ways that create comorbid conditions and pain that becomes “independent of the disease itself.”

Sensitized peripheral nerve fibers innervating a deeply infiltrating lesion on the left uterosacral ligament, for instance, can sensitize neurons in the spinal sacral segment. Branches of these nerve fibers can extend to other segments of the spinal cord, and, once sensitized themselves, turn on neurons in these other segments. There is a resultant remodeling of the central nervous system, in essence, and what is called “remote central sensitization.” The CNS becomes independent from peripheral neural processes.

I now explain to both patients and physicians that those who have had endometriosis for years have had an enduring “hand on the stove,” with a persistent signal to the CNS. Tight muscles are a hand on the stove, painful bladder syndrome is another hand on the stove, and SIBO is yet another. So are anxiety and depression.

The CNS becomes so upregulated and overloaded that messages branch out through the spinal cord to other available pathways and to other organs, muscles, and nerves. The CNS also starts firing on its own – and once it becomes its own pain generator, taking one hand off the stove (for instance, excising implants) while leaving multiple other hands on the hot stove won’t remove all pain. We must downregulate the CNS more broadly.

As I began addressing pain generators and instigators of CNS sensitization – and waiting for excision surgery until the CNS had sufficiently cooled – I saw that my patients had a better chance of more significant and lasting pain relief.
 

Pearls for a multimodal approach

My initial physical exam includes an assessment of the pelvic floor for overly tight musculature. An abdominal exam will usually reveal whether there is asymmetry of the abdominal wall muscles, which typically informs me of the likelihood of tightness and pulling on either side of the pelvic anatomy. On the internal exam, then, the pelvic floor muscles can be palpated and assessed. These findings will guide my referrals and my discussions with patients about the value of pelvic floor physical therapy. The cervix should be in the midline of the vagina – equidistant from the left and right vaginal fornices. If the cervix is pulled away from this midline, and a palpation of a thickened uterosacral ligament reproduces pain, endometriosis is 90% likely.

Patients who report significant “burning” pain that’s suggestive of neuropathic pain should be referred to a physical medicine rehabilitation physician or a pain specialist who can help downregulate their CNS. And patients who have symptoms of depression, anxiety disorders (including obsessive-compulsive disorder), or posttraumatic stress disorder should be referred to pain therapists, psychologists, or other mental health professionals, preferably well before surgery. I will also often discuss mindfulness practices and give my patients “meditation challenges” to achieve during the presurgical phase.

Additional points of emphasis about a multidisciplinary, multimodal approach include:

Advanced pelvic floor therapy: Therapists with specialized training in pelvic health and manual therapy utilize a range of techniques and modalities to release tension in affected muscles, fascia, nerves, and bone, and in doing so, they help to downregulate the CNS. Myofascial release, myofascial trigger point release, neural mobilization, and visceral mobilization are among these techniques. In addition to using manual therapy, many of these therapists may also employ neuromuscular reeducation and other techniques that will be helpful for the longer term.

It is important to identify physical therapists who have training in this approach; women with endometriosis often have a history of treatment by physical therapists whose focus is on incontinence and muscle strengthening (that is, Kegel exercises), which is the opposite of what endometriosis patients need.

Treating SIBO: Symptoms commonly associated with SIBO often overlap with symptoms of irritable bowel syndrome (IBS) – namely constipation, diarrhea (or both), and bloating. Indeed, many patients with undiagnosed endometriosis have been diagnosed with IBS. I send every patient who has one of these symptoms for SIBO breath testing, which utilizes carbohydrate substrates (glucose or lactulose) and measures hydrogen and/or methane in the breath.

SIBO is typically treated with rifampin, which stays in the small bowel and will not negatively affect beneficial bacteria, with or without neomycin. Gastroenterologists with more integrative practices also consider the use of herbals in addition to – or instead of – antibiotics. It can sometimes take months or a couple of years to correct SIBO, depending on how long the patient has been affected, but with presurgical diagnosis and a start on treatment, we can remove or at least tone down another instigator of CNS sensitization.

I estimate that 80% of my patients have tested positive for SIBO. Notably, in a testament to the systemic nature of endometriosis, a study published in 2009 of 355 women undergoing operative laparoscopy for suspected endometriosis found that 90% had gastrointestinal symptoms, but only 7.6% of the vast majority whose endometriosis was confirmed were found to have endometrial implants on the bowel itself.⁵

Addressing bladder issues: I routinely administer the PUF (Pain, Urgency, Frequency) questionnaire as part of my intake package and follow it up with conversation. For just about every patient with painful bladder syndrome, pelvic floor physical therapy in combination with a low-acid, low-potassium diet will work effectively together to reduce symptoms and pain. The IC Network offers a helpful food list, and patients can be counseled to choose foods that are also anti-inflammatory. When referrals to a urologist for bladder instillations are possible, these can be helpful as well.

Our communication with patients

Our patients need to have their symptoms and pain validated and to understand why we’re recommending these measures before surgery. Some education is necessary. Few patients will go to an integrative nutritionist, for example, if we just write a referral without explaining how years of inflammation and disruption in the gut can affect the whole body – including mental health – and that it can be corrected over time.

Also necessary is an appreciation of the fact that patients with delayed diagnoses have lived with gastrointestinal and other symptoms and patterns for so long – and often have mothers whose endometriosis caused similar symptoms – that some of their own experiences can seem almost “normal.” A patient whose mother had bowel movements every 7 days may think that 4-5 day intervals are acceptable, for instance. This means we have to carefully consider how we ask our questions.

I always ask my patients as we’re going into surgery, what percentage better are you? I’ve long aimed for at least 30% improvement, but most of the time, with pelvic floor therapy and as many other pain-generator–focused measures as possible, we’re getting them 70% better.

Excision surgery will remove the inflammation that has helped fuel the SIBO and other coconditions. Then, everything done to prepare the body must continue for some time. Certain practices, such as eating an anti-inflammatory diet, should be lifelong.

One day, it is hoped, a pediatrician or other physician will suspect endometriosis early on. The patient will see the surgeon within several months of the onset of pain, and we won’t need to unravel layers of pain generation and CNS upregulation before operating. But until this happens and we shorten the diagnostic delay, we must consider the benefits of presurgical preparation.
 

References

1. Orbuch I, Stein A. Beating Endo: How to Reclaim Your Life From Endometriosis. (New York: HarperCollins, 2019).

2. Healey M et al. J Minim Invasive Gynecol. 2014;21(6):999-1004.

3. Pundir J et al. J Minim Invasive Gynecol. 2017;24(5):747-56.

4. Stratton P, Berkley KJ. Hum Repro Update. 2011;17(3):327-46.

5. Maroun P et al. Aust N Z J Obstet Gynaecol. 2009;49(4):411-4.

Dr. Orbuch is a minimally invasive gynecologic surgeon in Los Angeles who specializes in endometriosis. She has no conflicts of interest to report.

In recent weeks, you may have noticed some familiar headlines about red wine and cardiovascular health. Why the sudden return of these stories? Because of an article recently published in the American Journal of Clinical Nutrition.

Funded in part by a grant from the São Paulo Research Foundation (FAPESP), the “Wine Flora Study” was carried out by prominent researchers from institutions in South America, Europe, and the United States: University of São Paulo; State University of Campinas, São Paulo; University of Brasília; University of Verona (Italy); Austrian Institute of Technology, Tulln; and Harvard Medical School, Boston. The team looked into the effects of red wine on gut flora and plasma levels of trimethylamine-N-oxide (TMAO). And what they found was quite interesting.
 

The study

Previous results have pointed to the beneficial effect that red wine has on the gut microbiome.

The Wine Flora Study involved 42 men (average age, 60 years) with documented coronary artery disease. The trial encompassed two 3-week interventions. In one, the participants consumed 250 mL of red wine per day; the red wine sample had an alcohol content (% v) of 12.75. The Brazilian Wine Institute produced and supplied the red wine: a 2014 Merlot bottled in August 2016 and customized for the study. The second intervention involved alcohol abstention.

Each intervention was preceded by a 2-week washout period. Because certain foods and drinks could interfere with the results, the participants were instructed not to consume alcoholic beverages, fermented foods (yogurt, kombucha, soy lecithin, kefir, sauerkraut, and other fermented vegetables), synthetic prebiotics (insulin, fructooligosaccharides), fiber, dairy, food polyphenols (grapes, grape juice, cranberries, strawberries), and probiotics.

At each intervention, the gut microbiota was analyzed via 16S ribosomal RNA highthroughput sequencing. This method makes it possible to identify bacterial species. The plasma metabolome of 20 randomly selected participants was evaluated by ultra–high-performance liquid chromatography with tandem mass spectrometry. In this method, liquid chromatography separates the compounds, and a mass spectrometer is used to analyze them.

One of the metabolites of interest was TMAO, which is produced from the trimethylamine released when gut bacteria process protein-rich foods. TMAO has been identified as playing a role in the development of atherosclerosis.
 

Results

After red wine consumption, there was significant remodeling of the gut microbiota, with a difference in beta diversity and predominance of Parasutterella, Ruminococcaceae, several Bacteroides species, and Prevotella.

Plasma metabolomic analysis revealed significant changes in metabolites after red wine consumption, consistent with improved redox homeostasis, which is involved in the oxidative stress that promotes atherosclerosis.

Plasma TMAO, however, did not differ between red wine intervention and alcohol abstention.
 

Implications

The researchers concluded that modulation of the gut microbiota may contribute to the putative cardiovascular benefits of moderate red wine consumption. But, as they were careful to point out in the very title of the study, a red wine intervention does not modify plasma TMAO. They also mentioned that the 3-week period may have been too short for the findings to serve as the basis for promoting any meaningful modification. In addition, the team emphasized that these data remain hypothesisgenerating and pave the way for future research.

In an interview with FAPESP, the study’s corresponding author, Protásio Lemos da Luz, MD, PhD, warned about the risks associated with drinking too much alcohol (> 8.5 oz., or 250 mL, of wine daily).

It should be kept in mind that, in Brazil, people do not drink nearly as much wine as they do beer or liquor. Furthermore, the evidence that is available does not provide confirmation of the existence or the extent of the protective health effects associated with light or moderate alcohol intake.

This article was translated from the Medscape Portuguese edition. A version appeared on Medscape.com.

In recent weeks, you may have noticed some familiar headlines about red wine and cardiovascular health. Why the sudden return of these stories? Because of an article recently published in the American Journal of Clinical Nutrition.

Funded in part by a grant from the São Paulo Research Foundation (FAPESP), the “Wine Flora Study” was carried out by prominent researchers from institutions in South America, Europe, and the United States: University of São Paulo; State University of Campinas, São Paulo; University of Brasília; University of Verona (Italy); Austrian Institute of Technology, Tulln; and Harvard Medical School, Boston. The team looked into the effects of red wine on gut flora and plasma levels of trimethylamine-N-oxide (TMAO). And what they found was quite interesting.
 

The study

Previous results have pointed to the beneficial effect that red wine has on the gut microbiome.

The Wine Flora Study involved 42 men (average age, 60 years) with documented coronary artery disease. The trial encompassed two 3-week interventions. In one, the participants consumed 250 mL of red wine per day; the red wine sample had an alcohol content (% v) of 12.75. The Brazilian Wine Institute produced and supplied the red wine: a 2014 Merlot bottled in August 2016 and customized for the study. The second intervention involved alcohol abstention.

Each intervention was preceded by a 2-week washout period. Because certain foods and drinks could interfere with the results, the participants were instructed not to consume alcoholic beverages, fermented foods (yogurt, kombucha, soy lecithin, kefir, sauerkraut, and other fermented vegetables), synthetic prebiotics (insulin, fructooligosaccharides), fiber, dairy, food polyphenols (grapes, grape juice, cranberries, strawberries), and probiotics.

At each intervention, the gut microbiota was analyzed via 16S ribosomal RNA highthroughput sequencing. This method makes it possible to identify bacterial species. The plasma metabolome of 20 randomly selected participants was evaluated by ultra–high-performance liquid chromatography with tandem mass spectrometry. In this method, liquid chromatography separates the compounds, and a mass spectrometer is used to analyze them.

One of the metabolites of interest was TMAO, which is produced from the trimethylamine released when gut bacteria process protein-rich foods. TMAO has been identified as playing a role in the development of atherosclerosis.
 

Results

After red wine consumption, there was significant remodeling of the gut microbiota, with a difference in beta diversity and predominance of Parasutterella, Ruminococcaceae, several Bacteroides species, and Prevotella.

Plasma metabolomic analysis revealed significant changes in metabolites after red wine consumption, consistent with improved redox homeostasis, which is involved in the oxidative stress that promotes atherosclerosis.

Plasma TMAO, however, did not differ between red wine intervention and alcohol abstention.
 

Implications

The researchers concluded that modulation of the gut microbiota may contribute to the putative cardiovascular benefits of moderate red wine consumption. But, as they were careful to point out in the very title of the study, a red wine intervention does not modify plasma TMAO. They also mentioned that the 3-week period may have been too short for the findings to serve as the basis for promoting any meaningful modification. In addition, the team emphasized that these data remain hypothesisgenerating and pave the way for future research.

In an interview with FAPESP, the study’s corresponding author, Protásio Lemos da Luz, MD, PhD, warned about the risks associated with drinking too much alcohol (> 8.5 oz., or 250 mL, of wine daily).

It should be kept in mind that, in Brazil, people do not drink nearly as much wine as they do beer or liquor. Furthermore, the evidence that is available does not provide confirmation of the existence or the extent of the protective health effects associated with light or moderate alcohol intake.

This article was translated from the Medscape Portuguese edition. A version appeared on Medscape.com.

In recent weeks, you may have noticed some familiar headlines about red wine and cardiovascular health. Why the sudden return of these stories? Because of an article recently published in the American Journal of Clinical Nutrition.

Funded in part by a grant from the São Paulo Research Foundation (FAPESP), the “Wine Flora Study” was carried out by prominent researchers from institutions in South America, Europe, and the United States: University of São Paulo; State University of Campinas, São Paulo; University of Brasília; University of Verona (Italy); Austrian Institute of Technology, Tulln; and Harvard Medical School, Boston. The team looked into the effects of red wine on gut flora and plasma levels of trimethylamine-N-oxide (TMAO). And what they found was quite interesting.
 

The study

Previous results have pointed to the beneficial effect that red wine has on the gut microbiome.

The Wine Flora Study involved 42 men (average age, 60 years) with documented coronary artery disease. The trial encompassed two 3-week interventions. In one, the participants consumed 250 mL of red wine per day; the red wine sample had an alcohol content (% v) of 12.75. The Brazilian Wine Institute produced and supplied the red wine: a 2014 Merlot bottled in August 2016 and customized for the study. The second intervention involved alcohol abstention.

Each intervention was preceded by a 2-week washout period. Because certain foods and drinks could interfere with the results, the participants were instructed not to consume alcoholic beverages, fermented foods (yogurt, kombucha, soy lecithin, kefir, sauerkraut, and other fermented vegetables), synthetic prebiotics (insulin, fructooligosaccharides), fiber, dairy, food polyphenols (grapes, grape juice, cranberries, strawberries), and probiotics.

At each intervention, the gut microbiota was analyzed via 16S ribosomal RNA highthroughput sequencing. This method makes it possible to identify bacterial species. The plasma metabolome of 20 randomly selected participants was evaluated by ultra–high-performance liquid chromatography with tandem mass spectrometry. In this method, liquid chromatography separates the compounds, and a mass spectrometer is used to analyze them.

One of the metabolites of interest was TMAO, which is produced from the trimethylamine released when gut bacteria process protein-rich foods. TMAO has been identified as playing a role in the development of atherosclerosis.
 

Results

After red wine consumption, there was significant remodeling of the gut microbiota, with a difference in beta diversity and predominance of Parasutterella, Ruminococcaceae, several Bacteroides species, and Prevotella.

Plasma metabolomic analysis revealed significant changes in metabolites after red wine consumption, consistent with improved redox homeostasis, which is involved in the oxidative stress that promotes atherosclerosis.

Plasma TMAO, however, did not differ between red wine intervention and alcohol abstention.
 

Implications

The researchers concluded that modulation of the gut microbiota may contribute to the putative cardiovascular benefits of moderate red wine consumption. But, as they were careful to point out in the very title of the study, a red wine intervention does not modify plasma TMAO. They also mentioned that the 3-week period may have been too short for the findings to serve as the basis for promoting any meaningful modification. In addition, the team emphasized that these data remain hypothesisgenerating and pave the way for future research.

In an interview with FAPESP, the study’s corresponding author, Protásio Lemos da Luz, MD, PhD, warned about the risks associated with drinking too much alcohol (> 8.5 oz., or 250 mL, of wine daily).

It should be kept in mind that, in Brazil, people do not drink nearly as much wine as they do beer or liquor. Furthermore, the evidence that is available does not provide confirmation of the existence or the extent of the protective health effects associated with light or moderate alcohol intake.

This article was translated from the Medscape Portuguese edition. A version appeared on Medscape.com.

A recent report in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association suggested that, at least for now, we need to lower the bar in Alzheimer’s disease drug trials.

Their point is that there’s no consensus on “clinically meaningful benefit.” Does it mean a complete cure for Alzheimer’s disease, with reversal of deficits? Or stopping disease progression where it is? Or just slowing things down enough that it means something to patients, family members, and caregivers?

The last one is, realistically, where we are now.

The problem with this is that many nonmedical people equate “treatment” with “cure,” which isn’t close to the truth for many diseases. In Alzheimer’s disease, it’s even trickier to figure out. There’s a disparity between imaging (which suggests something that should be quite effective) and clinical results (which aren’t nearly as impressive as the PET scans).

So when I prescribe any of the Alzheimer’s medications, I make it pretty clear to patients, and more importantly the patient’s family, what they can and can’t expect. This isn’t easy, because most will come back a month later, tell me their loved one is no better, and want to try something else. So I have to explain it again. These people aren’t stupid. They’re hopeful, and also facing an impossible question. “Better” is a lot easier to judge than “slowed progression.”

“Better” is a great word for migraines. Or seizures. Or Parkinson’s disease. These are condition where patients and families can tell us whether they’ve seen an improvement.

But with the current treatments for Alzheimer’s disease we’re asking patients and families “do you think you’ve gotten any worse than you would have if you hadn’t taken the drug at all?”

That’s an impossible question to answer, unless you’re following people with objective cognitive data over time and comparing them against a placebo group, which is how these drugs got here in the first place – we know they do that.

But to a family watching their loved ones go downhill, such reassurances aren’t what they want to hear.

Regrettably, it’s where things stand. While I want to strive for absolute success in these things, today it’s simply not possible. Maybe it never will be, though I hope it is.

But, for now, I agree that we need to reframe what we’re going to consider clinically meaningful. Sometimes you have to settle for a flight of stairs instead of an elevator, but still hope that you’ll get to the top. It just takes longer, and it’s better than not going anywhere at all.

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

A recent report in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association suggested that, at least for now, we need to lower the bar in Alzheimer’s disease drug trials.

Their point is that there’s no consensus on “clinically meaningful benefit.” Does it mean a complete cure for Alzheimer’s disease, with reversal of deficits? Or stopping disease progression where it is? Or just slowing things down enough that it means something to patients, family members, and caregivers?

The last one is, realistically, where we are now.

The problem with this is that many nonmedical people equate “treatment” with “cure,” which isn’t close to the truth for many diseases. In Alzheimer’s disease, it’s even trickier to figure out. There’s a disparity between imaging (which suggests something that should be quite effective) and clinical results (which aren’t nearly as impressive as the PET scans).

So when I prescribe any of the Alzheimer’s medications, I make it pretty clear to patients, and more importantly the patient’s family, what they can and can’t expect. This isn’t easy, because most will come back a month later, tell me their loved one is no better, and want to try something else. So I have to explain it again. These people aren’t stupid. They’re hopeful, and also facing an impossible question. “Better” is a lot easier to judge than “slowed progression.”

“Better” is a great word for migraines. Or seizures. Or Parkinson’s disease. These are condition where patients and families can tell us whether they’ve seen an improvement.

But with the current treatments for Alzheimer’s disease we’re asking patients and families “do you think you’ve gotten any worse than you would have if you hadn’t taken the drug at all?”

That’s an impossible question to answer, unless you’re following people with objective cognitive data over time and comparing them against a placebo group, which is how these drugs got here in the first place – we know they do that.

But to a family watching their loved ones go downhill, such reassurances aren’t what they want to hear.

Regrettably, it’s where things stand. While I want to strive for absolute success in these things, today it’s simply not possible. Maybe it never will be, though I hope it is.

But, for now, I agree that we need to reframe what we’re going to consider clinically meaningful. Sometimes you have to settle for a flight of stairs instead of an elevator, but still hope that you’ll get to the top. It just takes longer, and it’s better than not going anywhere at all.

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

A recent report in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association suggested that, at least for now, we need to lower the bar in Alzheimer’s disease drug trials.

Their point is that there’s no consensus on “clinically meaningful benefit.” Does it mean a complete cure for Alzheimer’s disease, with reversal of deficits? Or stopping disease progression where it is? Or just slowing things down enough that it means something to patients, family members, and caregivers?

The last one is, realistically, where we are now.

The problem with this is that many nonmedical people equate “treatment” with “cure,” which isn’t close to the truth for many diseases. In Alzheimer’s disease, it’s even trickier to figure out. There’s a disparity between imaging (which suggests something that should be quite effective) and clinical results (which aren’t nearly as impressive as the PET scans).

So when I prescribe any of the Alzheimer’s medications, I make it pretty clear to patients, and more importantly the patient’s family, what they can and can’t expect. This isn’t easy, because most will come back a month later, tell me their loved one is no better, and want to try something else. So I have to explain it again. These people aren’t stupid. They’re hopeful, and also facing an impossible question. “Better” is a lot easier to judge than “slowed progression.”

“Better” is a great word for migraines. Or seizures. Or Parkinson’s disease. These are condition where patients and families can tell us whether they’ve seen an improvement.

But with the current treatments for Alzheimer’s disease we’re asking patients and families “do you think you’ve gotten any worse than you would have if you hadn’t taken the drug at all?”

That’s an impossible question to answer, unless you’re following people with objective cognitive data over time and comparing them against a placebo group, which is how these drugs got here in the first place – we know they do that.

But to a family watching their loved ones go downhill, such reassurances aren’t what they want to hear.

Regrettably, it’s where things stand. While I want to strive for absolute success in these things, today it’s simply not possible. Maybe it never will be, though I hope it is.

But, for now, I agree that we need to reframe what we’re going to consider clinically meaningful. Sometimes you have to settle for a flight of stairs instead of an elevator, but still hope that you’ll get to the top. It just takes longer, and it’s better than not going anywhere at all.

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

Last night I invested an hour and a half watching the first half of the Super Bowl ... because ... well, just because. As exciting as it might have been to watch, investing another 2 hours on the second half would have kept me up well past my bedtime. As I lay in bed with the thwack-thwack-thud of helmets hitting pads still reverberating in my ears, my thoughts drifted to the ever-shifting landscape of concussion management.

More than 2 decades ago, concussions were just beginning to exit the dark ages when loss of consciousness was the defining symptom or sign that most folks (and here I am including physicians) used to separate the run-of-the-mill stinger or bell-ringer from a “real” concussion.

The new era dawned with the appearance of clinics devoted to concussion management and the development of protocols that limited everything from physical exertion to reading and screen time. Schools were coaxed into subjecting their athletes to preparticipation testing sessions with the hope that creating a baseline cognitive assessment would somehow make the diagnosis and management of concussion feel more scientific. Many of the recommended management strategies were based on the intuitive but flawed notion of “brain rest.” If reading or bright lights aggravate patient’s symptoms, they should be avoided but otherwise resting the brain doesn’t seem to make sense.

Fortunately, there were, and hopefully will continue to be, clinicians willing to question hastily developed management protocols. One recent cohort study from Canada has found that, surprisingly, (to some experts), “early return to school was associated with a lower symptom burden” This association held true for both age groups the researches studied (8-12 years and 13-18 years). The authors conclude that delayed return to school “may be detrimental to recovery.” In this study, early return to school was defined as less than 3 days.

In another study, this one in the journal Pediatrics, the authors found that “the association of early screen time with postconcussion symptoms is not linear.” Their conclusion was that the best approach to clinical management of concussion should include a moderate amount of screen time.

After reading both of these studies I am heartened that we are now hearing voices suggesting a return to concussion management based on careful observation of the individual patient and common sense. A concussed brain is not a torn hamstring or a broken clavicle that under most circumstances will heal in a predictable amount of time. It is prudent to exclude the concussed patient from activities that carry a significant risk of reinjury until the symptoms have subsided. However, postconcussion symptoms are often vague and can be mistaken for or aggravated by a host of other conditions including learning disabilities, anxiety, and depression.

I hope that our experience with the COVID pandemic has taught us that removing children from school and their usual activities can have a serious negative effect on their emotional health and academic achievement. This seems to be particularly true for the young people who were already struggling to adjust to being a student. Getting out of the habit of going to school often intensifies the anxieties of an emotionally or academically challenged student. Each day away from the school atmosphere can compound the symptoms that may or may not have been triggered by the concussion.

The message here is clear that, whether we are talking about concussions or appendectomies or mononucleosis, the sooner we can return the child to something close to their old normal the more successful we will be in a helping them adjust to the new normal.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Last night I invested an hour and a half watching the first half of the Super Bowl ... because ... well, just because. As exciting as it might have been to watch, investing another 2 hours on the second half would have kept me up well past my bedtime. As I lay in bed with the thwack-thwack-thud of helmets hitting pads still reverberating in my ears, my thoughts drifted to the ever-shifting landscape of concussion management.

More than 2 decades ago, concussions were just beginning to exit the dark ages when loss of consciousness was the defining symptom or sign that most folks (and here I am including physicians) used to separate the run-of-the-mill stinger or bell-ringer from a “real” concussion.

The new era dawned with the appearance of clinics devoted to concussion management and the development of protocols that limited everything from physical exertion to reading and screen time. Schools were coaxed into subjecting their athletes to preparticipation testing sessions with the hope that creating a baseline cognitive assessment would somehow make the diagnosis and management of concussion feel more scientific. Many of the recommended management strategies were based on the intuitive but flawed notion of “brain rest.” If reading or bright lights aggravate patient’s symptoms, they should be avoided but otherwise resting the brain doesn’t seem to make sense.

Fortunately, there were, and hopefully will continue to be, clinicians willing to question hastily developed management protocols. One recent cohort study from Canada has found that, surprisingly, (to some experts), “early return to school was associated with a lower symptom burden” This association held true for both age groups the researches studied (8-12 years and 13-18 years). The authors conclude that delayed return to school “may be detrimental to recovery.” In this study, early return to school was defined as less than 3 days.

In another study, this one in the journal Pediatrics, the authors found that “the association of early screen time with postconcussion symptoms is not linear.” Their conclusion was that the best approach to clinical management of concussion should include a moderate amount of screen time.

After reading both of these studies I am heartened that we are now hearing voices suggesting a return to concussion management based on careful observation of the individual patient and common sense. A concussed brain is not a torn hamstring or a broken clavicle that under most circumstances will heal in a predictable amount of time. It is prudent to exclude the concussed patient from activities that carry a significant risk of reinjury until the symptoms have subsided. However, postconcussion symptoms are often vague and can be mistaken for or aggravated by a host of other conditions including learning disabilities, anxiety, and depression.

I hope that our experience with the COVID pandemic has taught us that removing children from school and their usual activities can have a serious negative effect on their emotional health and academic achievement. This seems to be particularly true for the young people who were already struggling to adjust to being a student. Getting out of the habit of going to school often intensifies the anxieties of an emotionally or academically challenged student. Each day away from the school atmosphere can compound the symptoms that may or may not have been triggered by the concussion.

The message here is clear that, whether we are talking about concussions or appendectomies or mononucleosis, the sooner we can return the child to something close to their old normal the more successful we will be in a helping them adjust to the new normal.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

Last night I invested an hour and a half watching the first half of the Super Bowl ... because ... well, just because. As exciting as it might have been to watch, investing another 2 hours on the second half would have kept me up well past my bedtime. As I lay in bed with the thwack-thwack-thud of helmets hitting pads still reverberating in my ears, my thoughts drifted to the ever-shifting landscape of concussion management.

More than 2 decades ago, concussions were just beginning to exit the dark ages when loss of consciousness was the defining symptom or sign that most folks (and here I am including physicians) used to separate the run-of-the-mill stinger or bell-ringer from a “real” concussion.

The new era dawned with the appearance of clinics devoted to concussion management and the development of protocols that limited everything from physical exertion to reading and screen time. Schools were coaxed into subjecting their athletes to preparticipation testing sessions with the hope that creating a baseline cognitive assessment would somehow make the diagnosis and management of concussion feel more scientific. Many of the recommended management strategies were based on the intuitive but flawed notion of “brain rest.” If reading or bright lights aggravate patient’s symptoms, they should be avoided but otherwise resting the brain doesn’t seem to make sense.

Fortunately, there were, and hopefully will continue to be, clinicians willing to question hastily developed management protocols. One recent cohort study from Canada has found that, surprisingly, (to some experts), “early return to school was associated with a lower symptom burden” This association held true for both age groups the researches studied (8-12 years and 13-18 years). The authors conclude that delayed return to school “may be detrimental to recovery.” In this study, early return to school was defined as less than 3 days.

In another study, this one in the journal Pediatrics, the authors found that “the association of early screen time with postconcussion symptoms is not linear.” Their conclusion was that the best approach to clinical management of concussion should include a moderate amount of screen time.

After reading both of these studies I am heartened that we are now hearing voices suggesting a return to concussion management based on careful observation of the individual patient and common sense. A concussed brain is not a torn hamstring or a broken clavicle that under most circumstances will heal in a predictable amount of time. It is prudent to exclude the concussed patient from activities that carry a significant risk of reinjury until the symptoms have subsided. However, postconcussion symptoms are often vague and can be mistaken for or aggravated by a host of other conditions including learning disabilities, anxiety, and depression.

I hope that our experience with the COVID pandemic has taught us that removing children from school and their usual activities can have a serious negative effect on their emotional health and academic achievement. This seems to be particularly true for the young people who were already struggling to adjust to being a student. Getting out of the habit of going to school often intensifies the anxieties of an emotionally or academically challenged student. Each day away from the school atmosphere can compound the symptoms that may or may not have been triggered by the concussion.

The message here is clear that, whether we are talking about concussions or appendectomies or mononucleosis, the sooner we can return the child to something close to their old normal the more successful we will be in a helping them adjust to the new normal.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

If the pandemic served as a window into our health, what it revealed was a U.S. population that is not only sick but also seemingly only getting sicker. Life expectancy is falling precipitously. Three-fourths of Americans are overweight or obese, half have diabetes or prediabetes, and a majority are metabolically unhealthy. Furthermore, the rates of allergic, inflammatory, and autoimmune diseases are rising at rates of 3%-9% per year in the West, far faster than the speed of genetic change in this population.

Of course, diet and lifestyle are major factors behind such trends, but a grossly underappreciated driver in what ails us is the role of environmental toxins and endocrine-disrupting chemicals. In years past, these factors have largely evaded the traditional Western medical establishment; however, mounting evidence now supports their significance in fertility, metabolic health, and cancer.

Although several industrial chemicals and toxins have been identified as carcinogens and have subsequently been regulated, many more remain persistent in the environment and continue to be freely used. It is therefore incumbent upon both the general public and clinicians to be knowledgeable about these exposures. Here, we review some of the most common exposures and the substantial health risks associated with them, along with some general guidance around best practices for how to minimize exposure.
 

Microplastics

“Microplastics” is a term used to describe small fragments or particles of plastic breakdown or microbeads from household or personal care products, measuring less than 5 mm in length.

Plastic waste is accumulating at alarming and devastating proportions – by 2050, it is estimated that by weight, there will be more plastic than fish in the oceans. That translates into hundreds of thousands of tons of microplastics and trillions of these particles in the seas. A recent study demonstrated that microplastics were present in the bloodstream in the majority of 22 otherwise healthy participants.

Since the 1950s, plastic exposure has been shown to promote tumorigenesis in animal studies, and in vitro studies have demonstrated the toxicity of microplastics at the cellular level. However, it is not well known whether the plastic itself is toxic or if it simply serves as a carrier for other environmental toxins to bioaccumulate.

According to Tasha Stoiber, a senior scientist at the Environmental Working Group, “Microplastics have been widely detected in fish and seafood, as well as other products like bottled water, beer, honey, and tap water.” The EWG states there are no formal advisories on fish consumption to avoid exposure to microplastics at the moment.

Pressure also is mounting for a ban on microbeads in personal care products.

Until such bans are put in place, it is advised to avoid single-use plastics, favor reusable tote bags for grocery shopping rather than plastic bags, and opt for loose leaf tea or paper tea bags rather than mesh-based alternatives.
 

Phthalates

Phthalates are chemicals used to make plastics soft and durable, as well as to bind fragrances. They are commonly found in household items such as vinyl (for example, flooring, shower curtains) and fragrances, air fresheners, and perfumes.

Phthalates are known hormone-disrupting chemicals, exposure to which has been associated with abnormal sexual and brain development in children, as well as lower levels of testosterone in men. Exposures are thought to occur via inhalation, ingestion, and skin contact; however, fasting studies demonstrate that a majority of exposure is probably food related.

To avoid phthalate exposures, recommendations include avoiding polyvinyl chloride plastics (particularly food containers, plastic wrap, and children’s toys), which are identifiable by the recycle code number 3, as well as air fresheners and fragranced products.

The EWG’s Skin Deep database provides an important resource on phthalate-free personal care products.

Despite pressure from consumer advocacy groups, the U.S. Food and Drug Administration has not yet banned phthalates in food packaging.
 

Bisphenol A (BPA)

BPA is a chemical additive used to make clear and hard polycarbonate plastics, as well as epoxy and thermal papers. BPA is one of the highest-volume chemicals, with roughly 6 billion pounds produced each year. BPA is traditionally found in many clear plastic bottles and sippy cups, as well as in the lining of canned foods.

Structurally, BPA acts as an estrogen mimetic and has been associated with cardiovascular disease, obesity, and male sexual dysfunction. Since 2012, BPA has been banned in sippy cups and baby bottles, but there is some debate as to whether its replacements (bisphenol S and bisphenol F) are any safer; they appear to have similar hormonal effects as BPA.

As with phthalates, the majority of ingestion is thought to be food related. BPA has been found in more than 90% of a representative study population in the United States.

Guidance advises avoiding polycarbonate plastics (identifiable with the recycling code number 7), as well as avoiding handling thermal papers such as tickets and receipts, if possible. Food and beverages should be stored in glass or stainless steel. If plastic must be used, opt for polycarbonate- and polyvinyl chloride–free plastics, and food and beverages should never be reheated in plastic containers or wrapping. Canned foods should ideally be avoided, particularly canned tunas and condensed soups. If canned products are bought, they should ideally be BPA free.
 

Dioxins and polychlorinated biphenyls (PCBs)

Dioxins are mainly the byproducts of industrial practices; they are released after incineration, trash burning, and fires. PCBs, which are somewhat structurally related to dioxins, were previously found in products such as flame retardants and coolants. Dioxins and PCBs are often grouped in the same category under the umbrella term “persistent organic pollutants” because they break down slowly and remain in the environment even after emissions have been curbed.

Tetrachlorodibenzodioxin, perhaps the best-known dioxin, is a known carcinogen. Dioxins also have been associated with a host of health implications in development, immunity, and reproductive and endocrine systems. Higher levels of PCB exposure have also been associated with an increased risk for mortality from cardiovascular disease.

Notably, dioxin emissions have been reduced by 90% since the 1980s, and the U.S. Environmental Protection Agency has banned the use of PCBs in industrial manufacturing since 1979. However, environmental dioxins and PCBs still enter the food chain and accumulate in fat.

The best ways to avoid exposures are through limiting meat, fish, and dairy consumption and trimming the skin and fat from meats. The level of dioxins and PCBs found in meat, eggs, fish, and dairy are approximately 5-10 times higher than they are in plant-based foods. Research has shown that farmed salmon is likely to be the most PCB-contaminated protein source in the U.S. diet; however, newer forms of land-based and sustainable aquaculture probably avoid this exposure.
 

Pesticides

The growth of modern monoculture agriculture in the United States over the past century has coincided with a dramatic surge in the use of industrial pesticides. In fact, over 90% of the U.S. population have pesticides in their urine and blood, regardless of where they live. Exposures are thought to be food related.

Approximately 1 billion pounds of pesticides are used annually in the United States, including nearly 300 million pounds of glyphosate, which has been identified as a probable carcinogen by European agencies. The EPA has not yet reached this conclusion, although the matter is currently being litigated.

A large European prospective cohort trial demonstrated a lower risk for cancer in those with a greater frequency of self-reported organic food consumption. In addition to cancer risk, relatively elevated blood levels of a pesticide known as beta-hexachlorocyclohexane (B-HCH) are associated with higher all-cause mortality. Also, exposure to DDE – a metabolite of DDT, a chlorinated pesticide heavily used in the 1940s-1960s that still persists in the environment today – has been shown to increase the risk for Alzheimer’s-type dementia as well as overall cognitive decline.

Because these chlorinated pesticides are often fat soluble, they seem to accumulate in animal products. Therefore, people consuming a vegetarian diet have been found to have lower levels of B-HCH. This has led to the recommendation that consumers of produce should favor organic over conventional, if possible. Here too, the EWG provides an important resource to consumers in the form of shopper guides regarding pesticides in produce.
 

Per- and polyfluoroalkyl substances (PFAS)

PFAS are a group of fluorinated compounds discovered in the 1930s. Their chemical composition includes a durable carbon-fluoride bond, giving them a persistence within the environment that has led to their being referred to as “forever chemicals.”

PFAS have been detected in the blood of 98% of Americans, and in the rainwater of locations as far afield as Tibet and Antarctica. Even low levels of exposure have been associated with an increased risk for cancer, liver disease, low birth weight, and hormonal disruption.

The properties of PFAS also make them both durable at very high heat and water repellent. Notoriously, the chemical was used by 3M to make Scotchgard for carpets and fabrics and by Dupont to make Teflon for nonstick coating of pots and pans. Although perfluorooctanoic acid (PFOA) was removed from nonstick cookware in 2013, PFAS – a family of thousands of synthetic compounds – remain common in fast-food packaging, water- and stain-repellent clothing, firefighting foam, and personal care products. PFAS are released into the environment during the breakdown of these consumer and industrial products, as well as from dumping from waste facilities.

Alarmingly, the EWG notes that up to 200 million Americans may be exposed to PFAS in their drinking water. In March 2021, the EPA announced that they will be regulating PFAS in drinking water; however, the regulations have not been finalized. Currently, it is up to individual states to test for its presence in the water. The EWG has compiled a map of all known PFAS contamination sites.

To avoid or prevent exposures from PFAS, recommendations include filtering tap water with either reverse osmosis or activated carbon filters, as well as avoiding fast food and carry-out food, if possible, and consumer products labeled as “water resistant,” “stain-resistant,” and “nonstick.”

In a testament to how harmful these chemicals are, the EPA recently revised their lifetime health advisories for PFAS, such as PFOA, to 0.004 parts per trillion, which is more than 10,000 times smaller than the previous limit of 70 parts per trillion. The EPA also has proposed formally designating certain PFAS chemicals as “hazardous substances.”

Dr. Goel, clinical assistant professor of medicine at Weill Cornell Medicine, New York, has disclosed no relevant financial relationships. A version of this article originally appeared on Medscape.com.

If the pandemic served as a window into our health, what it revealed was a U.S. population that is not only sick but also seemingly only getting sicker. Life expectancy is falling precipitously. Three-fourths of Americans are overweight or obese, half have diabetes or prediabetes, and a majority are metabolically unhealthy. Furthermore, the rates of allergic, inflammatory, and autoimmune diseases are rising at rates of 3%-9% per year in the West, far faster than the speed of genetic change in this population.

Of course, diet and lifestyle are major factors behind such trends, but a grossly underappreciated driver in what ails us is the role of environmental toxins and endocrine-disrupting chemicals. In years past, these factors have largely evaded the traditional Western medical establishment; however, mounting evidence now supports their significance in fertility, metabolic health, and cancer.

Although several industrial chemicals and toxins have been identified as carcinogens and have subsequently been regulated, many more remain persistent in the environment and continue to be freely used. It is therefore incumbent upon both the general public and clinicians to be knowledgeable about these exposures. Here, we review some of the most common exposures and the substantial health risks associated with them, along with some general guidance around best practices for how to minimize exposure.
 

Microplastics

“Microplastics” is a term used to describe small fragments or particles of plastic breakdown or microbeads from household or personal care products, measuring less than 5 mm in length.

Plastic waste is accumulating at alarming and devastating proportions – by 2050, it is estimated that by weight, there will be more plastic than fish in the oceans. That translates into hundreds of thousands of tons of microplastics and trillions of these particles in the seas. A recent study demonstrated that microplastics were present in the bloodstream in the majority of 22 otherwise healthy participants.

Since the 1950s, plastic exposure has been shown to promote tumorigenesis in animal studies, and in vitro studies have demonstrated the toxicity of microplastics at the cellular level. However, it is not well known whether the plastic itself is toxic or if it simply serves as a carrier for other environmental toxins to bioaccumulate.

According to Tasha Stoiber, a senior scientist at the Environmental Working Group, “Microplastics have been widely detected in fish and seafood, as well as other products like bottled water, beer, honey, and tap water.” The EWG states there are no formal advisories on fish consumption to avoid exposure to microplastics at the moment.

Pressure also is mounting for a ban on microbeads in personal care products.

Until such bans are put in place, it is advised to avoid single-use plastics, favor reusable tote bags for grocery shopping rather than plastic bags, and opt for loose leaf tea or paper tea bags rather than mesh-based alternatives.
 

Phthalates

Phthalates are chemicals used to make plastics soft and durable, as well as to bind fragrances. They are commonly found in household items such as vinyl (for example, flooring, shower curtains) and fragrances, air fresheners, and perfumes.

Phthalates are known hormone-disrupting chemicals, exposure to which has been associated with abnormal sexual and brain development in children, as well as lower levels of testosterone in men. Exposures are thought to occur via inhalation, ingestion, and skin contact; however, fasting studies demonstrate that a majority of exposure is probably food related.

To avoid phthalate exposures, recommendations include avoiding polyvinyl chloride plastics (particularly food containers, plastic wrap, and children’s toys), which are identifiable by the recycle code number 3, as well as air fresheners and fragranced products.

The EWG’s Skin Deep database provides an important resource on phthalate-free personal care products.

Despite pressure from consumer advocacy groups, the U.S. Food and Drug Administration has not yet banned phthalates in food packaging.
 

Bisphenol A (BPA)

BPA is a chemical additive used to make clear and hard polycarbonate plastics, as well as epoxy and thermal papers. BPA is one of the highest-volume chemicals, with roughly 6 billion pounds produced each year. BPA is traditionally found in many clear plastic bottles and sippy cups, as well as in the lining of canned foods.

Structurally, BPA acts as an estrogen mimetic and has been associated with cardiovascular disease, obesity, and male sexual dysfunction. Since 2012, BPA has been banned in sippy cups and baby bottles, but there is some debate as to whether its replacements (bisphenol S and bisphenol F) are any safer; they appear to have similar hormonal effects as BPA.

As with phthalates, the majority of ingestion is thought to be food related. BPA has been found in more than 90% of a representative study population in the United States.

Guidance advises avoiding polycarbonate plastics (identifiable with the recycling code number 7), as well as avoiding handling thermal papers such as tickets and receipts, if possible. Food and beverages should be stored in glass or stainless steel. If plastic must be used, opt for polycarbonate- and polyvinyl chloride–free plastics, and food and beverages should never be reheated in plastic containers or wrapping. Canned foods should ideally be avoided, particularly canned tunas and condensed soups. If canned products are bought, they should ideally be BPA free.
 

Dioxins and polychlorinated biphenyls (PCBs)

Dioxins are mainly the byproducts of industrial practices; they are released after incineration, trash burning, and fires. PCBs, which are somewhat structurally related to dioxins, were previously found in products such as flame retardants and coolants. Dioxins and PCBs are often grouped in the same category under the umbrella term “persistent organic pollutants” because they break down slowly and remain in the environment even after emissions have been curbed.

Tetrachlorodibenzodioxin, perhaps the best-known dioxin, is a known carcinogen. Dioxins also have been associated with a host of health implications in development, immunity, and reproductive and endocrine systems. Higher levels of PCB exposure have also been associated with an increased risk for mortality from cardiovascular disease.

Notably, dioxin emissions have been reduced by 90% since the 1980s, and the U.S. Environmental Protection Agency has banned the use of PCBs in industrial manufacturing since 1979. However, environmental dioxins and PCBs still enter the food chain and accumulate in fat.

The best ways to avoid exposures are through limiting meat, fish, and dairy consumption and trimming the skin and fat from meats. The level of dioxins and PCBs found in meat, eggs, fish, and dairy are approximately 5-10 times higher than they are in plant-based foods. Research has shown that farmed salmon is likely to be the most PCB-contaminated protein source in the U.S. diet; however, newer forms of land-based and sustainable aquaculture probably avoid this exposure.
 

Pesticides

The growth of modern monoculture agriculture in the United States over the past century has coincided with a dramatic surge in the use of industrial pesticides. In fact, over 90% of the U.S. population have pesticides in their urine and blood, regardless of where they live. Exposures are thought to be food related.

Approximately 1 billion pounds of pesticides are used annually in the United States, including nearly 300 million pounds of glyphosate, which has been identified as a probable carcinogen by European agencies. The EPA has not yet reached this conclusion, although the matter is currently being litigated.

A large European prospective cohort trial demonstrated a lower risk for cancer in those with a greater frequency of self-reported organic food consumption. In addition to cancer risk, relatively elevated blood levels of a pesticide known as beta-hexachlorocyclohexane (B-HCH) are associated with higher all-cause mortality. Also, exposure to DDE – a metabolite of DDT, a chlorinated pesticide heavily used in the 1940s-1960s that still persists in the environment today – has been shown to increase the risk for Alzheimer’s-type dementia as well as overall cognitive decline.

Because these chlorinated pesticides are often fat soluble, they seem to accumulate in animal products. Therefore, people consuming a vegetarian diet have been found to have lower levels of B-HCH. This has led to the recommendation that consumers of produce should favor organic over conventional, if possible. Here too, the EWG provides an important resource to consumers in the form of shopper guides regarding pesticides in produce.
 

Per- and polyfluoroalkyl substances (PFAS)

PFAS are a group of fluorinated compounds discovered in the 1930s. Their chemical composition includes a durable carbon-fluoride bond, giving them a persistence within the environment that has led to their being referred to as “forever chemicals.”

PFAS have been detected in the blood of 98% of Americans, and in the rainwater of locations as far afield as Tibet and Antarctica. Even low levels of exposure have been associated with an increased risk for cancer, liver disease, low birth weight, and hormonal disruption.

The properties of PFAS also make them both durable at very high heat and water repellent. Notoriously, the chemical was used by 3M to make Scotchgard for carpets and fabrics and by Dupont to make Teflon for nonstick coating of pots and pans. Although perfluorooctanoic acid (PFOA) was removed from nonstick cookware in 2013, PFAS – a family of thousands of synthetic compounds – remain common in fast-food packaging, water- and stain-repellent clothing, firefighting foam, and personal care products. PFAS are released into the environment during the breakdown of these consumer and industrial products, as well as from dumping from waste facilities.

Alarmingly, the EWG notes that up to 200 million Americans may be exposed to PFAS in their drinking water. In March 2021, the EPA announced that they will be regulating PFAS in drinking water; however, the regulations have not been finalized. Currently, it is up to individual states to test for its presence in the water. The EWG has compiled a map of all known PFAS contamination sites.

To avoid or prevent exposures from PFAS, recommendations include filtering tap water with either reverse osmosis or activated carbon filters, as well as avoiding fast food and carry-out food, if possible, and consumer products labeled as “water resistant,” “stain-resistant,” and “nonstick.”

In a testament to how harmful these chemicals are, the EPA recently revised their lifetime health advisories for PFAS, such as PFOA, to 0.004 parts per trillion, which is more than 10,000 times smaller than the previous limit of 70 parts per trillion. The EPA also has proposed formally designating certain PFAS chemicals as “hazardous substances.”

Dr. Goel, clinical assistant professor of medicine at Weill Cornell Medicine, New York, has disclosed no relevant financial relationships. A version of this article originally appeared on Medscape.com.

If the pandemic served as a window into our health, what it revealed was a U.S. population that is not only sick but also seemingly only getting sicker. Life expectancy is falling precipitously. Three-fourths of Americans are overweight or obese, half have diabetes or prediabetes, and a majority are metabolically unhealthy. Furthermore, the rates of allergic, inflammatory, and autoimmune diseases are rising at rates of 3%-9% per year in the West, far faster than the speed of genetic change in this population.

Of course, diet and lifestyle are major factors behind such trends, but a grossly underappreciated driver in what ails us is the role of environmental toxins and endocrine-disrupting chemicals. In years past, these factors have largely evaded the traditional Western medical establishment; however, mounting evidence now supports their significance in fertility, metabolic health, and cancer.

Although several industrial chemicals and toxins have been identified as carcinogens and have subsequently been regulated, many more remain persistent in the environment and continue to be freely used. It is therefore incumbent upon both the general public and clinicians to be knowledgeable about these exposures. Here, we review some of the most common exposures and the substantial health risks associated with them, along with some general guidance around best practices for how to minimize exposure.
 

Microplastics

“Microplastics” is a term used to describe small fragments or particles of plastic breakdown or microbeads from household or personal care products, measuring less than 5 mm in length.

Plastic waste is accumulating at alarming and devastating proportions – by 2050, it is estimated that by weight, there will be more plastic than fish in the oceans. That translates into hundreds of thousands of tons of microplastics and trillions of these particles in the seas. A recent study demonstrated that microplastics were present in the bloodstream in the majority of 22 otherwise healthy participants.

Since the 1950s, plastic exposure has been shown to promote tumorigenesis in animal studies, and in vitro studies have demonstrated the toxicity of microplastics at the cellular level. However, it is not well known whether the plastic itself is toxic or if it simply serves as a carrier for other environmental toxins to bioaccumulate.

According to Tasha Stoiber, a senior scientist at the Environmental Working Group, “Microplastics have been widely detected in fish and seafood, as well as other products like bottled water, beer, honey, and tap water.” The EWG states there are no formal advisories on fish consumption to avoid exposure to microplastics at the moment.

Pressure also is mounting for a ban on microbeads in personal care products.

Until such bans are put in place, it is advised to avoid single-use plastics, favor reusable tote bags for grocery shopping rather than plastic bags, and opt for loose leaf tea or paper tea bags rather than mesh-based alternatives.
 

Phthalates

Phthalates are chemicals used to make plastics soft and durable, as well as to bind fragrances. They are commonly found in household items such as vinyl (for example, flooring, shower curtains) and fragrances, air fresheners, and perfumes.

Phthalates are known hormone-disrupting chemicals, exposure to which has been associated with abnormal sexual and brain development in children, as well as lower levels of testosterone in men. Exposures are thought to occur via inhalation, ingestion, and skin contact; however, fasting studies demonstrate that a majority of exposure is probably food related.

To avoid phthalate exposures, recommendations include avoiding polyvinyl chloride plastics (particularly food containers, plastic wrap, and children’s toys), which are identifiable by the recycle code number 3, as well as air fresheners and fragranced products.

The EWG’s Skin Deep database provides an important resource on phthalate-free personal care products.

Despite pressure from consumer advocacy groups, the U.S. Food and Drug Administration has not yet banned phthalates in food packaging.
 

Bisphenol A (BPA)

BPA is a chemical additive used to make clear and hard polycarbonate plastics, as well as epoxy and thermal papers. BPA is one of the highest-volume chemicals, with roughly 6 billion pounds produced each year. BPA is traditionally found in many clear plastic bottles and sippy cups, as well as in the lining of canned foods.

Structurally, BPA acts as an estrogen mimetic and has been associated with cardiovascular disease, obesity, and male sexual dysfunction. Since 2012, BPA has been banned in sippy cups and baby bottles, but there is some debate as to whether its replacements (bisphenol S and bisphenol F) are any safer; they appear to have similar hormonal effects as BPA.

As with phthalates, the majority of ingestion is thought to be food related. BPA has been found in more than 90% of a representative study population in the United States.

Guidance advises avoiding polycarbonate plastics (identifiable with the recycling code number 7), as well as avoiding handling thermal papers such as tickets and receipts, if possible. Food and beverages should be stored in glass or stainless steel. If plastic must be used, opt for polycarbonate- and polyvinyl chloride–free plastics, and food and beverages should never be reheated in plastic containers or wrapping. Canned foods should ideally be avoided, particularly canned tunas and condensed soups. If canned products are bought, they should ideally be BPA free.
 

Dioxins and polychlorinated biphenyls (PCBs)

Dioxins are mainly the byproducts of industrial practices; they are released after incineration, trash burning, and fires. PCBs, which are somewhat structurally related to dioxins, were previously found in products such as flame retardants and coolants. Dioxins and PCBs are often grouped in the same category under the umbrella term “persistent organic pollutants” because they break down slowly and remain in the environment even after emissions have been curbed.

Tetrachlorodibenzodioxin, perhaps the best-known dioxin, is a known carcinogen. Dioxins also have been associated with a host of health implications in development, immunity, and reproductive and endocrine systems. Higher levels of PCB exposure have also been associated with an increased risk for mortality from cardiovascular disease.

Notably, dioxin emissions have been reduced by 90% since the 1980s, and the U.S. Environmental Protection Agency has banned the use of PCBs in industrial manufacturing since 1979. However, environmental dioxins and PCBs still enter the food chain and accumulate in fat.

The best ways to avoid exposures are through limiting meat, fish, and dairy consumption and trimming the skin and fat from meats. The level of dioxins and PCBs found in meat, eggs, fish, and dairy are approximately 5-10 times higher than they are in plant-based foods. Research has shown that farmed salmon is likely to be the most PCB-contaminated protein source in the U.S. diet; however, newer forms of land-based and sustainable aquaculture probably avoid this exposure.
 

Pesticides

The growth of modern monoculture agriculture in the United States over the past century has coincided with a dramatic surge in the use of industrial pesticides. In fact, over 90% of the U.S. population have pesticides in their urine and blood, regardless of where they live. Exposures are thought to be food related.

Approximately 1 billion pounds of pesticides are used annually in the United States, including nearly 300 million pounds of glyphosate, which has been identified as a probable carcinogen by European agencies. The EPA has not yet reached this conclusion, although the matter is currently being litigated.

A large European prospective cohort trial demonstrated a lower risk for cancer in those with a greater frequency of self-reported organic food consumption. In addition to cancer risk, relatively elevated blood levels of a pesticide known as beta-hexachlorocyclohexane (B-HCH) are associated with higher all-cause mortality. Also, exposure to DDE – a metabolite of DDT, a chlorinated pesticide heavily used in the 1940s-1960s that still persists in the environment today – has been shown to increase the risk for Alzheimer’s-type dementia as well as overall cognitive decline.

Because these chlorinated pesticides are often fat soluble, they seem to accumulate in animal products. Therefore, people consuming a vegetarian diet have been found to have lower levels of B-HCH. This has led to the recommendation that consumers of produce should favor organic over conventional, if possible. Here too, the EWG provides an important resource to consumers in the form of shopper guides regarding pesticides in produce.
 

Per- and polyfluoroalkyl substances (PFAS)

PFAS are a group of fluorinated compounds discovered in the 1930s. Their chemical composition includes a durable carbon-fluoride bond, giving them a persistence within the environment that has led to their being referred to as “forever chemicals.”

PFAS have been detected in the blood of 98% of Americans, and in the rainwater of locations as far afield as Tibet and Antarctica. Even low levels of exposure have been associated with an increased risk for cancer, liver disease, low birth weight, and hormonal disruption.

The properties of PFAS also make them both durable at very high heat and water repellent. Notoriously, the chemical was used by 3M to make Scotchgard for carpets and fabrics and by Dupont to make Teflon for nonstick coating of pots and pans. Although perfluorooctanoic acid (PFOA) was removed from nonstick cookware in 2013, PFAS – a family of thousands of synthetic compounds – remain common in fast-food packaging, water- and stain-repellent clothing, firefighting foam, and personal care products. PFAS are released into the environment during the breakdown of these consumer and industrial products, as well as from dumping from waste facilities.

Alarmingly, the EWG notes that up to 200 million Americans may be exposed to PFAS in their drinking water. In March 2021, the EPA announced that they will be regulating PFAS in drinking water; however, the regulations have not been finalized. Currently, it is up to individual states to test for its presence in the water. The EWG has compiled a map of all known PFAS contamination sites.

To avoid or prevent exposures from PFAS, recommendations include filtering tap water with either reverse osmosis or activated carbon filters, as well as avoiding fast food and carry-out food, if possible, and consumer products labeled as “water resistant,” “stain-resistant,” and “nonstick.”

In a testament to how harmful these chemicals are, the EPA recently revised their lifetime health advisories for PFAS, such as PFOA, to 0.004 parts per trillion, which is more than 10,000 times smaller than the previous limit of 70 parts per trillion. The EPA also has proposed formally designating certain PFAS chemicals as “hazardous substances.”

Dr. Goel, clinical assistant professor of medicine at Weill Cornell Medicine, New York, has disclosed no relevant financial relationships. A version of this article originally appeared on Medscape.com.