It’s Oscars weekend, so for the second annual Meddy Awards – a very self-congratulatory and very tongue-in-cheek version of the Oscars – we celebrate outstanding medical performances and events in motion pictures throughout history. Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...

Best depiction of emergency medicine’s rollercoaster

M*A*S*H (1970)

The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.

Best ‘is there a doctor in the house?’ moment

Field of Dreams (1989)

When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.

Most unethical doctor

Elvis (2022)

No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”

Best self-use of a defibrillator

Casino Royale (2006)

We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.

Best worst patient lying about an injury

Tár (2022)

Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.

Best therapy for a speech disorder

The King’s Speech (2010)

Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”

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

It’s Oscars weekend, so for the second annual Meddy Awards – a very self-congratulatory and very tongue-in-cheek version of the Oscars – we celebrate outstanding medical performances and events in motion pictures throughout history. Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...

Best depiction of emergency medicine’s rollercoaster

M*A*S*H (1970)

The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.

Best ‘is there a doctor in the house?’ moment

Field of Dreams (1989)

When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.

Most unethical doctor

Elvis (2022)

No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”

Best self-use of a defibrillator

Casino Royale (2006)

We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.

Best worst patient lying about an injury

Tár (2022)

Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.

Best therapy for a speech disorder

The King’s Speech (2010)

Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”

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

It’s Oscars weekend, so for the second annual Meddy Awards – a very self-congratulatory and very tongue-in-cheek version of the Oscars – we celebrate outstanding medical performances and events in motion pictures throughout history. Without further ado (or comedy skits or musical numbers or extended tributes or commercials), the Meddys go to ...

Best depiction of emergency medicine’s rollercoaster

M*A*S*H (1970)

The original film, not the TV show, jumps from Frank Burns being hauled away in a straitjacket to a soldier’s spurting neck wound. Hawkeye Pierce calmly steps in and we see the entire sequence of him applying pressure, then stepping back to gown-and-glove (“it’s going to spurt a bit”), then jumping back in with arterial sutures, quipping, “Baby, we’re gonna see some stitchin’ like you never saw before.” After that, cocktail hour. Yes, medicine in Hollywood can be overdramatized and even inaccurate, but Robert Altman’s take on the novel by former U.S. Army surgeon Richard Hooker still stands tall for just how crazy emergency medicine can be.

Best ‘is there a doctor in the house?’ moment

Field of Dreams (1989)

When Ray Kinsella’s daughter gets knocked off the back of the bleachers, everything stops. No one knows what to do … except Doc “Moonlight” Graham, who gives up his life’s (and afterlife’s) dream to step off the field and save the girl from choking to death. Burt Lancaster, in his final movie role, embodies everything people wish a doctor to be: Calm, kind, and able to offer a quick, effective solution to a crisis. “Hey rookie! You were good.” Yes, he sure was.

Most unethical doctor

Elvis (2022)

No doctor wants to be remembered as the guy who killed Elvis. But that legacy clings to Dr. George Nichopoulos, Elvis’s personal physician in the 1970s. In Elvis, Dr. Nichopoulos, played by Tony Nixon, hovers in the background, enabling the King’s worsening addictions. Taking late-night calls for narcotics and injecting the unconscious star with stimulants, “unethical” is an understatement for the fictional “Dr. Nick.” The real Dr. Nichopoulos was acquitted of wrongdoing in Elvis’ death, although there is little doubt that the thousands of medication doses he prescribed played a role. When his license was finally revoked for overprescribing in the 1990s, the obliging doc reportedly claimed, “I cared too much.”

Best self-use of a defibrillator

Casino Royale (2006)

We expect backlash in the post-award press conference since James Bond technically only attempted to self-defibrillate in the passenger seat of his car. He never attached the device to the leads. Vesper Lynd had to pick up his slack and save the day. Also, supporters of fellow self-defibrillating nominee Jason Statham in Crank will no doubt raise a stink on Twitter. But we stand by our choice because it was such an, ahem, heart-stopper of a scene.

Best worst patient lying about an injury

Tár (2022)

Love it or hate it, few recent movies have been as polarizing as Tár. Cate Blanchett’s portrayal of a musical genius might be toweringly brilliant or outrageously offensive (or both) depending on whom you ask. But clearly the character has a loose relationship with facts. More than a few doctors might have raised an eyebrow had Lydia Tár appeared with injuries to her face, claiming to have been attacked in a mugging. In reality, Lydia tripped and fell while pursuing an attractive young cellist into a hazardous basement. Did she lie to protect her image, preserve her marriage, or – like many patients – avoid a lecture on unhealthy behavior? We pick D, all of the above.

Best therapy for a speech disorder

The King’s Speech (2010)

Public speaking might cause anxiety for many of us, but how about doing it in front of a global radio audience while wrestling with a speech disorder? Based on a true story, The King’s Speech revealed that terrifying experience for England’s King George VI. Enter Lionel Logue, played by Geoffrey Rush. Irreverent, unconventional, and untrained, the Australian pioneer in speech and language therapy uses a range of strategies – some of which are still used today – to help the royal find his voice. But when singing, shouting swear words, and provoking rage don’t do the trick, Mr. Logue turns to psychotherapy to unearth the childhood traumas at the root of the king’s disability. Experience, as Mr. Logue tells his patient, matters just as much as “letters after your name.”

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

Of all the consequences of climate change, here’s one nobody counted on.

A team of European researchers digging into Siberian permafrost discovered and revived 13 types of prehistoric viruses. As the ancient frozen ground slowly loses its “perma” label because of rising temperatures, more and more microbes that have never encountered modern humans are resurfacing.

The researchers coined the isn’t-that-just-great term “zombie viruses” to describe previously dormant viruses that had been frozen in ice for tens of thousands of years – 27,000 to 48,500 years, in fact.

The first question is obvious: This is fascinating, but is it a good idea? We’re still dealing with a certain mutating virus our immune systems have never encountered before.

The second question: What does it mean?
 

No humans were harmed in this study

The quick answer: The viruses observed here were only able to infect amoebae. But viruses that can infect humans do indeed exist in environments like permafrost.

The possibility that an unearthed, unknown virus will one day appear from seemingly nowhere and result in another pandemic is not necessarily zero.

“There is an objective risk, and it is increasing,” says Jean-Michel Claverie, PhD, the lead researcher and an emeritus professor of genomics and bioinformatics at Aix-Marseille University in France. “However, we cannot put a number on this probability, specifically because we refuse to work with and revive human- and animal-infecting viruses. It would be much too dangerous.”

Based on Dr. Claverie and his team’s results, human- and animal-infecting viruses can indeed survive deep within the permafrost for extended periods of time. 

“From our research, we can deduce that other viruses present in the permafrost are likely still infectious,” says Dr. Claverie. “By sequencing the total DNA, we can detect the presence of viruses similar to those infecting animals or humans today.”

That said, the chances of something catastrophic happening from, say, humans exposed to thawed permafrost are slim. “[The microbes] would be quick to decay once they’re exposed to heat, UV light, and oxygen,” he says.

Also, in places like Siberia where permafrost exists, people generally do not. So, some science fiction-inspired fears (we see you, fans of John Carpenter’s “The Thing”) are pretty unfounded. But if more people or companies begin to migrate toward the areas where these microbes are being released, the chances of a virus successfully infecting a host could be greater.
 

But what if ...

So, what would happen – hypothetically – if the next deadly virus to overtake our planet came from the Arctic permafrost? Would we even be remotely prepared?

“There is a small risk that a frozen virus that gets unearthed is able to start an infection chain that ends up in humans,” says Adrian Liston, PhD, an immunologist and senior group leader at the Babraham Institute, a life sciences research institute at the University of Cambridge in England. Dr. Liston was not involved in the research discussed here. “On the one hand, we would not have preexisting immunity against it, so the initial ability to combat the infection is low. On the other hand, the virus would not be adapted to infect (modern-day) humans, so the chance of an initial infection being successful for the virus is extremely low.”

That’s something a lot of folks don’t understand: Today’s viruses and other infectious microbes are infectious only because they exist today. They have evolved to work within our modern immune systems – for either good or ill.

“ ‘Entry events’ do happen, very rarely, and they can shape human evolution,” says Dr. Liston. “Major examples would be smallpox (a virus) and tuberculosis (a bacteria), which strongly influenced human evolution when they entered our species, selecting for the type of immune system that was able to fight them and killing off individuals with the ‘wrong’ type of immune system.”

And not all organisms are harmful.

“There are many, many microbes that are beneficial to humans,” Dr. Liston says. “But generally speaking, these are microbes that have evolved for millions of years to work in harmony with our body, such as our microbiome, or have been selected for thousands of years to do beneficial chores for us, like yeast in making bread or brewing beer.”

Some random frozen microbe is unlikely to affect us directly, but if it does, it is far more likely to be bad, Dr. Liston says.

For now, at least, we can rest easy knowing that Dr. Claverie and his team have no plans to revive dangerous viruses or retrieve more samples. “Because of the Russian-Ukrainian war, all of our collaborations have stopped. We are now focused on studying the viruses already in our lab and understanding how they replicate and interact with their cellular hosts,” he says.

If anything, zombie viruses can at least remind us about the constant increasing effects that climate change will have on our lives and planet in the near future.

“The most important take-home message is that climate change is going to create unexpected problems,” says Dr. Liston. “It isn’t simply changes to weather, climate events, and sea levels rising. A whole cascade of secondary problems will be generated. New infections, some of which could go pandemic, are almost certainly going to happen because of climate change.”

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

Of all the consequences of climate change, here’s one nobody counted on.

A team of European researchers digging into Siberian permafrost discovered and revived 13 types of prehistoric viruses. As the ancient frozen ground slowly loses its “perma” label because of rising temperatures, more and more microbes that have never encountered modern humans are resurfacing.

The researchers coined the isn’t-that-just-great term “zombie viruses” to describe previously dormant viruses that had been frozen in ice for tens of thousands of years – 27,000 to 48,500 years, in fact.

The first question is obvious: This is fascinating, but is it a good idea? We’re still dealing with a certain mutating virus our immune systems have never encountered before.

The second question: What does it mean?
 

No humans were harmed in this study

The quick answer: The viruses observed here were only able to infect amoebae. But viruses that can infect humans do indeed exist in environments like permafrost.

The possibility that an unearthed, unknown virus will one day appear from seemingly nowhere and result in another pandemic is not necessarily zero.

“There is an objective risk, and it is increasing,” says Jean-Michel Claverie, PhD, the lead researcher and an emeritus professor of genomics and bioinformatics at Aix-Marseille University in France. “However, we cannot put a number on this probability, specifically because we refuse to work with and revive human- and animal-infecting viruses. It would be much too dangerous.”

Based on Dr. Claverie and his team’s results, human- and animal-infecting viruses can indeed survive deep within the permafrost for extended periods of time. 

“From our research, we can deduce that other viruses present in the permafrost are likely still infectious,” says Dr. Claverie. “By sequencing the total DNA, we can detect the presence of viruses similar to those infecting animals or humans today.”

That said, the chances of something catastrophic happening from, say, humans exposed to thawed permafrost are slim. “[The microbes] would be quick to decay once they’re exposed to heat, UV light, and oxygen,” he says.

Also, in places like Siberia where permafrost exists, people generally do not. So, some science fiction-inspired fears (we see you, fans of John Carpenter’s “The Thing”) are pretty unfounded. But if more people or companies begin to migrate toward the areas where these microbes are being released, the chances of a virus successfully infecting a host could be greater.
 

But what if ...

So, what would happen – hypothetically – if the next deadly virus to overtake our planet came from the Arctic permafrost? Would we even be remotely prepared?

“There is a small risk that a frozen virus that gets unearthed is able to start an infection chain that ends up in humans,” says Adrian Liston, PhD, an immunologist and senior group leader at the Babraham Institute, a life sciences research institute at the University of Cambridge in England. Dr. Liston was not involved in the research discussed here. “On the one hand, we would not have preexisting immunity against it, so the initial ability to combat the infection is low. On the other hand, the virus would not be adapted to infect (modern-day) humans, so the chance of an initial infection being successful for the virus is extremely low.”

That’s something a lot of folks don’t understand: Today’s viruses and other infectious microbes are infectious only because they exist today. They have evolved to work within our modern immune systems – for either good or ill.

“ ‘Entry events’ do happen, very rarely, and they can shape human evolution,” says Dr. Liston. “Major examples would be smallpox (a virus) and tuberculosis (a bacteria), which strongly influenced human evolution when they entered our species, selecting for the type of immune system that was able to fight them and killing off individuals with the ‘wrong’ type of immune system.”

And not all organisms are harmful.

“There are many, many microbes that are beneficial to humans,” Dr. Liston says. “But generally speaking, these are microbes that have evolved for millions of years to work in harmony with our body, such as our microbiome, or have been selected for thousands of years to do beneficial chores for us, like yeast in making bread or brewing beer.”

Some random frozen microbe is unlikely to affect us directly, but if it does, it is far more likely to be bad, Dr. Liston says.

For now, at least, we can rest easy knowing that Dr. Claverie and his team have no plans to revive dangerous viruses or retrieve more samples. “Because of the Russian-Ukrainian war, all of our collaborations have stopped. We are now focused on studying the viruses already in our lab and understanding how they replicate and interact with their cellular hosts,” he says.

If anything, zombie viruses can at least remind us about the constant increasing effects that climate change will have on our lives and planet in the near future.

“The most important take-home message is that climate change is going to create unexpected problems,” says Dr. Liston. “It isn’t simply changes to weather, climate events, and sea levels rising. A whole cascade of secondary problems will be generated. New infections, some of which could go pandemic, are almost certainly going to happen because of climate change.”

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

Of all the consequences of climate change, here’s one nobody counted on.

A team of European researchers digging into Siberian permafrost discovered and revived 13 types of prehistoric viruses. As the ancient frozen ground slowly loses its “perma” label because of rising temperatures, more and more microbes that have never encountered modern humans are resurfacing.

The researchers coined the isn’t-that-just-great term “zombie viruses” to describe previously dormant viruses that had been frozen in ice for tens of thousands of years – 27,000 to 48,500 years, in fact.

The first question is obvious: This is fascinating, but is it a good idea? We’re still dealing with a certain mutating virus our immune systems have never encountered before.

The second question: What does it mean?
 

No humans were harmed in this study

The quick answer: The viruses observed here were only able to infect amoebae. But viruses that can infect humans do indeed exist in environments like permafrost.

The possibility that an unearthed, unknown virus will one day appear from seemingly nowhere and result in another pandemic is not necessarily zero.

“There is an objective risk, and it is increasing,” says Jean-Michel Claverie, PhD, the lead researcher and an emeritus professor of genomics and bioinformatics at Aix-Marseille University in France. “However, we cannot put a number on this probability, specifically because we refuse to work with and revive human- and animal-infecting viruses. It would be much too dangerous.”

Based on Dr. Claverie and his team’s results, human- and animal-infecting viruses can indeed survive deep within the permafrost for extended periods of time. 

“From our research, we can deduce that other viruses present in the permafrost are likely still infectious,” says Dr. Claverie. “By sequencing the total DNA, we can detect the presence of viruses similar to those infecting animals or humans today.”

That said, the chances of something catastrophic happening from, say, humans exposed to thawed permafrost are slim. “[The microbes] would be quick to decay once they’re exposed to heat, UV light, and oxygen,” he says.

Also, in places like Siberia where permafrost exists, people generally do not. So, some science fiction-inspired fears (we see you, fans of John Carpenter’s “The Thing”) are pretty unfounded. But if more people or companies begin to migrate toward the areas where these microbes are being released, the chances of a virus successfully infecting a host could be greater.
 

But what if ...

So, what would happen – hypothetically – if the next deadly virus to overtake our planet came from the Arctic permafrost? Would we even be remotely prepared?

“There is a small risk that a frozen virus that gets unearthed is able to start an infection chain that ends up in humans,” says Adrian Liston, PhD, an immunologist and senior group leader at the Babraham Institute, a life sciences research institute at the University of Cambridge in England. Dr. Liston was not involved in the research discussed here. “On the one hand, we would not have preexisting immunity against it, so the initial ability to combat the infection is low. On the other hand, the virus would not be adapted to infect (modern-day) humans, so the chance of an initial infection being successful for the virus is extremely low.”

That’s something a lot of folks don’t understand: Today’s viruses and other infectious microbes are infectious only because they exist today. They have evolved to work within our modern immune systems – for either good or ill.

“ ‘Entry events’ do happen, very rarely, and they can shape human evolution,” says Dr. Liston. “Major examples would be smallpox (a virus) and tuberculosis (a bacteria), which strongly influenced human evolution when they entered our species, selecting for the type of immune system that was able to fight them and killing off individuals with the ‘wrong’ type of immune system.”

And not all organisms are harmful.

“There are many, many microbes that are beneficial to humans,” Dr. Liston says. “But generally speaking, these are microbes that have evolved for millions of years to work in harmony with our body, such as our microbiome, or have been selected for thousands of years to do beneficial chores for us, like yeast in making bread or brewing beer.”

Some random frozen microbe is unlikely to affect us directly, but if it does, it is far more likely to be bad, Dr. Liston says.

For now, at least, we can rest easy knowing that Dr. Claverie and his team have no plans to revive dangerous viruses or retrieve more samples. “Because of the Russian-Ukrainian war, all of our collaborations have stopped. We are now focused on studying the viruses already in our lab and understanding how they replicate and interact with their cellular hosts,” he says.

If anything, zombie viruses can at least remind us about the constant increasing effects that climate change will have on our lives and planet in the near future.

“The most important take-home message is that climate change is going to create unexpected problems,” says Dr. Liston. “It isn’t simply changes to weather, climate events, and sea levels rising. A whole cascade of secondary problems will be generated. New infections, some of which could go pandemic, are almost certainly going to happen because of climate change.”

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

The suggestion that long-term endurance exercise may lead to a paradoxical increase in coronary atherosclerosis has been raised again by a new study.

In the Master@Heart study, lifelong endurance athletes had more coronary plaques, including more noncalcified plaques, than fit and healthy individuals with a similarly low cardiovascular risk profile.

The study was presented at the joint scientific sessions of the American College of Cardiology and the World Heart Federation. It was also simultaneously published online in the European Heart Journal.

“We consistently see higher plaque burden in lifelong endurance athletes. This is regardless of the plaque type, whether it is calcified, mixed, noncalcified, in the proximal segment or causing more than 50% stenosis,” concluded Ruben De Bosscher, MD, Catholic University of Leuven (Belgium), during his presentation.

The researchers suggested that all the information to date suggests there may be a “reverse J-shaped” dose-response relationship between exercise and coronary atherosclerosis.

Dr. De Bosscher added that “the worst thing you can do is nothing at all. As soon as you do a little bit of exercise – just brisk walking or jogging up to 3 hours a week – it seems that’s where you get the most benefit. And after that, we tend to see an increase in coronary plaque burden.”

The discussant of the study at the ACC session, Michael Emery, MD, codirector of the Sports Cardiology Center at the Cleveland Clinic, asked how this information should be translated into advice for the general public, given that it is known that endurance athletes show much improved mortality.

“That is a very good question,” Dr. De Bosscher replied. “Yes, we do see less events and adverse outcomes in endurance athletes, but that is compared to the whole population, including those that are unhealthy and do not exercise.

“If we only look at healthy individuals who do exercise but at varying levels, the question is, do we then see the same relationship?” he asked. “There is increasing evidence that there may be a point of diminished returns – and at a certain point, an increased cardiovascular risk is seen in endurance athletes.”

On advice to the public, Dr. De Bosscher added, “one of the main findings here is that, despite having a very healthy lifestyle style and exercising a lot, no one is granted immunity to coronary atherosclerosis. It would seem that the most benefit occurs in individuals doing a moderate amount of exercise – up to about 3 hours a week.”

In a comment, Dr. Emery noted: “This continues to be a ‘hot topic,’ although I continue to be underwhelmed, given a lack of hard outcomes, and I worry about the wrong take-home message being sent, that too much exercise will do more harm than good.”

He added that fitness still matters regardless of calcium score, and he would not advise people to stop exercising, because “the better your fitness, the better the outcome.”

However, he acknowledged that “the study does nicely illustrate that exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear, honestly).”

Also commenting, Paul D. Thompson, MD, Hartford (Conn.) Hospital, who has studied the cardiac implications of exercise for many years, said: “The problem we have in the U.S. and in most developed countries is not too much exercise but rather that most people don’t exercise very much at all.”

He noted that the Master@Heart study as an “important contribution” to the field.

“We have seen in previous trials that lifelong endurance athletes appear to have more deposition of cholesterol in their coronary arteries than you would expect,” he said. “But, while prior studies suggested that most of the deposits in endurance athletes were the safer type of highly calcified plaques, this study shows that the plaques in endurance athletes are not quite as benign as we had previously thought.”

It’s not clear what this means though, he added, because “despite these findings, it’s pretty clear that endurance athletes live longer than most people. But do they live longer because of the amount of exercise they do or because they are just hardier than the rest of us?”

He does not believe the study should be interpreted to mean that endurance exercise is dangerous. “We don’t have great evidence for that. This is a finding in a coronary artery. We don’t have outcome data.”

However, he added, “it doesn’t seem like you have to do a lot of extreme sport to get the cardiovascular benefits of exercise. All the studies show that the greatest benefits happen in people who go from doing very little to doing a moderate amount of exercise. Then it seems to plateau.”

Dr. Thompson pointed out that the most recent physical activity guidelines in the United States recommend between 150 and 300 minutes of moderate exercise, such as brisk walking, or 75-150 minutes a week of vigorous activity, such as running.

But he does not believe this study should put people off participating in endurance exercise, noting that many individuals engage in high levels of vigorous exercise for other reasons, not necessarily for their cardiovascular health.

“If people want to do more – for competitive reasons or if it makes them feel good – I say go ahead and do it,” Dr. Thompson added. “You should enjoy your life. But if you’re doing high levels of endurance exercise for your health and you’re miserable doing it, you may be wasting your time, as it doesn’t look as these more extreme levels of exercise do you any good. Does it do you any harm? We don’t have evidence yet to conclude that.”

In his presentation, Dr. De Bosscher noted that previous studies have reported higher calcium scores in athletes as well as more coronary plaques, compared with control persons. But the atherosclerotic lesions observed in the athletes were predominantly calcified plaques that were considered more stable and less prone to rupture, whereas nonathletes had predominantly mixed plaques that were considered less stable and more prone to rupture.

He pointed out, however, that these studies had limitations in that they included some individuals with other cardiovascular risk factors, such as smoking and intake of statins or antihypertensive drugs; they did not always assess the association between exercise and coronary atherosclerosis in a dose-response relationship; and while they reported the relative difference in plaque types, they didn’t report the absolute prevalence in calcified, noncalcified, and mixed plaques.

The Master@Heart study aimed to look at this question in a more comprehensive way.

The observational cohort study evaluated coronary atherosclerosis in 191 lifelong master endurance athletes, 191 late-onset athletes (endurance sports initiation after age 30 years), and 176 healthy nonathletes who engaged in no more than 3 hours a week of exercise. All participants were male and had a low cardiovascular risk profile. The median age was 55 in the three groups.

Maximal oxygen uptake (VO_2max) was used to quantify fitness. Lifelong and late-onset athletes had higher percentage predicted VO_2max than nonathletes (159 vs. 155 vs. 122).

There was no significant difference between the three groups with regard to age, weight, blood pressure cholesterol levels, or hemoglobin A1c levels. While the control group had a healthy body mass index and body fat percentage (19%), both groups of athletes were significantly leaner (body fat percentage, 14%-15%).

The exercise performed by the lifelong and late-onset endurance athletes was similar – mainly cycling and running. The endurance athletes reported an average of 10-11 hours of exercise per week, compared with 1 hour per week for the control persons. Only 22% of the control group reported engaging in no exercise at all; the others reported jogging, cycling, or engaging in nonendurance exercise, such as tennis.

Results showed that the overall coronary plaque burden assessed by segment stenosis score and segment-involvement score was higher among lifelong athletes than control persons (between-group difference, 0.86 and 0.65, respectively).

In comparison to control persons, lifelong endurance sport participation was associated with having one or more of each of the following, compared with a healthy nonathletic lifestyle:

• More than one coronary plaque (odds ratio, 1.86; 95% confidence interval, 1.17-2.94)
• More than one proximal plaque (OR, 1.96; 95% CI, 1.24-3.11)
• More than one calcified plaque (OR, 1.58; 95% CI, 1.01-2.49)
• More than one calcified proximal plaque (OR, 2.07; 95% CI, 1.28-3.35)
• More than one noncalcified plaque (OR, 1.95; 95% CI, 1.12-3.40)
• More than one noncalcified proximal plaque (OR, 2.80; 95% CI, 1.39-5.65)
• More than one mixed plaque (OR, 1.78; 95% CI, 1.06-2.99)

In comparison with late-onset athletes, at least 50% stenosis in any coronary segment (OR, 2.79; 95% CI, 1.20-6.50) and at least 50% stenosis in a proximal segment (OR, 5.92; 95% CI, 1.22 – 28.80) were more prevalent among lifelong athletes.

Vulnerable plaques, as defined by the presence of at least two high-risk features, were uncommon in all groups, but a lifelong athletic lifestyle was associated with a lower prevalence (OR, 0.11; 95% CI, 0.01-0.98).

In their article in the European Heart Journal, the researchers noted that the Master@Heart study is the largest and most comprehensive study to assess the dose-response relationship between intensive endurance exercise and coronary atherosclerosis.

“The findings do not support the hypothesis that highly trained endurance athletes have a more benign plaque composition to explain their lower risk of cardiovascular events compared to nonathletes,” they wrote.

“As studies on the impact of physical activity in the upper range are lacking, our data open the question on whether coronary events are indeed less prevalent in this high-end exercise cohort, and if that is the case, on what explains the paradox,” they concluded. “More and longitudinal research at the higher end of the endurance exercise spectrum is definitely needed.”

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

The suggestion that long-term endurance exercise may lead to a paradoxical increase in coronary atherosclerosis has been raised again by a new study.

In the Master@Heart study, lifelong endurance athletes had more coronary plaques, including more noncalcified plaques, than fit and healthy individuals with a similarly low cardiovascular risk profile.

The study was presented at the joint scientific sessions of the American College of Cardiology and the World Heart Federation. It was also simultaneously published online in the European Heart Journal.

“We consistently see higher plaque burden in lifelong endurance athletes. This is regardless of the plaque type, whether it is calcified, mixed, noncalcified, in the proximal segment or causing more than 50% stenosis,” concluded Ruben De Bosscher, MD, Catholic University of Leuven (Belgium), during his presentation.

The researchers suggested that all the information to date suggests there may be a “reverse J-shaped” dose-response relationship between exercise and coronary atherosclerosis.

Dr. De Bosscher added that “the worst thing you can do is nothing at all. As soon as you do a little bit of exercise – just brisk walking or jogging up to 3 hours a week – it seems that’s where you get the most benefit. And after that, we tend to see an increase in coronary plaque burden.”

The discussant of the study at the ACC session, Michael Emery, MD, codirector of the Sports Cardiology Center at the Cleveland Clinic, asked how this information should be translated into advice for the general public, given that it is known that endurance athletes show much improved mortality.

“That is a very good question,” Dr. De Bosscher replied. “Yes, we do see less events and adverse outcomes in endurance athletes, but that is compared to the whole population, including those that are unhealthy and do not exercise.

“If we only look at healthy individuals who do exercise but at varying levels, the question is, do we then see the same relationship?” he asked. “There is increasing evidence that there may be a point of diminished returns – and at a certain point, an increased cardiovascular risk is seen in endurance athletes.”

On advice to the public, Dr. De Bosscher added, “one of the main findings here is that, despite having a very healthy lifestyle style and exercising a lot, no one is granted immunity to coronary atherosclerosis. It would seem that the most benefit occurs in individuals doing a moderate amount of exercise – up to about 3 hours a week.”

In a comment, Dr. Emery noted: “This continues to be a ‘hot topic,’ although I continue to be underwhelmed, given a lack of hard outcomes, and I worry about the wrong take-home message being sent, that too much exercise will do more harm than good.”

He added that fitness still matters regardless of calcium score, and he would not advise people to stop exercising, because “the better your fitness, the better the outcome.”

However, he acknowledged that “the study does nicely illustrate that exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear, honestly).”

Also commenting, Paul D. Thompson, MD, Hartford (Conn.) Hospital, who has studied the cardiac implications of exercise for many years, said: “The problem we have in the U.S. and in most developed countries is not too much exercise but rather that most people don’t exercise very much at all.”

He noted that the Master@Heart study as an “important contribution” to the field.

“We have seen in previous trials that lifelong endurance athletes appear to have more deposition of cholesterol in their coronary arteries than you would expect,” he said. “But, while prior studies suggested that most of the deposits in endurance athletes were the safer type of highly calcified plaques, this study shows that the plaques in endurance athletes are not quite as benign as we had previously thought.”

It’s not clear what this means though, he added, because “despite these findings, it’s pretty clear that endurance athletes live longer than most people. But do they live longer because of the amount of exercise they do or because they are just hardier than the rest of us?”

He does not believe the study should be interpreted to mean that endurance exercise is dangerous. “We don’t have great evidence for that. This is a finding in a coronary artery. We don’t have outcome data.”

However, he added, “it doesn’t seem like you have to do a lot of extreme sport to get the cardiovascular benefits of exercise. All the studies show that the greatest benefits happen in people who go from doing very little to doing a moderate amount of exercise. Then it seems to plateau.”

Dr. Thompson pointed out that the most recent physical activity guidelines in the United States recommend between 150 and 300 minutes of moderate exercise, such as brisk walking, or 75-150 minutes a week of vigorous activity, such as running.

But he does not believe this study should put people off participating in endurance exercise, noting that many individuals engage in high levels of vigorous exercise for other reasons, not necessarily for their cardiovascular health.

“If people want to do more – for competitive reasons or if it makes them feel good – I say go ahead and do it,” Dr. Thompson added. “You should enjoy your life. But if you’re doing high levels of endurance exercise for your health and you’re miserable doing it, you may be wasting your time, as it doesn’t look as these more extreme levels of exercise do you any good. Does it do you any harm? We don’t have evidence yet to conclude that.”

In his presentation, Dr. De Bosscher noted that previous studies have reported higher calcium scores in athletes as well as more coronary plaques, compared with control persons. But the atherosclerotic lesions observed in the athletes were predominantly calcified plaques that were considered more stable and less prone to rupture, whereas nonathletes had predominantly mixed plaques that were considered less stable and more prone to rupture.

He pointed out, however, that these studies had limitations in that they included some individuals with other cardiovascular risk factors, such as smoking and intake of statins or antihypertensive drugs; they did not always assess the association between exercise and coronary atherosclerosis in a dose-response relationship; and while they reported the relative difference in plaque types, they didn’t report the absolute prevalence in calcified, noncalcified, and mixed plaques.

The Master@Heart study aimed to look at this question in a more comprehensive way.

The observational cohort study evaluated coronary atherosclerosis in 191 lifelong master endurance athletes, 191 late-onset athletes (endurance sports initiation after age 30 years), and 176 healthy nonathletes who engaged in no more than 3 hours a week of exercise. All participants were male and had a low cardiovascular risk profile. The median age was 55 in the three groups.

Maximal oxygen uptake (VO_2max) was used to quantify fitness. Lifelong and late-onset athletes had higher percentage predicted VO_2max than nonathletes (159 vs. 155 vs. 122).

There was no significant difference between the three groups with regard to age, weight, blood pressure cholesterol levels, or hemoglobin A1c levels. While the control group had a healthy body mass index and body fat percentage (19%), both groups of athletes were significantly leaner (body fat percentage, 14%-15%).

The exercise performed by the lifelong and late-onset endurance athletes was similar – mainly cycling and running. The endurance athletes reported an average of 10-11 hours of exercise per week, compared with 1 hour per week for the control persons. Only 22% of the control group reported engaging in no exercise at all; the others reported jogging, cycling, or engaging in nonendurance exercise, such as tennis.

Results showed that the overall coronary plaque burden assessed by segment stenosis score and segment-involvement score was higher among lifelong athletes than control persons (between-group difference, 0.86 and 0.65, respectively).

In comparison to control persons, lifelong endurance sport participation was associated with having one or more of each of the following, compared with a healthy nonathletic lifestyle:

• More than one coronary plaque (odds ratio, 1.86; 95% confidence interval, 1.17-2.94)
• More than one proximal plaque (OR, 1.96; 95% CI, 1.24-3.11)
• More than one calcified plaque (OR, 1.58; 95% CI, 1.01-2.49)
• More than one calcified proximal plaque (OR, 2.07; 95% CI, 1.28-3.35)
• More than one noncalcified plaque (OR, 1.95; 95% CI, 1.12-3.40)
• More than one noncalcified proximal plaque (OR, 2.80; 95% CI, 1.39-5.65)
• More than one mixed plaque (OR, 1.78; 95% CI, 1.06-2.99)

In comparison with late-onset athletes, at least 50% stenosis in any coronary segment (OR, 2.79; 95% CI, 1.20-6.50) and at least 50% stenosis in a proximal segment (OR, 5.92; 95% CI, 1.22 – 28.80) were more prevalent among lifelong athletes.

Vulnerable plaques, as defined by the presence of at least two high-risk features, were uncommon in all groups, but a lifelong athletic lifestyle was associated with a lower prevalence (OR, 0.11; 95% CI, 0.01-0.98).

In their article in the European Heart Journal, the researchers noted that the Master@Heart study is the largest and most comprehensive study to assess the dose-response relationship between intensive endurance exercise and coronary atherosclerosis.

“The findings do not support the hypothesis that highly trained endurance athletes have a more benign plaque composition to explain their lower risk of cardiovascular events compared to nonathletes,” they wrote.

“As studies on the impact of physical activity in the upper range are lacking, our data open the question on whether coronary events are indeed less prevalent in this high-end exercise cohort, and if that is the case, on what explains the paradox,” they concluded. “More and longitudinal research at the higher end of the endurance exercise spectrum is definitely needed.”

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

The suggestion that long-term endurance exercise may lead to a paradoxical increase in coronary atherosclerosis has been raised again by a new study.

In the Master@Heart study, lifelong endurance athletes had more coronary plaques, including more noncalcified plaques, than fit and healthy individuals with a similarly low cardiovascular risk profile.

The study was presented at the joint scientific sessions of the American College of Cardiology and the World Heart Federation. It was also simultaneously published online in the European Heart Journal.

“We consistently see higher plaque burden in lifelong endurance athletes. This is regardless of the plaque type, whether it is calcified, mixed, noncalcified, in the proximal segment or causing more than 50% stenosis,” concluded Ruben De Bosscher, MD, Catholic University of Leuven (Belgium), during his presentation.

The researchers suggested that all the information to date suggests there may be a “reverse J-shaped” dose-response relationship between exercise and coronary atherosclerosis.

Dr. De Bosscher added that “the worst thing you can do is nothing at all. As soon as you do a little bit of exercise – just brisk walking or jogging up to 3 hours a week – it seems that’s where you get the most benefit. And after that, we tend to see an increase in coronary plaque burden.”

The discussant of the study at the ACC session, Michael Emery, MD, codirector of the Sports Cardiology Center at the Cleveland Clinic, asked how this information should be translated into advice for the general public, given that it is known that endurance athletes show much improved mortality.

“That is a very good question,” Dr. De Bosscher replied. “Yes, we do see less events and adverse outcomes in endurance athletes, but that is compared to the whole population, including those that are unhealthy and do not exercise.

“If we only look at healthy individuals who do exercise but at varying levels, the question is, do we then see the same relationship?” he asked. “There is increasing evidence that there may be a point of diminished returns – and at a certain point, an increased cardiovascular risk is seen in endurance athletes.”

On advice to the public, Dr. De Bosscher added, “one of the main findings here is that, despite having a very healthy lifestyle style and exercising a lot, no one is granted immunity to coronary atherosclerosis. It would seem that the most benefit occurs in individuals doing a moderate amount of exercise – up to about 3 hours a week.”

In a comment, Dr. Emery noted: “This continues to be a ‘hot topic,’ although I continue to be underwhelmed, given a lack of hard outcomes, and I worry about the wrong take-home message being sent, that too much exercise will do more harm than good.”

He added that fitness still matters regardless of calcium score, and he would not advise people to stop exercising, because “the better your fitness, the better the outcome.”

However, he acknowledged that “the study does nicely illustrate that exercise does not make you immune from heart disease (which is a message a lot of athletes need to hear, honestly).”

Also commenting, Paul D. Thompson, MD, Hartford (Conn.) Hospital, who has studied the cardiac implications of exercise for many years, said: “The problem we have in the U.S. and in most developed countries is not too much exercise but rather that most people don’t exercise very much at all.”

He noted that the Master@Heart study as an “important contribution” to the field.

“We have seen in previous trials that lifelong endurance athletes appear to have more deposition of cholesterol in their coronary arteries than you would expect,” he said. “But, while prior studies suggested that most of the deposits in endurance athletes were the safer type of highly calcified plaques, this study shows that the plaques in endurance athletes are not quite as benign as we had previously thought.”

It’s not clear what this means though, he added, because “despite these findings, it’s pretty clear that endurance athletes live longer than most people. But do they live longer because of the amount of exercise they do or because they are just hardier than the rest of us?”

He does not believe the study should be interpreted to mean that endurance exercise is dangerous. “We don’t have great evidence for that. This is a finding in a coronary artery. We don’t have outcome data.”

However, he added, “it doesn’t seem like you have to do a lot of extreme sport to get the cardiovascular benefits of exercise. All the studies show that the greatest benefits happen in people who go from doing very little to doing a moderate amount of exercise. Then it seems to plateau.”

Dr. Thompson pointed out that the most recent physical activity guidelines in the United States recommend between 150 and 300 minutes of moderate exercise, such as brisk walking, or 75-150 minutes a week of vigorous activity, such as running.

But he does not believe this study should put people off participating in endurance exercise, noting that many individuals engage in high levels of vigorous exercise for other reasons, not necessarily for their cardiovascular health.

“If people want to do more – for competitive reasons or if it makes them feel good – I say go ahead and do it,” Dr. Thompson added. “You should enjoy your life. But if you’re doing high levels of endurance exercise for your health and you’re miserable doing it, you may be wasting your time, as it doesn’t look as these more extreme levels of exercise do you any good. Does it do you any harm? We don’t have evidence yet to conclude that.”

In his presentation, Dr. De Bosscher noted that previous studies have reported higher calcium scores in athletes as well as more coronary plaques, compared with control persons. But the atherosclerotic lesions observed in the athletes were predominantly calcified plaques that were considered more stable and less prone to rupture, whereas nonathletes had predominantly mixed plaques that were considered less stable and more prone to rupture.

He pointed out, however, that these studies had limitations in that they included some individuals with other cardiovascular risk factors, such as smoking and intake of statins or antihypertensive drugs; they did not always assess the association between exercise and coronary atherosclerosis in a dose-response relationship; and while they reported the relative difference in plaque types, they didn’t report the absolute prevalence in calcified, noncalcified, and mixed plaques.

The Master@Heart study aimed to look at this question in a more comprehensive way.

The observational cohort study evaluated coronary atherosclerosis in 191 lifelong master endurance athletes, 191 late-onset athletes (endurance sports initiation after age 30 years), and 176 healthy nonathletes who engaged in no more than 3 hours a week of exercise. All participants were male and had a low cardiovascular risk profile. The median age was 55 in the three groups.

Maximal oxygen uptake (VO_2max) was used to quantify fitness. Lifelong and late-onset athletes had higher percentage predicted VO_2max than nonathletes (159 vs. 155 vs. 122).

There was no significant difference between the three groups with regard to age, weight, blood pressure cholesterol levels, or hemoglobin A1c levels. While the control group had a healthy body mass index and body fat percentage (19%), both groups of athletes were significantly leaner (body fat percentage, 14%-15%).

The exercise performed by the lifelong and late-onset endurance athletes was similar – mainly cycling and running. The endurance athletes reported an average of 10-11 hours of exercise per week, compared with 1 hour per week for the control persons. Only 22% of the control group reported engaging in no exercise at all; the others reported jogging, cycling, or engaging in nonendurance exercise, such as tennis.

Results showed that the overall coronary plaque burden assessed by segment stenosis score and segment-involvement score was higher among lifelong athletes than control persons (between-group difference, 0.86 and 0.65, respectively).

In comparison to control persons, lifelong endurance sport participation was associated with having one or more of each of the following, compared with a healthy nonathletic lifestyle:

• More than one coronary plaque (odds ratio, 1.86; 95% confidence interval, 1.17-2.94)
• More than one proximal plaque (OR, 1.96; 95% CI, 1.24-3.11)
• More than one calcified plaque (OR, 1.58; 95% CI, 1.01-2.49)
• More than one calcified proximal plaque (OR, 2.07; 95% CI, 1.28-3.35)
• More than one noncalcified plaque (OR, 1.95; 95% CI, 1.12-3.40)
• More than one noncalcified proximal plaque (OR, 2.80; 95% CI, 1.39-5.65)
• More than one mixed plaque (OR, 1.78; 95% CI, 1.06-2.99)

In comparison with late-onset athletes, at least 50% stenosis in any coronary segment (OR, 2.79; 95% CI, 1.20-6.50) and at least 50% stenosis in a proximal segment (OR, 5.92; 95% CI, 1.22 – 28.80) were more prevalent among lifelong athletes.

Vulnerable plaques, as defined by the presence of at least two high-risk features, were uncommon in all groups, but a lifelong athletic lifestyle was associated with a lower prevalence (OR, 0.11; 95% CI, 0.01-0.98).

In their article in the European Heart Journal, the researchers noted that the Master@Heart study is the largest and most comprehensive study to assess the dose-response relationship between intensive endurance exercise and coronary atherosclerosis.

“The findings do not support the hypothesis that highly trained endurance athletes have a more benign plaque composition to explain their lower risk of cardiovascular events compared to nonathletes,” they wrote.

“As studies on the impact of physical activity in the upper range are lacking, our data open the question on whether coronary events are indeed less prevalent in this high-end exercise cohort, and if that is the case, on what explains the paradox,” they concluded. “More and longitudinal research at the higher end of the endurance exercise spectrum is definitely needed.”

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

Josh struggled for more than a decade with what his doctors had told him was irritable bowel syndrome (IBS). But curiously, the 39-year-old’s flare-ups were caused by some foods that aren’t typical IBS triggers. Peanuts and shellfish caused “stabbing” abdominal pains, and he would feel lightheaded after simply inhaling the scent of them. He also had severe constipation that lasted up to a week and rectal mucous discharges.

So, Josh (not his real name) sought the care of New York gastroenterologist Yevgenia Pashinsky, MD. She conducted a comprehensive nutritional assessment and sent him for allergy testing. The results: Josh had a little-known condition called systemic nickel allergy syndrome (SNAS), which can mimic some of the symptoms of IBS.

Dr. Pashinsky, of the department of medicine at Icahn School of Medicine at Mount Sinai, New York, and a partner with New York Gastroenterology Associates, presented Josh’s case as part of a seminar on SNAS and IBS “mimickers” at the Food and Nutrition Conference and Expo in Orlando last October, sponsored by the Academy of Nutrition and Dietetics.

She and two registered dietitians in her practice, Suzie Finkel, MS, RD, CDN, and Tamara Duker Freuman, MS, RD, CDN, told seminar attendees that SNAS is rarely diagnosed and can be mistaken for IBS. They noted that it probably strikes more people than doctors suspect.

“Systemic nickel allergy is present in at least 10% of the U.S. population (and much higher in some subgroups),” Dr. Pashinsky told this news organization. “But its connection to GI symptoms and functional GI disorders is still being learned about.

“I think of nickel allergy and other allergic disorders when, in addition to GI symptoms, the patient reports skin and mucous membrane involvement along with their abdominal reactions,” she said.

For patients like Josh with SNAS, the diagnosis and treatment of this condition are surprisingly simple and effective.

“Josh had these really [unusual] symptoms and nontraditional IBS food triggers,” Ms. Finkel said in an interview. “So, that’s a situation where, as dietitians we say, ‘Hmm, that’s weird; if you have IBS, then peanuts and shrimp shouldn’t really cause an issue here.’ But this might be something physicians might not be attuned to because it’s not part of their training.”

Ms. Finkel said that Josh was referred to an allergist. Josh tested positive for skin sensitization to nickel, and he was started on a low-nickel diet, which improved his symptoms.

“So, that was this happy ending,” she added.

The upshot?

“Doctors who treat IBS patients [who are not responding to treatment] need to consider the possibility that they have SNAS and send them for allergy testing,” Ms. Finkel said. “If they come back positive, simple dietary changes can address it.”
 

An underrecognized condition

There has been very little research regarding SNAS in patients with IBS, and there are no standard guidelines for diagnosing and treating it.

What’s more, many gastroenterologists aren’t familiar with it. More than a dozen gastroenterologists who were contacted for comment declined to be interviewed because they didn’t know about SNAS – or enough about it to provide useful information for the story.

Ms. Finkel said she’s not surprised that many gastroenterologists don’t know much about how SNAS can mimic IBS, which is why she and her colleagues presented the seminar last October in Orlando. “It’s really an allergy and not a GI disease. It manifests with GI symptoms, but the root is not in the digestive tract; the root is in a true allergy – a clinical allergy – to nickel.”

Complicating the issue is that people who have IBS and those with SNAS typically share some common symptoms.

Like IBS, SNAS can cause GI symptoms – such as cramping, abdominal pain, heartburn, constipation, gaseous distension, and mucus in the stool. It can be triggered by certain fresh, cooked, and canned foods.

But the food triggers that cause SNAS are not usually those that cause IBS symptoms. Rather, SNAS flare-ups are nearly always triggered by foods with high levels of nickel. Examples include apricots, artichokes, asparagus, beans, cauliflower, chickpeas, cocoa/chocolate, figs, lentils, licorice, oats, onions, peas, peanuts, potatoes, spinach, tomatoes, and tea.

According to the American Academy of Allergy, Asthma & Immunology, a distinguishing feature of SNAS is that it can cause allergic contact dermatitis when a person touches something made with nickel. Coins, jewelry, eyeglasses, home fixtures, keys, zippers, dental devices, and even stainless-steel cookware can contain allergy-triggering nickel.

What Ms. Finkel sees the most are skin reactions from touching a surface containing nickel or from ingesting it, she said.

The other immediate symptom is abdominal pain or changes in bowel movements, such as diarrhea, she added.

Christopher Randolph, MD, an allergist based in Connecticut, told this news organization that it’s important for doctors to realize that patients who have a skin reaction to nickel may also have inflammatory GI symptoms.

“We definitely need more controlled studies,” said Dr. Randolph, of the department of allergy and immunology at Yale University, New Haven, Conn. “But the takeaway here is for patients and certainly providers to be mindful that you can have systemic reactions to nickel, even though you implicate only the contact dermatitis.”
 

Diagnosis and treatment recommendations

Skin patch allergy testing – in which a person’s skin is exposed to nickel – can quickly determine whether a patient with IBS is actually experiencing inflammatory reactions to dietary nickel and would benefit from a low-nickel or no-nickel diet, research shows.

For these patients, Dr. Pashinsky recommends the following:

• Avoiding high-nickel foods.
• Limiting canned foods.
• Using nonstainless cookware, especially for acidic foods.
• Boiling foods for potential nickel reduction, especially grains and vegetables.
• Running the tap before using water to drink or cook with first thing in the morning.

Dr. Pashisky and her team also recommend the following guidelines for doctors:

• Ask patients if symptoms occur immediately after eating certain high-nickel foods or worsen with a low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diet.
• Determine whether a patient is not responding to typical medical and dietary interventions used to treat IBS.
• Conduct a food/symptom history to identify potential nickel allergy triggers.
• Try a low-nickel dietary intervention to see whether a patient’s symptoms improve in a week or two.
• Refer the patient for additional diagnostic skin-patch testing or treatment.

A multidisciplinary approach

Ms. Finkel said it’s important for doctors, particularly gastroenterologists who treat patients for suspected GI disorders to consider nickel allergy as a cause.

“SNAS is this overlooked condition ... and the research is really in its nascency here,” Ms. Finkel said.

“I would say only give [a low- or no-nickel diet] consideration if the high-nickel foods are a possible trigger,” she said. “It is very specific, looking at their diet history, to have a clear hypothesis based on what their triggers are. It’s not something to try out lightly because it’s a very restrictive diet, so I would never put a patient on a diet that I didn’t think was necessary.”

Ms. Finkel added that treatment of SNAS requires a multidisciplinary approach with a gastroenterologist, an allergist, and a dietitian.

Doctors and dietitians have distinct roles in identifying and treating these patients, Ms. Finkel said.

“If there is a suspicion of IBS symptoms and the patient is not responding to first-line treatments, then it is worth having the input of a dietitian and an allergist,” she said.

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

Josh struggled for more than a decade with what his doctors had told him was irritable bowel syndrome (IBS). But curiously, the 39-year-old’s flare-ups were caused by some foods that aren’t typical IBS triggers. Peanuts and shellfish caused “stabbing” abdominal pains, and he would feel lightheaded after simply inhaling the scent of them. He also had severe constipation that lasted up to a week and rectal mucous discharges.

So, Josh (not his real name) sought the care of New York gastroenterologist Yevgenia Pashinsky, MD. She conducted a comprehensive nutritional assessment and sent him for allergy testing. The results: Josh had a little-known condition called systemic nickel allergy syndrome (SNAS), which can mimic some of the symptoms of IBS.

Dr. Pashinsky, of the department of medicine at Icahn School of Medicine at Mount Sinai, New York, and a partner with New York Gastroenterology Associates, presented Josh’s case as part of a seminar on SNAS and IBS “mimickers” at the Food and Nutrition Conference and Expo in Orlando last October, sponsored by the Academy of Nutrition and Dietetics.

She and two registered dietitians in her practice, Suzie Finkel, MS, RD, CDN, and Tamara Duker Freuman, MS, RD, CDN, told seminar attendees that SNAS is rarely diagnosed and can be mistaken for IBS. They noted that it probably strikes more people than doctors suspect.

“Systemic nickel allergy is present in at least 10% of the U.S. population (and much higher in some subgroups),” Dr. Pashinsky told this news organization. “But its connection to GI symptoms and functional GI disorders is still being learned about.

“I think of nickel allergy and other allergic disorders when, in addition to GI symptoms, the patient reports skin and mucous membrane involvement along with their abdominal reactions,” she said.

For patients like Josh with SNAS, the diagnosis and treatment of this condition are surprisingly simple and effective.

“Josh had these really [unusual] symptoms and nontraditional IBS food triggers,” Ms. Finkel said in an interview. “So, that’s a situation where, as dietitians we say, ‘Hmm, that’s weird; if you have IBS, then peanuts and shrimp shouldn’t really cause an issue here.’ But this might be something physicians might not be attuned to because it’s not part of their training.”

Ms. Finkel said that Josh was referred to an allergist. Josh tested positive for skin sensitization to nickel, and he was started on a low-nickel diet, which improved his symptoms.

“So, that was this happy ending,” she added.

The upshot?

“Doctors who treat IBS patients [who are not responding to treatment] need to consider the possibility that they have SNAS and send them for allergy testing,” Ms. Finkel said. “If they come back positive, simple dietary changes can address it.”
 

An underrecognized condition

There has been very little research regarding SNAS in patients with IBS, and there are no standard guidelines for diagnosing and treating it.

What’s more, many gastroenterologists aren’t familiar with it. More than a dozen gastroenterologists who were contacted for comment declined to be interviewed because they didn’t know about SNAS – or enough about it to provide useful information for the story.

Ms. Finkel said she’s not surprised that many gastroenterologists don’t know much about how SNAS can mimic IBS, which is why she and her colleagues presented the seminar last October in Orlando. “It’s really an allergy and not a GI disease. It manifests with GI symptoms, but the root is not in the digestive tract; the root is in a true allergy – a clinical allergy – to nickel.”

Complicating the issue is that people who have IBS and those with SNAS typically share some common symptoms.

Like IBS, SNAS can cause GI symptoms – such as cramping, abdominal pain, heartburn, constipation, gaseous distension, and mucus in the stool. It can be triggered by certain fresh, cooked, and canned foods.

But the food triggers that cause SNAS are not usually those that cause IBS symptoms. Rather, SNAS flare-ups are nearly always triggered by foods with high levels of nickel. Examples include apricots, artichokes, asparagus, beans, cauliflower, chickpeas, cocoa/chocolate, figs, lentils, licorice, oats, onions, peas, peanuts, potatoes, spinach, tomatoes, and tea.

According to the American Academy of Allergy, Asthma & Immunology, a distinguishing feature of SNAS is that it can cause allergic contact dermatitis when a person touches something made with nickel. Coins, jewelry, eyeglasses, home fixtures, keys, zippers, dental devices, and even stainless-steel cookware can contain allergy-triggering nickel.

What Ms. Finkel sees the most are skin reactions from touching a surface containing nickel or from ingesting it, she said.

The other immediate symptom is abdominal pain or changes in bowel movements, such as diarrhea, she added.

Christopher Randolph, MD, an allergist based in Connecticut, told this news organization that it’s important for doctors to realize that patients who have a skin reaction to nickel may also have inflammatory GI symptoms.

“We definitely need more controlled studies,” said Dr. Randolph, of the department of allergy and immunology at Yale University, New Haven, Conn. “But the takeaway here is for patients and certainly providers to be mindful that you can have systemic reactions to nickel, even though you implicate only the contact dermatitis.”
 

Diagnosis and treatment recommendations

Skin patch allergy testing – in which a person’s skin is exposed to nickel – can quickly determine whether a patient with IBS is actually experiencing inflammatory reactions to dietary nickel and would benefit from a low-nickel or no-nickel diet, research shows.

For these patients, Dr. Pashinsky recommends the following:

• Avoiding high-nickel foods.
• Limiting canned foods.
• Using nonstainless cookware, especially for acidic foods.
• Boiling foods for potential nickel reduction, especially grains and vegetables.
• Running the tap before using water to drink or cook with first thing in the morning.

Dr. Pashisky and her team also recommend the following guidelines for doctors:

• Ask patients if symptoms occur immediately after eating certain high-nickel foods or worsen with a low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diet.
• Determine whether a patient is not responding to typical medical and dietary interventions used to treat IBS.
• Conduct a food/symptom history to identify potential nickel allergy triggers.
• Try a low-nickel dietary intervention to see whether a patient’s symptoms improve in a week or two.
• Refer the patient for additional diagnostic skin-patch testing or treatment.

A multidisciplinary approach

Ms. Finkel said it’s important for doctors, particularly gastroenterologists who treat patients for suspected GI disorders to consider nickel allergy as a cause.

“SNAS is this overlooked condition ... and the research is really in its nascency here,” Ms. Finkel said.

“I would say only give [a low- or no-nickel diet] consideration if the high-nickel foods are a possible trigger,” she said. “It is very specific, looking at their diet history, to have a clear hypothesis based on what their triggers are. It’s not something to try out lightly because it’s a very restrictive diet, so I would never put a patient on a diet that I didn’t think was necessary.”

Ms. Finkel added that treatment of SNAS requires a multidisciplinary approach with a gastroenterologist, an allergist, and a dietitian.

Doctors and dietitians have distinct roles in identifying and treating these patients, Ms. Finkel said.

“If there is a suspicion of IBS symptoms and the patient is not responding to first-line treatments, then it is worth having the input of a dietitian and an allergist,” she said.

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

Josh struggled for more than a decade with what his doctors had told him was irritable bowel syndrome (IBS). But curiously, the 39-year-old’s flare-ups were caused by some foods that aren’t typical IBS triggers. Peanuts and shellfish caused “stabbing” abdominal pains, and he would feel lightheaded after simply inhaling the scent of them. He also had severe constipation that lasted up to a week and rectal mucous discharges.

So, Josh (not his real name) sought the care of New York gastroenterologist Yevgenia Pashinsky, MD. She conducted a comprehensive nutritional assessment and sent him for allergy testing. The results: Josh had a little-known condition called systemic nickel allergy syndrome (SNAS), which can mimic some of the symptoms of IBS.

Dr. Pashinsky, of the department of medicine at Icahn School of Medicine at Mount Sinai, New York, and a partner with New York Gastroenterology Associates, presented Josh’s case as part of a seminar on SNAS and IBS “mimickers” at the Food and Nutrition Conference and Expo in Orlando last October, sponsored by the Academy of Nutrition and Dietetics.

She and two registered dietitians in her practice, Suzie Finkel, MS, RD, CDN, and Tamara Duker Freuman, MS, RD, CDN, told seminar attendees that SNAS is rarely diagnosed and can be mistaken for IBS. They noted that it probably strikes more people than doctors suspect.

“Systemic nickel allergy is present in at least 10% of the U.S. population (and much higher in some subgroups),” Dr. Pashinsky told this news organization. “But its connection to GI symptoms and functional GI disorders is still being learned about.

“I think of nickel allergy and other allergic disorders when, in addition to GI symptoms, the patient reports skin and mucous membrane involvement along with their abdominal reactions,” she said.

For patients like Josh with SNAS, the diagnosis and treatment of this condition are surprisingly simple and effective.

“Josh had these really [unusual] symptoms and nontraditional IBS food triggers,” Ms. Finkel said in an interview. “So, that’s a situation where, as dietitians we say, ‘Hmm, that’s weird; if you have IBS, then peanuts and shrimp shouldn’t really cause an issue here.’ But this might be something physicians might not be attuned to because it’s not part of their training.”

Ms. Finkel said that Josh was referred to an allergist. Josh tested positive for skin sensitization to nickel, and he was started on a low-nickel diet, which improved his symptoms.

“So, that was this happy ending,” she added.

The upshot?

“Doctors who treat IBS patients [who are not responding to treatment] need to consider the possibility that they have SNAS and send them for allergy testing,” Ms. Finkel said. “If they come back positive, simple dietary changes can address it.”
 

An underrecognized condition

There has been very little research regarding SNAS in patients with IBS, and there are no standard guidelines for diagnosing and treating it.

What’s more, many gastroenterologists aren’t familiar with it. More than a dozen gastroenterologists who were contacted for comment declined to be interviewed because they didn’t know about SNAS – or enough about it to provide useful information for the story.

Ms. Finkel said she’s not surprised that many gastroenterologists don’t know much about how SNAS can mimic IBS, which is why she and her colleagues presented the seminar last October in Orlando. “It’s really an allergy and not a GI disease. It manifests with GI symptoms, but the root is not in the digestive tract; the root is in a true allergy – a clinical allergy – to nickel.”

Complicating the issue is that people who have IBS and those with SNAS typically share some common symptoms.

Like IBS, SNAS can cause GI symptoms – such as cramping, abdominal pain, heartburn, constipation, gaseous distension, and mucus in the stool. It can be triggered by certain fresh, cooked, and canned foods.

But the food triggers that cause SNAS are not usually those that cause IBS symptoms. Rather, SNAS flare-ups are nearly always triggered by foods with high levels of nickel. Examples include apricots, artichokes, asparagus, beans, cauliflower, chickpeas, cocoa/chocolate, figs, lentils, licorice, oats, onions, peas, peanuts, potatoes, spinach, tomatoes, and tea.

According to the American Academy of Allergy, Asthma & Immunology, a distinguishing feature of SNAS is that it can cause allergic contact dermatitis when a person touches something made with nickel. Coins, jewelry, eyeglasses, home fixtures, keys, zippers, dental devices, and even stainless-steel cookware can contain allergy-triggering nickel.

What Ms. Finkel sees the most are skin reactions from touching a surface containing nickel or from ingesting it, she said.

The other immediate symptom is abdominal pain or changes in bowel movements, such as diarrhea, she added.

Christopher Randolph, MD, an allergist based in Connecticut, told this news organization that it’s important for doctors to realize that patients who have a skin reaction to nickel may also have inflammatory GI symptoms.

“We definitely need more controlled studies,” said Dr. Randolph, of the department of allergy and immunology at Yale University, New Haven, Conn. “But the takeaway here is for patients and certainly providers to be mindful that you can have systemic reactions to nickel, even though you implicate only the contact dermatitis.”
 

Diagnosis and treatment recommendations

Skin patch allergy testing – in which a person’s skin is exposed to nickel – can quickly determine whether a patient with IBS is actually experiencing inflammatory reactions to dietary nickel and would benefit from a low-nickel or no-nickel diet, research shows.

For these patients, Dr. Pashinsky recommends the following:

• Avoiding high-nickel foods.
• Limiting canned foods.
• Using nonstainless cookware, especially for acidic foods.
• Boiling foods for potential nickel reduction, especially grains and vegetables.
• Running the tap before using water to drink or cook with first thing in the morning.

Dr. Pashisky and her team also recommend the following guidelines for doctors:

• Ask patients if symptoms occur immediately after eating certain high-nickel foods or worsen with a low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diet.
• Determine whether a patient is not responding to typical medical and dietary interventions used to treat IBS.
• Conduct a food/symptom history to identify potential nickel allergy triggers.
• Try a low-nickel dietary intervention to see whether a patient’s symptoms improve in a week or two.
• Refer the patient for additional diagnostic skin-patch testing or treatment.

A multidisciplinary approach

Ms. Finkel said it’s important for doctors, particularly gastroenterologists who treat patients for suspected GI disorders to consider nickel allergy as a cause.

“SNAS is this overlooked condition ... and the research is really in its nascency here,” Ms. Finkel said.

“I would say only give [a low- or no-nickel diet] consideration if the high-nickel foods are a possible trigger,” she said. “It is very specific, looking at their diet history, to have a clear hypothesis based on what their triggers are. It’s not something to try out lightly because it’s a very restrictive diet, so I would never put a patient on a diet that I didn’t think was necessary.”

Ms. Finkel added that treatment of SNAS requires a multidisciplinary approach with a gastroenterologist, an allergist, and a dietitian.

Doctors and dietitians have distinct roles in identifying and treating these patients, Ms. Finkel said.

“If there is a suspicion of IBS symptoms and the patient is not responding to first-line treatments, then it is worth having the input of a dietitian and an allergist,” she said.

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

In this issue, Regn and colleagues (page 78) have provided a concise resource for primary care professionals (PCPs) on a lesser known sleep disorder that is increasingly common in veterans.¹ Their review provides a basic understanding of central sleep apnea (CSA) and a systematic clinical approach to diagnosis and treatment in primary care. We applaud the authors for providing education on sleep disorders to the Federal Practitioner audience, since sleep disorders are prevalent among military service members and veterans, with significant implications for health, wellness, productivity, and cost. The American workforce has a long-held sense of pride in working hard, often at the expense of sleep. Early work start times are common in the military and federal government, and sleep medicine specialists have the expertise necessary to diagnose and treat the myriad of sleep disorders that have come to light recently. A massive shortage of sleep medicine specialists limits the evidence-based sleep treatment implementations in medical care.

Medicine has become increasingly complex, necessitating a highly connected web of people, resources, institutions, and processes to keep up with the demands of growing information and technology. The evolution of a systems approach to health care built momentum during the 21st century.1-3 The National Academy of Medicine has published 2 reports that raised concerns about the quality and safety of medical care.4,5 With this expansion, the potential for medical errors at individual components or relationship nodes between actors in the medical system also has grown. Medical errors encompass more than acts of commission and can also take the form of acts of omission by failing to diagnosis and appropriately treat before long-term or irrevocable health consequences occur. A systems approach seeks to aid clinical decision making to improve the quality of medical care and patient outcomes in an otherwise complex medical system that can be difficult to navigate.

Although awareness of obstructive sleep apnea (OSA) has increased, CSA has not received the same level of attention and may not be recognized by PCPs. A lack of education about CSA can contribute to acts of omission in a health care setting. Although CSA is ultimately diagnosed and managed in specialty care sleep medicine clinics, PCPs play an instrumental role in referring patients for evaluation and then collaborating with specialists to optimize care and outcomes. The multidisciplinary approach of CSA management is important because it overlaps with many conditions that are commonly seen in primary care, including obesity, chronic pain, congestive heart failure (CHF), chronic kidney disease, and hypothyroidism. These chronic conditions are also prevalent among veterans. In a national cross-sectional study, veterans had higher prevalence rates of chronic health conditions, including cardiovascular disease and kidney disease, compared with nonveterans (odds ratios, 1.4 and 1.2, respectively).⁶

It is important to understand the relationship between CSA and chronic medical conditions because recognizing the signs of CSA can lead to identification of underlying medical conditions. Likewise, the chronic medical conditions that lead to CSA may cue the PCP’s clinical suspicion for CSA and lead to specialty care referrals if needed. The clinician also serves a significant role in the management of CSA by optimizing medical care for the underlying condition prior to pursuing additional specialty care treatments like positive airway pressure (PAP). For example, PCPs are often involved in the management of atrial fibrillation and cardiac dysfunction, which can minimize or exacerbate CSA. PCPs should also be aware of which drugs are associated with the presentation of CSA as withdrawal or reduction of the medication can resolve symptoms without further evaluation by a specialist.

The review by Regn and colleagues updates readers on developments—and lack thereof—in the literature. Treatment options for CSA have been limited. For most patients, continuous PAP (CPAP), which is the gold standard treatment for OSA, is not an effective CSA treatment. Earlier specialty guidelines endorsed adaptive servo-ventilation (ASV), a more sophisticated respiratory assist device, for treating CSA. In 2015, the SERVE-HF trial examined the effects of ASV in combination with guideline-based medical treatment on survival and cardiovascular outcomes for patients who had CSA and HF with reduced ejection fraction.⁷ They found that ASV had no significant effect on the primary endpoints of first event of death from any cause, lifesaving cardiovascular intervention, or unplanned hospitalization for worsening HF. However, all-cause and cardiovascular mortality were both increased with ASV. There has not been a more recent large clinical trial that either refutes or reinforces those findings (ADVENT-HF found that ASV effectively treated CSA and OSA in patients with CHF but had no impact on the primary endpoint of mortality).^7,8 We are unlikely to see more studies soon that will put this issue to rest and change the guidance that is currently available for ASV use.

Regn and colleagues also provide an update on the use of acetazolamide as to assist in CSA treatment. This should be done cautiously and potentially deferred to subspecialists in sleep medicine, cardiology, or nephrology. The theoretical benefit of acetazolamide in CSA is based on its promotion of excretion of sodium bicarbonate, leading to metabolic acidosis, which can stimulate central respiratory drive. Since CSA is characterized by episodic loss of central respiratory drive, it seems logical that a respiratory stimulant would provide benefit. However, acetazolamide is not approved by the US Food and Drug Administration for CSA.⁹ In those with impaired respiratory mechanics, CHF, chronic obstructive pulmonary disease, and obesity hypoventilation syndrome, this medication has the potential for harm by adding metabolic acidosis to a patient with concurrent respiratory acidosis or respiratory constraints that limit their ability to compensate effectively for additional acid-base derangements.

It is worth noting that Regn and colleagues do not make claims outside the intended scope. It accomplishes the mission of providing all PCPs with an updated streamlined summary for diagnosing and treating CSA. Such tools are important in an age of growing medical information technology because it can improve the quality of medical care and ultimately, patient outcomes with timely diagnosis and treatment. This is particularly significant in a veteran population with a high burden of chronic medical conditions and polypharmacy.

In this issue, Regn and colleagues (page 78) have provided a concise resource for primary care professionals (PCPs) on a lesser known sleep disorder that is increasingly common in veterans.¹ Their review provides a basic understanding of central sleep apnea (CSA) and a systematic clinical approach to diagnosis and treatment in primary care. We applaud the authors for providing education on sleep disorders to the Federal Practitioner audience, since sleep disorders are prevalent among military service members and veterans, with significant implications for health, wellness, productivity, and cost. The American workforce has a long-held sense of pride in working hard, often at the expense of sleep. Early work start times are common in the military and federal government, and sleep medicine specialists have the expertise necessary to diagnose and treat the myriad of sleep disorders that have come to light recently. A massive shortage of sleep medicine specialists limits the evidence-based sleep treatment implementations in medical care.

Medicine has become increasingly complex, necessitating a highly connected web of people, resources, institutions, and processes to keep up with the demands of growing information and technology. The evolution of a systems approach to health care built momentum during the 21st century.1-3 The National Academy of Medicine has published 2 reports that raised concerns about the quality and safety of medical care.4,5 With this expansion, the potential for medical errors at individual components or relationship nodes between actors in the medical system also has grown. Medical errors encompass more than acts of commission and can also take the form of acts of omission by failing to diagnosis and appropriately treat before long-term or irrevocable health consequences occur. A systems approach seeks to aid clinical decision making to improve the quality of medical care and patient outcomes in an otherwise complex medical system that can be difficult to navigate.

Although awareness of obstructive sleep apnea (OSA) has increased, CSA has not received the same level of attention and may not be recognized by PCPs. A lack of education about CSA can contribute to acts of omission in a health care setting. Although CSA is ultimately diagnosed and managed in specialty care sleep medicine clinics, PCPs play an instrumental role in referring patients for evaluation and then collaborating with specialists to optimize care and outcomes. The multidisciplinary approach of CSA management is important because it overlaps with many conditions that are commonly seen in primary care, including obesity, chronic pain, congestive heart failure (CHF), chronic kidney disease, and hypothyroidism. These chronic conditions are also prevalent among veterans. In a national cross-sectional study, veterans had higher prevalence rates of chronic health conditions, including cardiovascular disease and kidney disease, compared with nonveterans (odds ratios, 1.4 and 1.2, respectively).⁶

It is important to understand the relationship between CSA and chronic medical conditions because recognizing the signs of CSA can lead to identification of underlying medical conditions. Likewise, the chronic medical conditions that lead to CSA may cue the PCP’s clinical suspicion for CSA and lead to specialty care referrals if needed. The clinician also serves a significant role in the management of CSA by optimizing medical care for the underlying condition prior to pursuing additional specialty care treatments like positive airway pressure (PAP). For example, PCPs are often involved in the management of atrial fibrillation and cardiac dysfunction, which can minimize or exacerbate CSA. PCPs should also be aware of which drugs are associated with the presentation of CSA as withdrawal or reduction of the medication can resolve symptoms without further evaluation by a specialist.

The review by Regn and colleagues updates readers on developments—and lack thereof—in the literature. Treatment options for CSA have been limited. For most patients, continuous PAP (CPAP), which is the gold standard treatment for OSA, is not an effective CSA treatment. Earlier specialty guidelines endorsed adaptive servo-ventilation (ASV), a more sophisticated respiratory assist device, for treating CSA. In 2015, the SERVE-HF trial examined the effects of ASV in combination with guideline-based medical treatment on survival and cardiovascular outcomes for patients who had CSA and HF with reduced ejection fraction.⁷ They found that ASV had no significant effect on the primary endpoints of first event of death from any cause, lifesaving cardiovascular intervention, or unplanned hospitalization for worsening HF. However, all-cause and cardiovascular mortality were both increased with ASV. There has not been a more recent large clinical trial that either refutes or reinforces those findings (ADVENT-HF found that ASV effectively treated CSA and OSA in patients with CHF but had no impact on the primary endpoint of mortality).^7,8 We are unlikely to see more studies soon that will put this issue to rest and change the guidance that is currently available for ASV use.

Regn and colleagues also provide an update on the use of acetazolamide as to assist in CSA treatment. This should be done cautiously and potentially deferred to subspecialists in sleep medicine, cardiology, or nephrology. The theoretical benefit of acetazolamide in CSA is based on its promotion of excretion of sodium bicarbonate, leading to metabolic acidosis, which can stimulate central respiratory drive. Since CSA is characterized by episodic loss of central respiratory drive, it seems logical that a respiratory stimulant would provide benefit. However, acetazolamide is not approved by the US Food and Drug Administration for CSA.⁹ In those with impaired respiratory mechanics, CHF, chronic obstructive pulmonary disease, and obesity hypoventilation syndrome, this medication has the potential for harm by adding metabolic acidosis to a patient with concurrent respiratory acidosis or respiratory constraints that limit their ability to compensate effectively for additional acid-base derangements.

It is worth noting that Regn and colleagues do not make claims outside the intended scope. It accomplishes the mission of providing all PCPs with an updated streamlined summary for diagnosing and treating CSA. Such tools are important in an age of growing medical information technology because it can improve the quality of medical care and ultimately, patient outcomes with timely diagnosis and treatment. This is particularly significant in a veteran population with a high burden of chronic medical conditions and polypharmacy.

In this issue, Regn and colleagues (page 78) have provided a concise resource for primary care professionals (PCPs) on a lesser known sleep disorder that is increasingly common in veterans.¹ Their review provides a basic understanding of central sleep apnea (CSA) and a systematic clinical approach to diagnosis and treatment in primary care. We applaud the authors for providing education on sleep disorders to the Federal Practitioner audience, since sleep disorders are prevalent among military service members and veterans, with significant implications for health, wellness, productivity, and cost. The American workforce has a long-held sense of pride in working hard, often at the expense of sleep. Early work start times are common in the military and federal government, and sleep medicine specialists have the expertise necessary to diagnose and treat the myriad of sleep disorders that have come to light recently. A massive shortage of sleep medicine specialists limits the evidence-based sleep treatment implementations in medical care.

Medicine has become increasingly complex, necessitating a highly connected web of people, resources, institutions, and processes to keep up with the demands of growing information and technology. The evolution of a systems approach to health care built momentum during the 21st century.1-3 The National Academy of Medicine has published 2 reports that raised concerns about the quality and safety of medical care.4,5 With this expansion, the potential for medical errors at individual components or relationship nodes between actors in the medical system also has grown. Medical errors encompass more than acts of commission and can also take the form of acts of omission by failing to diagnosis and appropriately treat before long-term or irrevocable health consequences occur. A systems approach seeks to aid clinical decision making to improve the quality of medical care and patient outcomes in an otherwise complex medical system that can be difficult to navigate.

Although awareness of obstructive sleep apnea (OSA) has increased, CSA has not received the same level of attention and may not be recognized by PCPs. A lack of education about CSA can contribute to acts of omission in a health care setting. Although CSA is ultimately diagnosed and managed in specialty care sleep medicine clinics, PCPs play an instrumental role in referring patients for evaluation and then collaborating with specialists to optimize care and outcomes. The multidisciplinary approach of CSA management is important because it overlaps with many conditions that are commonly seen in primary care, including obesity, chronic pain, congestive heart failure (CHF), chronic kidney disease, and hypothyroidism. These chronic conditions are also prevalent among veterans. In a national cross-sectional study, veterans had higher prevalence rates of chronic health conditions, including cardiovascular disease and kidney disease, compared with nonveterans (odds ratios, 1.4 and 1.2, respectively).⁶

It is important to understand the relationship between CSA and chronic medical conditions because recognizing the signs of CSA can lead to identification of underlying medical conditions. Likewise, the chronic medical conditions that lead to CSA may cue the PCP’s clinical suspicion for CSA and lead to specialty care referrals if needed. The clinician also serves a significant role in the management of CSA by optimizing medical care for the underlying condition prior to pursuing additional specialty care treatments like positive airway pressure (PAP). For example, PCPs are often involved in the management of atrial fibrillation and cardiac dysfunction, which can minimize or exacerbate CSA. PCPs should also be aware of which drugs are associated with the presentation of CSA as withdrawal or reduction of the medication can resolve symptoms without further evaluation by a specialist.

The review by Regn and colleagues updates readers on developments—and lack thereof—in the literature. Treatment options for CSA have been limited. For most patients, continuous PAP (CPAP), which is the gold standard treatment for OSA, is not an effective CSA treatment. Earlier specialty guidelines endorsed adaptive servo-ventilation (ASV), a more sophisticated respiratory assist device, for treating CSA. In 2015, the SERVE-HF trial examined the effects of ASV in combination with guideline-based medical treatment on survival and cardiovascular outcomes for patients who had CSA and HF with reduced ejection fraction.⁷ They found that ASV had no significant effect on the primary endpoints of first event of death from any cause, lifesaving cardiovascular intervention, or unplanned hospitalization for worsening HF. However, all-cause and cardiovascular mortality were both increased with ASV. There has not been a more recent large clinical trial that either refutes or reinforces those findings (ADVENT-HF found that ASV effectively treated CSA and OSA in patients with CHF but had no impact on the primary endpoint of mortality).^7,8 We are unlikely to see more studies soon that will put this issue to rest and change the guidance that is currently available for ASV use.

Regn and colleagues also provide an update on the use of acetazolamide as to assist in CSA treatment. This should be done cautiously and potentially deferred to subspecialists in sleep medicine, cardiology, or nephrology. The theoretical benefit of acetazolamide in CSA is based on its promotion of excretion of sodium bicarbonate, leading to metabolic acidosis, which can stimulate central respiratory drive. Since CSA is characterized by episodic loss of central respiratory drive, it seems logical that a respiratory stimulant would provide benefit. However, acetazolamide is not approved by the US Food and Drug Administration for CSA.⁹ In those with impaired respiratory mechanics, CHF, chronic obstructive pulmonary disease, and obesity hypoventilation syndrome, this medication has the potential for harm by adding metabolic acidosis to a patient with concurrent respiratory acidosis or respiratory constraints that limit their ability to compensate effectively for additional acid-base derangements.

It is worth noting that Regn and colleagues do not make claims outside the intended scope. It accomplishes the mission of providing all PCPs with an updated streamlined summary for diagnosing and treating CSA. Such tools are important in an age of growing medical information technology because it can improve the quality of medical care and ultimately, patient outcomes with timely diagnosis and treatment. This is particularly significant in a veteran population with a high burden of chronic medical conditions and polypharmacy.

Sleep Medicine Network

Home-Based Mechanical Ventilation & Neuromuscular Disease Section

Novel therapies for neuromuscular disease: What are the respiratory and sleep implications?

The natural history of respiratory impairment in children and adults with progressive neuromuscular disease (NMD) often follows a predictable progression. Muscle weakness leads to sleep-disordered breathing and sleep-related hypoventilation, followed by diurnal hypoventilation, and, ultimately leads to respiratory failure. A number of disease-specific and society guidelines provide protocols for anticipatory respiratory monitoring, such as the role of polysomnography, pulmonary function testing, and respiratory muscle strength testing. They also guide the treatment of respiratory symptoms, such as when to initiate cough augmentation and assisted ventilation.

The emergence of disease-modifying therapies over the last decade has changed the landscape of a number of neuromuscular diseases, including spinal muscular atrophy (SMA) and Duchenne muscular dystrophy. There are now cases of children with SMA type 1, who subsequent to treatment, are walking independently. Studies examining the impact of these therapies on motor function use standardized assessments, but there are limited studies assessing pulmonary and sleep outcomes (Gurbani N, et al. Pediatr Pulmonol. 2021;56[4]:700).

Researchers are also assessing the role of home testing to diagnose hypoventilation (Shi J, et al. Sleep Med. 2023;101:221-7) and using tools like positive airway pressure device data to guide treatment with noninvasive ventilation (Perrem L et al. Pediatr Pulmonol. 2020;55[1]:58-67). While these advances in therapy are exciting, we still do not know what the long-term respiratory function, prognosis, or disease progression may be. Questions remain regarding how to best monitor, and at what frequency to assess, the respiratory status in these patients.

Moshe Y. Prero, MD
Section Member-at-Large

Sleep Medicine Network

Home-Based Mechanical Ventilation & Neuromuscular Disease Section

Novel therapies for neuromuscular disease: What are the respiratory and sleep implications?

The natural history of respiratory impairment in children and adults with progressive neuromuscular disease (NMD) often follows a predictable progression. Muscle weakness leads to sleep-disordered breathing and sleep-related hypoventilation, followed by diurnal hypoventilation, and, ultimately leads to respiratory failure. A number of disease-specific and society guidelines provide protocols for anticipatory respiratory monitoring, such as the role of polysomnography, pulmonary function testing, and respiratory muscle strength testing. They also guide the treatment of respiratory symptoms, such as when to initiate cough augmentation and assisted ventilation.

The emergence of disease-modifying therapies over the last decade has changed the landscape of a number of neuromuscular diseases, including spinal muscular atrophy (SMA) and Duchenne muscular dystrophy. There are now cases of children with SMA type 1, who subsequent to treatment, are walking independently. Studies examining the impact of these therapies on motor function use standardized assessments, but there are limited studies assessing pulmonary and sleep outcomes (Gurbani N, et al. Pediatr Pulmonol. 2021;56[4]:700).

Researchers are also assessing the role of home testing to diagnose hypoventilation (Shi J, et al. Sleep Med. 2023;101:221-7) and using tools like positive airway pressure device data to guide treatment with noninvasive ventilation (Perrem L et al. Pediatr Pulmonol. 2020;55[1]:58-67). While these advances in therapy are exciting, we still do not know what the long-term respiratory function, prognosis, or disease progression may be. Questions remain regarding how to best monitor, and at what frequency to assess, the respiratory status in these patients.

Moshe Y. Prero, MD
Section Member-at-Large

Sleep Medicine Network

Home-Based Mechanical Ventilation & Neuromuscular Disease Section

Novel therapies for neuromuscular disease: What are the respiratory and sleep implications?

The natural history of respiratory impairment in children and adults with progressive neuromuscular disease (NMD) often follows a predictable progression. Muscle weakness leads to sleep-disordered breathing and sleep-related hypoventilation, followed by diurnal hypoventilation, and, ultimately leads to respiratory failure. A number of disease-specific and society guidelines provide protocols for anticipatory respiratory monitoring, such as the role of polysomnography, pulmonary function testing, and respiratory muscle strength testing. They also guide the treatment of respiratory symptoms, such as when to initiate cough augmentation and assisted ventilation.

The emergence of disease-modifying therapies over the last decade has changed the landscape of a number of neuromuscular diseases, including spinal muscular atrophy (SMA) and Duchenne muscular dystrophy. There are now cases of children with SMA type 1, who subsequent to treatment, are walking independently. Studies examining the impact of these therapies on motor function use standardized assessments, but there are limited studies assessing pulmonary and sleep outcomes (Gurbani N, et al. Pediatr Pulmonol. 2021;56[4]:700).

Researchers are also assessing the role of home testing to diagnose hypoventilation (Shi J, et al. Sleep Med. 2023;101:221-7) and using tools like positive airway pressure device data to guide treatment with noninvasive ventilation (Perrem L et al. Pediatr Pulmonol. 2020;55[1]:58-67). While these advances in therapy are exciting, we still do not know what the long-term respiratory function, prognosis, or disease progression may be. Questions remain regarding how to best monitor, and at what frequency to assess, the respiratory status in these patients.

Moshe Y. Prero, MD
Section Member-at-Large

Despite their convenience and low cost, handheld point-of-care (POC) devices lack precision for measuring neonatal bilirubin and need refinement in order to tailor jaundice management in newborns, a systematic review and meta-analysis reports in JAMA Pediatrics. Lauren E.H. Westenberg, MD, of the division of neonatology at Erasmus MC Sophia Children’s Hospital in Rotterdam, the Netherlands, and colleagues reported that POC meters tended to underestimate neonatal bilirubin levels, compared with conventional laboratory-based quantification.

A.H. Westenberg

Furthermore, pooled estimates from 10 studies found these devices to be too imprecise overall, with substantial outer-confidence bounds. On the plus side, Dr. Westenberg’s group said POC bilirubin testing was as much as 60 times faster than lab measurement, and used 40-60 times less blood. “Conventional laboratory-based bilirubin quantification usually requires up to 500 mcL, but sometimes even 1,500 mcL, while POC tests require up to 50 mcL, which means less stress for the baby,” Dr. Westenberg said in an interview. “Especially when infants are cared for at home, it usually takes a few hours between deciding to quantify bilirubin and obtaining the test result. Meanwhile, bilirubin levels may rise unnoticed.”

On the positive side, POC devices are useful where laboratories in low-resource areas may be remote, poorly equipped, and not always able to provide an accurate bilirubin level. “As a result, the diagnosis of jaundice relies mainly on visual inspection, which is known to be unreliable,” she said. POC devices, however, need near-perfect conditions for optimal use, and results can be affected by humidity, preanalytic conditions such as test strip saturation, and hematocrit.

Yet results from these devices have recently proven to have acceptable accuracy, resulting, for example, in the same clinical decisions as the reference standard in 90.7% of times according to a 2022 study in a hospital in Malawi.

Nevertheless, the authors concluded that the devices’ imprecision limits their widespread use in neonatal jaundice management, especially when accurate lab-based bilirubin quantification is available. Results from these POC tests should be interpreted with caution, Dr. Westenberg said. In terms of clinical decision-making, POC devices entail a risk of missing neonates with jaundice who need phototherapy or, in the case of overestimation, of starting phototherapy too early.

The study

The meta-analysis included nine cross-sectional and one prospective cohort study representing 3,122 neonates in Europe, Africa, and East and Southeast Asia. Two tests with 30-minute turnaround times were evaluated in neonates 0-28 days old. The Bilistick device was evaluated in eight studies and the BiliSpec (now called BiliDX) in just two studies. Three of the studies had a high risk of bias.

A total of 3,122 measurements paired with lab quantification showed a pooled mean difference in total bilirubin levels for the POC devices of –14 micromol/L, with pooled 95% confidence bounds (CBs) of –106 to 78 micromol/L. For the Bilistick, the pooled mean difference was –17 micromol/L (95% CBs, –114 to 80 micromol/L). Of the two devices, the Bilistick was more likely to have a failed quantification against the reference standard.
 

Context for POC devices

Commenting on the meta-analysis but not involved in it, Rebecca Richards-Kortum, PhD, a professor of biomedical engineering at Rice University in Houston, noted that both devices were developed specifically to address needs in low-resource settings. “I don’t think the meta-analysis acknowledges this rationale sufficiently,” she said. “It feels like this paper is comparing apples to oranges and then criticizing the apples for not being oranges,” said Dr. Richards-Kortum, who helped develop the BiliSpec test.

John D. and Catherine T. MacArthur Foundation

Similarly, Anne S. Lee, MD, MPH, an associate professor of pediatrics at Brigham and Women’s Hospital in Boston, and not a participant in the meta-analysis, also stressed that POC devices are designed for scenarios where lab-based results are not widely available. “In a broad sense, the devices fill an important gap, both in low- and middle-income countries, as well as in the U.S. when laboratory capacity is not readily available,” said Dr. Lee. She was involved the development of the Bili-ruler icterometer, which proved to be diagnostically accurate in Bangladeshi newborns.

“Access to this technology is a critical way to address health disparities even in the U.S.,” Dr. Lee continued. “We have heard of the need for this technology from the Indian health services and Alaskan health services, where decisions are made to airlift a child based on a visual inspection alone.”

More broadly, however, cautioned Dr. Westenberg, the total allowable error and the permissible limits of uncertainty in neonatal bilirubin quantification need to be defined – irrespective of the method used. “Accurate measurement of bilirubin is difficult as has been demonstrated in so-called external quality assessment (EQA) programs that exist for laboratory-based bilirubin methods,” she said. “EQA programs for POC bilirubin devices that include a reference method as a gold standard may contribute to adaptation of the device and improving POC test imprecision.”

This work was supported by the Netherlands Organization for Health Research and Development. The authors had no conflicts of interest to disclose. Dr. Richards-Kortum and Dr. Lee have both been involved in the development of POC devices for assessing neonatal bilirubin levels.
 

Despite their convenience and low cost, handheld point-of-care (POC) devices lack precision for measuring neonatal bilirubin and need refinement in order to tailor jaundice management in newborns, a systematic review and meta-analysis reports in JAMA Pediatrics. Lauren E.H. Westenberg, MD, of the division of neonatology at Erasmus MC Sophia Children’s Hospital in Rotterdam, the Netherlands, and colleagues reported that POC meters tended to underestimate neonatal bilirubin levels, compared with conventional laboratory-based quantification.

A.H. Westenberg

Furthermore, pooled estimates from 10 studies found these devices to be too imprecise overall, with substantial outer-confidence bounds. On the plus side, Dr. Westenberg’s group said POC bilirubin testing was as much as 60 times faster than lab measurement, and used 40-60 times less blood. “Conventional laboratory-based bilirubin quantification usually requires up to 500 mcL, but sometimes even 1,500 mcL, while POC tests require up to 50 mcL, which means less stress for the baby,” Dr. Westenberg said in an interview. “Especially when infants are cared for at home, it usually takes a few hours between deciding to quantify bilirubin and obtaining the test result. Meanwhile, bilirubin levels may rise unnoticed.”

On the positive side, POC devices are useful where laboratories in low-resource areas may be remote, poorly equipped, and not always able to provide an accurate bilirubin level. “As a result, the diagnosis of jaundice relies mainly on visual inspection, which is known to be unreliable,” she said. POC devices, however, need near-perfect conditions for optimal use, and results can be affected by humidity, preanalytic conditions such as test strip saturation, and hematocrit.

Yet results from these devices have recently proven to have acceptable accuracy, resulting, for example, in the same clinical decisions as the reference standard in 90.7% of times according to a 2022 study in a hospital in Malawi.

Nevertheless, the authors concluded that the devices’ imprecision limits their widespread use in neonatal jaundice management, especially when accurate lab-based bilirubin quantification is available. Results from these POC tests should be interpreted with caution, Dr. Westenberg said. In terms of clinical decision-making, POC devices entail a risk of missing neonates with jaundice who need phototherapy or, in the case of overestimation, of starting phototherapy too early.

The study

The meta-analysis included nine cross-sectional and one prospective cohort study representing 3,122 neonates in Europe, Africa, and East and Southeast Asia. Two tests with 30-minute turnaround times were evaluated in neonates 0-28 days old. The Bilistick device was evaluated in eight studies and the BiliSpec (now called BiliDX) in just two studies. Three of the studies had a high risk of bias.

A total of 3,122 measurements paired with lab quantification showed a pooled mean difference in total bilirubin levels for the POC devices of –14 micromol/L, with pooled 95% confidence bounds (CBs) of –106 to 78 micromol/L. For the Bilistick, the pooled mean difference was –17 micromol/L (95% CBs, –114 to 80 micromol/L). Of the two devices, the Bilistick was more likely to have a failed quantification against the reference standard.
 

Context for POC devices

Commenting on the meta-analysis but not involved in it, Rebecca Richards-Kortum, PhD, a professor of biomedical engineering at Rice University in Houston, noted that both devices were developed specifically to address needs in low-resource settings. “I don’t think the meta-analysis acknowledges this rationale sufficiently,” she said. “It feels like this paper is comparing apples to oranges and then criticizing the apples for not being oranges,” said Dr. Richards-Kortum, who helped develop the BiliSpec test.

John D. and Catherine T. MacArthur Foundation

Similarly, Anne S. Lee, MD, MPH, an associate professor of pediatrics at Brigham and Women’s Hospital in Boston, and not a participant in the meta-analysis, also stressed that POC devices are designed for scenarios where lab-based results are not widely available. “In a broad sense, the devices fill an important gap, both in low- and middle-income countries, as well as in the U.S. when laboratory capacity is not readily available,” said Dr. Lee. She was involved the development of the Bili-ruler icterometer, which proved to be diagnostically accurate in Bangladeshi newborns.

“Access to this technology is a critical way to address health disparities even in the U.S.,” Dr. Lee continued. “We have heard of the need for this technology from the Indian health services and Alaskan health services, where decisions are made to airlift a child based on a visual inspection alone.”

More broadly, however, cautioned Dr. Westenberg, the total allowable error and the permissible limits of uncertainty in neonatal bilirubin quantification need to be defined – irrespective of the method used. “Accurate measurement of bilirubin is difficult as has been demonstrated in so-called external quality assessment (EQA) programs that exist for laboratory-based bilirubin methods,” she said. “EQA programs for POC bilirubin devices that include a reference method as a gold standard may contribute to adaptation of the device and improving POC test imprecision.”

This work was supported by the Netherlands Organization for Health Research and Development. The authors had no conflicts of interest to disclose. Dr. Richards-Kortum and Dr. Lee have both been involved in the development of POC devices for assessing neonatal bilirubin levels.
 

Despite their convenience and low cost, handheld point-of-care (POC) devices lack precision for measuring neonatal bilirubin and need refinement in order to tailor jaundice management in newborns, a systematic review and meta-analysis reports in JAMA Pediatrics. Lauren E.H. Westenberg, MD, of the division of neonatology at Erasmus MC Sophia Children’s Hospital in Rotterdam, the Netherlands, and colleagues reported that POC meters tended to underestimate neonatal bilirubin levels, compared with conventional laboratory-based quantification.

A.H. Westenberg

Furthermore, pooled estimates from 10 studies found these devices to be too imprecise overall, with substantial outer-confidence bounds. On the plus side, Dr. Westenberg’s group said POC bilirubin testing was as much as 60 times faster than lab measurement, and used 40-60 times less blood. “Conventional laboratory-based bilirubin quantification usually requires up to 500 mcL, but sometimes even 1,500 mcL, while POC tests require up to 50 mcL, which means less stress for the baby,” Dr. Westenberg said in an interview. “Especially when infants are cared for at home, it usually takes a few hours between deciding to quantify bilirubin and obtaining the test result. Meanwhile, bilirubin levels may rise unnoticed.”

On the positive side, POC devices are useful where laboratories in low-resource areas may be remote, poorly equipped, and not always able to provide an accurate bilirubin level. “As a result, the diagnosis of jaundice relies mainly on visual inspection, which is known to be unreliable,” she said. POC devices, however, need near-perfect conditions for optimal use, and results can be affected by humidity, preanalytic conditions such as test strip saturation, and hematocrit.

Yet results from these devices have recently proven to have acceptable accuracy, resulting, for example, in the same clinical decisions as the reference standard in 90.7% of times according to a 2022 study in a hospital in Malawi.

Nevertheless, the authors concluded that the devices’ imprecision limits their widespread use in neonatal jaundice management, especially when accurate lab-based bilirubin quantification is available. Results from these POC tests should be interpreted with caution, Dr. Westenberg said. In terms of clinical decision-making, POC devices entail a risk of missing neonates with jaundice who need phototherapy or, in the case of overestimation, of starting phototherapy too early.

The study

The meta-analysis included nine cross-sectional and one prospective cohort study representing 3,122 neonates in Europe, Africa, and East and Southeast Asia. Two tests with 30-minute turnaround times were evaluated in neonates 0-28 days old. The Bilistick device was evaluated in eight studies and the BiliSpec (now called BiliDX) in just two studies. Three of the studies had a high risk of bias.

A total of 3,122 measurements paired with lab quantification showed a pooled mean difference in total bilirubin levels for the POC devices of –14 micromol/L, with pooled 95% confidence bounds (CBs) of –106 to 78 micromol/L. For the Bilistick, the pooled mean difference was –17 micromol/L (95% CBs, –114 to 80 micromol/L). Of the two devices, the Bilistick was more likely to have a failed quantification against the reference standard.
 

Context for POC devices

Commenting on the meta-analysis but not involved in it, Rebecca Richards-Kortum, PhD, a professor of biomedical engineering at Rice University in Houston, noted that both devices were developed specifically to address needs in low-resource settings. “I don’t think the meta-analysis acknowledges this rationale sufficiently,” she said. “It feels like this paper is comparing apples to oranges and then criticizing the apples for not being oranges,” said Dr. Richards-Kortum, who helped develop the BiliSpec test.

John D. and Catherine T. MacArthur Foundation

Similarly, Anne S. Lee, MD, MPH, an associate professor of pediatrics at Brigham and Women’s Hospital in Boston, and not a participant in the meta-analysis, also stressed that POC devices are designed for scenarios where lab-based results are not widely available. “In a broad sense, the devices fill an important gap, both in low- and middle-income countries, as well as in the U.S. when laboratory capacity is not readily available,” said Dr. Lee. She was involved the development of the Bili-ruler icterometer, which proved to be diagnostically accurate in Bangladeshi newborns.

“Access to this technology is a critical way to address health disparities even in the U.S.,” Dr. Lee continued. “We have heard of the need for this technology from the Indian health services and Alaskan health services, where decisions are made to airlift a child based on a visual inspection alone.”

More broadly, however, cautioned Dr. Westenberg, the total allowable error and the permissible limits of uncertainty in neonatal bilirubin quantification need to be defined – irrespective of the method used. “Accurate measurement of bilirubin is difficult as has been demonstrated in so-called external quality assessment (EQA) programs that exist for laboratory-based bilirubin methods,” she said. “EQA programs for POC bilirubin devices that include a reference method as a gold standard may contribute to adaptation of the device and improving POC test imprecision.”

This work was supported by the Netherlands Organization for Health Research and Development. The authors had no conflicts of interest to disclose. Dr. Richards-Kortum and Dr. Lee have both been involved in the development of POC devices for assessing neonatal bilirubin levels.
 

Radiation dermatitis is one of the most common side effects of radiotherapy for women with breast cancer. Results from a phase 3 trial add to previous evidence from smaller trials that show that a silicone-based film can protect skin from this side effect. 

But it is not being used much in clinical practice. Instead, radiation dermatitis is usually treated after the fact, most often with aqueous creams.

The product is Mepitel film, from Swedish medical device company Mölnlycke Health Care.

It should be used for women who are at high risk for developing radiation dermatitis, said Edward Chow, MBBS, PhD, of the department of radiation oncology, Odette Cancer Centre, Sunnybrook Health Sciences Centre, Toronto, who was the senior author of the phase 3 study published recently in the Journal of Clinical Oncology.

“Other doctors think that because radiation dermatitis isn’t life-threatening it isn’t as important, but the condition does affect the quality of life for patients,” Dr. Chow said. “If we can lessen the pain and discomfort, why wouldn’t we as physicians?”

Dr. Chow’s open-label, multicenter trial was conducted in 376 women with large breasts (bra cup size C or larger) who were undergoing radiotherapy after lumpectomy or mastectomy. The primary endpoint was grade 2 or 3 radiation dermatitis using the Common Terminology Criteria for Adverse Events. (Grade 2 is described as moderate, whereas grade 3 is severe.) 

The film significantly reduced the incidence of grade 2 or 3 radiation dermatitis, down to  15.5% compared with 45.6% in patients receiving standard care (odds ratio, 0.20, 95% confidence interval, 0.12-0.34, P < .0001). 

There was also a significant reduction in grade 3 radiation dermatitis (2.8% vs. 13.6%; OR, 0.19; P < .0002) and moist desquamation (8% vs. 19.2%; OR, 0.36; P = .002).

“The film was remarkably effective and helped protect patients from potentially debilitating side effects,” commented Corey Speers, MD, PhD, a radiation oncologist with University Hospitals, Cleveland, who saw the study data presented during a plenary session at the annual meeting of the American Society of Clinical Oncology.

He believes that preventing radiation dermatitis before it develops is the best way to care for patients. 

“[Radiation dermatitis] is usually associated with pain and discomfort and can lead to more serious issues like infection or delayed wound healing, and unfortunately, there aren’t effective treatments for it once it’s developed, so preventing it is our most effective strategy,” Dr. Speers said. 

One reason for the film not being used much could be that it takes time apply the film, suggested Patries Herst, PhD, department of radiation therapy, University of Otago, Wellington, New Zealand. She was the lead author of a study published in 2014 that also analyzed the effectiveness of the film in preventing radiation dermatitis.

In their trial, a research radiation therapist applied the film to women when they were starting their radiotherapy. The film is applied to a portion of the breast or chest wall, and Dr. Herst emphasized the importance of applying the film correctly, making sure the film is not stretched during application and not overlapping other pieces of the film, while also making sure that it conforms to the breast shape. The film was replaced when it would curl too much around the sides, approximately every 1 or 2 weeks. 

“Radiation therapy itself is very short. And so you have about 10 minutes for every patient,” she explained.

“But applying the film adds 20-30 minutes and it’s really awkward to apply properly,” Dr. Herst said. “You have to tap it in and then have to maybe cut it so that it fits better. And hospitals say, ‘We don’t have the time’ and that is still the biggest issue that we’re seeing right now.”

In Dr. Chow’s study, the average time spent applying the film on lumpectomy patients was 55 minutes and was slightly shorter at 45 minutes for mastectomy patients. He acknowledged that it does take time that staff at most hospitals and clinics simply don’t have.

Dr. Chow suggested that perhaps a family member or other caregiver could apply the film, and he referenced an educational video from the manufacturer that provides in-depth instructions on the correct way to apply the film for radiotherapy patients. However, this could lead to errors and a waste of product if not the film was not applied properly. 

The cost of Mepitel film may also be a deterrent. Dr. Chow’s study noted that, during the entire course of radiotherapy, the cost for the film was about $80-$100 per patient. However, he believes the benefits outweigh the cost. 

In addition, there have been issues with supplies, and it has been difficult for people to get their hands on the actual product.

Currently, the Mayo Clinic is also conducting a study testing Mepitel Film for radiation dermatitis in breast cancer patients following mastectomy. Mayo Clinic principal investigator Kimberly Corbin, MD, could not go into great detail about the ongoing trial, but she said it has been difficult to get the product. 

“We have been using the film at Mayo for a number of years,” Dr. Corbin said, but we “have found that it is challenging to get supplies.”

“While we have generally been able to have some supply established through our store here, we know that is not typical and it is difficult for patients to access,” she said. In addition, “there are not a ton of centers with experience in application.”

A representative with Mölnlycke Health Care, Allyson Bower-Willner, could not comment on the distribution of Mepitel film in the United States or if the company plans to increase the amount of product shipped. The film is available “to a limited set of customers,” she said.

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

Radiation dermatitis is one of the most common side effects of radiotherapy for women with breast cancer. Results from a phase 3 trial add to previous evidence from smaller trials that show that a silicone-based film can protect skin from this side effect. 

But it is not being used much in clinical practice. Instead, radiation dermatitis is usually treated after the fact, most often with aqueous creams.

The product is Mepitel film, from Swedish medical device company Mölnlycke Health Care.

It should be used for women who are at high risk for developing radiation dermatitis, said Edward Chow, MBBS, PhD, of the department of radiation oncology, Odette Cancer Centre, Sunnybrook Health Sciences Centre, Toronto, who was the senior author of the phase 3 study published recently in the Journal of Clinical Oncology.

“Other doctors think that because radiation dermatitis isn’t life-threatening it isn’t as important, but the condition does affect the quality of life for patients,” Dr. Chow said. “If we can lessen the pain and discomfort, why wouldn’t we as physicians?”

Dr. Chow’s open-label, multicenter trial was conducted in 376 women with large breasts (bra cup size C or larger) who were undergoing radiotherapy after lumpectomy or mastectomy. The primary endpoint was grade 2 or 3 radiation dermatitis using the Common Terminology Criteria for Adverse Events. (Grade 2 is described as moderate, whereas grade 3 is severe.) 

The film significantly reduced the incidence of grade 2 or 3 radiation dermatitis, down to  15.5% compared with 45.6% in patients receiving standard care (odds ratio, 0.20, 95% confidence interval, 0.12-0.34, P < .0001). 

There was also a significant reduction in grade 3 radiation dermatitis (2.8% vs. 13.6%; OR, 0.19; P < .0002) and moist desquamation (8% vs. 19.2%; OR, 0.36; P = .002).

“The film was remarkably effective and helped protect patients from potentially debilitating side effects,” commented Corey Speers, MD, PhD, a radiation oncologist with University Hospitals, Cleveland, who saw the study data presented during a plenary session at the annual meeting of the American Society of Clinical Oncology.

He believes that preventing radiation dermatitis before it develops is the best way to care for patients. 

“[Radiation dermatitis] is usually associated with pain and discomfort and can lead to more serious issues like infection or delayed wound healing, and unfortunately, there aren’t effective treatments for it once it’s developed, so preventing it is our most effective strategy,” Dr. Speers said. 

One reason for the film not being used much could be that it takes time apply the film, suggested Patries Herst, PhD, department of radiation therapy, University of Otago, Wellington, New Zealand. She was the lead author of a study published in 2014 that also analyzed the effectiveness of the film in preventing radiation dermatitis.

In their trial, a research radiation therapist applied the film to women when they were starting their radiotherapy. The film is applied to a portion of the breast or chest wall, and Dr. Herst emphasized the importance of applying the film correctly, making sure the film is not stretched during application and not overlapping other pieces of the film, while also making sure that it conforms to the breast shape. The film was replaced when it would curl too much around the sides, approximately every 1 or 2 weeks. 

“Radiation therapy itself is very short. And so you have about 10 minutes for every patient,” she explained.

“But applying the film adds 20-30 minutes and it’s really awkward to apply properly,” Dr. Herst said. “You have to tap it in and then have to maybe cut it so that it fits better. And hospitals say, ‘We don’t have the time’ and that is still the biggest issue that we’re seeing right now.”

In Dr. Chow’s study, the average time spent applying the film on lumpectomy patients was 55 minutes and was slightly shorter at 45 minutes for mastectomy patients. He acknowledged that it does take time that staff at most hospitals and clinics simply don’t have.

Dr. Chow suggested that perhaps a family member or other caregiver could apply the film, and he referenced an educational video from the manufacturer that provides in-depth instructions on the correct way to apply the film for radiotherapy patients. However, this could lead to errors and a waste of product if not the film was not applied properly. 

The cost of Mepitel film may also be a deterrent. Dr. Chow’s study noted that, during the entire course of radiotherapy, the cost for the film was about $80-$100 per patient. However, he believes the benefits outweigh the cost. 

In addition, there have been issues with supplies, and it has been difficult for people to get their hands on the actual product.

Currently, the Mayo Clinic is also conducting a study testing Mepitel Film for radiation dermatitis in breast cancer patients following mastectomy. Mayo Clinic principal investigator Kimberly Corbin, MD, could not go into great detail about the ongoing trial, but she said it has been difficult to get the product. 

“We have been using the film at Mayo for a number of years,” Dr. Corbin said, but we “have found that it is challenging to get supplies.”

“While we have generally been able to have some supply established through our store here, we know that is not typical and it is difficult for patients to access,” she said. In addition, “there are not a ton of centers with experience in application.”

A representative with Mölnlycke Health Care, Allyson Bower-Willner, could not comment on the distribution of Mepitel film in the United States or if the company plans to increase the amount of product shipped. The film is available “to a limited set of customers,” she said.

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

Radiation dermatitis is one of the most common side effects of radiotherapy for women with breast cancer. Results from a phase 3 trial add to previous evidence from smaller trials that show that a silicone-based film can protect skin from this side effect. 

But it is not being used much in clinical practice. Instead, radiation dermatitis is usually treated after the fact, most often with aqueous creams.

The product is Mepitel film, from Swedish medical device company Mölnlycke Health Care.

It should be used for women who are at high risk for developing radiation dermatitis, said Edward Chow, MBBS, PhD, of the department of radiation oncology, Odette Cancer Centre, Sunnybrook Health Sciences Centre, Toronto, who was the senior author of the phase 3 study published recently in the Journal of Clinical Oncology.

“Other doctors think that because radiation dermatitis isn’t life-threatening it isn’t as important, but the condition does affect the quality of life for patients,” Dr. Chow said. “If we can lessen the pain and discomfort, why wouldn’t we as physicians?”

Dr. Chow’s open-label, multicenter trial was conducted in 376 women with large breasts (bra cup size C or larger) who were undergoing radiotherapy after lumpectomy or mastectomy. The primary endpoint was grade 2 or 3 radiation dermatitis using the Common Terminology Criteria for Adverse Events. (Grade 2 is described as moderate, whereas grade 3 is severe.) 

The film significantly reduced the incidence of grade 2 or 3 radiation dermatitis, down to  15.5% compared with 45.6% in patients receiving standard care (odds ratio, 0.20, 95% confidence interval, 0.12-0.34, P < .0001). 

There was also a significant reduction in grade 3 radiation dermatitis (2.8% vs. 13.6%; OR, 0.19; P < .0002) and moist desquamation (8% vs. 19.2%; OR, 0.36; P = .002).

“The film was remarkably effective and helped protect patients from potentially debilitating side effects,” commented Corey Speers, MD, PhD, a radiation oncologist with University Hospitals, Cleveland, who saw the study data presented during a plenary session at the annual meeting of the American Society of Clinical Oncology.

He believes that preventing radiation dermatitis before it develops is the best way to care for patients. 

“[Radiation dermatitis] is usually associated with pain and discomfort and can lead to more serious issues like infection or delayed wound healing, and unfortunately, there aren’t effective treatments for it once it’s developed, so preventing it is our most effective strategy,” Dr. Speers said. 

One reason for the film not being used much could be that it takes time apply the film, suggested Patries Herst, PhD, department of radiation therapy, University of Otago, Wellington, New Zealand. She was the lead author of a study published in 2014 that also analyzed the effectiveness of the film in preventing radiation dermatitis.

In their trial, a research radiation therapist applied the film to women when they were starting their radiotherapy. The film is applied to a portion of the breast or chest wall, and Dr. Herst emphasized the importance of applying the film correctly, making sure the film is not stretched during application and not overlapping other pieces of the film, while also making sure that it conforms to the breast shape. The film was replaced when it would curl too much around the sides, approximately every 1 or 2 weeks. 

“Radiation therapy itself is very short. And so you have about 10 minutes for every patient,” she explained.

“But applying the film adds 20-30 minutes and it’s really awkward to apply properly,” Dr. Herst said. “You have to tap it in and then have to maybe cut it so that it fits better. And hospitals say, ‘We don’t have the time’ and that is still the biggest issue that we’re seeing right now.”

In Dr. Chow’s study, the average time spent applying the film on lumpectomy patients was 55 minutes and was slightly shorter at 45 minutes for mastectomy patients. He acknowledged that it does take time that staff at most hospitals and clinics simply don’t have.

Dr. Chow suggested that perhaps a family member or other caregiver could apply the film, and he referenced an educational video from the manufacturer that provides in-depth instructions on the correct way to apply the film for radiotherapy patients. However, this could lead to errors and a waste of product if not the film was not applied properly. 

The cost of Mepitel film may also be a deterrent. Dr. Chow’s study noted that, during the entire course of radiotherapy, the cost for the film was about $80-$100 per patient. However, he believes the benefits outweigh the cost. 

In addition, there have been issues with supplies, and it has been difficult for people to get their hands on the actual product.

Currently, the Mayo Clinic is also conducting a study testing Mepitel Film for radiation dermatitis in breast cancer patients following mastectomy. Mayo Clinic principal investigator Kimberly Corbin, MD, could not go into great detail about the ongoing trial, but she said it has been difficult to get the product. 

“We have been using the film at Mayo for a number of years,” Dr. Corbin said, but we “have found that it is challenging to get supplies.”

“While we have generally been able to have some supply established through our store here, we know that is not typical and it is difficult for patients to access,” she said. In addition, “there are not a ton of centers with experience in application.”

A representative with Mölnlycke Health Care, Allyson Bower-Willner, could not comment on the distribution of Mepitel film in the United States or if the company plans to increase the amount of product shipped. The film is available “to a limited set of customers,” she said.

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

Several years after xylazine first began appearing as an additive in illicit street drugs – and as its use spreads nationwide – the Food and Drug Administration says it will more closely monitor imports.

The agency issued an import alert, which gives it the power to detain raw ingredients or bulk finished product if the shipments are suspected to be in violation of the law. Xylazine was first approved by the FDA in 1972 as a sedative and analgesic for use only in animals.

bankrx/Getty Images

It is increasingly being detected and is usually mixed with fentanyl, cocaine, methamphetamine, and other illicit drugs. A January 2023 study by Nashville-based testing company Aegis Sciences found xylazine in 413 of about 60,000 urine samples and in 25 of 39 states that submitted tests. The vast majority of xylazine-positive samples also tested positive for fentanyl.

The FDA said it would continue to ensure the availability of xylazine for veterinary use, and the American Veterinary Medicine Association said in a statement that it “supports such efforts to combat illicit drug use.”

FDA Commissioner Robert M. Califf, MD, said in a statement that the agency “remains concerned about the increasing prevalence of xylazine mixed with illicit drugs, and this action is one part of broader efforts the agency is undertaking to address this issue.”

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

Several years after xylazine first began appearing as an additive in illicit street drugs – and as its use spreads nationwide – the Food and Drug Administration says it will more closely monitor imports.

The agency issued an import alert, which gives it the power to detain raw ingredients or bulk finished product if the shipments are suspected to be in violation of the law. Xylazine was first approved by the FDA in 1972 as a sedative and analgesic for use only in animals.

bankrx/Getty Images

It is increasingly being detected and is usually mixed with fentanyl, cocaine, methamphetamine, and other illicit drugs. A January 2023 study by Nashville-based testing company Aegis Sciences found xylazine in 413 of about 60,000 urine samples and in 25 of 39 states that submitted tests. The vast majority of xylazine-positive samples also tested positive for fentanyl.

The FDA said it would continue to ensure the availability of xylazine for veterinary use, and the American Veterinary Medicine Association said in a statement that it “supports such efforts to combat illicit drug use.”

FDA Commissioner Robert M. Califf, MD, said in a statement that the agency “remains concerned about the increasing prevalence of xylazine mixed with illicit drugs, and this action is one part of broader efforts the agency is undertaking to address this issue.”

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

Several years after xylazine first began appearing as an additive in illicit street drugs – and as its use spreads nationwide – the Food and Drug Administration says it will more closely monitor imports.

The agency issued an import alert, which gives it the power to detain raw ingredients or bulk finished product if the shipments are suspected to be in violation of the law. Xylazine was first approved by the FDA in 1972 as a sedative and analgesic for use only in animals.

bankrx/Getty Images

It is increasingly being detected and is usually mixed with fentanyl, cocaine, methamphetamine, and other illicit drugs. A January 2023 study by Nashville-based testing company Aegis Sciences found xylazine in 413 of about 60,000 urine samples and in 25 of 39 states that submitted tests. The vast majority of xylazine-positive samples also tested positive for fentanyl.

The FDA said it would continue to ensure the availability of xylazine for veterinary use, and the American Veterinary Medicine Association said in a statement that it “supports such efforts to combat illicit drug use.”

FDA Commissioner Robert M. Califf, MD, said in a statement that the agency “remains concerned about the increasing prevalence of xylazine mixed with illicit drugs, and this action is one part of broader efforts the agency is undertaking to address this issue.”

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