Sports Medicine

In 1974, Tommy John of the Los Angeles Dodgers was 31 and a 12-year veteran of Major League Baseball when he became the unwitting vanguard of a revolution in baseball and orthopedics. Fifty years later, Mr. John might not be a candidate for the latest advances to a procedure that bears his name.

The southpaw pitcher had faced the abrupt end of his career when, after one fateful delivery, he found himself unable to throw to home. So he took a gamble on the surgical equivalent of a Hail Mary: the reconstruction of a torn ligament in his pitching elbow.

The experiment was a wild success. Mr. John pitched— and better than he had before — for another 14 seasons, retiring in 1989 at the age of 46. How much better? After the surgery, he tallied three 20-win seasons compared with none before the operation, and he finished among the top five vote-getters for the annual Cy Young Award three times. He was named an All-Star once before the surgery and three times after.

The triumph notwithstanding, Tommy John now cautions against Tommy John surgery. What’s given him and clinicians pause is a trend in recent years of ever-younger athletes who undergo the procedure.

Along with the surgical improvements in repairing a torn ulnar collateral ligament (UCL) is a demographic shift toward school-aged athletes who get it. By 2014, one study concluded that 67.4% of UCL reconstruction surgeries were performed on athletes between 16 and 20 years of age. Some patients are still in Little League when they undergo the procedure.

Experts say these athletes have weakened their UCLs through overuse. They disagree on whether to call it an “epidemic,” but if it is, “the vaccine is awareness” against throwing too hard and too often, said Eric Makhni, MD, an orthopedic surgeon at Henry Ford Health in Detroit.
 

From Career-Ending to Routine

Mr. John’s entry into baseball and orthopedic lore was initially slow, but the trickle turned into a tide. After Frank Jobe, MD, swapped a healthy tendon from John’s right wrist for his worn and torn left UCL on September 25, 1974, he didn’t perform his second surgery for another 1194 days. By the time “Tommy John surgery” became a recognized phrase, Mr. John was still active but only 14 professional baseball players had undergone the operation.

Prior to the start of spring training this year, an oft-cited database listed 366 pro players who’d undergone the operation. 

“Before Tommy John, that was a career-ending injury,” said Grant E. Garrigues, MD, an orthopedic surgeon at Midwest Orthopaedics at RUSH in Chicago, who called Mr. John “a pure revolutionary.”

Tommy John surgery is “the only one that I can think of that is named after the patient rather than the doctor who first did it,” said Patrick McCulloch, MD, an orthopedic surgeon in Houston and a team physician for the Astros.

Dr. McCulloch, who performs about 25 UCL repairs a year, said that by recent estimates, one-third of pro pitchers had had some sort of surgical repair. He hesitated to call the increasing number of operations an epidemic but acknowledged that the ingredients exist for more elbow trauma among baseball players.

“More people are playing more often, and people are bigger and stronger and throwing harder,” he said.

Either way, Dr. McCulloch said, “the procedure is a victim of its own success” because it is “just done phenomenally well.”

The surgery is now commonplace — perhaps too commonplace, said David W. Altchek, MD, attending surgeon and co-chief emeritus at Hospital for Special Surgery in New York City.

Dr. Altchek played a key role in the popularity of the operation. Twenty-two years after Mr. John’s surgery, he helped develop a variation of the procedure called the docking technique. 

Whereas Dr. Jobe sutured Mr. John’s replacement graft to itself, “we developed a different way of tying it over a bone bridge, which was more secure and more easy to tension,” Dr. Altchek explained.

The advance meant less drilling into bone and enabled surgeons to avoid moving a problem-free ulnar nerve or removing the flexor-pronator muscle that protects the elbow from stress. “The trauma of the surgery is significantly less,” he said. “We just made it a lot easier very quickly,” cutting the surgery time from 2 hours to 30-40 minutes.

Maybe the surgery became too easy, said Dr. Altchek, who estimates he has done 2000 of them over the past 30 years. “I don’t want to condemn my colleagues, but there are a lot of people doing the surgery,” he said. “And not a lot of people are doing a lot of them, and they don’t know the nuances of doing the surgery.”

The older procedures are known as the “full Tommy John”; each has a 12- to 18-month healing process, with a success rate of 80%-85%. Pitchers typically sit out a season while recovering.

Brandon Erickson, MD, an orthopedic surgeon at Rothman Orthopaedic Institute in New York City, said that in younger patients he has recently turned more often to the suture of the future: an internal brace that provides a repair rather than reconstruction.

The procedure, pioneered by Felix H. Savoie III, MD, the Ray J. Haddad Professor of Orthopaedics at Tulane University School of Medicine in New Orleans, and Jeffrey R. Dugas, MD, of Andrews Sports Medicine & Orthopaedic Center in Birmingham, Alabama, uses collagen-coated tape that looks like a shoelace and provides a scaffold that Dr. McCulloch said “is inductive to healing and growth of ligament tissue.”

The brace is intended for an “overhead” athlete (mostly baseball players but also javelin throwers and gymnasts) whose UCL is torn on only one side but is otherwise in good shape. In a pitcher the same age as Mr. John was when Dr. Jobe performed the first procedure, “that ligament may not be of very good quality,” Dr. McCulloch said. “It may have thickened. It may have calcifications.” But for a high-school junior with aspirations to pitch in college or beyond without “way too many miles on the elbow,” the approach is a good fit. The healing process is as little as 6 months.

“The ones who have a good ligament are very likely to do well,” said Dr. Erickson, an assistant team doctor for the Philadelphia Phillies.

“If the patient’s ligament is generally ‘good’ with only a tear, the InternalBrace procedure may be used to repair the native ligament. On the other end of the spectrum, if the patient’s ligament is torn and degenerative the surgeon may opt to do a UCL reconstruction using an auto or allograft — ie, Tommy John surgery,” Allen Holowecky, senior product manager of Arthrex of Naples, Florida, the maker of the InternalBrace, told this news organization. “Before UCL repair, Tommy John surgery was the only real treatment option. We tend to see repairs done on younger patients since their ligament hasn’t seen years of use-damage.”
 

Calls for Caution

Tommy John III wanted to play baseball like his dad until near-fatal complications from shoulder surgery altered his path. He was drawn to chiropractic and consults on injury prevention. “All surgeries and all medical interventions are cut first, ask questions later,” he said. “I was born with that.”

He saw his dad’s slow, heroic comeback from the surgery and described him as the perfect candidate for Dr. Jobe’s experiment. Tommy John spent his recovery time squeezing Silly Putty and throwing tennis balls. “He was willing to do anything necessary. He wanted to throw. That was his brush.” When the son was recovering from his own injury, “he said, ‘Learn the knuckleball.’ I said, ‘I don’t want to. I’ve reached my point.’ ”

He said he tells young patients with UCL injuries to rest. But instead “we have year-round sports with the promise that the more you play, the better,” he said. “They’re over-activitied.”

According to the American Academy of Orthopaedic Surgeons, 6.4 million children and adolescents in the United States played organized baseball in 2022, down from 11.5 million in 2014. Nearly half of pitchers played in a league with no maximum pitch counts, and 43.5% pitched on consecutive days, the group said.

How many UCL repair or reconstruction surgeries are performed on youth athletes each year is unclear. A 2019 study, however, found that although baseball injuries decreased between 2006 and 2016, the elbow was “the only location of injury that saw an increase.”

Dr. Garrigues said some parents of throwing athletes have asked about prophylactic Tommy John surgery for their children. He said it shouldn’t apply to pitchers.

“People have taken it a little too far,” he said. Dr. Garrigues and others argue against children throwing weighted balls when coming back from surgery. Instead, “we’re shutting them down,” he said.

Throwing any pitch is an act of violence on the body, Dr. Garrigues said, with the elbow taking the final brunt of the force. “These pitchers are functioning at the absolute limits of what the human body can take,” he said. “There’s only so many bullets in a gun,” which is why pitchers often feel the twinge of a torn UCL on a routine pitch.

Dr. Makhni suggested cross-training for pitchers in the off-season instead of playing baseball year-round. “If you play soccer, your footwork is going to be better,” he said.

“Kids shouldn’t be doing this all year round,” said Rebecca Carl, MD, associate professor of pediatrics at Northwestern University Feinberg School of Medicine in Chicago. “We are recommending that kids take 2 or 3 months off.” In the off-season, she urges them to strengthen their backs and cores. 

Such advice can “feel like a bombshell,” said Dr. Carl, who chairs the Council on Sports Medicine and Fitness for the American Academy of Pediatrics. ‘Some started at a very young age. They go to camps. If I say to a teenager, ‘If you do this, I can keep you from getting injured,’ they think, ‘I won’t be injured.’” Most parents, however, understand the risk of “doing too much, too soon.”

Justin Orenduff, a former pitching prospect until his arm blew out, has made a career teaching head-to-toe pitching mechanics. He founded DVS Baseball, which uses software to teach pitchers how to properly use every muscle, starting with the orientation of the back foot. He, too, argues against pitching year-round. “Everyone on that travel team expects to get their fair share of playing time,” he said. “It just never stops.”

Organized baseball is paying attention. It has come up with the Pitch Smart program that gives maximum pitch counts for young players, but experts said children often get around that by belonging to several leagues.

Dr. Altchek said some surgeons have added platelet-rich plasma, stem cells, and bone marrow during surgery to quicken the slow healing time from UCL replacement. But he said, “it has to heal. Can you speed up biology?”

Dr. McCulloch said that, all the advances in Tommy John surgery aside, “the next frontier is really trying to crack the code on prevention.”

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

In 1974, Tommy John of the Los Angeles Dodgers was 31 and a 12-year veteran of Major League Baseball when he became the unwitting vanguard of a revolution in baseball and orthopedics. Fifty years later, Mr. John might not be a candidate for the latest advances to a procedure that bears his name.

The southpaw pitcher had faced the abrupt end of his career when, after one fateful delivery, he found himself unable to throw to home. So he took a gamble on the surgical equivalent of a Hail Mary: the reconstruction of a torn ligament in his pitching elbow.

The experiment was a wild success. Mr. John pitched— and better than he had before — for another 14 seasons, retiring in 1989 at the age of 46. How much better? After the surgery, he tallied three 20-win seasons compared with none before the operation, and he finished among the top five vote-getters for the annual Cy Young Award three times. He was named an All-Star once before the surgery and three times after.

The triumph notwithstanding, Tommy John now cautions against Tommy John surgery. What’s given him and clinicians pause is a trend in recent years of ever-younger athletes who undergo the procedure.

Along with the surgical improvements in repairing a torn ulnar collateral ligament (UCL) is a demographic shift toward school-aged athletes who get it. By 2014, one study concluded that 67.4% of UCL reconstruction surgeries were performed on athletes between 16 and 20 years of age. Some patients are still in Little League when they undergo the procedure.

Experts say these athletes have weakened their UCLs through overuse. They disagree on whether to call it an “epidemic,” but if it is, “the vaccine is awareness” against throwing too hard and too often, said Eric Makhni, MD, an orthopedic surgeon at Henry Ford Health in Detroit.
 

From Career-Ending to Routine

Mr. John’s entry into baseball and orthopedic lore was initially slow, but the trickle turned into a tide. After Frank Jobe, MD, swapped a healthy tendon from John’s right wrist for his worn and torn left UCL on September 25, 1974, he didn’t perform his second surgery for another 1194 days. By the time “Tommy John surgery” became a recognized phrase, Mr. John was still active but only 14 professional baseball players had undergone the operation.

Prior to the start of spring training this year, an oft-cited database listed 366 pro players who’d undergone the operation. 

“Before Tommy John, that was a career-ending injury,” said Grant E. Garrigues, MD, an orthopedic surgeon at Midwest Orthopaedics at RUSH in Chicago, who called Mr. John “a pure revolutionary.”

Tommy John surgery is “the only one that I can think of that is named after the patient rather than the doctor who first did it,” said Patrick McCulloch, MD, an orthopedic surgeon in Houston and a team physician for the Astros.

Dr. McCulloch, who performs about 25 UCL repairs a year, said that by recent estimates, one-third of pro pitchers had had some sort of surgical repair. He hesitated to call the increasing number of operations an epidemic but acknowledged that the ingredients exist for more elbow trauma among baseball players.

“More people are playing more often, and people are bigger and stronger and throwing harder,” he said.

Either way, Dr. McCulloch said, “the procedure is a victim of its own success” because it is “just done phenomenally well.”

The surgery is now commonplace — perhaps too commonplace, said David W. Altchek, MD, attending surgeon and co-chief emeritus at Hospital for Special Surgery in New York City.

Dr. Altchek played a key role in the popularity of the operation. Twenty-two years after Mr. John’s surgery, he helped develop a variation of the procedure called the docking technique. 

Whereas Dr. Jobe sutured Mr. John’s replacement graft to itself, “we developed a different way of tying it over a bone bridge, which was more secure and more easy to tension,” Dr. Altchek explained.

The advance meant less drilling into bone and enabled surgeons to avoid moving a problem-free ulnar nerve or removing the flexor-pronator muscle that protects the elbow from stress. “The trauma of the surgery is significantly less,” he said. “We just made it a lot easier very quickly,” cutting the surgery time from 2 hours to 30-40 minutes.

Maybe the surgery became too easy, said Dr. Altchek, who estimates he has done 2000 of them over the past 30 years. “I don’t want to condemn my colleagues, but there are a lot of people doing the surgery,” he said. “And not a lot of people are doing a lot of them, and they don’t know the nuances of doing the surgery.”

The older procedures are known as the “full Tommy John”; each has a 12- to 18-month healing process, with a success rate of 80%-85%. Pitchers typically sit out a season while recovering.

Brandon Erickson, MD, an orthopedic surgeon at Rothman Orthopaedic Institute in New York City, said that in younger patients he has recently turned more often to the suture of the future: an internal brace that provides a repair rather than reconstruction.

The procedure, pioneered by Felix H. Savoie III, MD, the Ray J. Haddad Professor of Orthopaedics at Tulane University School of Medicine in New Orleans, and Jeffrey R. Dugas, MD, of Andrews Sports Medicine & Orthopaedic Center in Birmingham, Alabama, uses collagen-coated tape that looks like a shoelace and provides a scaffold that Dr. McCulloch said “is inductive to healing and growth of ligament tissue.”

The brace is intended for an “overhead” athlete (mostly baseball players but also javelin throwers and gymnasts) whose UCL is torn on only one side but is otherwise in good shape. In a pitcher the same age as Mr. John was when Dr. Jobe performed the first procedure, “that ligament may not be of very good quality,” Dr. McCulloch said. “It may have thickened. It may have calcifications.” But for a high-school junior with aspirations to pitch in college or beyond without “way too many miles on the elbow,” the approach is a good fit. The healing process is as little as 6 months.

“The ones who have a good ligament are very likely to do well,” said Dr. Erickson, an assistant team doctor for the Philadelphia Phillies.

“If the patient’s ligament is generally ‘good’ with only a tear, the InternalBrace procedure may be used to repair the native ligament. On the other end of the spectrum, if the patient’s ligament is torn and degenerative the surgeon may opt to do a UCL reconstruction using an auto or allograft — ie, Tommy John surgery,” Allen Holowecky, senior product manager of Arthrex of Naples, Florida, the maker of the InternalBrace, told this news organization. “Before UCL repair, Tommy John surgery was the only real treatment option. We tend to see repairs done on younger patients since their ligament hasn’t seen years of use-damage.”
 

Calls for Caution

Tommy John III wanted to play baseball like his dad until near-fatal complications from shoulder surgery altered his path. He was drawn to chiropractic and consults on injury prevention. “All surgeries and all medical interventions are cut first, ask questions later,” he said. “I was born with that.”

He saw his dad’s slow, heroic comeback from the surgery and described him as the perfect candidate for Dr. Jobe’s experiment. Tommy John spent his recovery time squeezing Silly Putty and throwing tennis balls. “He was willing to do anything necessary. He wanted to throw. That was his brush.” When the son was recovering from his own injury, “he said, ‘Learn the knuckleball.’ I said, ‘I don’t want to. I’ve reached my point.’ ”

He said he tells young patients with UCL injuries to rest. But instead “we have year-round sports with the promise that the more you play, the better,” he said. “They’re over-activitied.”

According to the American Academy of Orthopaedic Surgeons, 6.4 million children and adolescents in the United States played organized baseball in 2022, down from 11.5 million in 2014. Nearly half of pitchers played in a league with no maximum pitch counts, and 43.5% pitched on consecutive days, the group said.

How many UCL repair or reconstruction surgeries are performed on youth athletes each year is unclear. A 2019 study, however, found that although baseball injuries decreased between 2006 and 2016, the elbow was “the only location of injury that saw an increase.”

Dr. Garrigues said some parents of throwing athletes have asked about prophylactic Tommy John surgery for their children. He said it shouldn’t apply to pitchers.

“People have taken it a little too far,” he said. Dr. Garrigues and others argue against children throwing weighted balls when coming back from surgery. Instead, “we’re shutting them down,” he said.

Throwing any pitch is an act of violence on the body, Dr. Garrigues said, with the elbow taking the final brunt of the force. “These pitchers are functioning at the absolute limits of what the human body can take,” he said. “There’s only so many bullets in a gun,” which is why pitchers often feel the twinge of a torn UCL on a routine pitch.

Dr. Makhni suggested cross-training for pitchers in the off-season instead of playing baseball year-round. “If you play soccer, your footwork is going to be better,” he said.

“Kids shouldn’t be doing this all year round,” said Rebecca Carl, MD, associate professor of pediatrics at Northwestern University Feinberg School of Medicine in Chicago. “We are recommending that kids take 2 or 3 months off.” In the off-season, she urges them to strengthen their backs and cores. 

Such advice can “feel like a bombshell,” said Dr. Carl, who chairs the Council on Sports Medicine and Fitness for the American Academy of Pediatrics. ‘Some started at a very young age. They go to camps. If I say to a teenager, ‘If you do this, I can keep you from getting injured,’ they think, ‘I won’t be injured.’” Most parents, however, understand the risk of “doing too much, too soon.”

Justin Orenduff, a former pitching prospect until his arm blew out, has made a career teaching head-to-toe pitching mechanics. He founded DVS Baseball, which uses software to teach pitchers how to properly use every muscle, starting with the orientation of the back foot. He, too, argues against pitching year-round. “Everyone on that travel team expects to get their fair share of playing time,” he said. “It just never stops.”

Organized baseball is paying attention. It has come up with the Pitch Smart program that gives maximum pitch counts for young players, but experts said children often get around that by belonging to several leagues.

Dr. Altchek said some surgeons have added platelet-rich plasma, stem cells, and bone marrow during surgery to quicken the slow healing time from UCL replacement. But he said, “it has to heal. Can you speed up biology?”

Dr. McCulloch said that, all the advances in Tommy John surgery aside, “the next frontier is really trying to crack the code on prevention.”

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

In 1974, Tommy John of the Los Angeles Dodgers was 31 and a 12-year veteran of Major League Baseball when he became the unwitting vanguard of a revolution in baseball and orthopedics. Fifty years later, Mr. John might not be a candidate for the latest advances to a procedure that bears his name.

The southpaw pitcher had faced the abrupt end of his career when, after one fateful delivery, he found himself unable to throw to home. So he took a gamble on the surgical equivalent of a Hail Mary: the reconstruction of a torn ligament in his pitching elbow.

The experiment was a wild success. Mr. John pitched— and better than he had before — for another 14 seasons, retiring in 1989 at the age of 46. How much better? After the surgery, he tallied three 20-win seasons compared with none before the operation, and he finished among the top five vote-getters for the annual Cy Young Award three times. He was named an All-Star once before the surgery and three times after.

The triumph notwithstanding, Tommy John now cautions against Tommy John surgery. What’s given him and clinicians pause is a trend in recent years of ever-younger athletes who undergo the procedure.

Along with the surgical improvements in repairing a torn ulnar collateral ligament (UCL) is a demographic shift toward school-aged athletes who get it. By 2014, one study concluded that 67.4% of UCL reconstruction surgeries were performed on athletes between 16 and 20 years of age. Some patients are still in Little League when they undergo the procedure.

Experts say these athletes have weakened their UCLs through overuse. They disagree on whether to call it an “epidemic,” but if it is, “the vaccine is awareness” against throwing too hard and too often, said Eric Makhni, MD, an orthopedic surgeon at Henry Ford Health in Detroit.
 

From Career-Ending to Routine

Mr. John’s entry into baseball and orthopedic lore was initially slow, but the trickle turned into a tide. After Frank Jobe, MD, swapped a healthy tendon from John’s right wrist for his worn and torn left UCL on September 25, 1974, he didn’t perform his second surgery for another 1194 days. By the time “Tommy John surgery” became a recognized phrase, Mr. John was still active but only 14 professional baseball players had undergone the operation.

Prior to the start of spring training this year, an oft-cited database listed 366 pro players who’d undergone the operation. 

“Before Tommy John, that was a career-ending injury,” said Grant E. Garrigues, MD, an orthopedic surgeon at Midwest Orthopaedics at RUSH in Chicago, who called Mr. John “a pure revolutionary.”

Tommy John surgery is “the only one that I can think of that is named after the patient rather than the doctor who first did it,” said Patrick McCulloch, MD, an orthopedic surgeon in Houston and a team physician for the Astros.

Dr. McCulloch, who performs about 25 UCL repairs a year, said that by recent estimates, one-third of pro pitchers had had some sort of surgical repair. He hesitated to call the increasing number of operations an epidemic but acknowledged that the ingredients exist for more elbow trauma among baseball players.

“More people are playing more often, and people are bigger and stronger and throwing harder,” he said.

Either way, Dr. McCulloch said, “the procedure is a victim of its own success” because it is “just done phenomenally well.”

The surgery is now commonplace — perhaps too commonplace, said David W. Altchek, MD, attending surgeon and co-chief emeritus at Hospital for Special Surgery in New York City.

Dr. Altchek played a key role in the popularity of the operation. Twenty-two years after Mr. John’s surgery, he helped develop a variation of the procedure called the docking technique. 

Whereas Dr. Jobe sutured Mr. John’s replacement graft to itself, “we developed a different way of tying it over a bone bridge, which was more secure and more easy to tension,” Dr. Altchek explained.

The advance meant less drilling into bone and enabled surgeons to avoid moving a problem-free ulnar nerve or removing the flexor-pronator muscle that protects the elbow from stress. “The trauma of the surgery is significantly less,” he said. “We just made it a lot easier very quickly,” cutting the surgery time from 2 hours to 30-40 minutes.

Maybe the surgery became too easy, said Dr. Altchek, who estimates he has done 2000 of them over the past 30 years. “I don’t want to condemn my colleagues, but there are a lot of people doing the surgery,” he said. “And not a lot of people are doing a lot of them, and they don’t know the nuances of doing the surgery.”

The older procedures are known as the “full Tommy John”; each has a 12- to 18-month healing process, with a success rate of 80%-85%. Pitchers typically sit out a season while recovering.

Brandon Erickson, MD, an orthopedic surgeon at Rothman Orthopaedic Institute in New York City, said that in younger patients he has recently turned more often to the suture of the future: an internal brace that provides a repair rather than reconstruction.

The procedure, pioneered by Felix H. Savoie III, MD, the Ray J. Haddad Professor of Orthopaedics at Tulane University School of Medicine in New Orleans, and Jeffrey R. Dugas, MD, of Andrews Sports Medicine & Orthopaedic Center in Birmingham, Alabama, uses collagen-coated tape that looks like a shoelace and provides a scaffold that Dr. McCulloch said “is inductive to healing and growth of ligament tissue.”

The brace is intended for an “overhead” athlete (mostly baseball players but also javelin throwers and gymnasts) whose UCL is torn on only one side but is otherwise in good shape. In a pitcher the same age as Mr. John was when Dr. Jobe performed the first procedure, “that ligament may not be of very good quality,” Dr. McCulloch said. “It may have thickened. It may have calcifications.” But for a high-school junior with aspirations to pitch in college or beyond without “way too many miles on the elbow,” the approach is a good fit. The healing process is as little as 6 months.

“The ones who have a good ligament are very likely to do well,” said Dr. Erickson, an assistant team doctor for the Philadelphia Phillies.

“If the patient’s ligament is generally ‘good’ with only a tear, the InternalBrace procedure may be used to repair the native ligament. On the other end of the spectrum, if the patient’s ligament is torn and degenerative the surgeon may opt to do a UCL reconstruction using an auto or allograft — ie, Tommy John surgery,” Allen Holowecky, senior product manager of Arthrex of Naples, Florida, the maker of the InternalBrace, told this news organization. “Before UCL repair, Tommy John surgery was the only real treatment option. We tend to see repairs done on younger patients since their ligament hasn’t seen years of use-damage.”
 

Calls for Caution

Tommy John III wanted to play baseball like his dad until near-fatal complications from shoulder surgery altered his path. He was drawn to chiropractic and consults on injury prevention. “All surgeries and all medical interventions are cut first, ask questions later,” he said. “I was born with that.”

He saw his dad’s slow, heroic comeback from the surgery and described him as the perfect candidate for Dr. Jobe’s experiment. Tommy John spent his recovery time squeezing Silly Putty and throwing tennis balls. “He was willing to do anything necessary. He wanted to throw. That was his brush.” When the son was recovering from his own injury, “he said, ‘Learn the knuckleball.’ I said, ‘I don’t want to. I’ve reached my point.’ ”

He said he tells young patients with UCL injuries to rest. But instead “we have year-round sports with the promise that the more you play, the better,” he said. “They’re over-activitied.”

According to the American Academy of Orthopaedic Surgeons, 6.4 million children and adolescents in the United States played organized baseball in 2022, down from 11.5 million in 2014. Nearly half of pitchers played in a league with no maximum pitch counts, and 43.5% pitched on consecutive days, the group said.

How many UCL repair or reconstruction surgeries are performed on youth athletes each year is unclear. A 2019 study, however, found that although baseball injuries decreased between 2006 and 2016, the elbow was “the only location of injury that saw an increase.”

Dr. Garrigues said some parents of throwing athletes have asked about prophylactic Tommy John surgery for their children. He said it shouldn’t apply to pitchers.

“People have taken it a little too far,” he said. Dr. Garrigues and others argue against children throwing weighted balls when coming back from surgery. Instead, “we’re shutting them down,” he said.

Throwing any pitch is an act of violence on the body, Dr. Garrigues said, with the elbow taking the final brunt of the force. “These pitchers are functioning at the absolute limits of what the human body can take,” he said. “There’s only so many bullets in a gun,” which is why pitchers often feel the twinge of a torn UCL on a routine pitch.

Dr. Makhni suggested cross-training for pitchers in the off-season instead of playing baseball year-round. “If you play soccer, your footwork is going to be better,” he said.

“Kids shouldn’t be doing this all year round,” said Rebecca Carl, MD, associate professor of pediatrics at Northwestern University Feinberg School of Medicine in Chicago. “We are recommending that kids take 2 or 3 months off.” In the off-season, she urges them to strengthen their backs and cores. 

Such advice can “feel like a bombshell,” said Dr. Carl, who chairs the Council on Sports Medicine and Fitness for the American Academy of Pediatrics. ‘Some started at a very young age. They go to camps. If I say to a teenager, ‘If you do this, I can keep you from getting injured,’ they think, ‘I won’t be injured.’” Most parents, however, understand the risk of “doing too much, too soon.”

Justin Orenduff, a former pitching prospect until his arm blew out, has made a career teaching head-to-toe pitching mechanics. He founded DVS Baseball, which uses software to teach pitchers how to properly use every muscle, starting with the orientation of the back foot. He, too, argues against pitching year-round. “Everyone on that travel team expects to get their fair share of playing time,” he said. “It just never stops.”

Organized baseball is paying attention. It has come up with the Pitch Smart program that gives maximum pitch counts for young players, but experts said children often get around that by belonging to several leagues.

Dr. Altchek said some surgeons have added platelet-rich plasma, stem cells, and bone marrow during surgery to quicken the slow healing time from UCL replacement. But he said, “it has to heal. Can you speed up biology?”

Dr. McCulloch said that, all the advances in Tommy John surgery aside, “the next frontier is really trying to crack the code on prevention.”

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

TOPLINE:

A new study shows sudden cardiac deaths among collegiate athletes decreased over a recent 20-year period, but risks are still elevated among males, Black players, and basketball players, suggesting more intensive screening among these groups is needed.

METHODOLOGY:

• The study examined incidence and surrounding circumstances of sudden cardiac death (SCD) among student athletes who competed in at least one varsity sport at National Collegiate Athletic Association (NCAA) Division I, II, or III institutions in the 20 years from July 1, 2002, to June 30, 2022.
• Researchers determined causes of death and gathered demographic characteristics using multiple methods, including review of autopsy and other official documents, Internet searches, and contacts to next of kin, coaches, athletic trainers, coroners, medical examiners, scholarship foundations, and physicians involved in the case.
• SCD was defined as sudden unexpected death attributable to a cardiac cause, or a sudden death in a structurally normal heart with no other explanation for death and a history consistent with cardiac-related death that occurred within an hour of symptom onset, or an unwitnessed death occurring within 24 hours of the person being alive.
• Researchers calculated incidence rates over a typical 4-year collegiate career and reported these as athlete-years.

TAKEAWAY:

• The incidence of SCD, which accounted for 13% of the 1102 total deaths during the study period, decreased over time, with a 5-year incidence rate ratio (IRR) of 0.71 (95% CI, 0.61-0.82), while noncardiovascular deaths remained stable.
• IRR for males versus females was 3.79 (95% CI, 2.45-5.88) and for Black versus White athletes was 2.79 (95% CI, 1.98-3.94).
• Basketball and football players were at increased risk of SCD; for example, the incidence rate among Division I Black male basketball athletes was 1:1924 per 4-year athlete-years.
• The most common postmortem finding was autopsy-negative sudden unexplained death, at 19%, followed by idiopathic left ventricular hypertrophy/possible cardiomyopathy (17%) and hypertrophic cardiomyopathy (13%), with no cases of death attributable to COVID-19 myocarditis.

IN PRACTICE:

Although the reason for the decrease in SCD is unknown, “our data suggest that strategies to reduce SCD among competing athletes may be having a positive effect,” wrote the authors. More intensive screening strategies among groups with high SCD incidence may be warranted, they added.

SOURCE:

The study was conducted by Bradley J. Petek, MD, Sports Cardiology Program, Knight Cardiovascular Institute, Oregon Health & Science University, Portland. It was published online November 13 in Circulation and presented at the American Heart Association scientific sessions (abstract 479).

LIMITATIONS:

Some cases of SCD may have been missed as there is no mandatory reporting system in the United States. Approaches to cardiac autopsy and reporting varied significantly. The cause of death was unknown in 16 cases, and postmortem genetic testing was available for only 3% of athletes. As the study didn’t have data on resuscitated sudden cardiac arrest or preparticipation cardiovascular screening practices and findings, definitive conclusions couldn’t be drawn regarding causal factors underlying the decreased incidence of SCD.

DISCLOSURES:

There was no outside funding source. Dr. Petek has reported no relevant financial relationships. Disclosures for the other authors are listed with the article.

A version of this article appeared on Medscape.com.

TOPLINE:

A new study shows sudden cardiac deaths among collegiate athletes decreased over a recent 20-year period, but risks are still elevated among males, Black players, and basketball players, suggesting more intensive screening among these groups is needed.

METHODOLOGY:

• The study examined incidence and surrounding circumstances of sudden cardiac death (SCD) among student athletes who competed in at least one varsity sport at National Collegiate Athletic Association (NCAA) Division I, II, or III institutions in the 20 years from July 1, 2002, to June 30, 2022.
• Researchers determined causes of death and gathered demographic characteristics using multiple methods, including review of autopsy and other official documents, Internet searches, and contacts to next of kin, coaches, athletic trainers, coroners, medical examiners, scholarship foundations, and physicians involved in the case.
• SCD was defined as sudden unexpected death attributable to a cardiac cause, or a sudden death in a structurally normal heart with no other explanation for death and a history consistent with cardiac-related death that occurred within an hour of symptom onset, or an unwitnessed death occurring within 24 hours of the person being alive.
• Researchers calculated incidence rates over a typical 4-year collegiate career and reported these as athlete-years.

TAKEAWAY:

• The incidence of SCD, which accounted for 13% of the 1102 total deaths during the study period, decreased over time, with a 5-year incidence rate ratio (IRR) of 0.71 (95% CI, 0.61-0.82), while noncardiovascular deaths remained stable.
• IRR for males versus females was 3.79 (95% CI, 2.45-5.88) and for Black versus White athletes was 2.79 (95% CI, 1.98-3.94).
• Basketball and football players were at increased risk of SCD; for example, the incidence rate among Division I Black male basketball athletes was 1:1924 per 4-year athlete-years.
• The most common postmortem finding was autopsy-negative sudden unexplained death, at 19%, followed by idiopathic left ventricular hypertrophy/possible cardiomyopathy (17%) and hypertrophic cardiomyopathy (13%), with no cases of death attributable to COVID-19 myocarditis.

IN PRACTICE:

Although the reason for the decrease in SCD is unknown, “our data suggest that strategies to reduce SCD among competing athletes may be having a positive effect,” wrote the authors. More intensive screening strategies among groups with high SCD incidence may be warranted, they added.

SOURCE:

The study was conducted by Bradley J. Petek, MD, Sports Cardiology Program, Knight Cardiovascular Institute, Oregon Health & Science University, Portland. It was published online November 13 in Circulation and presented at the American Heart Association scientific sessions (abstract 479).

LIMITATIONS:

Some cases of SCD may have been missed as there is no mandatory reporting system in the United States. Approaches to cardiac autopsy and reporting varied significantly. The cause of death was unknown in 16 cases, and postmortem genetic testing was available for only 3% of athletes. As the study didn’t have data on resuscitated sudden cardiac arrest or preparticipation cardiovascular screening practices and findings, definitive conclusions couldn’t be drawn regarding causal factors underlying the decreased incidence of SCD.

DISCLOSURES:

There was no outside funding source. Dr. Petek has reported no relevant financial relationships. Disclosures for the other authors are listed with the article.

A version of this article appeared on Medscape.com.

TOPLINE:

A new study shows sudden cardiac deaths among collegiate athletes decreased over a recent 20-year period, but risks are still elevated among males, Black players, and basketball players, suggesting more intensive screening among these groups is needed.

METHODOLOGY:

• The study examined incidence and surrounding circumstances of sudden cardiac death (SCD) among student athletes who competed in at least one varsity sport at National Collegiate Athletic Association (NCAA) Division I, II, or III institutions in the 20 years from July 1, 2002, to June 30, 2022.
• Researchers determined causes of death and gathered demographic characteristics using multiple methods, including review of autopsy and other official documents, Internet searches, and contacts to next of kin, coaches, athletic trainers, coroners, medical examiners, scholarship foundations, and physicians involved in the case.
• SCD was defined as sudden unexpected death attributable to a cardiac cause, or a sudden death in a structurally normal heart with no other explanation for death and a history consistent with cardiac-related death that occurred within an hour of symptom onset, or an unwitnessed death occurring within 24 hours of the person being alive.
• Researchers calculated incidence rates over a typical 4-year collegiate career and reported these as athlete-years.

TAKEAWAY:

• The incidence of SCD, which accounted for 13% of the 1102 total deaths during the study period, decreased over time, with a 5-year incidence rate ratio (IRR) of 0.71 (95% CI, 0.61-0.82), while noncardiovascular deaths remained stable.
• IRR for males versus females was 3.79 (95% CI, 2.45-5.88) and for Black versus White athletes was 2.79 (95% CI, 1.98-3.94).
• Basketball and football players were at increased risk of SCD; for example, the incidence rate among Division I Black male basketball athletes was 1:1924 per 4-year athlete-years.
• The most common postmortem finding was autopsy-negative sudden unexplained death, at 19%, followed by idiopathic left ventricular hypertrophy/possible cardiomyopathy (17%) and hypertrophic cardiomyopathy (13%), with no cases of death attributable to COVID-19 myocarditis.

IN PRACTICE:

Although the reason for the decrease in SCD is unknown, “our data suggest that strategies to reduce SCD among competing athletes may be having a positive effect,” wrote the authors. More intensive screening strategies among groups with high SCD incidence may be warranted, they added.

SOURCE:

The study was conducted by Bradley J. Petek, MD, Sports Cardiology Program, Knight Cardiovascular Institute, Oregon Health & Science University, Portland. It was published online November 13 in Circulation and presented at the American Heart Association scientific sessions (abstract 479).

LIMITATIONS:

Some cases of SCD may have been missed as there is no mandatory reporting system in the United States. Approaches to cardiac autopsy and reporting varied significantly. The cause of death was unknown in 16 cases, and postmortem genetic testing was available for only 3% of athletes. As the study didn’t have data on resuscitated sudden cardiac arrest or preparticipation cardiovascular screening practices and findings, definitive conclusions couldn’t be drawn regarding causal factors underlying the decreased incidence of SCD.

DISCLOSURES:

There was no outside funding source. Dr. Petek has reported no relevant financial relationships. Disclosures for the other authors are listed with the article.

A version of this article appeared on Medscape.com.

If a patient’s prostate-specific antigen (PSA) spikes 2 points in just 90 days, what is your first thought? This patient has a strong likelihood of aggressive prostate cancer, right? If that same patient also presents with severe, burning bone pain with no precipitating trauma to the area and rest and over-the-counter  painkillers are not helping, you’d think, “check for metastases,” right?

That patient was me in late January 2023.

As a research scientist member of the American Urological Association, I knew enough to know I had to consult my urologist ASAP.

With the above symptoms, I’ll admit I was scared. Fortunately, if that’s the right word, I was no stranger to a rapid, dramatic spike in PSA. In 2021 I was temporarily living in a new city, and I wanted to form a relationship with a good local urologist. The urologist that I was referred to gave me a thorough consultation, including a vigorous digital rectal exam (DRE) and sent me across the street for a blood draw.

To my shock, my PSA had spiked over 2 points, to 9.9 from 7.8 a few months earlier. I freaked. Had my 3-cm tumor burst out into an aggressive cancer? Research on PubMed provided an array of studies showing what could cause PSA to suddenly rise, including a DRE performed 72 hours before the blood draw.1 A week later, my PSA was back down to its normal 7.6. 

But in January 2023, I had none of those previously reported experiences that could suddenly trigger a spike in PSA, like a DRE or riding on a thin bicycle seat for a few hours before the lab visit. 
 

The COVID effect

I went back to PubMed and found a new circumstance that could cause a surge in PSA: COVID-19. A recent study² of 91 men with benign prostatic hypertrophy by researchers in Turkey found that PSA spiked from 0 to 5 points during the COVID infection period and up to 2 points higher 3 months after the infection had cleared. I had tested positive for COVID-19 in mid-December 2022, 4 weeks before my 9.9 PSA reading.

Using Google translate, I communicated with the team in Turkey and found out that the PSA spike can last up to 6 months.

That study helps explain why my PSA dropped over 1.5 points to 8.5 just 2 weeks after the 9.9 reading, with the expectation that it would return to its previous normal of 7.8 within 6 months of infection with SARS-CoV-2. To be safe, my urologist scheduled another PSA test in May, along with an updated multiparametric MRI, which may be followed by an in-bore MRI-guided biopsy of the 3-cm tumor if the mass has enlarged.
 

COVID-19 pain

What about my burning bone pain in my upper right humerus and right rotator cuff that was not precipitated by trauma or strain? A radiograph found no evidence of metastasis, thank goodness. And my research showed that several studies³ have found that COVID-19 can cause burning musculoskeletal pain, including enthesopathy, which is what I had per the radiology report. So my PSA spike and searing pain were likely consequences of the infection.

To avoid the risk for a gross misdiagnosis after a radical spike in PSA, the informed urologist should ask the patient if he has had COVID-19 in the previous 6 months. Overlooking that question could lead to the wrong diagnostic decisions about a rapid jump in PSA or unexplained bone pain.

References

1. Bossens MM et al. Eur J Cancer. 1995;31A:682-5.

2. Cinislioglu AE et al. Urology. 2022;159:16-21.

3. Ciaffi J et al. Joint Bone Spine. 2021;88:105158.

Dr. Keller is founder of the Keller Research Institute, Jacksonville, Fla. He reported serving as a research scientist for the American Urological Association, serving on the advisory board of Active Surveillance Patient’s International, and serving on the boards of numerous nonprofit organizations.

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

If a patient’s prostate-specific antigen (PSA) spikes 2 points in just 90 days, what is your first thought? This patient has a strong likelihood of aggressive prostate cancer, right? If that same patient also presents with severe, burning bone pain with no precipitating trauma to the area and rest and over-the-counter  painkillers are not helping, you’d think, “check for metastases,” right?

That patient was me in late January 2023.

As a research scientist member of the American Urological Association, I knew enough to know I had to consult my urologist ASAP.

With the above symptoms, I’ll admit I was scared. Fortunately, if that’s the right word, I was no stranger to a rapid, dramatic spike in PSA. In 2021 I was temporarily living in a new city, and I wanted to form a relationship with a good local urologist. The urologist that I was referred to gave me a thorough consultation, including a vigorous digital rectal exam (DRE) and sent me across the street for a blood draw.

To my shock, my PSA had spiked over 2 points, to 9.9 from 7.8 a few months earlier. I freaked. Had my 3-cm tumor burst out into an aggressive cancer? Research on PubMed provided an array of studies showing what could cause PSA to suddenly rise, including a DRE performed 72 hours before the blood draw.1 A week later, my PSA was back down to its normal 7.6. 

But in January 2023, I had none of those previously reported experiences that could suddenly trigger a spike in PSA, like a DRE or riding on a thin bicycle seat for a few hours before the lab visit. 
 

The COVID effect

I went back to PubMed and found a new circumstance that could cause a surge in PSA: COVID-19. A recent study² of 91 men with benign prostatic hypertrophy by researchers in Turkey found that PSA spiked from 0 to 5 points during the COVID infection period and up to 2 points higher 3 months after the infection had cleared. I had tested positive for COVID-19 in mid-December 2022, 4 weeks before my 9.9 PSA reading.

Using Google translate, I communicated with the team in Turkey and found out that the PSA spike can last up to 6 months.

That study helps explain why my PSA dropped over 1.5 points to 8.5 just 2 weeks after the 9.9 reading, with the expectation that it would return to its previous normal of 7.8 within 6 months of infection with SARS-CoV-2. To be safe, my urologist scheduled another PSA test in May, along with an updated multiparametric MRI, which may be followed by an in-bore MRI-guided biopsy of the 3-cm tumor if the mass has enlarged.
 

COVID-19 pain

What about my burning bone pain in my upper right humerus and right rotator cuff that was not precipitated by trauma or strain? A radiograph found no evidence of metastasis, thank goodness. And my research showed that several studies³ have found that COVID-19 can cause burning musculoskeletal pain, including enthesopathy, which is what I had per the radiology report. So my PSA spike and searing pain were likely consequences of the infection.

To avoid the risk for a gross misdiagnosis after a radical spike in PSA, the informed urologist should ask the patient if he has had COVID-19 in the previous 6 months. Overlooking that question could lead to the wrong diagnostic decisions about a rapid jump in PSA or unexplained bone pain.

References

1. Bossens MM et al. Eur J Cancer. 1995;31A:682-5.

2. Cinislioglu AE et al. Urology. 2022;159:16-21.

3. Ciaffi J et al. Joint Bone Spine. 2021;88:105158.

Dr. Keller is founder of the Keller Research Institute, Jacksonville, Fla. He reported serving as a research scientist for the American Urological Association, serving on the advisory board of Active Surveillance Patient’s International, and serving on the boards of numerous nonprofit organizations.

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

If a patient’s prostate-specific antigen (PSA) spikes 2 points in just 90 days, what is your first thought? This patient has a strong likelihood of aggressive prostate cancer, right? If that same patient also presents with severe, burning bone pain with no precipitating trauma to the area and rest and over-the-counter  painkillers are not helping, you’d think, “check for metastases,” right?

That patient was me in late January 2023.

As a research scientist member of the American Urological Association, I knew enough to know I had to consult my urologist ASAP.

With the above symptoms, I’ll admit I was scared. Fortunately, if that’s the right word, I was no stranger to a rapid, dramatic spike in PSA. In 2021 I was temporarily living in a new city, and I wanted to form a relationship with a good local urologist. The urologist that I was referred to gave me a thorough consultation, including a vigorous digital rectal exam (DRE) and sent me across the street for a blood draw.

To my shock, my PSA had spiked over 2 points, to 9.9 from 7.8 a few months earlier. I freaked. Had my 3-cm tumor burst out into an aggressive cancer? Research on PubMed provided an array of studies showing what could cause PSA to suddenly rise, including a DRE performed 72 hours before the blood draw.1 A week later, my PSA was back down to its normal 7.6. 

But in January 2023, I had none of those previously reported experiences that could suddenly trigger a spike in PSA, like a DRE or riding on a thin bicycle seat for a few hours before the lab visit. 
 

The COVID effect

I went back to PubMed and found a new circumstance that could cause a surge in PSA: COVID-19. A recent study² of 91 men with benign prostatic hypertrophy by researchers in Turkey found that PSA spiked from 0 to 5 points during the COVID infection period and up to 2 points higher 3 months after the infection had cleared. I had tested positive for COVID-19 in mid-December 2022, 4 weeks before my 9.9 PSA reading.

Using Google translate, I communicated with the team in Turkey and found out that the PSA spike can last up to 6 months.

That study helps explain why my PSA dropped over 1.5 points to 8.5 just 2 weeks after the 9.9 reading, with the expectation that it would return to its previous normal of 7.8 within 6 months of infection with SARS-CoV-2. To be safe, my urologist scheduled another PSA test in May, along with an updated multiparametric MRI, which may be followed by an in-bore MRI-guided biopsy of the 3-cm tumor if the mass has enlarged.
 

COVID-19 pain

What about my burning bone pain in my upper right humerus and right rotator cuff that was not precipitated by trauma or strain? A radiograph found no evidence of metastasis, thank goodness. And my research showed that several studies³ have found that COVID-19 can cause burning musculoskeletal pain, including enthesopathy, which is what I had per the radiology report. So my PSA spike and searing pain were likely consequences of the infection.

To avoid the risk for a gross misdiagnosis after a radical spike in PSA, the informed urologist should ask the patient if he has had COVID-19 in the previous 6 months. Overlooking that question could lead to the wrong diagnostic decisions about a rapid jump in PSA or unexplained bone pain.

References

1. Bossens MM et al. Eur J Cancer. 1995;31A:682-5.

2. Cinislioglu AE et al. Urology. 2022;159:16-21.

3. Ciaffi J et al. Joint Bone Spine. 2021;88:105158.

Dr. Keller is founder of the Keller Research Institute, Jacksonville, Fla. He reported serving as a research scientist for the American Urological Association, serving on the advisory board of Active Surveillance Patient’s International, and serving on the boards of numerous nonprofit organizations.

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

High school students are injuring themselves more severely even as overall injury rates have declined, according to a new study presented at the annual meeting of the American Academy of Orthopaedic Surgeons.

The study compared injuries from a 4-year period ending in 2019 to data from 2005 and 2006. The overall rate of injuries dropped 9%, from 2.51 injuries per 1,000 athletic games or practices to 2.29 per 1,000; injuries requiring less than 1 week of recovery time fell by 13%. But, the number of head and neck injuries increased by 10%, injuries requiring surgery increased by 1%, and injuries leading to medical disqualification jumped by 11%. 

“It’s wonderful that the injury rate is declining,” said Jordan Neoma Pizzarro, a medical student at George Washington University, Washington, who led the study. “But the data does suggest that the injuries that are happening are worse.”

The increases may also reflect increased education and awareness of how to detect concussions and other injuries that need medical attention, said Micah Lissy, MD, MS, an orthopedic surgeon specializing in sports medicine at Michigan State University, East Lansing. Dr. Lissy cautioned against physicians and others taking the data at face value. 

“We need to be implementing preventive measures wherever possible, but I think we can also consider that there may be some confounding factors in the data,” Dr. Lissy told this news organization. 

Ms. Pizzarro and her team analyzed data collected from athletic trainers at 100 high schools across the country for the ongoing National Health School Sports-Related Injury Surveillance Study.

Athletes participating in sports such as football, soccer, basketball, volleyball, and softball were included in the analysis. Trainers report the number of injuries for every competition and practice, also known as “athletic exposures.”

Boys’ football carried the highest injury rate, with 3.96 injuries per 1,000 AEs, amounting to 44% of all injuries reported. Girls’ soccer and boys’ wrestling followed, with injury rates of 2.65 and 1.56, respectively. 

Sprains and strains accounted for 37% of injuries, followed by concussions (21.6%). The head and/or face was the most injured body site, followed by the ankles and/or knees. Most injuries took place during competitions rather than in practices (relative risk, 3.39; 95% confidence interval, 3.28-3.49; P < .05).

Ms. Pizzarro said that an overall increase in intensity, physical contact, and collisions may account for the spike in more severe injuries.

“Kids are encouraged to specialize in one sport early on and stick with it year-round,” she said. “They’re probably becoming more agile and better athletes, but they’re probably also getting more competitive.” 

Dr. Lissy, who has worked with high school athletes as a surgeon, physical therapist, athletic trainer, and coach, said that some of the increases in severity of injuries may reflect trends in sports over the past two decades: Student athletes have become stronger and faster and have put on more muscle mass. 

“When you have something that’s much larger, moving much faster and with more force, you’re going to have more force when you bump into things,” he said. “This can lead to more significant injuries.”

The study was independently supported. Study authors report no relevant financial relationships. 

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

High school students are injuring themselves more severely even as overall injury rates have declined, according to a new study presented at the annual meeting of the American Academy of Orthopaedic Surgeons.

The study compared injuries from a 4-year period ending in 2019 to data from 2005 and 2006. The overall rate of injuries dropped 9%, from 2.51 injuries per 1,000 athletic games or practices to 2.29 per 1,000; injuries requiring less than 1 week of recovery time fell by 13%. But, the number of head and neck injuries increased by 10%, injuries requiring surgery increased by 1%, and injuries leading to medical disqualification jumped by 11%. 

“It’s wonderful that the injury rate is declining,” said Jordan Neoma Pizzarro, a medical student at George Washington University, Washington, who led the study. “But the data does suggest that the injuries that are happening are worse.”

The increases may also reflect increased education and awareness of how to detect concussions and other injuries that need medical attention, said Micah Lissy, MD, MS, an orthopedic surgeon specializing in sports medicine at Michigan State University, East Lansing. Dr. Lissy cautioned against physicians and others taking the data at face value. 

“We need to be implementing preventive measures wherever possible, but I think we can also consider that there may be some confounding factors in the data,” Dr. Lissy told this news organization. 

Ms. Pizzarro and her team analyzed data collected from athletic trainers at 100 high schools across the country for the ongoing National Health School Sports-Related Injury Surveillance Study.

Athletes participating in sports such as football, soccer, basketball, volleyball, and softball were included in the analysis. Trainers report the number of injuries for every competition and practice, also known as “athletic exposures.”

Boys’ football carried the highest injury rate, with 3.96 injuries per 1,000 AEs, amounting to 44% of all injuries reported. Girls’ soccer and boys’ wrestling followed, with injury rates of 2.65 and 1.56, respectively. 

Sprains and strains accounted for 37% of injuries, followed by concussions (21.6%). The head and/or face was the most injured body site, followed by the ankles and/or knees. Most injuries took place during competitions rather than in practices (relative risk, 3.39; 95% confidence interval, 3.28-3.49; P < .05).

Ms. Pizzarro said that an overall increase in intensity, physical contact, and collisions may account for the spike in more severe injuries.

“Kids are encouraged to specialize in one sport early on and stick with it year-round,” she said. “They’re probably becoming more agile and better athletes, but they’re probably also getting more competitive.” 

Dr. Lissy, who has worked with high school athletes as a surgeon, physical therapist, athletic trainer, and coach, said that some of the increases in severity of injuries may reflect trends in sports over the past two decades: Student athletes have become stronger and faster and have put on more muscle mass. 

“When you have something that’s much larger, moving much faster and with more force, you’re going to have more force when you bump into things,” he said. “This can lead to more significant injuries.”

The study was independently supported. Study authors report no relevant financial relationships. 

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

High school students are injuring themselves more severely even as overall injury rates have declined, according to a new study presented at the annual meeting of the American Academy of Orthopaedic Surgeons.

The study compared injuries from a 4-year period ending in 2019 to data from 2005 and 2006. The overall rate of injuries dropped 9%, from 2.51 injuries per 1,000 athletic games or practices to 2.29 per 1,000; injuries requiring less than 1 week of recovery time fell by 13%. But, the number of head and neck injuries increased by 10%, injuries requiring surgery increased by 1%, and injuries leading to medical disqualification jumped by 11%. 

“It’s wonderful that the injury rate is declining,” said Jordan Neoma Pizzarro, a medical student at George Washington University, Washington, who led the study. “But the data does suggest that the injuries that are happening are worse.”

The increases may also reflect increased education and awareness of how to detect concussions and other injuries that need medical attention, said Micah Lissy, MD, MS, an orthopedic surgeon specializing in sports medicine at Michigan State University, East Lansing. Dr. Lissy cautioned against physicians and others taking the data at face value. 

“We need to be implementing preventive measures wherever possible, but I think we can also consider that there may be some confounding factors in the data,” Dr. Lissy told this news organization. 

Ms. Pizzarro and her team analyzed data collected from athletic trainers at 100 high schools across the country for the ongoing National Health School Sports-Related Injury Surveillance Study.

Athletes participating in sports such as football, soccer, basketball, volleyball, and softball were included in the analysis. Trainers report the number of injuries for every competition and practice, also known as “athletic exposures.”

Boys’ football carried the highest injury rate, with 3.96 injuries per 1,000 AEs, amounting to 44% of all injuries reported. Girls’ soccer and boys’ wrestling followed, with injury rates of 2.65 and 1.56, respectively. 

Sprains and strains accounted for 37% of injuries, followed by concussions (21.6%). The head and/or face was the most injured body site, followed by the ankles and/or knees. Most injuries took place during competitions rather than in practices (relative risk, 3.39; 95% confidence interval, 3.28-3.49; P < .05).

Ms. Pizzarro said that an overall increase in intensity, physical contact, and collisions may account for the spike in more severe injuries.

“Kids are encouraged to specialize in one sport early on and stick with it year-round,” she said. “They’re probably becoming more agile and better athletes, but they’re probably also getting more competitive.” 

Dr. Lissy, who has worked with high school athletes as a surgeon, physical therapist, athletic trainer, and coach, said that some of the increases in severity of injuries may reflect trends in sports over the past two decades: Student athletes have become stronger and faster and have put on more muscle mass. 

“When you have something that’s much larger, moving much faster and with more force, you’re going to have more force when you bump into things,” he said. “This can lead to more significant injuries.”

The study was independently supported. Study authors report no relevant financial relationships. 

A version of this article originally 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.

Children who experience migraine headaches in the aftermath of a concussion are more likely to experience prolonged symptoms of the head injury than are those with other forms of headache or no headaches at all, researchers have found.

“Early assessment of headache – and whether it has migraine features – after concussion can be helpful in predicting which children are at risk for poor outcomes and identifying children who require targeted intervention,” said senior author Keith Owen Yeates, PhD, the Ronald and Irene Ward Chair in Pediatric Brain Injury Professor and head of the department of psychology at the University of Calgary (Alta.). “Posttraumatic headache, especially when it involves migraine features, is a strong predictor of persisting symptoms and poorer quality of life after childhood concussion.”

Approximately 840,000 children per year visit an emergency department in the United States after having a traumatic brain injury. As many as 90% of those visits are considered to involve a concussion, according to the investigators. Although most children recover quickly, approximately one-third continue to report symptoms a month after the event.

Posttraumatic headache occurs in up to 90% of children, most commonly with features of migraine.

The new study, published in JAMA Network Open, was a secondary analysis of the Advancing Concussion Assessment in Pediatrics (A-CAP) prospective cohort study. The study was conducted at five emergency departments in Canada from September 2016 to July 2019 and included children and adolescents aged 8-17 years who presented with acute concussion or an orthopedic injury.

Children were included in the concussion group if they had a history of blunt head trauma resulting in at least one of three criteria consistent with the World Health Organization definition of mild traumatic brain injury. The criteria include loss of consciousness for less than 30 minutes, a Glasgow Coma Scale score of 13 or 14, or at least one acute sign or symptom of concussion, as noted by emergency clinicians.

Patients were excluded from the concussion group if they had deteriorating neurologic status, underwent neurosurgical intervention, had posttraumatic amnesia that lasted more than 24 hours, or had a score higher than 4 on the Abbreviated Injury Scale (AIS). The orthopedic injury group included patients without symptoms of concussion and with blunt trauma associated with an AIS 13 score of 4 or less. Patients were excluded from both groups if they had an overnight hospitalization for traumatic brain injury, a concussion within the past 3 months, or a neurodevelopmental disorder.

The researchers analyzed data from 928 children of 967 enrolled in the study. The median age was 12.2 years, and 41.3% were female. The final study cohort included 239 children with orthopedic injuries but no headache, 160 with a concussion and no headache, 134 with a concussion and nonmigraine headaches, and 254 with a concussion and migraine headaches.

Children with posttraumatic migraines 10 days after a concussion had the most severe symptoms and worst quality of life 3 months following their head trauma, the researchers found. Children without headaches within 10 days after concussion had the best 3-month outcomes, comparable to those with orthopedic injuries alone.

The researchers said the strengths of their study included its large population and its inclusion of various causes of head trauma, not just sports-related concussions. Limitations included self-reports of headaches instead of a physician diagnosis and lack of control for clinical interventions that might have affected the outcomes.

Charles Tator, MD, PhD, director of the Canadian Concussion Centre at Toronto Western Hospital, said the findings were unsurprising.

“Headaches are the most common symptom after concussion,” Dr. Tator, who was not involved in the latest research, told this news organization. “In my practice and research with concussed kids 11 and up and with adults, those with preconcussion history of migraine are the most difficult to treat because their headaches don’t improve unless specific measures are taken.”

Dr. Tator, who also is a professor of neurosurgery at the University of Toronto, said clinicians who treat concussions must determine which type of headaches children are experiencing – and refer as early as possible for migraine prevention or treatment and medication, as warranted.

“Early recognition after concussion that migraine headaches are occurring will save kids a lot of suffering,” he said.

The study was supported by a Canadian Institute of Health Research Foundation Grant and by funds from the Alberta Children’s Hospital Foundation and the Alberta Children’s Hospital Research Institute. Dr. Tator has disclosed no relevant financial relationships.
 

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

Children who experience migraine headaches in the aftermath of a concussion are more likely to experience prolonged symptoms of the head injury than are those with other forms of headache or no headaches at all, researchers have found.

“Early assessment of headache – and whether it has migraine features – after concussion can be helpful in predicting which children are at risk for poor outcomes and identifying children who require targeted intervention,” said senior author Keith Owen Yeates, PhD, the Ronald and Irene Ward Chair in Pediatric Brain Injury Professor and head of the department of psychology at the University of Calgary (Alta.). “Posttraumatic headache, especially when it involves migraine features, is a strong predictor of persisting symptoms and poorer quality of life after childhood concussion.”

Approximately 840,000 children per year visit an emergency department in the United States after having a traumatic brain injury. As many as 90% of those visits are considered to involve a concussion, according to the investigators. Although most children recover quickly, approximately one-third continue to report symptoms a month after the event.

Posttraumatic headache occurs in up to 90% of children, most commonly with features of migraine.

The new study, published in JAMA Network Open, was a secondary analysis of the Advancing Concussion Assessment in Pediatrics (A-CAP) prospective cohort study. The study was conducted at five emergency departments in Canada from September 2016 to July 2019 and included children and adolescents aged 8-17 years who presented with acute concussion or an orthopedic injury.

Children were included in the concussion group if they had a history of blunt head trauma resulting in at least one of three criteria consistent with the World Health Organization definition of mild traumatic brain injury. The criteria include loss of consciousness for less than 30 minutes, a Glasgow Coma Scale score of 13 or 14, or at least one acute sign or symptom of concussion, as noted by emergency clinicians.

Patients were excluded from the concussion group if they had deteriorating neurologic status, underwent neurosurgical intervention, had posttraumatic amnesia that lasted more than 24 hours, or had a score higher than 4 on the Abbreviated Injury Scale (AIS). The orthopedic injury group included patients without symptoms of concussion and with blunt trauma associated with an AIS 13 score of 4 or less. Patients were excluded from both groups if they had an overnight hospitalization for traumatic brain injury, a concussion within the past 3 months, or a neurodevelopmental disorder.

The researchers analyzed data from 928 children of 967 enrolled in the study. The median age was 12.2 years, and 41.3% were female. The final study cohort included 239 children with orthopedic injuries but no headache, 160 with a concussion and no headache, 134 with a concussion and nonmigraine headaches, and 254 with a concussion and migraine headaches.

Children with posttraumatic migraines 10 days after a concussion had the most severe symptoms and worst quality of life 3 months following their head trauma, the researchers found. Children without headaches within 10 days after concussion had the best 3-month outcomes, comparable to those with orthopedic injuries alone.

The researchers said the strengths of their study included its large population and its inclusion of various causes of head trauma, not just sports-related concussions. Limitations included self-reports of headaches instead of a physician diagnosis and lack of control for clinical interventions that might have affected the outcomes.

Charles Tator, MD, PhD, director of the Canadian Concussion Centre at Toronto Western Hospital, said the findings were unsurprising.

“Headaches are the most common symptom after concussion,” Dr. Tator, who was not involved in the latest research, told this news organization. “In my practice and research with concussed kids 11 and up and with adults, those with preconcussion history of migraine are the most difficult to treat because their headaches don’t improve unless specific measures are taken.”

Dr. Tator, who also is a professor of neurosurgery at the University of Toronto, said clinicians who treat concussions must determine which type of headaches children are experiencing – and refer as early as possible for migraine prevention or treatment and medication, as warranted.

“Early recognition after concussion that migraine headaches are occurring will save kids a lot of suffering,” he said.

The study was supported by a Canadian Institute of Health Research Foundation Grant and by funds from the Alberta Children’s Hospital Foundation and the Alberta Children’s Hospital Research Institute. Dr. Tator has disclosed no relevant financial relationships.
 

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

Children who experience migraine headaches in the aftermath of a concussion are more likely to experience prolonged symptoms of the head injury than are those with other forms of headache or no headaches at all, researchers have found.

“Early assessment of headache – and whether it has migraine features – after concussion can be helpful in predicting which children are at risk for poor outcomes and identifying children who require targeted intervention,” said senior author Keith Owen Yeates, PhD, the Ronald and Irene Ward Chair in Pediatric Brain Injury Professor and head of the department of psychology at the University of Calgary (Alta.). “Posttraumatic headache, especially when it involves migraine features, is a strong predictor of persisting symptoms and poorer quality of life after childhood concussion.”

Approximately 840,000 children per year visit an emergency department in the United States after having a traumatic brain injury. As many as 90% of those visits are considered to involve a concussion, according to the investigators. Although most children recover quickly, approximately one-third continue to report symptoms a month after the event.

Posttraumatic headache occurs in up to 90% of children, most commonly with features of migraine.

The new study, published in JAMA Network Open, was a secondary analysis of the Advancing Concussion Assessment in Pediatrics (A-CAP) prospective cohort study. The study was conducted at five emergency departments in Canada from September 2016 to July 2019 and included children and adolescents aged 8-17 years who presented with acute concussion or an orthopedic injury.

Children were included in the concussion group if they had a history of blunt head trauma resulting in at least one of three criteria consistent with the World Health Organization definition of mild traumatic brain injury. The criteria include loss of consciousness for less than 30 minutes, a Glasgow Coma Scale score of 13 or 14, or at least one acute sign or symptom of concussion, as noted by emergency clinicians.

Patients were excluded from the concussion group if they had deteriorating neurologic status, underwent neurosurgical intervention, had posttraumatic amnesia that lasted more than 24 hours, or had a score higher than 4 on the Abbreviated Injury Scale (AIS). The orthopedic injury group included patients without symptoms of concussion and with blunt trauma associated with an AIS 13 score of 4 or less. Patients were excluded from both groups if they had an overnight hospitalization for traumatic brain injury, a concussion within the past 3 months, or a neurodevelopmental disorder.

The researchers analyzed data from 928 children of 967 enrolled in the study. The median age was 12.2 years, and 41.3% were female. The final study cohort included 239 children with orthopedic injuries but no headache, 160 with a concussion and no headache, 134 with a concussion and nonmigraine headaches, and 254 with a concussion and migraine headaches.

Children with posttraumatic migraines 10 days after a concussion had the most severe symptoms and worst quality of life 3 months following their head trauma, the researchers found. Children without headaches within 10 days after concussion had the best 3-month outcomes, comparable to those with orthopedic injuries alone.

The researchers said the strengths of their study included its large population and its inclusion of various causes of head trauma, not just sports-related concussions. Limitations included self-reports of headaches instead of a physician diagnosis and lack of control for clinical interventions that might have affected the outcomes.

Charles Tator, MD, PhD, director of the Canadian Concussion Centre at Toronto Western Hospital, said the findings were unsurprising.

“Headaches are the most common symptom after concussion,” Dr. Tator, who was not involved in the latest research, told this news organization. “In my practice and research with concussed kids 11 and up and with adults, those with preconcussion history of migraine are the most difficult to treat because their headaches don’t improve unless specific measures are taken.”

Dr. Tator, who also is a professor of neurosurgery at the University of Toronto, said clinicians who treat concussions must determine which type of headaches children are experiencing – and refer as early as possible for migraine prevention or treatment and medication, as warranted.

“Early recognition after concussion that migraine headaches are occurring will save kids a lot of suffering,” he said.

The study was supported by a Canadian Institute of Health Research Foundation Grant and by funds from the Alberta Children’s Hospital Foundation and the Alberta Children’s Hospital Research Institute. Dr. Tator has disclosed no relevant financial relationships.
 

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

This discussion was recorded on Jan. 9, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert D. Glatter, medical adviser for Medscape Emergency Medicine. Today, we have Dr. Paul E. Pepe, an emergency medicine physician based in Florida and a highly recognized expert in emergency medical services (EMS), critical care, sports and event medicine, and resuscitation. Also joining us is Dr. Michael S. (“Mick”) Malloy, an emergency medicine physician based in Ireland, also an expert in prehospital care, resuscitation, and sports and event medicine. Welcome, gentlemen.

Dr. Pepe: Thanks for having us here.

Dr. Glatter: We have a serious event to discuss today. We’re going to be talking about what happened to Damar Hamlin, the Buffalo Bills safety who went down suffering a cardiac arrest in front of millions of people. Although we don’t know the exact cause of the events that transpired, the goal of our discussion is to guide our audience through a systematic approach to evaluation and management of an athlete suffering blunt force chest and neck trauma, and then suffering a cardiac arrest. We do know, obviously, that Damar was successfully resuscitated, thanks to the medical staff and trainers.

Almost 50 years ago, Chuck Hughes, a Detroit Lions receiver, went down and died with just a minute to go in the game and, unfortunately, didn’t survive.

Paul, can you tell me your impressions after viewing the replay of the events that evening? What were the most likely causes of this syncopal event and the subsequent cardiac arrest?

Dr. Pepe: We don’t know anything specifically. It’s being kept private about what the events were. It’s a little bit complicated in a sense that he basically had an extended resuscitation in the hospital. My experience has been that most people that have ventricular fibrillation, from whatever cause, will most likely be waking up on the field if you get to them. I’ve had personal experience with that.

More importantly than when it starts, when someone goes down on the field, both Dr. Malloy and I take a broader view. We don’t get tunnel vision and think, “Oh, it was a traumatic event,” or “It was cardiac event,” and we just have our minds open. There are many things that could make you stop breathing on the field. It could be a neck or a severe head injury, and then any kind of other internal injury that occurs.

When I saw in the video that Damar Hamlin stood up, that made it a less likely to be a spinal injury. He seemed to be physically functioning, and then he suddenly collapsed. That went along with something that looks like a ventricular fibrillation or ventricular tachycardia type of event and made me think right away that it was commotio cordis. I’m not a Latin scholar, but commotio is like commotion. A literal translation might be an agitation of the heart. I was thinking that he probably got hit somewhere in the middle of the chest at the right moment where the heart is resetting in that repolarization phase, like an R-on-T phenomenon, and then caused this sudden ventricular dysrhythmia.

Most people associate it to that because we have a couple of dozen cases a year of people getting hockey pucks or a baseball hitting their chest, which is very common with adolescents. On the other hand, you can’t get it from a blunt injury like this, and it was too early for it to be, say, a direct cardiac contusion, unless there was a direct injury there. It just happened so quickly.

In Europe, they’ve had a large amount of experience with this same kind of problem before, even just from a direct shoulder hit, for example. Mick Malloy is the dean of the faculty of sports and exercise medicine at the Royal College of Surgeons in Ireland and has vast experience, and now he is the person overseeing the procedures for this. Mick, have you had those kinds of experiences as well?

Dr. Molloy: Yes. It’s something that has occurred over recent decades and has been more recognized. I note that in professional sports, it’s a very different thing because you’ve got such huge teams and teams trained to respond very quickly. And that’s the most important thing in this scenario – having a team that is well functioning as a high-class emergency response team ready to get out on to that field very quickly after the person collapses, getting the automated external defibrillator (AED) on, and then recognizing whether there needs to be a shock given or not. The machine will tell you all that.

In our scenario, we run courses called CARES (Care of the Athlete Resuscitation and Emergencies in Sport) to make sure that our team physicians and team physiotherapists and trainers are all speaking as one when an emergency arises.

I don’t worry so much about the professional sport. It’s more with the amateur sports and the kids sports that I get a bit more concerned because there isn’t the same level of medical care there. Having everybody trained in basic life support would be very important to reduce unnecessary deaths from these types of conditions.

As Paul mentioned, there is a very specific cardiac cause in some of these circumstances, where you get hit just at the wrong time and that hit occurs at a particular electrical point in time. It causes this ventricular fibrillation, and the only real treatment there is the defibrillator as quickly as possible.

Dr. Glatter: What you’re saying ultimately is an important part about rapid defibrillation, and at first, cardiopulmonary resuscitation (CPR). People are concerned about whether they should begin CPR. We’re talking about out-of-hospital cardiac arrest that is outside of a football stadium, for example. Some people are obsessed with taking a person’s pulse, and that’s been a point of contention. If someone is unconscious and not breathing, we should start CPR. Wouldn›t you agree? They will wake up quickly if you begin chest compressions if they’re not necessary.

Dr. Pepe: I tell people, just do it. You’re right, people will wake up and feel it if they don’t need it.

Getting back to Mick’s point of having things ready to go, for example, 8 years ago, we had a professional player on the bench who suddenly collapsed right there in front of the entire audience. We immediately did CPR, and we got the AED on. We shocked him and he was ready, willing, and able to get back on the bench again. It turns out he had underlying coronary artery disease, but we got him back right away.

I did an initial study where we placed an AED in a public place at the Chicago O’Hare Airport to see if the public would use these. Most cardiac arrests occur at home, of course, but in public places, that was a good place to try it. We had almost 10 cases the first year. What was fascinating was that we had almost no survivors over the previous decade, even though there were paramedics at the airport. When we put these out there, we had nine people go down that first year, and six people who had never operated an AED or seen one before knew to get one and use it. Every one of those people survived neurologically intact, and almost every person was waking up before traditional responders got there. That’s how effective this is, but you need to know where the AED is.

Dr. Glatter: How to turn it on, where it is, and how to operate it.

Dr. Pepe: That was the point: These rescuers saved lives in the first year, and it was tremendous. Two points I make about it are that one, you need to know where it is, and two, just go turn it on. It gives you the instructions to follow through; just be in the Nike mode, because it basically won’t hurt a person. It’s rare that there’s ever been any complication of that. The machine algorithms are so good.

Dr. Glatter: Mick, I want to turn to you about the European experience. Specifically in Denmark, we know that there’s a large public health initiative to have AEDs accessible. There have been studies showing that when the public is engaged, especially with studies looking at an app when access is available, survivability doubled in the past 10 years from having access to AEDs. What’s your experience in Ireland in terms of public access to defibrillators?

Dr. Molloy: We’ve got two different streams here. There was a big push to have more AEDs at all sports venues. That was great, but some of the sporting clubs put them inside the locked door. I said that there’s no point to that because nobody can access it. You need to have an external building and you need to leave it open. If somebody needs to use it, they need to know how to get it, open it, and get away, and not get in through a locked door to get access to a defibrillator. We have AEDs now in most stadiums and even in small rural areas, where you might have only 200 people turn up for a game.

From another public access side, if you dial in – in our scenario, it’s 112, not 911 –we have Community First Responder groups. In the rural areas, you have local people who’ve been trained in basic life support and community first response who have AEDs. They’ll have periods of the day where they come home from work as a teacher, a nurse, a policeman, or a fireman, and they turn on an app on their phone and say, “I’m available for the next 5 hours.” If there’s a cardiac arrest rung in within 5 miles of their community, they will drive directly there with the AED that they have. We’ve had numerous saves from that in the country because it could take 40 minutes to get an EMS vehicle there, and obviously, time is crucial in these scenarios. Our dispatchers will talk people through CPR, and then the community responders arrive with the AED. It has been a fantastic initiative.

Dr. Pepe: In many places, people have apps on their phones where they’re locked into the system, and it will go off and tell them there is something nearby and even GPS them into it, and it’s been fantastic.

The two points I want to make to responding to what we just heard Dean Malloy say is one, we always have a designated spot to have these in various places. If I’m at City Hall, we always have them near the red elevators on every floor and down at security. In all the public high schools, we always have one right below the clock where everybody can see it. We set it up in a very standardized form that anybody and everybody will know where it is at the time an event happens.

The other point he made about having the response teams is fantastic. I live in a large high rise and there are two complexes with many people here, and many are older, so there’s going to be a higher risk for having an event. In fact, we’ve just had one recently. The concept we developed here was a community emergency response team, where we sometimes have doctors, nurses, and paramedics who live here be on call and be responsible, or you could try to find an AED. More importantly, we made sure everybody here knew where they were and where to get them. We’ve got most of the people trained, and we’re doing more training in what actions to take during these periods of time when such events happen.

Dr. Glatter: Yes, it’s critical. I wanted to point out that we’ve looked at the use of drones, especially here in the United States. There have been some pilot studies looking at their utility in the setting of out-of-hospital cardiac arrest. I want to get both of your thoughts on this and the feasibility of this.

Dr. Molloy: In a rural area, it’s a fantastic idea. You’re going to get something there as the crow flies very quickly. You probably have to look at exactly in, say, a rural area like Ireland of 32,000 square kilometers, how many you›ll have to put, what kind of distances they can realistically cover, and make sure the batteries are charged. Certainly, that’s a very good initiative because with the AEDs, you can’t do anything wrong. You can’t give a shock unless a shock needs to be given. The machine directs you what to do, so somebody who has had no training can pick one of these out of the box and start to work with it quickly and confidently that they can’t do anything wrong.

It’s a great idea. It would be a little expensive potentially at the moment in getting the drones and having that volume of drones around. In the U.S., you have completely different air traffic than we have, and in cities, you have more helicopters flying around. We certainly wouldn’t have that in our cities because that could cause a challenge if you’ve got drones flying around as well. It’s about making it safe that nothing else can go wrong from a drone in somebody else’s flight path.

Dr. Pepe: In my experience, the earlier the intervention, the better the results. There is a limit here in terms of the drones if they just can’t get there soon enough. Having said that, we are so fortunate in the city of Seattle to have most citizens knowing CPR, and we’d get that person resuscitated because they were doing such a good job with the CPR up front.

That’s why you’re going to see the Buffalo Bills player survive neurologically intact – because he did get immediate treatment right then and there. In the future, we may even have some better devices that will actually even restore normal blood flow right then and there while you’re still in cardiac arrest. There are limitations in every case. But on the other hand, it’s exciting and it paid off in this case recently.

Dr. Molloy: Just a point of interest coming from this small little country over here. The first portable defibrillator was developed in Belfast, Ireland, in the back of a cardiac response car. Despite us being a tiny little country, we do have some advances ahead of the United States.
 

Dr. Pepe: That was a breakthrough. Dr. Frank Pantridge and John Geddes did this great work and that caught the imagination of everybody here. At first, they were just going out to give people oxygen and sedate them for their chest pain. It turned out that their defibrillators are what made the difference as they went out there. Absolutely, I have to acknowledge the folks in Ireland for giving us this. Many of the EMS systems got started because of the article they published in The Lancet back in 1967.

Dr. Glatter: I wanted to briefly talk about screening of the athletes at the high school/college level, but also at the professional level. Obviously, there are issues, including the risk for false-positives in terms of low incidence, but there are also false negatives, as the case with Christian Eriksen, who had a cardiac arrest in 2021 and who has been through extensive testing. We can debate the validity of such testing, but I wanted to get both of your takes on the utility of screening in such a population.

Dr. Molloy: That’s a very emotive subject. False-positives are difficult because you’re now saying to somebody that they can’t compete in your sport at a decent level. The difficult part is telling somebody that this is the end of their career.

The false-negative is a little bit more difficult. I don’t know Christian Eriksen and I’m not involved in his team in any way, but that is a one-point examination, and you’re dependent on the scale of the process interpreting the ECG, which is again only a couple of seconds and that particular arrhythmia may not have shown up on that.

Also, athletes, by nature of what they’re doing, are operating at 99% of efficiency on a frequent basis. They are at the peak of their physiologic fitness, and it does make them a little bit more prone to picking up viral illnesses from time to time. They may get a small viral myopericarditis, which causes a new arrhythmia that nobody knew about. They had the screening 2 or 3 years ago, and they now developed a new problem because of what they do, which just may not show up.

I was actually surprised that the gentleman came through it very well, which is fantastic. He wasn’t allowed to play football in the country where he was employed, and he has now moved to another country and is playing football with a defibrillator inserted. I don’t know what the rules are in American football where you can play with implantable defibrillators. I’m not so sure it’s a great idea to do that.

Dr. Pepe: One thing that we should bring up is that there are athletes with underlying cardiomyopathies or hypertrophies and things like that, but that was unlikely in this case. It’s possible, but it’s unlikely, because it would have manifested itself before. In terms of screening, I’ve met some very smart medical doctors who have run those tests, and they have been very encouraged even at the high school levels to have screenings done, whether it’s electrocardiography, echocardiography, and so on. I have to reiterate what Dr Malloy just said in that it may have its downsides as well. If you can pick up real obvious cases, I think that may be of value.

Dr. Glatter: I want to conclude and get some pearls and takeaways from each of you regarding the events that transpired and what our audience can really hold onto.

Dr. Molloy: Look at Formula One in the past 50 years. In Formula One, in the beginning it was a 2-minute job to change a tire. Now, they have this down where they’re measuring in fractions of a second and criticizing each other if one guy is 2.6 seconds and the other guy is 2.9 seconds. For me, that’s phenomenal. It takes me 25 minutes to change a tire.

We’ve looked at that from a resuscitation perspective, and we now do pit crew resuscitation before our events. We’ve planned our team and know who’s going to be occupying what role. After the events at the UEFA championships, we had a new rule brought in by UEFA where they handed me a new document saying, “This is what we would like you to do for resuscitation.” It was a three-man triangle, and I said, “No, we’re not going to do that here.” And they said, “Why, you have to; it’s our rule.”

I said, “No, our rule in Ireland is we have a six-person triangle. We’re not downing our standards because of what you have internationally. You’re covering games in some very low-resource environments, I know that. We have a particular standard here that we’re sticking to. We have a six-person group. We know what we’re all doing; we come very quickly to those downed players and get involved and we’ve had good outcomes, so we’re not going to change the standards.”

That’s the thing: You need to practice these things. The players don’t go out on the weekend and do a move for the very first time without practicing it hundreds of times. We need to look at it the same way as the medical team who are looking after that group of players and the crowd because we also look after the crowd.

A particular challenge in some of our stadiums is that the upper decks are so steep, and it’s very hard to get a patient onto a trolley and do CPR as you’re bringing them down to a zone to get them flat. We’ve had to come up with some innovative techniques to try and do that and accommodate that using some of the mechanical CPR devices. That’s the result you’ll only get from having practiced these events and trying to extricate patients. We want to check response times, so you have to practice your response team activity very frequently.

Dr. Pepe: There are two points made by Mick that I want to react to. One, the pit crew approach is critical in so many ways. We do the same thing in what we call the medical first attack, where we knew who the A, B, and C person would be. When we took it out to the NBA trainers, I recommended for them to have a similar approach so that if an event does happen right in the middle of prime time, they are coordinated.

The second point is that we do mass-gathering medicine. It’s not just the sportspeople on the field or the entertainers that we’re looking after; it is the people in the stands. We will see a cardiac arrest once a month. If you think about it, you might see a cardiac arrest occur in any community on a regular basis. Now you’ve got 100,000 people in one stadium, and something is bound to go wrong over those 3 or 4 hours where they are there and may have a critical emergency. Preparation for all of that is really important as well.

The final point is that on a day-to-day basis, most cardiac arrests do occur in the home. Granted, 80% of them are nonshockable cases, but the people who are more apt to survive are going to be the ones who have an electrical event. In fact, when we looked at our data years ago, we found that, of the cases of people with ventricular fibrillation that we resuscitated, half didn’t even have heart damage. Their enzymes were normal. It was a pure electrical event, and they were more resuscitable. They may have an underlying problem, but we can fix that once we get them back.

Everybody needs to know how to do bystander CPR, and second, we must make sure we have AEDs strategically placed, as I alluded to before. We also go out to other parts of the community and give them advice. All those things must be put in place, but more importantly, just get the training and make the training simple. It’s really a “just do it” philosophy, but make it simple.

For example, when I teach a course, I can do it in 15 minutes, and people retain it because I keep reiterating things like, “Okay, there’s one thing you need to know about choking: Pop the cork.” You give them a physiologic image of what’s happening. Everybody says, “I remember you saying to just do it, pop the cork.”

With AEDs, know where it is – that’s why we should have it in standardized places. Go get it, turn it on, and then follow the instructions. Also, the most important thing is making sure you’re doing quality compressions; and there are videos that can help you with that, as well as classes that you can take that will get you through it.

Dr. Glatter: Absolutely. The public still has the misconception that you need to do mouth-to-mouth resuscitation. The message has not permeated through society that you don’t need to do mouth-to-mouth. Hands-only CPR is the gold standard now.

Dr. Pepe: If people have a reversible cause like ventricular fibrillation, often they’re already gasping, which is better than a delivered breath, by the way. Most important, then, are the compressions to make sure you have oxygen going up to the brain, because you’re still theoretically loaded with oxygen in your bloodstream if you had a sudden cardiac arrest from a ventricular fibrillation.

Your points are well taken, and we found that we had better outcomes when we just gave instructions to do compressions only, and that became the standard. Mick, you’ve had some experiences with that as well.

Dr. Molloy: If we’re going to have a long-term benefit from all this, we have to start doing this in elementary school and teaching kids basic life support and some basic health messaging.

I remember trying to get this across to a teacher one day and the teacher saying, “But why would we teach young kids to resuscitate each other?” I said, “I think you forget that the only 60-year-old person in the room is you. You train them, and we train them. They’re the ones who are going to respond and keep you alive. That’s the way you should be looking at this.” That completely changed the mindset of whether we should be doing this for the kids or not.

Dr. Pepe: In fact, what we find is that that’s exactly who gets saved. I had case after case where the kids at the school had learned CPR and saved the teachers or the administrator at the high school or elementary school. It’s a fantastic point that you bring up, Dr. Malloy.

Dr. Glatter: One other brief thing we can interject here is that the team was excellent on field in that they evaluated Damar Hamlin in a primary survey sense of ABCs (i.e., airway, breathing, and circulation) for things like a tension pneumothorax. In the sense in which he was hit, there are reversible causes. Making sure he didn’t have a tension pneumothorax that caused the arrest, in my mind, was critical.

Dr. Pepe: We do the same thing on a day-to-day basis with a car wreck, because it could be that the person had ventricular fibrillation and then had the wreck. It’s not always trauma. That’s a fantastic point that you’re making. That’s exactly what I think happened, and that’s what we do.

Dr. Glatter: Well, thank you, gentlemen. This was an informative and helpful discussion for our audience. I appreciate your time and expertise.



Dr. Glatter, is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes.

Dr. Pepe is a professor of internal medicine, surgery, pediatrics, public health, and emergency medicine at University of Texas Health Science Center in Houston. He’s also a global coordinator of the U.S. Metropolitan Municipalities EMS Medical Directors (“Eagles”) Coalition.

Dr. Molloy works clinically as a consultant in emergency medicine in Wexford General Hospital, part of the Ireland East Hospital Group (IEHG). Internationally, he is a member of the Disaster Medicine Section of the European Society of Emergency Medicine (EUSEM) and has been appointed by the Irish Medical Organization (IMO) as one of two Irish delegates to serve on the European Board and Section of Emergency Medicine of the European Union of Medical Specialists (UEMS), having served for a number of years on its predecessor, the Multidisciplinary Joint Committee on Emergency Medicine.

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

This discussion was recorded on Jan. 9, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert D. Glatter, medical adviser for Medscape Emergency Medicine. Today, we have Dr. Paul E. Pepe, an emergency medicine physician based in Florida and a highly recognized expert in emergency medical services (EMS), critical care, sports and event medicine, and resuscitation. Also joining us is Dr. Michael S. (“Mick”) Malloy, an emergency medicine physician based in Ireland, also an expert in prehospital care, resuscitation, and sports and event medicine. Welcome, gentlemen.

Dr. Pepe: Thanks for having us here.

Dr. Glatter: We have a serious event to discuss today. We’re going to be talking about what happened to Damar Hamlin, the Buffalo Bills safety who went down suffering a cardiac arrest in front of millions of people. Although we don’t know the exact cause of the events that transpired, the goal of our discussion is to guide our audience through a systematic approach to evaluation and management of an athlete suffering blunt force chest and neck trauma, and then suffering a cardiac arrest. We do know, obviously, that Damar was successfully resuscitated, thanks to the medical staff and trainers.

Almost 50 years ago, Chuck Hughes, a Detroit Lions receiver, went down and died with just a minute to go in the game and, unfortunately, didn’t survive.

Paul, can you tell me your impressions after viewing the replay of the events that evening? What were the most likely causes of this syncopal event and the subsequent cardiac arrest?

Dr. Pepe: We don’t know anything specifically. It’s being kept private about what the events were. It’s a little bit complicated in a sense that he basically had an extended resuscitation in the hospital. My experience has been that most people that have ventricular fibrillation, from whatever cause, will most likely be waking up on the field if you get to them. I’ve had personal experience with that.

More importantly than when it starts, when someone goes down on the field, both Dr. Malloy and I take a broader view. We don’t get tunnel vision and think, “Oh, it was a traumatic event,” or “It was cardiac event,” and we just have our minds open. There are many things that could make you stop breathing on the field. It could be a neck or a severe head injury, and then any kind of other internal injury that occurs.

When I saw in the video that Damar Hamlin stood up, that made it a less likely to be a spinal injury. He seemed to be physically functioning, and then he suddenly collapsed. That went along with something that looks like a ventricular fibrillation or ventricular tachycardia type of event and made me think right away that it was commotio cordis. I’m not a Latin scholar, but commotio is like commotion. A literal translation might be an agitation of the heart. I was thinking that he probably got hit somewhere in the middle of the chest at the right moment where the heart is resetting in that repolarization phase, like an R-on-T phenomenon, and then caused this sudden ventricular dysrhythmia.

Most people associate it to that because we have a couple of dozen cases a year of people getting hockey pucks or a baseball hitting their chest, which is very common with adolescents. On the other hand, you can’t get it from a blunt injury like this, and it was too early for it to be, say, a direct cardiac contusion, unless there was a direct injury there. It just happened so quickly.

In Europe, they’ve had a large amount of experience with this same kind of problem before, even just from a direct shoulder hit, for example. Mick Malloy is the dean of the faculty of sports and exercise medicine at the Royal College of Surgeons in Ireland and has vast experience, and now he is the person overseeing the procedures for this. Mick, have you had those kinds of experiences as well?

Dr. Molloy: Yes. It’s something that has occurred over recent decades and has been more recognized. I note that in professional sports, it’s a very different thing because you’ve got such huge teams and teams trained to respond very quickly. And that’s the most important thing in this scenario – having a team that is well functioning as a high-class emergency response team ready to get out on to that field very quickly after the person collapses, getting the automated external defibrillator (AED) on, and then recognizing whether there needs to be a shock given or not. The machine will tell you all that.

In our scenario, we run courses called CARES (Care of the Athlete Resuscitation and Emergencies in Sport) to make sure that our team physicians and team physiotherapists and trainers are all speaking as one when an emergency arises.

I don’t worry so much about the professional sport. It’s more with the amateur sports and the kids sports that I get a bit more concerned because there isn’t the same level of medical care there. Having everybody trained in basic life support would be very important to reduce unnecessary deaths from these types of conditions.

As Paul mentioned, there is a very specific cardiac cause in some of these circumstances, where you get hit just at the wrong time and that hit occurs at a particular electrical point in time. It causes this ventricular fibrillation, and the only real treatment there is the defibrillator as quickly as possible.

Dr. Glatter: What you’re saying ultimately is an important part about rapid defibrillation, and at first, cardiopulmonary resuscitation (CPR). People are concerned about whether they should begin CPR. We’re talking about out-of-hospital cardiac arrest that is outside of a football stadium, for example. Some people are obsessed with taking a person’s pulse, and that’s been a point of contention. If someone is unconscious and not breathing, we should start CPR. Wouldn›t you agree? They will wake up quickly if you begin chest compressions if they’re not necessary.

Dr. Pepe: I tell people, just do it. You’re right, people will wake up and feel it if they don’t need it.

Getting back to Mick’s point of having things ready to go, for example, 8 years ago, we had a professional player on the bench who suddenly collapsed right there in front of the entire audience. We immediately did CPR, and we got the AED on. We shocked him and he was ready, willing, and able to get back on the bench again. It turns out he had underlying coronary artery disease, but we got him back right away.

I did an initial study where we placed an AED in a public place at the Chicago O’Hare Airport to see if the public would use these. Most cardiac arrests occur at home, of course, but in public places, that was a good place to try it. We had almost 10 cases the first year. What was fascinating was that we had almost no survivors over the previous decade, even though there were paramedics at the airport. When we put these out there, we had nine people go down that first year, and six people who had never operated an AED or seen one before knew to get one and use it. Every one of those people survived neurologically intact, and almost every person was waking up before traditional responders got there. That’s how effective this is, but you need to know where the AED is.

Dr. Glatter: How to turn it on, where it is, and how to operate it.

Dr. Pepe: That was the point: These rescuers saved lives in the first year, and it was tremendous. Two points I make about it are that one, you need to know where it is, and two, just go turn it on. It gives you the instructions to follow through; just be in the Nike mode, because it basically won’t hurt a person. It’s rare that there’s ever been any complication of that. The machine algorithms are so good.

Dr. Glatter: Mick, I want to turn to you about the European experience. Specifically in Denmark, we know that there’s a large public health initiative to have AEDs accessible. There have been studies showing that when the public is engaged, especially with studies looking at an app when access is available, survivability doubled in the past 10 years from having access to AEDs. What’s your experience in Ireland in terms of public access to defibrillators?

Dr. Molloy: We’ve got two different streams here. There was a big push to have more AEDs at all sports venues. That was great, but some of the sporting clubs put them inside the locked door. I said that there’s no point to that because nobody can access it. You need to have an external building and you need to leave it open. If somebody needs to use it, they need to know how to get it, open it, and get away, and not get in through a locked door to get access to a defibrillator. We have AEDs now in most stadiums and even in small rural areas, where you might have only 200 people turn up for a game.

From another public access side, if you dial in – in our scenario, it’s 112, not 911 –we have Community First Responder groups. In the rural areas, you have local people who’ve been trained in basic life support and community first response who have AEDs. They’ll have periods of the day where they come home from work as a teacher, a nurse, a policeman, or a fireman, and they turn on an app on their phone and say, “I’m available for the next 5 hours.” If there’s a cardiac arrest rung in within 5 miles of their community, they will drive directly there with the AED that they have. We’ve had numerous saves from that in the country because it could take 40 minutes to get an EMS vehicle there, and obviously, time is crucial in these scenarios. Our dispatchers will talk people through CPR, and then the community responders arrive with the AED. It has been a fantastic initiative.

Dr. Pepe: In many places, people have apps on their phones where they’re locked into the system, and it will go off and tell them there is something nearby and even GPS them into it, and it’s been fantastic.

The two points I want to make to responding to what we just heard Dean Malloy say is one, we always have a designated spot to have these in various places. If I’m at City Hall, we always have them near the red elevators on every floor and down at security. In all the public high schools, we always have one right below the clock where everybody can see it. We set it up in a very standardized form that anybody and everybody will know where it is at the time an event happens.

The other point he made about having the response teams is fantastic. I live in a large high rise and there are two complexes with many people here, and many are older, so there’s going to be a higher risk for having an event. In fact, we’ve just had one recently. The concept we developed here was a community emergency response team, where we sometimes have doctors, nurses, and paramedics who live here be on call and be responsible, or you could try to find an AED. More importantly, we made sure everybody here knew where they were and where to get them. We’ve got most of the people trained, and we’re doing more training in what actions to take during these periods of time when such events happen.

Dr. Glatter: Yes, it’s critical. I wanted to point out that we’ve looked at the use of drones, especially here in the United States. There have been some pilot studies looking at their utility in the setting of out-of-hospital cardiac arrest. I want to get both of your thoughts on this and the feasibility of this.

Dr. Molloy: In a rural area, it’s a fantastic idea. You’re going to get something there as the crow flies very quickly. You probably have to look at exactly in, say, a rural area like Ireland of 32,000 square kilometers, how many you›ll have to put, what kind of distances they can realistically cover, and make sure the batteries are charged. Certainly, that’s a very good initiative because with the AEDs, you can’t do anything wrong. You can’t give a shock unless a shock needs to be given. The machine directs you what to do, so somebody who has had no training can pick one of these out of the box and start to work with it quickly and confidently that they can’t do anything wrong.

It’s a great idea. It would be a little expensive potentially at the moment in getting the drones and having that volume of drones around. In the U.S., you have completely different air traffic than we have, and in cities, you have more helicopters flying around. We certainly wouldn’t have that in our cities because that could cause a challenge if you’ve got drones flying around as well. It’s about making it safe that nothing else can go wrong from a drone in somebody else’s flight path.

Dr. Pepe: In my experience, the earlier the intervention, the better the results. There is a limit here in terms of the drones if they just can’t get there soon enough. Having said that, we are so fortunate in the city of Seattle to have most citizens knowing CPR, and we’d get that person resuscitated because they were doing such a good job with the CPR up front.

That’s why you’re going to see the Buffalo Bills player survive neurologically intact – because he did get immediate treatment right then and there. In the future, we may even have some better devices that will actually even restore normal blood flow right then and there while you’re still in cardiac arrest. There are limitations in every case. But on the other hand, it’s exciting and it paid off in this case recently.

Dr. Molloy: Just a point of interest coming from this small little country over here. The first portable defibrillator was developed in Belfast, Ireland, in the back of a cardiac response car. Despite us being a tiny little country, we do have some advances ahead of the United States.
 

Dr. Pepe: That was a breakthrough. Dr. Frank Pantridge and John Geddes did this great work and that caught the imagination of everybody here. At first, they were just going out to give people oxygen and sedate them for their chest pain. It turned out that their defibrillators are what made the difference as they went out there. Absolutely, I have to acknowledge the folks in Ireland for giving us this. Many of the EMS systems got started because of the article they published in The Lancet back in 1967.

Dr. Glatter: I wanted to briefly talk about screening of the athletes at the high school/college level, but also at the professional level. Obviously, there are issues, including the risk for false-positives in terms of low incidence, but there are also false negatives, as the case with Christian Eriksen, who had a cardiac arrest in 2021 and who has been through extensive testing. We can debate the validity of such testing, but I wanted to get both of your takes on the utility of screening in such a population.

Dr. Molloy: That’s a very emotive subject. False-positives are difficult because you’re now saying to somebody that they can’t compete in your sport at a decent level. The difficult part is telling somebody that this is the end of their career.

The false-negative is a little bit more difficult. I don’t know Christian Eriksen and I’m not involved in his team in any way, but that is a one-point examination, and you’re dependent on the scale of the process interpreting the ECG, which is again only a couple of seconds and that particular arrhythmia may not have shown up on that.

Also, athletes, by nature of what they’re doing, are operating at 99% of efficiency on a frequent basis. They are at the peak of their physiologic fitness, and it does make them a little bit more prone to picking up viral illnesses from time to time. They may get a small viral myopericarditis, which causes a new arrhythmia that nobody knew about. They had the screening 2 or 3 years ago, and they now developed a new problem because of what they do, which just may not show up.

I was actually surprised that the gentleman came through it very well, which is fantastic. He wasn’t allowed to play football in the country where he was employed, and he has now moved to another country and is playing football with a defibrillator inserted. I don’t know what the rules are in American football where you can play with implantable defibrillators. I’m not so sure it’s a great idea to do that.

Dr. Pepe: One thing that we should bring up is that there are athletes with underlying cardiomyopathies or hypertrophies and things like that, but that was unlikely in this case. It’s possible, but it’s unlikely, because it would have manifested itself before. In terms of screening, I’ve met some very smart medical doctors who have run those tests, and they have been very encouraged even at the high school levels to have screenings done, whether it’s electrocardiography, echocardiography, and so on. I have to reiterate what Dr Malloy just said in that it may have its downsides as well. If you can pick up real obvious cases, I think that may be of value.

Dr. Glatter: I want to conclude and get some pearls and takeaways from each of you regarding the events that transpired and what our audience can really hold onto.

Dr. Molloy: Look at Formula One in the past 50 years. In Formula One, in the beginning it was a 2-minute job to change a tire. Now, they have this down where they’re measuring in fractions of a second and criticizing each other if one guy is 2.6 seconds and the other guy is 2.9 seconds. For me, that’s phenomenal. It takes me 25 minutes to change a tire.

We’ve looked at that from a resuscitation perspective, and we now do pit crew resuscitation before our events. We’ve planned our team and know who’s going to be occupying what role. After the events at the UEFA championships, we had a new rule brought in by UEFA where they handed me a new document saying, “This is what we would like you to do for resuscitation.” It was a three-man triangle, and I said, “No, we’re not going to do that here.” And they said, “Why, you have to; it’s our rule.”

I said, “No, our rule in Ireland is we have a six-person triangle. We’re not downing our standards because of what you have internationally. You’re covering games in some very low-resource environments, I know that. We have a particular standard here that we’re sticking to. We have a six-person group. We know what we’re all doing; we come very quickly to those downed players and get involved and we’ve had good outcomes, so we’re not going to change the standards.”

That’s the thing: You need to practice these things. The players don’t go out on the weekend and do a move for the very first time without practicing it hundreds of times. We need to look at it the same way as the medical team who are looking after that group of players and the crowd because we also look after the crowd.

A particular challenge in some of our stadiums is that the upper decks are so steep, and it’s very hard to get a patient onto a trolley and do CPR as you’re bringing them down to a zone to get them flat. We’ve had to come up with some innovative techniques to try and do that and accommodate that using some of the mechanical CPR devices. That’s the result you’ll only get from having practiced these events and trying to extricate patients. We want to check response times, so you have to practice your response team activity very frequently.

Dr. Pepe: There are two points made by Mick that I want to react to. One, the pit crew approach is critical in so many ways. We do the same thing in what we call the medical first attack, where we knew who the A, B, and C person would be. When we took it out to the NBA trainers, I recommended for them to have a similar approach so that if an event does happen right in the middle of prime time, they are coordinated.

The second point is that we do mass-gathering medicine. It’s not just the sportspeople on the field or the entertainers that we’re looking after; it is the people in the stands. We will see a cardiac arrest once a month. If you think about it, you might see a cardiac arrest occur in any community on a regular basis. Now you’ve got 100,000 people in one stadium, and something is bound to go wrong over those 3 or 4 hours where they are there and may have a critical emergency. Preparation for all of that is really important as well.

The final point is that on a day-to-day basis, most cardiac arrests do occur in the home. Granted, 80% of them are nonshockable cases, but the people who are more apt to survive are going to be the ones who have an electrical event. In fact, when we looked at our data years ago, we found that, of the cases of people with ventricular fibrillation that we resuscitated, half didn’t even have heart damage. Their enzymes were normal. It was a pure electrical event, and they were more resuscitable. They may have an underlying problem, but we can fix that once we get them back.

Everybody needs to know how to do bystander CPR, and second, we must make sure we have AEDs strategically placed, as I alluded to before. We also go out to other parts of the community and give them advice. All those things must be put in place, but more importantly, just get the training and make the training simple. It’s really a “just do it” philosophy, but make it simple.

For example, when I teach a course, I can do it in 15 minutes, and people retain it because I keep reiterating things like, “Okay, there’s one thing you need to know about choking: Pop the cork.” You give them a physiologic image of what’s happening. Everybody says, “I remember you saying to just do it, pop the cork.”

With AEDs, know where it is – that’s why we should have it in standardized places. Go get it, turn it on, and then follow the instructions. Also, the most important thing is making sure you’re doing quality compressions; and there are videos that can help you with that, as well as classes that you can take that will get you through it.

Dr. Glatter: Absolutely. The public still has the misconception that you need to do mouth-to-mouth resuscitation. The message has not permeated through society that you don’t need to do mouth-to-mouth. Hands-only CPR is the gold standard now.

Dr. Pepe: If people have a reversible cause like ventricular fibrillation, often they’re already gasping, which is better than a delivered breath, by the way. Most important, then, are the compressions to make sure you have oxygen going up to the brain, because you’re still theoretically loaded with oxygen in your bloodstream if you had a sudden cardiac arrest from a ventricular fibrillation.

Your points are well taken, and we found that we had better outcomes when we just gave instructions to do compressions only, and that became the standard. Mick, you’ve had some experiences with that as well.

Dr. Molloy: If we’re going to have a long-term benefit from all this, we have to start doing this in elementary school and teaching kids basic life support and some basic health messaging.

I remember trying to get this across to a teacher one day and the teacher saying, “But why would we teach young kids to resuscitate each other?” I said, “I think you forget that the only 60-year-old person in the room is you. You train them, and we train them. They’re the ones who are going to respond and keep you alive. That’s the way you should be looking at this.” That completely changed the mindset of whether we should be doing this for the kids or not.

Dr. Pepe: In fact, what we find is that that’s exactly who gets saved. I had case after case where the kids at the school had learned CPR and saved the teachers or the administrator at the high school or elementary school. It’s a fantastic point that you bring up, Dr. Malloy.

Dr. Glatter: One other brief thing we can interject here is that the team was excellent on field in that they evaluated Damar Hamlin in a primary survey sense of ABCs (i.e., airway, breathing, and circulation) for things like a tension pneumothorax. In the sense in which he was hit, there are reversible causes. Making sure he didn’t have a tension pneumothorax that caused the arrest, in my mind, was critical.

Dr. Pepe: We do the same thing on a day-to-day basis with a car wreck, because it could be that the person had ventricular fibrillation and then had the wreck. It’s not always trauma. That’s a fantastic point that you’re making. That’s exactly what I think happened, and that’s what we do.

Dr. Glatter: Well, thank you, gentlemen. This was an informative and helpful discussion for our audience. I appreciate your time and expertise.



Dr. Glatter, is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes.

Dr. Pepe is a professor of internal medicine, surgery, pediatrics, public health, and emergency medicine at University of Texas Health Science Center in Houston. He’s also a global coordinator of the U.S. Metropolitan Municipalities EMS Medical Directors (“Eagles”) Coalition.

Dr. Molloy works clinically as a consultant in emergency medicine in Wexford General Hospital, part of the Ireland East Hospital Group (IEHG). Internationally, he is a member of the Disaster Medicine Section of the European Society of Emergency Medicine (EUSEM) and has been appointed by the Irish Medical Organization (IMO) as one of two Irish delegates to serve on the European Board and Section of Emergency Medicine of the European Union of Medical Specialists (UEMS), having served for a number of years on its predecessor, the Multidisciplinary Joint Committee on Emergency Medicine.

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

This discussion was recorded on Jan. 9, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert D. Glatter, medical adviser for Medscape Emergency Medicine. Today, we have Dr. Paul E. Pepe, an emergency medicine physician based in Florida and a highly recognized expert in emergency medical services (EMS), critical care, sports and event medicine, and resuscitation. Also joining us is Dr. Michael S. (“Mick”) Malloy, an emergency medicine physician based in Ireland, also an expert in prehospital care, resuscitation, and sports and event medicine. Welcome, gentlemen.

Dr. Pepe: Thanks for having us here.

Dr. Glatter: We have a serious event to discuss today. We’re going to be talking about what happened to Damar Hamlin, the Buffalo Bills safety who went down suffering a cardiac arrest in front of millions of people. Although we don’t know the exact cause of the events that transpired, the goal of our discussion is to guide our audience through a systematic approach to evaluation and management of an athlete suffering blunt force chest and neck trauma, and then suffering a cardiac arrest. We do know, obviously, that Damar was successfully resuscitated, thanks to the medical staff and trainers.

Almost 50 years ago, Chuck Hughes, a Detroit Lions receiver, went down and died with just a minute to go in the game and, unfortunately, didn’t survive.

Paul, can you tell me your impressions after viewing the replay of the events that evening? What were the most likely causes of this syncopal event and the subsequent cardiac arrest?

Dr. Pepe: We don’t know anything specifically. It’s being kept private about what the events were. It’s a little bit complicated in a sense that he basically had an extended resuscitation in the hospital. My experience has been that most people that have ventricular fibrillation, from whatever cause, will most likely be waking up on the field if you get to them. I’ve had personal experience with that.

More importantly than when it starts, when someone goes down on the field, both Dr. Malloy and I take a broader view. We don’t get tunnel vision and think, “Oh, it was a traumatic event,” or “It was cardiac event,” and we just have our minds open. There are many things that could make you stop breathing on the field. It could be a neck or a severe head injury, and then any kind of other internal injury that occurs.

When I saw in the video that Damar Hamlin stood up, that made it a less likely to be a spinal injury. He seemed to be physically functioning, and then he suddenly collapsed. That went along with something that looks like a ventricular fibrillation or ventricular tachycardia type of event and made me think right away that it was commotio cordis. I’m not a Latin scholar, but commotio is like commotion. A literal translation might be an agitation of the heart. I was thinking that he probably got hit somewhere in the middle of the chest at the right moment where the heart is resetting in that repolarization phase, like an R-on-T phenomenon, and then caused this sudden ventricular dysrhythmia.

Most people associate it to that because we have a couple of dozen cases a year of people getting hockey pucks or a baseball hitting their chest, which is very common with adolescents. On the other hand, you can’t get it from a blunt injury like this, and it was too early for it to be, say, a direct cardiac contusion, unless there was a direct injury there. It just happened so quickly.

In Europe, they’ve had a large amount of experience with this same kind of problem before, even just from a direct shoulder hit, for example. Mick Malloy is the dean of the faculty of sports and exercise medicine at the Royal College of Surgeons in Ireland and has vast experience, and now he is the person overseeing the procedures for this. Mick, have you had those kinds of experiences as well?

Dr. Molloy: Yes. It’s something that has occurred over recent decades and has been more recognized. I note that in professional sports, it’s a very different thing because you’ve got such huge teams and teams trained to respond very quickly. And that’s the most important thing in this scenario – having a team that is well functioning as a high-class emergency response team ready to get out on to that field very quickly after the person collapses, getting the automated external defibrillator (AED) on, and then recognizing whether there needs to be a shock given or not. The machine will tell you all that.

In our scenario, we run courses called CARES (Care of the Athlete Resuscitation and Emergencies in Sport) to make sure that our team physicians and team physiotherapists and trainers are all speaking as one when an emergency arises.

I don’t worry so much about the professional sport. It’s more with the amateur sports and the kids sports that I get a bit more concerned because there isn’t the same level of medical care there. Having everybody trained in basic life support would be very important to reduce unnecessary deaths from these types of conditions.

As Paul mentioned, there is a very specific cardiac cause in some of these circumstances, where you get hit just at the wrong time and that hit occurs at a particular electrical point in time. It causes this ventricular fibrillation, and the only real treatment there is the defibrillator as quickly as possible.

Dr. Glatter: What you’re saying ultimately is an important part about rapid defibrillation, and at first, cardiopulmonary resuscitation (CPR). People are concerned about whether they should begin CPR. We’re talking about out-of-hospital cardiac arrest that is outside of a football stadium, for example. Some people are obsessed with taking a person’s pulse, and that’s been a point of contention. If someone is unconscious and not breathing, we should start CPR. Wouldn›t you agree? They will wake up quickly if you begin chest compressions if they’re not necessary.

Dr. Pepe: I tell people, just do it. You’re right, people will wake up and feel it if they don’t need it.

Getting back to Mick’s point of having things ready to go, for example, 8 years ago, we had a professional player on the bench who suddenly collapsed right there in front of the entire audience. We immediately did CPR, and we got the AED on. We shocked him and he was ready, willing, and able to get back on the bench again. It turns out he had underlying coronary artery disease, but we got him back right away.

I did an initial study where we placed an AED in a public place at the Chicago O’Hare Airport to see if the public would use these. Most cardiac arrests occur at home, of course, but in public places, that was a good place to try it. We had almost 10 cases the first year. What was fascinating was that we had almost no survivors over the previous decade, even though there were paramedics at the airport. When we put these out there, we had nine people go down that first year, and six people who had never operated an AED or seen one before knew to get one and use it. Every one of those people survived neurologically intact, and almost every person was waking up before traditional responders got there. That’s how effective this is, but you need to know where the AED is.

Dr. Glatter: How to turn it on, where it is, and how to operate it.

Dr. Pepe: That was the point: These rescuers saved lives in the first year, and it was tremendous. Two points I make about it are that one, you need to know where it is, and two, just go turn it on. It gives you the instructions to follow through; just be in the Nike mode, because it basically won’t hurt a person. It’s rare that there’s ever been any complication of that. The machine algorithms are so good.

Dr. Glatter: Mick, I want to turn to you about the European experience. Specifically in Denmark, we know that there’s a large public health initiative to have AEDs accessible. There have been studies showing that when the public is engaged, especially with studies looking at an app when access is available, survivability doubled in the past 10 years from having access to AEDs. What’s your experience in Ireland in terms of public access to defibrillators?

Dr. Molloy: We’ve got two different streams here. There was a big push to have more AEDs at all sports venues. That was great, but some of the sporting clubs put them inside the locked door. I said that there’s no point to that because nobody can access it. You need to have an external building and you need to leave it open. If somebody needs to use it, they need to know how to get it, open it, and get away, and not get in through a locked door to get access to a defibrillator. We have AEDs now in most stadiums and even in small rural areas, where you might have only 200 people turn up for a game.

From another public access side, if you dial in – in our scenario, it’s 112, not 911 –we have Community First Responder groups. In the rural areas, you have local people who’ve been trained in basic life support and community first response who have AEDs. They’ll have periods of the day where they come home from work as a teacher, a nurse, a policeman, or a fireman, and they turn on an app on their phone and say, “I’m available for the next 5 hours.” If there’s a cardiac arrest rung in within 5 miles of their community, they will drive directly there with the AED that they have. We’ve had numerous saves from that in the country because it could take 40 minutes to get an EMS vehicle there, and obviously, time is crucial in these scenarios. Our dispatchers will talk people through CPR, and then the community responders arrive with the AED. It has been a fantastic initiative.

Dr. Pepe: In many places, people have apps on their phones where they’re locked into the system, and it will go off and tell them there is something nearby and even GPS them into it, and it’s been fantastic.

The two points I want to make to responding to what we just heard Dean Malloy say is one, we always have a designated spot to have these in various places. If I’m at City Hall, we always have them near the red elevators on every floor and down at security. In all the public high schools, we always have one right below the clock where everybody can see it. We set it up in a very standardized form that anybody and everybody will know where it is at the time an event happens.

The other point he made about having the response teams is fantastic. I live in a large high rise and there are two complexes with many people here, and many are older, so there’s going to be a higher risk for having an event. In fact, we’ve just had one recently. The concept we developed here was a community emergency response team, where we sometimes have doctors, nurses, and paramedics who live here be on call and be responsible, or you could try to find an AED. More importantly, we made sure everybody here knew where they were and where to get them. We’ve got most of the people trained, and we’re doing more training in what actions to take during these periods of time when such events happen.

Dr. Glatter: Yes, it’s critical. I wanted to point out that we’ve looked at the use of drones, especially here in the United States. There have been some pilot studies looking at their utility in the setting of out-of-hospital cardiac arrest. I want to get both of your thoughts on this and the feasibility of this.

Dr. Molloy: In a rural area, it’s a fantastic idea. You’re going to get something there as the crow flies very quickly. You probably have to look at exactly in, say, a rural area like Ireland of 32,000 square kilometers, how many you›ll have to put, what kind of distances they can realistically cover, and make sure the batteries are charged. Certainly, that’s a very good initiative because with the AEDs, you can’t do anything wrong. You can’t give a shock unless a shock needs to be given. The machine directs you what to do, so somebody who has had no training can pick one of these out of the box and start to work with it quickly and confidently that they can’t do anything wrong.

It’s a great idea. It would be a little expensive potentially at the moment in getting the drones and having that volume of drones around. In the U.S., you have completely different air traffic than we have, and in cities, you have more helicopters flying around. We certainly wouldn’t have that in our cities because that could cause a challenge if you’ve got drones flying around as well. It’s about making it safe that nothing else can go wrong from a drone in somebody else’s flight path.

Dr. Pepe: In my experience, the earlier the intervention, the better the results. There is a limit here in terms of the drones if they just can’t get there soon enough. Having said that, we are so fortunate in the city of Seattle to have most citizens knowing CPR, and we’d get that person resuscitated because they were doing such a good job with the CPR up front.

That’s why you’re going to see the Buffalo Bills player survive neurologically intact – because he did get immediate treatment right then and there. In the future, we may even have some better devices that will actually even restore normal blood flow right then and there while you’re still in cardiac arrest. There are limitations in every case. But on the other hand, it’s exciting and it paid off in this case recently.

Dr. Molloy: Just a point of interest coming from this small little country over here. The first portable defibrillator was developed in Belfast, Ireland, in the back of a cardiac response car. Despite us being a tiny little country, we do have some advances ahead of the United States.
 

Dr. Pepe: That was a breakthrough. Dr. Frank Pantridge and John Geddes did this great work and that caught the imagination of everybody here. At first, they were just going out to give people oxygen and sedate them for their chest pain. It turned out that their defibrillators are what made the difference as they went out there. Absolutely, I have to acknowledge the folks in Ireland for giving us this. Many of the EMS systems got started because of the article they published in The Lancet back in 1967.

Dr. Glatter: I wanted to briefly talk about screening of the athletes at the high school/college level, but also at the professional level. Obviously, there are issues, including the risk for false-positives in terms of low incidence, but there are also false negatives, as the case with Christian Eriksen, who had a cardiac arrest in 2021 and who has been through extensive testing. We can debate the validity of such testing, but I wanted to get both of your takes on the utility of screening in such a population.

Dr. Molloy: That’s a very emotive subject. False-positives are difficult because you’re now saying to somebody that they can’t compete in your sport at a decent level. The difficult part is telling somebody that this is the end of their career.

The false-negative is a little bit more difficult. I don’t know Christian Eriksen and I’m not involved in his team in any way, but that is a one-point examination, and you’re dependent on the scale of the process interpreting the ECG, which is again only a couple of seconds and that particular arrhythmia may not have shown up on that.

Also, athletes, by nature of what they’re doing, are operating at 99% of efficiency on a frequent basis. They are at the peak of their physiologic fitness, and it does make them a little bit more prone to picking up viral illnesses from time to time. They may get a small viral myopericarditis, which causes a new arrhythmia that nobody knew about. They had the screening 2 or 3 years ago, and they now developed a new problem because of what they do, which just may not show up.

I was actually surprised that the gentleman came through it very well, which is fantastic. He wasn’t allowed to play football in the country where he was employed, and he has now moved to another country and is playing football with a defibrillator inserted. I don’t know what the rules are in American football where you can play with implantable defibrillators. I’m not so sure it’s a great idea to do that.

Dr. Pepe: One thing that we should bring up is that there are athletes with underlying cardiomyopathies or hypertrophies and things like that, but that was unlikely in this case. It’s possible, but it’s unlikely, because it would have manifested itself before. In terms of screening, I’ve met some very smart medical doctors who have run those tests, and they have been very encouraged even at the high school levels to have screenings done, whether it’s electrocardiography, echocardiography, and so on. I have to reiterate what Dr Malloy just said in that it may have its downsides as well. If you can pick up real obvious cases, I think that may be of value.

Dr. Glatter: I want to conclude and get some pearls and takeaways from each of you regarding the events that transpired and what our audience can really hold onto.

Dr. Molloy: Look at Formula One in the past 50 years. In Formula One, in the beginning it was a 2-minute job to change a tire. Now, they have this down where they’re measuring in fractions of a second and criticizing each other if one guy is 2.6 seconds and the other guy is 2.9 seconds. For me, that’s phenomenal. It takes me 25 minutes to change a tire.

We’ve looked at that from a resuscitation perspective, and we now do pit crew resuscitation before our events. We’ve planned our team and know who’s going to be occupying what role. After the events at the UEFA championships, we had a new rule brought in by UEFA where they handed me a new document saying, “This is what we would like you to do for resuscitation.” It was a three-man triangle, and I said, “No, we’re not going to do that here.” And they said, “Why, you have to; it’s our rule.”

I said, “No, our rule in Ireland is we have a six-person triangle. We’re not downing our standards because of what you have internationally. You’re covering games in some very low-resource environments, I know that. We have a particular standard here that we’re sticking to. We have a six-person group. We know what we’re all doing; we come very quickly to those downed players and get involved and we’ve had good outcomes, so we’re not going to change the standards.”

That’s the thing: You need to practice these things. The players don’t go out on the weekend and do a move for the very first time without practicing it hundreds of times. We need to look at it the same way as the medical team who are looking after that group of players and the crowd because we also look after the crowd.

A particular challenge in some of our stadiums is that the upper decks are so steep, and it’s very hard to get a patient onto a trolley and do CPR as you’re bringing them down to a zone to get them flat. We’ve had to come up with some innovative techniques to try and do that and accommodate that using some of the mechanical CPR devices. That’s the result you’ll only get from having practiced these events and trying to extricate patients. We want to check response times, so you have to practice your response team activity very frequently.

Dr. Pepe: There are two points made by Mick that I want to react to. One, the pit crew approach is critical in so many ways. We do the same thing in what we call the medical first attack, where we knew who the A, B, and C person would be. When we took it out to the NBA trainers, I recommended for them to have a similar approach so that if an event does happen right in the middle of prime time, they are coordinated.

The second point is that we do mass-gathering medicine. It’s not just the sportspeople on the field or the entertainers that we’re looking after; it is the people in the stands. We will see a cardiac arrest once a month. If you think about it, you might see a cardiac arrest occur in any community on a regular basis. Now you’ve got 100,000 people in one stadium, and something is bound to go wrong over those 3 or 4 hours where they are there and may have a critical emergency. Preparation for all of that is really important as well.

The final point is that on a day-to-day basis, most cardiac arrests do occur in the home. Granted, 80% of them are nonshockable cases, but the people who are more apt to survive are going to be the ones who have an electrical event. In fact, when we looked at our data years ago, we found that, of the cases of people with ventricular fibrillation that we resuscitated, half didn’t even have heart damage. Their enzymes were normal. It was a pure electrical event, and they were more resuscitable. They may have an underlying problem, but we can fix that once we get them back.

Everybody needs to know how to do bystander CPR, and second, we must make sure we have AEDs strategically placed, as I alluded to before. We also go out to other parts of the community and give them advice. All those things must be put in place, but more importantly, just get the training and make the training simple. It’s really a “just do it” philosophy, but make it simple.

For example, when I teach a course, I can do it in 15 minutes, and people retain it because I keep reiterating things like, “Okay, there’s one thing you need to know about choking: Pop the cork.” You give them a physiologic image of what’s happening. Everybody says, “I remember you saying to just do it, pop the cork.”

With AEDs, know where it is – that’s why we should have it in standardized places. Go get it, turn it on, and then follow the instructions. Also, the most important thing is making sure you’re doing quality compressions; and there are videos that can help you with that, as well as classes that you can take that will get you through it.

Dr. Glatter: Absolutely. The public still has the misconception that you need to do mouth-to-mouth resuscitation. The message has not permeated through society that you don’t need to do mouth-to-mouth. Hands-only CPR is the gold standard now.

Dr. Pepe: If people have a reversible cause like ventricular fibrillation, often they’re already gasping, which is better than a delivered breath, by the way. Most important, then, are the compressions to make sure you have oxygen going up to the brain, because you’re still theoretically loaded with oxygen in your bloodstream if you had a sudden cardiac arrest from a ventricular fibrillation.

Your points are well taken, and we found that we had better outcomes when we just gave instructions to do compressions only, and that became the standard. Mick, you’ve had some experiences with that as well.

Dr. Molloy: If we’re going to have a long-term benefit from all this, we have to start doing this in elementary school and teaching kids basic life support and some basic health messaging.

I remember trying to get this across to a teacher one day and the teacher saying, “But why would we teach young kids to resuscitate each other?” I said, “I think you forget that the only 60-year-old person in the room is you. You train them, and we train them. They’re the ones who are going to respond and keep you alive. That’s the way you should be looking at this.” That completely changed the mindset of whether we should be doing this for the kids or not.

Dr. Pepe: In fact, what we find is that that’s exactly who gets saved. I had case after case where the kids at the school had learned CPR and saved the teachers or the administrator at the high school or elementary school. It’s a fantastic point that you bring up, Dr. Malloy.

Dr. Glatter: One other brief thing we can interject here is that the team was excellent on field in that they evaluated Damar Hamlin in a primary survey sense of ABCs (i.e., airway, breathing, and circulation) for things like a tension pneumothorax. In the sense in which he was hit, there are reversible causes. Making sure he didn’t have a tension pneumothorax that caused the arrest, in my mind, was critical.

Dr. Pepe: We do the same thing on a day-to-day basis with a car wreck, because it could be that the person had ventricular fibrillation and then had the wreck. It’s not always trauma. That’s a fantastic point that you’re making. That’s exactly what I think happened, and that’s what we do.

Dr. Glatter: Well, thank you, gentlemen. This was an informative and helpful discussion for our audience. I appreciate your time and expertise.



Dr. Glatter, is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes.

Dr. Pepe is a professor of internal medicine, surgery, pediatrics, public health, and emergency medicine at University of Texas Health Science Center in Houston. He’s also a global coordinator of the U.S. Metropolitan Municipalities EMS Medical Directors (“Eagles”) Coalition.

Dr. Molloy works clinically as a consultant in emergency medicine in Wexford General Hospital, part of the Ireland East Hospital Group (IEHG). Internationally, he is a member of the Disaster Medicine Section of the European Society of Emergency Medicine (EUSEM) and has been appointed by the Irish Medical Organization (IMO) as one of two Irish delegates to serve on the European Board and Section of Emergency Medicine of the European Union of Medical Specialists (UEMS), having served for a number of years on its predecessor, the Multidisciplinary Joint Committee on Emergency Medicine.

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

It started as a mountain biking excursion with two friends. When we drove into the trailhead parking lot, we saw several emergency vehicles. Then a helicopter passed overhead. As we got on our bikes, a police officer told us there’d been an accident out on the trail and to be careful because emergency personnel were going to be bringing in the patient. So we started the ride cautiously, ready to yield to emergency medical services.

Half a mile down the trail, we encountered another police officer. He asked if we would be willing to go back to get an oxygen tank from the ambulance and carry it out to the scene. The three of us turned around, went back to the parking lot and were able to snag a tank of oxygen. We put it in a backpack and biked out again.

We found the scene about a mile down the trail. An adult male was lying on his back in the dirt after a crash. His eyes were closed and he wasn’t moving except for occasional breaths. Six emergency medical personnel huddled around him, one assisting breaths with a bag mask. I didn’t introduce myself initially. I just listened to hear what was happening.

They were debating the dose of medication to give him in order to intubate. I knew the answer to that question, so I introduced myself. They were happy to have somebody else to assist.

They already had an IV in place and quite a lot of supplies. They administered the meds and the paramedic attempted to intubate through the mouth. Within a few seconds, she pulled the intubating blade out and said, “I’m not going to be able to get this. His tongue is too big.”

I took the blade myself and kneeled at the head of the victim. I made three attempts at intubating, and each time couldn’t view the landmarks. I wasn’t sure if his tongue was too large or if there was some traumatic injury. To make it more difficult, a lot of secretions clogged the airway. The paramedics had a portable suction, which was somewhat functional, but I still couldn’t visualize the landmarks.

I started asking about alternative methods of establishing an airway. They had an i-gel, which is a supraglottic device that goes into the back of the mouth. So, we placed it. But when we attached the bag, air still wasn’t getting into the lungs.

We removed it and put the bag mask back on. Now I was worried. We were having difficulty keeping his oxygen above 90%. I examined the chest and abdomen again. I was wondering if perhaps he was having some gastric distention, which can result from prolonged bagging, but that didn’t seem to be the case.

Bagging became progressively more difficult, and the oxygen slowly trended down through the 80s. Then the 70s. Heart rate dropped below 60 beats per minute. The trajectory was obvious.

That’s when I asked if they had the tools for a surgical airway.

No one thought the question was crazy. In fact, they pulled out a scalpel from an equipment bag.

But now I had to actually do it. I knelt next to the patient, trying to palpate the front of the neck to identify the correct location to cut. I had difficulty finding the appropriate landmarks there as well. Frustrating.

I glanced at the monitor. O₂ was now in the 60s. Later the paramedic told me the heart rate was down to 30.

One of the medics looked me in the eye and said, “We’ve got to do something. The time is now.” That helped me snap out of it and act. I made my large vertical incision on the front of the victim’s neck, which of course resulted in quite a bit of bleeding.

My two friends, who were watching, later told me this was the moment the intensity of the scene really increased (it was already pretty intense for me, thanks).

Next, I made the horizontal stab incision. Then I probed with my finger, but it seems the incision hadn’t reached the trachea. I had to make the stab much deeper than I would’ve thought.

And then air bubbled out through the blood. A paramedic was ready with the ET tube in hand and she put it through the incision. We attached the bag. We had air movement into the lungs, and within minutes the oxygen came up.

Not long after, the flight paramedics from the helicopter showed up, having jogged a mile through the woods. They seemed rather surprised to find a patient with a cricothyrotomy. We filled them in on the situation. Now we had to get the patient out of the woods (literally and figuratively).

The emergency responders had a really great transport device: A litter with one big wheel underneath in the middle so we could roll the patient down the mountain bike trail over rocks relatively safely. One person’s job was to hold the tube as we went since we didn’t have suture to hold it in place.

We got back to the parking lot and loaded him into the ambulance, which drove another mile to the helicopter, which then had to take him a hundred miles to the hospital.

To be honest, I thought the prognosis was poor. I suspected he had an intercranial bleed slowly squeezing his brain (that later turned out to not be the case). Even though we had established an airway, it took us so long to get him to the ambulance.

The director of the local EMS called me that evening and said the patient had made it to the hospital. I had never been a part of anything with this intensity. I definitely lost sleep over it. Partly just from the uncertainty of not knowing what the outcome would be. But also second-guessing if I had done everything that I could have.

The story doesn’t quite end there, however.

A week later, a friend of the patient called me. He had recovered well and was going to be discharged from the hospital. He’d chosen to share the story with the media, and the local TV station was going to interview him. They had asked if I would agree to be interviewed.

After the local news story ran, it was kind of a media blitz. In came numerous media requests. But honestly, the portrayal of the story made me feel really weird. It was overly dramatized and not entirely accurate. It really didn’t sit well with me.

Friends all over the country saw the story, and here’s what they got from the coverage:

I was biking behind the patient when he crashed.

I had my own tools. Even the patient himself was told I used my own blade to make the incision.

The true story is what I just told you: A half-dozen emergency medical personnel were already there when I arrived. It was a combination of all of us – together – in the right place at the right time.

A month later, the patient and his family drove to the city where I live to take me out to lunch. It was emotional. There were plenty of tears. His wife and daughter were expressing a lot of gratitude and had some gifts for me. I was able to get his version of the story and learned some details. He had facial trauma in the past with some reconstruction. I realized that perhaps those anatomical changes affected my ability to do the intubation.

I hope to never again have to do this outside of the hospital. But I suppose I’m more prepared than ever now. I’ve reviewed my cricothyrotomy technique many times since then.

I was trained as a family doctor and did clinic and hospital medicine for several years. It was only in 2020 that I transitioned to doing emergency medicine work in a rural hospital. So, 2 years earlier, I’m not sure I would’ve been able to do what I did that day. To me, it was almost symbolic of the transition of my practice to emergency medicine.

I’m still in touch with the patient. We’ve talked about biking together. That hasn’t happened yet, but it may very well happen someday.

Jesse Coenen, MD, is an emergency medicine physician at Hayward Area Memorial Hospital in Hayward, Wisc.

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

It started as a mountain biking excursion with two friends. When we drove into the trailhead parking lot, we saw several emergency vehicles. Then a helicopter passed overhead. As we got on our bikes, a police officer told us there’d been an accident out on the trail and to be careful because emergency personnel were going to be bringing in the patient. So we started the ride cautiously, ready to yield to emergency medical services.

Half a mile down the trail, we encountered another police officer. He asked if we would be willing to go back to get an oxygen tank from the ambulance and carry it out to the scene. The three of us turned around, went back to the parking lot and were able to snag a tank of oxygen. We put it in a backpack and biked out again.

We found the scene about a mile down the trail. An adult male was lying on his back in the dirt after a crash. His eyes were closed and he wasn’t moving except for occasional breaths. Six emergency medical personnel huddled around him, one assisting breaths with a bag mask. I didn’t introduce myself initially. I just listened to hear what was happening.

They were debating the dose of medication to give him in order to intubate. I knew the answer to that question, so I introduced myself. They were happy to have somebody else to assist.

They already had an IV in place and quite a lot of supplies. They administered the meds and the paramedic attempted to intubate through the mouth. Within a few seconds, she pulled the intubating blade out and said, “I’m not going to be able to get this. His tongue is too big.”

I took the blade myself and kneeled at the head of the victim. I made three attempts at intubating, and each time couldn’t view the landmarks. I wasn’t sure if his tongue was too large or if there was some traumatic injury. To make it more difficult, a lot of secretions clogged the airway. The paramedics had a portable suction, which was somewhat functional, but I still couldn’t visualize the landmarks.

I started asking about alternative methods of establishing an airway. They had an i-gel, which is a supraglottic device that goes into the back of the mouth. So, we placed it. But when we attached the bag, air still wasn’t getting into the lungs.

We removed it and put the bag mask back on. Now I was worried. We were having difficulty keeping his oxygen above 90%. I examined the chest and abdomen again. I was wondering if perhaps he was having some gastric distention, which can result from prolonged bagging, but that didn’t seem to be the case.

Bagging became progressively more difficult, and the oxygen slowly trended down through the 80s. Then the 70s. Heart rate dropped below 60 beats per minute. The trajectory was obvious.

That’s when I asked if they had the tools for a surgical airway.

No one thought the question was crazy. In fact, they pulled out a scalpel from an equipment bag.

But now I had to actually do it. I knelt next to the patient, trying to palpate the front of the neck to identify the correct location to cut. I had difficulty finding the appropriate landmarks there as well. Frustrating.

I glanced at the monitor. O₂ was now in the 60s. Later the paramedic told me the heart rate was down to 30.

One of the medics looked me in the eye and said, “We’ve got to do something. The time is now.” That helped me snap out of it and act. I made my large vertical incision on the front of the victim’s neck, which of course resulted in quite a bit of bleeding.

My two friends, who were watching, later told me this was the moment the intensity of the scene really increased (it was already pretty intense for me, thanks).

Next, I made the horizontal stab incision. Then I probed with my finger, but it seems the incision hadn’t reached the trachea. I had to make the stab much deeper than I would’ve thought.

And then air bubbled out through the blood. A paramedic was ready with the ET tube in hand and she put it through the incision. We attached the bag. We had air movement into the lungs, and within minutes the oxygen came up.

Not long after, the flight paramedics from the helicopter showed up, having jogged a mile through the woods. They seemed rather surprised to find a patient with a cricothyrotomy. We filled them in on the situation. Now we had to get the patient out of the woods (literally and figuratively).

The emergency responders had a really great transport device: A litter with one big wheel underneath in the middle so we could roll the patient down the mountain bike trail over rocks relatively safely. One person’s job was to hold the tube as we went since we didn’t have suture to hold it in place.

We got back to the parking lot and loaded him into the ambulance, which drove another mile to the helicopter, which then had to take him a hundred miles to the hospital.

To be honest, I thought the prognosis was poor. I suspected he had an intercranial bleed slowly squeezing his brain (that later turned out to not be the case). Even though we had established an airway, it took us so long to get him to the ambulance.

The director of the local EMS called me that evening and said the patient had made it to the hospital. I had never been a part of anything with this intensity. I definitely lost sleep over it. Partly just from the uncertainty of not knowing what the outcome would be. But also second-guessing if I had done everything that I could have.

The story doesn’t quite end there, however.

A week later, a friend of the patient called me. He had recovered well and was going to be discharged from the hospital. He’d chosen to share the story with the media, and the local TV station was going to interview him. They had asked if I would agree to be interviewed.

After the local news story ran, it was kind of a media blitz. In came numerous media requests. But honestly, the portrayal of the story made me feel really weird. It was overly dramatized and not entirely accurate. It really didn’t sit well with me.

Friends all over the country saw the story, and here’s what they got from the coverage:

I was biking behind the patient when he crashed.

I had my own tools. Even the patient himself was told I used my own blade to make the incision.

The true story is what I just told you: A half-dozen emergency medical personnel were already there when I arrived. It was a combination of all of us – together – in the right place at the right time.

A month later, the patient and his family drove to the city where I live to take me out to lunch. It was emotional. There were plenty of tears. His wife and daughter were expressing a lot of gratitude and had some gifts for me. I was able to get his version of the story and learned some details. He had facial trauma in the past with some reconstruction. I realized that perhaps those anatomical changes affected my ability to do the intubation.

I hope to never again have to do this outside of the hospital. But I suppose I’m more prepared than ever now. I’ve reviewed my cricothyrotomy technique many times since then.

I was trained as a family doctor and did clinic and hospital medicine for several years. It was only in 2020 that I transitioned to doing emergency medicine work in a rural hospital. So, 2 years earlier, I’m not sure I would’ve been able to do what I did that day. To me, it was almost symbolic of the transition of my practice to emergency medicine.

I’m still in touch with the patient. We’ve talked about biking together. That hasn’t happened yet, but it may very well happen someday.

Jesse Coenen, MD, is an emergency medicine physician at Hayward Area Memorial Hospital in Hayward, Wisc.

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

It started as a mountain biking excursion with two friends. When we drove into the trailhead parking lot, we saw several emergency vehicles. Then a helicopter passed overhead. As we got on our bikes, a police officer told us there’d been an accident out on the trail and to be careful because emergency personnel were going to be bringing in the patient. So we started the ride cautiously, ready to yield to emergency medical services.

Half a mile down the trail, we encountered another police officer. He asked if we would be willing to go back to get an oxygen tank from the ambulance and carry it out to the scene. The three of us turned around, went back to the parking lot and were able to snag a tank of oxygen. We put it in a backpack and biked out again.

We found the scene about a mile down the trail. An adult male was lying on his back in the dirt after a crash. His eyes were closed and he wasn’t moving except for occasional breaths. Six emergency medical personnel huddled around him, one assisting breaths with a bag mask. I didn’t introduce myself initially. I just listened to hear what was happening.

They were debating the dose of medication to give him in order to intubate. I knew the answer to that question, so I introduced myself. They were happy to have somebody else to assist.

They already had an IV in place and quite a lot of supplies. They administered the meds and the paramedic attempted to intubate through the mouth. Within a few seconds, she pulled the intubating blade out and said, “I’m not going to be able to get this. His tongue is too big.”

I took the blade myself and kneeled at the head of the victim. I made three attempts at intubating, and each time couldn’t view the landmarks. I wasn’t sure if his tongue was too large or if there was some traumatic injury. To make it more difficult, a lot of secretions clogged the airway. The paramedics had a portable suction, which was somewhat functional, but I still couldn’t visualize the landmarks.

I started asking about alternative methods of establishing an airway. They had an i-gel, which is a supraglottic device that goes into the back of the mouth. So, we placed it. But when we attached the bag, air still wasn’t getting into the lungs.

We removed it and put the bag mask back on. Now I was worried. We were having difficulty keeping his oxygen above 90%. I examined the chest and abdomen again. I was wondering if perhaps he was having some gastric distention, which can result from prolonged bagging, but that didn’t seem to be the case.

Bagging became progressively more difficult, and the oxygen slowly trended down through the 80s. Then the 70s. Heart rate dropped below 60 beats per minute. The trajectory was obvious.

That’s when I asked if they had the tools for a surgical airway.

No one thought the question was crazy. In fact, they pulled out a scalpel from an equipment bag.

But now I had to actually do it. I knelt next to the patient, trying to palpate the front of the neck to identify the correct location to cut. I had difficulty finding the appropriate landmarks there as well. Frustrating.

I glanced at the monitor. O₂ was now in the 60s. Later the paramedic told me the heart rate was down to 30.

One of the medics looked me in the eye and said, “We’ve got to do something. The time is now.” That helped me snap out of it and act. I made my large vertical incision on the front of the victim’s neck, which of course resulted in quite a bit of bleeding.

My two friends, who were watching, later told me this was the moment the intensity of the scene really increased (it was already pretty intense for me, thanks).

Next, I made the horizontal stab incision. Then I probed with my finger, but it seems the incision hadn’t reached the trachea. I had to make the stab much deeper than I would’ve thought.

And then air bubbled out through the blood. A paramedic was ready with the ET tube in hand and she put it through the incision. We attached the bag. We had air movement into the lungs, and within minutes the oxygen came up.

Not long after, the flight paramedics from the helicopter showed up, having jogged a mile through the woods. They seemed rather surprised to find a patient with a cricothyrotomy. We filled them in on the situation. Now we had to get the patient out of the woods (literally and figuratively).

The emergency responders had a really great transport device: A litter with one big wheel underneath in the middle so we could roll the patient down the mountain bike trail over rocks relatively safely. One person’s job was to hold the tube as we went since we didn’t have suture to hold it in place.

We got back to the parking lot and loaded him into the ambulance, which drove another mile to the helicopter, which then had to take him a hundred miles to the hospital.

To be honest, I thought the prognosis was poor. I suspected he had an intercranial bleed slowly squeezing his brain (that later turned out to not be the case). Even though we had established an airway, it took us so long to get him to the ambulance.

The director of the local EMS called me that evening and said the patient had made it to the hospital. I had never been a part of anything with this intensity. I definitely lost sleep over it. Partly just from the uncertainty of not knowing what the outcome would be. But also second-guessing if I had done everything that I could have.

The story doesn’t quite end there, however.

A week later, a friend of the patient called me. He had recovered well and was going to be discharged from the hospital. He’d chosen to share the story with the media, and the local TV station was going to interview him. They had asked if I would agree to be interviewed.

After the local news story ran, it was kind of a media blitz. In came numerous media requests. But honestly, the portrayal of the story made me feel really weird. It was overly dramatized and not entirely accurate. It really didn’t sit well with me.

Friends all over the country saw the story, and here’s what they got from the coverage:

I was biking behind the patient when he crashed.

I had my own tools. Even the patient himself was told I used my own blade to make the incision.

The true story is what I just told you: A half-dozen emergency medical personnel were already there when I arrived. It was a combination of all of us – together – in the right place at the right time.

A month later, the patient and his family drove to the city where I live to take me out to lunch. It was emotional. There were plenty of tears. His wife and daughter were expressing a lot of gratitude and had some gifts for me. I was able to get his version of the story and learned some details. He had facial trauma in the past with some reconstruction. I realized that perhaps those anatomical changes affected my ability to do the intubation.

I hope to never again have to do this outside of the hospital. But I suppose I’m more prepared than ever now. I’ve reviewed my cricothyrotomy technique many times since then.

I was trained as a family doctor and did clinic and hospital medicine for several years. It was only in 2020 that I transitioned to doing emergency medicine work in a rural hospital. So, 2 years earlier, I’m not sure I would’ve been able to do what I did that day. To me, it was almost symbolic of the transition of my practice to emergency medicine.

I’m still in touch with the patient. We’ve talked about biking together. That hasn’t happened yet, but it may very well happen someday.

Jesse Coenen, MD, is an emergency medicine physician at Hayward Area Memorial Hospital in Hayward, Wisc.

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

Practice has gone back and forth on whether atrial fibrillation (AFib) should be considered in the preoperative cardiovascular risk (CV) evaluation of patients slated for noncardiac surgery, and the Revised Cardiac Risk Index (RCRI), currently widely used as an assessment tool, doesn’t include the arrhythmia.

But consideration of preexisting AFib along with the RCRI predicted 30-day mortality more sharply than the RCRI alone in an analysis of data covering several million patients slated for such procedures.

ECG_Electrocardiogram_web.jpg

• 1.31 (95% CI, 1.30-1.33) for heart failure
• 1.40 (95% CI, 1.37-1.43) for stroke
• 1.59 (95% CI, 1.43-1.75) for systemic embolism
• 1.14 (95% CI, 1.13-1.16) for major bleeding  
• 0.81 (95% CI, 0.79-0.82) for MI

Those with preexisting AFib also had longer hospitalizations at a median 5 days, compared with 4 days for those without such AFib (P < .001).

The study has the limitations of most any retrospective cohort analysis. Other limitations, the report notes, include lack of information on any antiarrhythmic meds given during hospitalization or type of AFib.

For example, AFib that is permanent – compared with paroxysmal or persistent – may be associated with more atrial fibrosis, greater atrial dilatation, “and probably higher pressures inside the heart,” Dr. Mentias observed.

“That’s not always the case, but that’s the notion. So presumably people with persistent or permanent atrial fib would have more advanced heart disease, and that could imply more risk. But we did not have that kind of data.”

Dr. Mentias and Dr. Prasada report no relevant financial relationships; disclosures for the other authors are in the report. Dr. Curtis discloses serving on advisory boards for Abbott, Janssen Pharmaceuticals, Sanofi, and Milestone Pharmaceuticals; receiving honoraria for speaking from Medtronic and Zoll; and serving on a data-monitoring board for Medtronic. Dr. Korada reports he has no relevant financial relationships.

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

Practice has gone back and forth on whether atrial fibrillation (AFib) should be considered in the preoperative cardiovascular risk (CV) evaluation of patients slated for noncardiac surgery, and the Revised Cardiac Risk Index (RCRI), currently widely used as an assessment tool, doesn’t include the arrhythmia.

But consideration of preexisting AFib along with the RCRI predicted 30-day mortality more sharply than the RCRI alone in an analysis of data covering several million patients slated for such procedures.

ECG_Electrocardiogram_web.jpg

• 1.31 (95% CI, 1.30-1.33) for heart failure
• 1.40 (95% CI, 1.37-1.43) for stroke
• 1.59 (95% CI, 1.43-1.75) for systemic embolism
• 1.14 (95% CI, 1.13-1.16) for major bleeding  
• 0.81 (95% CI, 0.79-0.82) for MI

Those with preexisting AFib also had longer hospitalizations at a median 5 days, compared with 4 days for those without such AFib (P < .001).

The study has the limitations of most any retrospective cohort analysis. Other limitations, the report notes, include lack of information on any antiarrhythmic meds given during hospitalization or type of AFib.

For example, AFib that is permanent – compared with paroxysmal or persistent – may be associated with more atrial fibrosis, greater atrial dilatation, “and probably higher pressures inside the heart,” Dr. Mentias observed.

“That’s not always the case, but that’s the notion. So presumably people with persistent or permanent atrial fib would have more advanced heart disease, and that could imply more risk. But we did not have that kind of data.”

Dr. Mentias and Dr. Prasada report no relevant financial relationships; disclosures for the other authors are in the report. Dr. Curtis discloses serving on advisory boards for Abbott, Janssen Pharmaceuticals, Sanofi, and Milestone Pharmaceuticals; receiving honoraria for speaking from Medtronic and Zoll; and serving on a data-monitoring board for Medtronic. Dr. Korada reports he has no relevant financial relationships.

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

Practice has gone back and forth on whether atrial fibrillation (AFib) should be considered in the preoperative cardiovascular risk (CV) evaluation of patients slated for noncardiac surgery, and the Revised Cardiac Risk Index (RCRI), currently widely used as an assessment tool, doesn’t include the arrhythmia.

But consideration of preexisting AFib along with the RCRI predicted 30-day mortality more sharply than the RCRI alone in an analysis of data covering several million patients slated for such procedures.

ECG_Electrocardiogram_web.jpg

• 1.31 (95% CI, 1.30-1.33) for heart failure
• 1.40 (95% CI, 1.37-1.43) for stroke
• 1.59 (95% CI, 1.43-1.75) for systemic embolism
• 1.14 (95% CI, 1.13-1.16) for major bleeding  
• 0.81 (95% CI, 0.79-0.82) for MI

Those with preexisting AFib also had longer hospitalizations at a median 5 days, compared with 4 days for those without such AFib (P < .001).

The study has the limitations of most any retrospective cohort analysis. Other limitations, the report notes, include lack of information on any antiarrhythmic meds given during hospitalization or type of AFib.

For example, AFib that is permanent – compared with paroxysmal or persistent – may be associated with more atrial fibrosis, greater atrial dilatation, “and probably higher pressures inside the heart,” Dr. Mentias observed.

“That’s not always the case, but that’s the notion. So presumably people with persistent or permanent atrial fib would have more advanced heart disease, and that could imply more risk. But we did not have that kind of data.”

Dr. Mentias and Dr. Prasada report no relevant financial relationships; disclosures for the other authors are in the report. Dr. Curtis discloses serving on advisory boards for Abbott, Janssen Pharmaceuticals, Sanofi, and Milestone Pharmaceuticals; receiving honoraria for speaking from Medtronic and Zoll; and serving on a data-monitoring board for Medtronic. Dr. Korada reports he has no relevant financial relationships.

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

Knee and shoulder pain are common complaints for patients in the primary care office.

But identifying the source of the pain can be complicated,

and an accurate diagnosis of the underlying cause of discomfort is key to appropriate management – whether that involves simple home care options of ice and rest or a recommendation for a follow-up with a specialist.

Speaking at the annual meeting of the American College of Physicians, Greg Nakamoto, MD, department of orthopedics, Virginia Mason Medical Center, Seattle, discussed common knee and shoulder problems that patients often present with in the primary care setting, and offered tips on diagnosis and appropriate management.

The most common conditions causing knee pain are osteoarthritis and meniscal tears. “The differential for knee pain is broad,” Dr. Nakamoto said. “You have to have a way to divide it down, such as if it’s acute or chronic.”

The initial workup has several key components. The first steps: Determine the location of the pain – anterior, medial, lateral, posterior – and then whether it stems from an injury or is atraumatic.

“If you have to ask one question – ask where it hurts,” he said. “And is it from an injury or just wear and tear? That helps me when deciding if surgery is needed.”

Pain in the knee generally localizes well to the site of pathology, and knee pain of acute traumatic onset requires more scrutiny for problems best treated with early surgery. “This also helps establish whether radiographic findings are due to injury or degeneration,” Dr. Nakamoto said. “The presence of swelling guides the need for anti-inflammatories or cortisone.”

Palpating for tenderness along the joint line is important, as is palpating above and below the joint line, Dr. Nakamoto said.

“Tenderness limited to the joint line, combined with a meniscal exam maneuver that reproduces joint-line pain, is suggestive of pain from meniscal pathology,” he said.

Imaging is an important component of evaluating knee symptoms, and the question often arises as to when to order an MRI.

Dr. Nakamoto offered the following scenario: If significant osteoarthritis is evident on weight-bearing x-ray, treat the patient for the condition. However, if little or no osteoarthritis appears on x-ray, and if the onset of symptoms was traumatic and both patient history and physical examination suggest a meniscal tear, order an MRI.

An early MRI also is needed if the patient has had either atraumatic or traumatic onset of symptoms and their history and physical exams are suspicious for a mechanically locked or locking meniscus. For suspicion of a ruptured quadriceps or patellar tendon or a stress fracture, an MRI is needed urgently.

An MRI would be ordered later if the patient’s symptoms have not improved significantly after 3 months of conservative management.

Dr. Nakamoto stressed how common undiagnosed meniscus tears are in the general population. A third of men aged 50-59 years and nearly 20% of women in that age group have a tear, he said. “That number goes up to 56% and 51% in men and women aged 70-90 years, and 61% of these tears were in patients who were asymptomatic in the last month.”

In the setting of osteoarthritis, 76% of asymptomatic patients had a meniscus tear, and 91% of patients with symptomatic osteoarthritis had a meniscus tear, he added.

Treating knee pain

Treatment will vary depending on the underlying etiology of pain. For a possible meniscus tear, the recommendation is for a conservative intervention with ice, ibuprofen, knee immobilizer, and crutches, with a follow-up appointment in a week.

Three types of injections also can help:

• Cortisone for osteoarthritis or meniscus tears, swelling, and inflammation, and prophylaxis against inflammation.
• Viscosupplementation (intra‐articular hyaluronic acid) for chronic, baseline osteoarthritis symptoms.
• Regenerative therapies (platelet-rich plasma, stem cells, etc.) are used primarily for osteoarthritis (these do not regrow cartilage, but some patients report decreased pain).

The data on injections are mixed, Dr. Nakamoto said. For example, the results of a 2015 Cochrane review on cortisone injections for osteoarthritis reported that the benefits were small to moderate at 4‐6 weeks, and small to none at 13 weeks.  

“There is a lot of controversy for viscosupplementation despite all of the data on it,” he said. “But the recommendations from professional organizations are mixed.”

He noted that he has been using viscosupplementation since the 1990s, and some patients do benefit from it.

Shoulder pain

The most common causes of shoulder pain are adhesive capsulitis, rotator cuff tears and tendinopathy, and impingement.

As with knee pain, the same assessment routine largely applies.

First, pinpoint the location: Is the trouble spot the lateral shoulder and upper arm, the trapezial ridge, or the shoulder blade?

Next, assess pain on movement: Does the patient experience discomfort reaching overhead or behind the back, or moving at the glenohumeral joint/capsule and engaging the rotator cuff? Check for stiffness, weakness, and decreased range of motion in the rotator cuff.

Determine if the cause of the pain is traumatic or atraumatic and stems from an acute injury versus degeneration or overuse.

As with the knee, imaging is a major component of the assessment and typically involves the use of x-ray. An MRI may be required for evaluating full- and partial-thickness tears and when contemplating surgery.

MRI also is necessary for evaluating cases of acute, traumatic shoulder injury, and patients exhibiting disability suggestive of a rotator cuff tear in an otherwise healthy tendon.

Some pain can be treated with cortisone injections or regenerative therapies, which generally are given at the acromioclavicular or glenohumeral joints or in the subacromial space. A 2005 meta-analysis found that subacromial injections of corticosteroids are effective for improvement for rotator cuff tendinitis up to a 9‐month period.

Surgery may be warranted in some cases, Dr. Nakamoto said. These include adhesive capsulitis, rotator cuff tear, acute traumatic injury in an otherwise healthy tendon, and chronic (or acute-on-chronic) tears in a degenerative tendon following a trial of conservative therapy.

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

Knee and shoulder pain are common complaints for patients in the primary care office.

But identifying the source of the pain can be complicated,

and an accurate diagnosis of the underlying cause of discomfort is key to appropriate management – whether that involves simple home care options of ice and rest or a recommendation for a follow-up with a specialist.

Speaking at the annual meeting of the American College of Physicians, Greg Nakamoto, MD, department of orthopedics, Virginia Mason Medical Center, Seattle, discussed common knee and shoulder problems that patients often present with in the primary care setting, and offered tips on diagnosis and appropriate management.

The most common conditions causing knee pain are osteoarthritis and meniscal tears. “The differential for knee pain is broad,” Dr. Nakamoto said. “You have to have a way to divide it down, such as if it’s acute or chronic.”

The initial workup has several key components. The first steps: Determine the location of the pain – anterior, medial, lateral, posterior – and then whether it stems from an injury or is atraumatic.

“If you have to ask one question – ask where it hurts,” he said. “And is it from an injury or just wear and tear? That helps me when deciding if surgery is needed.”

Pain in the knee generally localizes well to the site of pathology, and knee pain of acute traumatic onset requires more scrutiny for problems best treated with early surgery. “This also helps establish whether radiographic findings are due to injury or degeneration,” Dr. Nakamoto said. “The presence of swelling guides the need for anti-inflammatories or cortisone.”

Palpating for tenderness along the joint line is important, as is palpating above and below the joint line, Dr. Nakamoto said.

“Tenderness limited to the joint line, combined with a meniscal exam maneuver that reproduces joint-line pain, is suggestive of pain from meniscal pathology,” he said.

Imaging is an important component of evaluating knee symptoms, and the question often arises as to when to order an MRI.

Dr. Nakamoto offered the following scenario: If significant osteoarthritis is evident on weight-bearing x-ray, treat the patient for the condition. However, if little or no osteoarthritis appears on x-ray, and if the onset of symptoms was traumatic and both patient history and physical examination suggest a meniscal tear, order an MRI.

An early MRI also is needed if the patient has had either atraumatic or traumatic onset of symptoms and their history and physical exams are suspicious for a mechanically locked or locking meniscus. For suspicion of a ruptured quadriceps or patellar tendon or a stress fracture, an MRI is needed urgently.

An MRI would be ordered later if the patient’s symptoms have not improved significantly after 3 months of conservative management.

Dr. Nakamoto stressed how common undiagnosed meniscus tears are in the general population. A third of men aged 50-59 years and nearly 20% of women in that age group have a tear, he said. “That number goes up to 56% and 51% in men and women aged 70-90 years, and 61% of these tears were in patients who were asymptomatic in the last month.”

In the setting of osteoarthritis, 76% of asymptomatic patients had a meniscus tear, and 91% of patients with symptomatic osteoarthritis had a meniscus tear, he added.

Treating knee pain

Treatment will vary depending on the underlying etiology of pain. For a possible meniscus tear, the recommendation is for a conservative intervention with ice, ibuprofen, knee immobilizer, and crutches, with a follow-up appointment in a week.

Three types of injections also can help:

• Cortisone for osteoarthritis or meniscus tears, swelling, and inflammation, and prophylaxis against inflammation.
• Viscosupplementation (intra‐articular hyaluronic acid) for chronic, baseline osteoarthritis symptoms.
• Regenerative therapies (platelet-rich plasma, stem cells, etc.) are used primarily for osteoarthritis (these do not regrow cartilage, but some patients report decreased pain).

The data on injections are mixed, Dr. Nakamoto said. For example, the results of a 2015 Cochrane review on cortisone injections for osteoarthritis reported that the benefits were small to moderate at 4‐6 weeks, and small to none at 13 weeks.  

“There is a lot of controversy for viscosupplementation despite all of the data on it,” he said. “But the recommendations from professional organizations are mixed.”

He noted that he has been using viscosupplementation since the 1990s, and some patients do benefit from it.

Shoulder pain

The most common causes of shoulder pain are adhesive capsulitis, rotator cuff tears and tendinopathy, and impingement.

As with knee pain, the same assessment routine largely applies.

First, pinpoint the location: Is the trouble spot the lateral shoulder and upper arm, the trapezial ridge, or the shoulder blade?

Next, assess pain on movement: Does the patient experience discomfort reaching overhead or behind the back, or moving at the glenohumeral joint/capsule and engaging the rotator cuff? Check for stiffness, weakness, and decreased range of motion in the rotator cuff.

Determine if the cause of the pain is traumatic or atraumatic and stems from an acute injury versus degeneration or overuse.

As with the knee, imaging is a major component of the assessment and typically involves the use of x-ray. An MRI may be required for evaluating full- and partial-thickness tears and when contemplating surgery.

MRI also is necessary for evaluating cases of acute, traumatic shoulder injury, and patients exhibiting disability suggestive of a rotator cuff tear in an otherwise healthy tendon.

Some pain can be treated with cortisone injections or regenerative therapies, which generally are given at the acromioclavicular or glenohumeral joints or in the subacromial space. A 2005 meta-analysis found that subacromial injections of corticosteroids are effective for improvement for rotator cuff tendinitis up to a 9‐month period.

Surgery may be warranted in some cases, Dr. Nakamoto said. These include adhesive capsulitis, rotator cuff tear, acute traumatic injury in an otherwise healthy tendon, and chronic (or acute-on-chronic) tears in a degenerative tendon following a trial of conservative therapy.

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

Knee and shoulder pain are common complaints for patients in the primary care office.

But identifying the source of the pain can be complicated,

and an accurate diagnosis of the underlying cause of discomfort is key to appropriate management – whether that involves simple home care options of ice and rest or a recommendation for a follow-up with a specialist.

Speaking at the annual meeting of the American College of Physicians, Greg Nakamoto, MD, department of orthopedics, Virginia Mason Medical Center, Seattle, discussed common knee and shoulder problems that patients often present with in the primary care setting, and offered tips on diagnosis and appropriate management.

The most common conditions causing knee pain are osteoarthritis and meniscal tears. “The differential for knee pain is broad,” Dr. Nakamoto said. “You have to have a way to divide it down, such as if it’s acute or chronic.”

The initial workup has several key components. The first steps: Determine the location of the pain – anterior, medial, lateral, posterior – and then whether it stems from an injury or is atraumatic.

“If you have to ask one question – ask where it hurts,” he said. “And is it from an injury or just wear and tear? That helps me when deciding if surgery is needed.”

Pain in the knee generally localizes well to the site of pathology, and knee pain of acute traumatic onset requires more scrutiny for problems best treated with early surgery. “This also helps establish whether radiographic findings are due to injury or degeneration,” Dr. Nakamoto said. “The presence of swelling guides the need for anti-inflammatories or cortisone.”

Palpating for tenderness along the joint line is important, as is palpating above and below the joint line, Dr. Nakamoto said.

“Tenderness limited to the joint line, combined with a meniscal exam maneuver that reproduces joint-line pain, is suggestive of pain from meniscal pathology,” he said.

Imaging is an important component of evaluating knee symptoms, and the question often arises as to when to order an MRI.

Dr. Nakamoto offered the following scenario: If significant osteoarthritis is evident on weight-bearing x-ray, treat the patient for the condition. However, if little or no osteoarthritis appears on x-ray, and if the onset of symptoms was traumatic and both patient history and physical examination suggest a meniscal tear, order an MRI.

An early MRI also is needed if the patient has had either atraumatic or traumatic onset of symptoms and their history and physical exams are suspicious for a mechanically locked or locking meniscus. For suspicion of a ruptured quadriceps or patellar tendon or a stress fracture, an MRI is needed urgently.

An MRI would be ordered later if the patient’s symptoms have not improved significantly after 3 months of conservative management.

Dr. Nakamoto stressed how common undiagnosed meniscus tears are in the general population. A third of men aged 50-59 years and nearly 20% of women in that age group have a tear, he said. “That number goes up to 56% and 51% in men and women aged 70-90 years, and 61% of these tears were in patients who were asymptomatic in the last month.”

In the setting of osteoarthritis, 76% of asymptomatic patients had a meniscus tear, and 91% of patients with symptomatic osteoarthritis had a meniscus tear, he added.

Treating knee pain

Treatment will vary depending on the underlying etiology of pain. For a possible meniscus tear, the recommendation is for a conservative intervention with ice, ibuprofen, knee immobilizer, and crutches, with a follow-up appointment in a week.

Three types of injections also can help:

• Cortisone for osteoarthritis or meniscus tears, swelling, and inflammation, and prophylaxis against inflammation.
• Viscosupplementation (intra‐articular hyaluronic acid) for chronic, baseline osteoarthritis symptoms.
• Regenerative therapies (platelet-rich plasma, stem cells, etc.) are used primarily for osteoarthritis (these do not regrow cartilage, but some patients report decreased pain).

The data on injections are mixed, Dr. Nakamoto said. For example, the results of a 2015 Cochrane review on cortisone injections for osteoarthritis reported that the benefits were small to moderate at 4‐6 weeks, and small to none at 13 weeks.  

“There is a lot of controversy for viscosupplementation despite all of the data on it,” he said. “But the recommendations from professional organizations are mixed.”

He noted that he has been using viscosupplementation since the 1990s, and some patients do benefit from it.

Shoulder pain

The most common causes of shoulder pain are adhesive capsulitis, rotator cuff tears and tendinopathy, and impingement.

As with knee pain, the same assessment routine largely applies.

First, pinpoint the location: Is the trouble spot the lateral shoulder and upper arm, the trapezial ridge, or the shoulder blade?

Next, assess pain on movement: Does the patient experience discomfort reaching overhead or behind the back, or moving at the glenohumeral joint/capsule and engaging the rotator cuff? Check for stiffness, weakness, and decreased range of motion in the rotator cuff.

Determine if the cause of the pain is traumatic or atraumatic and stems from an acute injury versus degeneration or overuse.

As with the knee, imaging is a major component of the assessment and typically involves the use of x-ray. An MRI may be required for evaluating full- and partial-thickness tears and when contemplating surgery.

MRI also is necessary for evaluating cases of acute, traumatic shoulder injury, and patients exhibiting disability suggestive of a rotator cuff tear in an otherwise healthy tendon.

Some pain can be treated with cortisone injections or regenerative therapies, which generally are given at the acromioclavicular or glenohumeral joints or in the subacromial space. A 2005 meta-analysis found that subacromial injections of corticosteroids are effective for improvement for rotator cuff tendinitis up to a 9‐month period.

Surgery may be warranted in some cases, Dr. Nakamoto said. These include adhesive capsulitis, rotator cuff tear, acute traumatic injury in an otherwise healthy tendon, and chronic (or acute-on-chronic) tears in a degenerative tendon following a trial of conservative therapy.

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