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How a concussion led a former football player/WWE star to a pioneering neuroscience career
On Oct. 5, 2022, at 10:24 a.m., Chris Nowinski, PhD, cofounder of the Boston-based Concussion Legacy Foundation (CLF), was in his home office when the email came through.
“I pounded my desk, shouted YES! and went to find my wife so I could pick her up and give her a big hug,” he recalled. “It was the culmination of 15 years of research and hard work.”
Robert Cantu, MD, who has been studying head trauma for 50+ years and has published more than 500 papers about it, compares the announcement to the 1964 Surgeon General’s report that linked cigarette smoking with lung cancer and heart disease. With the NIH and the Centers of Disease Control and Prevention (CDC) now in agreement about the risks of participating in impact sports and activities, he said, “We’ve reached a tipping point that should finally prompt deniers such as the NHL, NCAA, FIFA, World Rugby, the International Olympic Committee, and other [sports organizations] to remove all unnecessary head trauma from their sports.”
“A lot of the credit for this must go to Chris,” added Dr. Cantu, medical director and director of clinical research at the Cantu Concussion Center at Emerson Hospital in Concord, Mass. “Clinicians like myself can reach only so many people by writing papers and giving speeches at medical conferences. For this to happen, the message needed to get out to parents, athletes, and society in general. And Chris was the vehicle for doing that.”
Dr. Nowinski didn’t set out to be the messenger. He played football at Harvard in the late 1990s, making second-team All-Ivy as a defensive tackle his senior year. In 2000, he enrolled in Killer Kowalski’s Wrestling Institute and eventually joined Vince McMahon’s World Wrestling Entertainment (WWE).
There he played the role of 295-pound villain “Chris Harvard,” an intellectual snob who dressed in crimson tights and insulted the crowd’s IQ. “Roses are red. Violets are blue. The reason I’m talking so slowly is because no one in [insert name of town he was appearing in] has passed grade 2!”
“I’d often apply my education during a match,” he wrote in his book, “Head Games: Football’s Concussion Crisis.“ In a match in Bridgeport, Conn., I assaulted [my opponent] with a human skeleton, ripped off the skull, got down on bended knee, and began reciting Hamlet. Those were good times.”
Those good times ended abruptly, however, during a match with Bubba Ray Dudley at the Hartford Civic Center in Connecticut in 2003. Even though pro wrestling matches are rehearsed, and the blows aren’t real, accidents happen. Mr. Dudley mistakenly kicked Dr. Nowinski in the jaw with enough force to put him on his back and make the whole ring shake.
“Holy shit, kid! You okay?” asked the referee. Before a foggy Dr. Nowinski could reply, 300-pound Mr. Dudley crashed down on him, hooked his leg, and the ref began counting, “One! Two! …” Dr. Nowinski instinctively kicked out but had forgotten the rest of the script. He managed to finish the match and stagger backstage.
His coherence and awareness gradually returned, but a “throbbing headache” persisted. A locker room doctor said he might have a concussion and recommended he wait to see how he felt before wrestling in Albany, N.Y., the next evening.
The following day the headache had subsided, but he still felt “a little strange.” Nonetheless, he told the doctor he was fine and strutted out to again battle Bubba Ray, this time in a match where he eventually got thrown through a ringside table and suffered the Dudley Death Drop. Afterward, “I crawled backstage and laid down. The headache was much, much worse.”
An event and a process
Dr. Nowinski continued to insist he was “fine” and wrestled a few more matches in the following days before finally acknowledging something was wrong. He’d had his bell rung numerous times in football, but this was different. Even more worrisome, none of the doctors he consulted could give him any definitive answers. He finally found his way to Emerson Hospital, where Dr. Cantu was the chief of neurosurgery.
“I remember that day vividly,” said Dr. Cantu. “Chris was this big, strapping, handsome guy – a hell of an athlete whose star was rising. He didn’t realize that he’d suffered a series of concussions and that trying to push through them was the worst thing he could be doing.”
Concussions and their effects were misunderstood by many athletes, coaches, and even physicians back then. It was assumed that the quarter inch of bone surrounding the adult brain provided adequate protection from common sports impacts and that any aftereffects were temporary. A common treatment was smelling salts and a pat on the back as the athlete returned to action.
However, the brain floats inside the skull in a bath of cerebral fluid. Any significant impact causes it to slosh violently from side to side, damaging tissue, synapses, and cells resulting in inflammation that can manifest as confusion and brain fog.
“A concussion is actually not defined by a physical injury,” explained Dr. Nowinski, “but by a loss of brain function that is induced by trauma. Concussion is not just an event, but also a process.” It’s almost as if the person has suffered a small seizure.
Fortunately, most concussion symptoms resolve within 2 weeks, but in some cases, especially if there’s been additional head trauma, they can persist, causing anxiety, depression, anger, and/or sleep disorders. Known as postconcussion syndrome (PCS), this is what Dr. Nowinski was unknowingly suffering from when he consulted Dr. Cantu.
In fact, one night it an Indianapolis hotel, weeks after his initial concussion, he awoke to find himself on the floor and the room in shambles. His girlfriend was yelling his name and shaking him. She told him he’d been having a nightmare and had suddenly started screaming and tearing up the room. “I didn’t remember any of it,” he said.
Dr. Cantu eventually advised Dr. Nowinski against ever returning to the ring or any activity with the risk for head injury. Research shows that sustaining a single significant concussion increases the risk of subsequent more-severe brain injuries.
“My diagnosis could have sent Chris off the deep end because he could no longer do what he wanted to do with this life,” said Dr. Cantu. “But instead, he used it as a tool to find meaning for his life.”
Dr. Nowinski decided to use his experience as a teaching opportunity, not just for other athletes but also for sports organizations and the medical community.
His book, which focused on the NFL’s “tobacco-industry-like refusal to acknowledge the depths of the problem,” was published in 2006. A year later, Dr. Nowinski partnered with Dr. Cantu to found the Sports Legacy Institute, which eventually became the Concussion Legacy Foundation (CLF).
Cold calling for brain donations
Robert Stern, PhD, is another highly respected authority in the study of neurodegenerative disease. In 2007, he was directing the clinical core of Boston University’s Alzheimer’s Disease Center. After giving a lecture to a group of financial planners and elder-law attorneys one morning, he got a request for a private meeting from a fellow named Chris Nowinski.
“I’d never heard of him, but I agreed,” recalled Dr. Stern, a professor of neurology, neurosurgery, anatomy, and neurobiology at Boston University. “A few days later, this larger-than-life guy walked into our conference room at the BU School of Medicine, exuding a great deal of passion, intellect, and determination. He told me his story and then started talking about the long-term consequences of concussions in sports.”
Dr. Stern had seen patients with dementia pugilistica, the old-school term for CTE. These were mostly boxers with cognitive and behavioral impairment. “But I had not heard about football players,” he said. “I hadn’t put the two together. And as I was listening to Chris, I realized if what he was saying was true then it was not only a potentially huge public health issue, but it was also a potentially huge scientific issue in the field of neurodegenerative disease.”
Dr. Nowinski introduced Dr. Stern to Dr. Cantu, and together with Ann McKee, MD, professor of neurology and pathology at BU, they cofounded the Center for the Study of Traumatic Encephalopathy (CSTE) in 2008. It was the first center of its kind devoted to the study of CTE in the world.
One of Dr. Nowinski’s first jobs at the CSTE was soliciting and procuring brain donations. Since CTE is generally a progressive condition that can take decades to manifest, autopsy was the only way to detect it.
The brains of two former Pittsburgh Steelers, Mike Webster and Terry Long, had been examined after their untimely deaths. After immunostaining, investigators found both former NFL players had “protein misfolds” characteristic of CTE.
This finding drew a lot of public and scientific attention, given that Mr. Long died by suicide and Mr. Webster was homeless when he died of a heart attack. But more scientific evidence was needed to prove a causal link between the head trauma and CTE.
Dr. Nowinski scoured obituaries looking for potential brains to study. When he found one, he would cold call the family and try to convince them to donate it to science. The first brain he secured for the center belonged to John Grimsley, a former NFL linebacker who in 2008 died at age 45 of an accidental gunshot wound. Often, Dr. Nowinski would even be the courier, traveling to pick up the brain after it had been harvested.
Over the next 10 years, Dr. Nowinski and his research team secured 500 brain donations. The research that resulted was staggering. In the beginning only 45 cases of CTE had been identified in the world, but in the first 111 NFL players who were autopsied, 110 had the disorder.
Of the first 53 college football players autopsied, 48 had CTE. Although Dr. Nowinski’s initial focus was football, evidence of CTE was soon detected among athletes in boxing, hockey, soccer, and rugby, as well as in combat veterans. However, the National Football League and other governing sports bodies initially denied any connection between sport-related head trauma and CTE.
Cumulative damage
In 2017, after 7 years of study, Dr. Nowinski earned a PhD in neurology. As the scientific evidence continued to accumulate, two shifts occurred that Dr. Stern said represent Dr. Nowinski’s greatest contributions. First, concussion is now widely recognized as an acute brain injury with symptoms that need to be immediately diagnosed and addressed.
“This is a completely different story from where things were just 10 years ago,” said Dr. Stern, “and Chris played a central role, if not the central role, in raising awareness about that.”
All 50 states and the District of Columbia now have laws regarding sports-related concussion. And there are brain banks in Australia, Canada, New Zealand, Brazil, and the United Kingdom studying CTE. More than 2,500 athletes in a variety of sports, including NASCAR’s Dale Earnhardt Jr. and NFL hall of famer Nick Buoniconti, have publicly pledged to donate their brains to science after their deaths.
Second, said Dr. Stern, we now know that although concussions can contribute to CTE, they are not the sole cause. It’s repetitive subconcussive trauma, without symptoms of concussion, that do the most damage.
“These happen during every practice and in every game,” said Dr. Stern. In fact, it’s estimated that pro football players suffer thousands of subconcussive incidents over the course of their careers. So, a player doesn’t have to see stars or lose consciousness to suffer brain damage; small impacts can accumulate over time.
Understanding this point is crucial for making youth sports safer. “Chris has played a critical role in raising awareness here, too,” said Dr. Stern. “Allowing our kids to get hit in the head over and over can put them at greater risk for later problems, plus it just doesn’t make common sense.”
“The biggest misconception surrounding head trauma in sports,” said Dr. Nowinski, “is the belief among players, coaches, and even the medical and scientific communities that if you get hit in the head and don’t have any symptoms then you’re okay and there hasn’t been any damage. That couldn’t be further from the truth. We now know that people are suffering serious brain injuries due to the accumulated effect of subconcussive impacts, and we need to get the word out about that.”
A major initiative from the Concussion Legacy Foundation called “Stop Hitting Kids in the Head” has the goal of convincing every sport to eliminate repetitive head impacts in players under age 14 – the time when the skull and brain are still developing and most vulnerable – by 2026. In fact, Dr. Nowinski wrote that “there could be a lot of kids who are misdiagnosed and medicated for various behavioral or emotional problems that may actually be head injury–related.”
Starting in 2009, the NFL adopted a series of rule changes designed to better protect its players against repeated head trauma. Among them is a ban on spearing or leading with the helmet, penalties for hitting defenseless players, and more stringent return-to-play guidelines, including concussion protocols.
The NFL has also put more emphasis on flag football options for youngsters and, for the first time, showcased this alternative in the 2023 Pro Bowl. But Dr. Nowinski is pressuring the league to go further. “While acknowledging that the game causes CTE, the NFL still underwrites recruiting 5-year-olds to play tackle football,” he said. “In my opinion, that’s unethical, and it needs to be addressed.”
WWE one of the most responsive organizations
Dr. Nowinski said WWE has been one of the most responsive sports organizations for protecting athletes. A doctor is now ringside at every match as is an observer who knows the script, thereby allowing for instant medical intervention if something goes wrong. “Since everyone is trying to look like they have a concussion all the time, it takes a deep understanding of the business to recognize a real one,” he said.
But this hasn’t been the case with other sports. “I am eternally disappointed in the response of the professional sports industry to the knowledge of CTE and long-term concussion symptoms,” said Dr. Nowinski.
“For example, FIFA [international soccer’s governing body] still doesn’t allow doctors to evaluate [potentially concussed] players on the sidelines and put them back in the game with a free substitution [if they’re deemed okay]. Not giving players proper medical care for a brain injury is unethical,” he said. BU’s Center for the Study of Traumatic Encephalopathy diagnosed the first CTE case in soccer in 2012, and in 2015 Dr. Nowinski successfully lobbied U.S. Soccer to ban heading the ball before age 11.
“Unfortunately, many governing bodies have circled the wagons in denying their sport causes CTE,” he continued. “FIFA, World Rugby, the NHL, even the NCAA and International Olympic Committee refuse to acknowledge it and, therefore, aren’t taking any steps to prevent it. They see it as a threat to their business model. Hopefully, now that the NIH and CDC are aligned about the risks of head impact in sports, this will begin to change.”
Meanwhile, research is continuing. Scientists are getting closer to being able to diagnose CTE in living humans, with ongoing studies using PET scans, blood markers, and spinal fluid markers. In 2019, researchers identified tau proteins specific to CTE that they believe are distinct from those of Alzheimer’s and other neurodegenerative diseases. Next step would be developing a drug to slow the development of CTE once detected.
Nonetheless, athletes at all levels in impact sports still don’t fully appreciate the risks of repeated head trauma and especially subconcussive blows. “I talk to former NFL and college players every week,” said Dr. Stern. “Some tell me, ‘I love the sport, it gave me so much, and I would do it again, but I’m not letting my grandchildren play.’ But others say, ‘As long as they know the risks, they can make their own decision.’ “
Dr. Nowinski has a daughter who is 4 and a son who’s 2. Both play soccer but, thanks to dad, heading isn’t allowed in their age groups. If they continue playing sports, Dr. Nowinski said he’ll make sure they understand the risks and how to protect themselves. This is a conversation all parents should have with their kids at every level to make sure they play safe, he added.
Those in the medical community can also volunteer their time to explain head trauma to athletes, coaches, and school administrators to be sure they understand its seriousness and are doing everything to protect players.
As you watch this year’s Super Bowl, Dr. Nowinski and his team would like you to keep something in mind. Those young men on the field for your entertainment are receiving mild brain trauma repeatedly throughout the game.
Even if it’s not a huge hit that gets replayed and makes everyone gasp, even if no one gets ushered into the little sideline tent for a concussion screening, even if no one loses consciousness, brain damage is still occurring. Watch the heads of the players during every play and think about what’s going on inside their skulls regardless of how big and strong those helmets look.
A version of this article first appeared on Medscape.com.
On Oct. 5, 2022, at 10:24 a.m., Chris Nowinski, PhD, cofounder of the Boston-based Concussion Legacy Foundation (CLF), was in his home office when the email came through.
“I pounded my desk, shouted YES! and went to find my wife so I could pick her up and give her a big hug,” he recalled. “It was the culmination of 15 years of research and hard work.”
Robert Cantu, MD, who has been studying head trauma for 50+ years and has published more than 500 papers about it, compares the announcement to the 1964 Surgeon General’s report that linked cigarette smoking with lung cancer and heart disease. With the NIH and the Centers of Disease Control and Prevention (CDC) now in agreement about the risks of participating in impact sports and activities, he said, “We’ve reached a tipping point that should finally prompt deniers such as the NHL, NCAA, FIFA, World Rugby, the International Olympic Committee, and other [sports organizations] to remove all unnecessary head trauma from their sports.”
“A lot of the credit for this must go to Chris,” added Dr. Cantu, medical director and director of clinical research at the Cantu Concussion Center at Emerson Hospital in Concord, Mass. “Clinicians like myself can reach only so many people by writing papers and giving speeches at medical conferences. For this to happen, the message needed to get out to parents, athletes, and society in general. And Chris was the vehicle for doing that.”
Dr. Nowinski didn’t set out to be the messenger. He played football at Harvard in the late 1990s, making second-team All-Ivy as a defensive tackle his senior year. In 2000, he enrolled in Killer Kowalski’s Wrestling Institute and eventually joined Vince McMahon’s World Wrestling Entertainment (WWE).
There he played the role of 295-pound villain “Chris Harvard,” an intellectual snob who dressed in crimson tights and insulted the crowd’s IQ. “Roses are red. Violets are blue. The reason I’m talking so slowly is because no one in [insert name of town he was appearing in] has passed grade 2!”
“I’d often apply my education during a match,” he wrote in his book, “Head Games: Football’s Concussion Crisis.“ In a match in Bridgeport, Conn., I assaulted [my opponent] with a human skeleton, ripped off the skull, got down on bended knee, and began reciting Hamlet. Those were good times.”
Those good times ended abruptly, however, during a match with Bubba Ray Dudley at the Hartford Civic Center in Connecticut in 2003. Even though pro wrestling matches are rehearsed, and the blows aren’t real, accidents happen. Mr. Dudley mistakenly kicked Dr. Nowinski in the jaw with enough force to put him on his back and make the whole ring shake.
“Holy shit, kid! You okay?” asked the referee. Before a foggy Dr. Nowinski could reply, 300-pound Mr. Dudley crashed down on him, hooked his leg, and the ref began counting, “One! Two! …” Dr. Nowinski instinctively kicked out but had forgotten the rest of the script. He managed to finish the match and stagger backstage.
His coherence and awareness gradually returned, but a “throbbing headache” persisted. A locker room doctor said he might have a concussion and recommended he wait to see how he felt before wrestling in Albany, N.Y., the next evening.
The following day the headache had subsided, but he still felt “a little strange.” Nonetheless, he told the doctor he was fine and strutted out to again battle Bubba Ray, this time in a match where he eventually got thrown through a ringside table and suffered the Dudley Death Drop. Afterward, “I crawled backstage and laid down. The headache was much, much worse.”
An event and a process
Dr. Nowinski continued to insist he was “fine” and wrestled a few more matches in the following days before finally acknowledging something was wrong. He’d had his bell rung numerous times in football, but this was different. Even more worrisome, none of the doctors he consulted could give him any definitive answers. He finally found his way to Emerson Hospital, where Dr. Cantu was the chief of neurosurgery.
“I remember that day vividly,” said Dr. Cantu. “Chris was this big, strapping, handsome guy – a hell of an athlete whose star was rising. He didn’t realize that he’d suffered a series of concussions and that trying to push through them was the worst thing he could be doing.”
Concussions and their effects were misunderstood by many athletes, coaches, and even physicians back then. It was assumed that the quarter inch of bone surrounding the adult brain provided adequate protection from common sports impacts and that any aftereffects were temporary. A common treatment was smelling salts and a pat on the back as the athlete returned to action.
However, the brain floats inside the skull in a bath of cerebral fluid. Any significant impact causes it to slosh violently from side to side, damaging tissue, synapses, and cells resulting in inflammation that can manifest as confusion and brain fog.
“A concussion is actually not defined by a physical injury,” explained Dr. Nowinski, “but by a loss of brain function that is induced by trauma. Concussion is not just an event, but also a process.” It’s almost as if the person has suffered a small seizure.
Fortunately, most concussion symptoms resolve within 2 weeks, but in some cases, especially if there’s been additional head trauma, they can persist, causing anxiety, depression, anger, and/or sleep disorders. Known as postconcussion syndrome (PCS), this is what Dr. Nowinski was unknowingly suffering from when he consulted Dr. Cantu.
In fact, one night it an Indianapolis hotel, weeks after his initial concussion, he awoke to find himself on the floor and the room in shambles. His girlfriend was yelling his name and shaking him. She told him he’d been having a nightmare and had suddenly started screaming and tearing up the room. “I didn’t remember any of it,” he said.
Dr. Cantu eventually advised Dr. Nowinski against ever returning to the ring or any activity with the risk for head injury. Research shows that sustaining a single significant concussion increases the risk of subsequent more-severe brain injuries.
“My diagnosis could have sent Chris off the deep end because he could no longer do what he wanted to do with this life,” said Dr. Cantu. “But instead, he used it as a tool to find meaning for his life.”
Dr. Nowinski decided to use his experience as a teaching opportunity, not just for other athletes but also for sports organizations and the medical community.
His book, which focused on the NFL’s “tobacco-industry-like refusal to acknowledge the depths of the problem,” was published in 2006. A year later, Dr. Nowinski partnered with Dr. Cantu to found the Sports Legacy Institute, which eventually became the Concussion Legacy Foundation (CLF).
Cold calling for brain donations
Robert Stern, PhD, is another highly respected authority in the study of neurodegenerative disease. In 2007, he was directing the clinical core of Boston University’s Alzheimer’s Disease Center. After giving a lecture to a group of financial planners and elder-law attorneys one morning, he got a request for a private meeting from a fellow named Chris Nowinski.
“I’d never heard of him, but I agreed,” recalled Dr. Stern, a professor of neurology, neurosurgery, anatomy, and neurobiology at Boston University. “A few days later, this larger-than-life guy walked into our conference room at the BU School of Medicine, exuding a great deal of passion, intellect, and determination. He told me his story and then started talking about the long-term consequences of concussions in sports.”
Dr. Stern had seen patients with dementia pugilistica, the old-school term for CTE. These were mostly boxers with cognitive and behavioral impairment. “But I had not heard about football players,” he said. “I hadn’t put the two together. And as I was listening to Chris, I realized if what he was saying was true then it was not only a potentially huge public health issue, but it was also a potentially huge scientific issue in the field of neurodegenerative disease.”
Dr. Nowinski introduced Dr. Stern to Dr. Cantu, and together with Ann McKee, MD, professor of neurology and pathology at BU, they cofounded the Center for the Study of Traumatic Encephalopathy (CSTE) in 2008. It was the first center of its kind devoted to the study of CTE in the world.
One of Dr. Nowinski’s first jobs at the CSTE was soliciting and procuring brain donations. Since CTE is generally a progressive condition that can take decades to manifest, autopsy was the only way to detect it.
The brains of two former Pittsburgh Steelers, Mike Webster and Terry Long, had been examined after their untimely deaths. After immunostaining, investigators found both former NFL players had “protein misfolds” characteristic of CTE.
This finding drew a lot of public and scientific attention, given that Mr. Long died by suicide and Mr. Webster was homeless when he died of a heart attack. But more scientific evidence was needed to prove a causal link between the head trauma and CTE.
Dr. Nowinski scoured obituaries looking for potential brains to study. When he found one, he would cold call the family and try to convince them to donate it to science. The first brain he secured for the center belonged to John Grimsley, a former NFL linebacker who in 2008 died at age 45 of an accidental gunshot wound. Often, Dr. Nowinski would even be the courier, traveling to pick up the brain after it had been harvested.
Over the next 10 years, Dr. Nowinski and his research team secured 500 brain donations. The research that resulted was staggering. In the beginning only 45 cases of CTE had been identified in the world, but in the first 111 NFL players who were autopsied, 110 had the disorder.
Of the first 53 college football players autopsied, 48 had CTE. Although Dr. Nowinski’s initial focus was football, evidence of CTE was soon detected among athletes in boxing, hockey, soccer, and rugby, as well as in combat veterans. However, the National Football League and other governing sports bodies initially denied any connection between sport-related head trauma and CTE.
Cumulative damage
In 2017, after 7 years of study, Dr. Nowinski earned a PhD in neurology. As the scientific evidence continued to accumulate, two shifts occurred that Dr. Stern said represent Dr. Nowinski’s greatest contributions. First, concussion is now widely recognized as an acute brain injury with symptoms that need to be immediately diagnosed and addressed.
“This is a completely different story from where things were just 10 years ago,” said Dr. Stern, “and Chris played a central role, if not the central role, in raising awareness about that.”
All 50 states and the District of Columbia now have laws regarding sports-related concussion. And there are brain banks in Australia, Canada, New Zealand, Brazil, and the United Kingdom studying CTE. More than 2,500 athletes in a variety of sports, including NASCAR’s Dale Earnhardt Jr. and NFL hall of famer Nick Buoniconti, have publicly pledged to donate their brains to science after their deaths.
Second, said Dr. Stern, we now know that although concussions can contribute to CTE, they are not the sole cause. It’s repetitive subconcussive trauma, without symptoms of concussion, that do the most damage.
“These happen during every practice and in every game,” said Dr. Stern. In fact, it’s estimated that pro football players suffer thousands of subconcussive incidents over the course of their careers. So, a player doesn’t have to see stars or lose consciousness to suffer brain damage; small impacts can accumulate over time.
Understanding this point is crucial for making youth sports safer. “Chris has played a critical role in raising awareness here, too,” said Dr. Stern. “Allowing our kids to get hit in the head over and over can put them at greater risk for later problems, plus it just doesn’t make common sense.”
“The biggest misconception surrounding head trauma in sports,” said Dr. Nowinski, “is the belief among players, coaches, and even the medical and scientific communities that if you get hit in the head and don’t have any symptoms then you’re okay and there hasn’t been any damage. That couldn’t be further from the truth. We now know that people are suffering serious brain injuries due to the accumulated effect of subconcussive impacts, and we need to get the word out about that.”
A major initiative from the Concussion Legacy Foundation called “Stop Hitting Kids in the Head” has the goal of convincing every sport to eliminate repetitive head impacts in players under age 14 – the time when the skull and brain are still developing and most vulnerable – by 2026. In fact, Dr. Nowinski wrote that “there could be a lot of kids who are misdiagnosed and medicated for various behavioral or emotional problems that may actually be head injury–related.”
Starting in 2009, the NFL adopted a series of rule changes designed to better protect its players against repeated head trauma. Among them is a ban on spearing or leading with the helmet, penalties for hitting defenseless players, and more stringent return-to-play guidelines, including concussion protocols.
The NFL has also put more emphasis on flag football options for youngsters and, for the first time, showcased this alternative in the 2023 Pro Bowl. But Dr. Nowinski is pressuring the league to go further. “While acknowledging that the game causes CTE, the NFL still underwrites recruiting 5-year-olds to play tackle football,” he said. “In my opinion, that’s unethical, and it needs to be addressed.”
WWE one of the most responsive organizations
Dr. Nowinski said WWE has been one of the most responsive sports organizations for protecting athletes. A doctor is now ringside at every match as is an observer who knows the script, thereby allowing for instant medical intervention if something goes wrong. “Since everyone is trying to look like they have a concussion all the time, it takes a deep understanding of the business to recognize a real one,” he said.
But this hasn’t been the case with other sports. “I am eternally disappointed in the response of the professional sports industry to the knowledge of CTE and long-term concussion symptoms,” said Dr. Nowinski.
“For example, FIFA [international soccer’s governing body] still doesn’t allow doctors to evaluate [potentially concussed] players on the sidelines and put them back in the game with a free substitution [if they’re deemed okay]. Not giving players proper medical care for a brain injury is unethical,” he said. BU’s Center for the Study of Traumatic Encephalopathy diagnosed the first CTE case in soccer in 2012, and in 2015 Dr. Nowinski successfully lobbied U.S. Soccer to ban heading the ball before age 11.
“Unfortunately, many governing bodies have circled the wagons in denying their sport causes CTE,” he continued. “FIFA, World Rugby, the NHL, even the NCAA and International Olympic Committee refuse to acknowledge it and, therefore, aren’t taking any steps to prevent it. They see it as a threat to their business model. Hopefully, now that the NIH and CDC are aligned about the risks of head impact in sports, this will begin to change.”
Meanwhile, research is continuing. Scientists are getting closer to being able to diagnose CTE in living humans, with ongoing studies using PET scans, blood markers, and spinal fluid markers. In 2019, researchers identified tau proteins specific to CTE that they believe are distinct from those of Alzheimer’s and other neurodegenerative diseases. Next step would be developing a drug to slow the development of CTE once detected.
Nonetheless, athletes at all levels in impact sports still don’t fully appreciate the risks of repeated head trauma and especially subconcussive blows. “I talk to former NFL and college players every week,” said Dr. Stern. “Some tell me, ‘I love the sport, it gave me so much, and I would do it again, but I’m not letting my grandchildren play.’ But others say, ‘As long as they know the risks, they can make their own decision.’ “
Dr. Nowinski has a daughter who is 4 and a son who’s 2. Both play soccer but, thanks to dad, heading isn’t allowed in their age groups. If they continue playing sports, Dr. Nowinski said he’ll make sure they understand the risks and how to protect themselves. This is a conversation all parents should have with their kids at every level to make sure they play safe, he added.
Those in the medical community can also volunteer their time to explain head trauma to athletes, coaches, and school administrators to be sure they understand its seriousness and are doing everything to protect players.
As you watch this year’s Super Bowl, Dr. Nowinski and his team would like you to keep something in mind. Those young men on the field for your entertainment are receiving mild brain trauma repeatedly throughout the game.
Even if it’s not a huge hit that gets replayed and makes everyone gasp, even if no one gets ushered into the little sideline tent for a concussion screening, even if no one loses consciousness, brain damage is still occurring. Watch the heads of the players during every play and think about what’s going on inside their skulls regardless of how big and strong those helmets look.
A version of this article first appeared on Medscape.com.
On Oct. 5, 2022, at 10:24 a.m., Chris Nowinski, PhD, cofounder of the Boston-based Concussion Legacy Foundation (CLF), was in his home office when the email came through.
“I pounded my desk, shouted YES! and went to find my wife so I could pick her up and give her a big hug,” he recalled. “It was the culmination of 15 years of research and hard work.”
Robert Cantu, MD, who has been studying head trauma for 50+ years and has published more than 500 papers about it, compares the announcement to the 1964 Surgeon General’s report that linked cigarette smoking with lung cancer and heart disease. With the NIH and the Centers of Disease Control and Prevention (CDC) now in agreement about the risks of participating in impact sports and activities, he said, “We’ve reached a tipping point that should finally prompt deniers such as the NHL, NCAA, FIFA, World Rugby, the International Olympic Committee, and other [sports organizations] to remove all unnecessary head trauma from their sports.”
“A lot of the credit for this must go to Chris,” added Dr. Cantu, medical director and director of clinical research at the Cantu Concussion Center at Emerson Hospital in Concord, Mass. “Clinicians like myself can reach only so many people by writing papers and giving speeches at medical conferences. For this to happen, the message needed to get out to parents, athletes, and society in general. And Chris was the vehicle for doing that.”
Dr. Nowinski didn’t set out to be the messenger. He played football at Harvard in the late 1990s, making second-team All-Ivy as a defensive tackle his senior year. In 2000, he enrolled in Killer Kowalski’s Wrestling Institute and eventually joined Vince McMahon’s World Wrestling Entertainment (WWE).
There he played the role of 295-pound villain “Chris Harvard,” an intellectual snob who dressed in crimson tights and insulted the crowd’s IQ. “Roses are red. Violets are blue. The reason I’m talking so slowly is because no one in [insert name of town he was appearing in] has passed grade 2!”
“I’d often apply my education during a match,” he wrote in his book, “Head Games: Football’s Concussion Crisis.“ In a match in Bridgeport, Conn., I assaulted [my opponent] with a human skeleton, ripped off the skull, got down on bended knee, and began reciting Hamlet. Those were good times.”
Those good times ended abruptly, however, during a match with Bubba Ray Dudley at the Hartford Civic Center in Connecticut in 2003. Even though pro wrestling matches are rehearsed, and the blows aren’t real, accidents happen. Mr. Dudley mistakenly kicked Dr. Nowinski in the jaw with enough force to put him on his back and make the whole ring shake.
“Holy shit, kid! You okay?” asked the referee. Before a foggy Dr. Nowinski could reply, 300-pound Mr. Dudley crashed down on him, hooked his leg, and the ref began counting, “One! Two! …” Dr. Nowinski instinctively kicked out but had forgotten the rest of the script. He managed to finish the match and stagger backstage.
His coherence and awareness gradually returned, but a “throbbing headache” persisted. A locker room doctor said he might have a concussion and recommended he wait to see how he felt before wrestling in Albany, N.Y., the next evening.
The following day the headache had subsided, but he still felt “a little strange.” Nonetheless, he told the doctor he was fine and strutted out to again battle Bubba Ray, this time in a match where he eventually got thrown through a ringside table and suffered the Dudley Death Drop. Afterward, “I crawled backstage and laid down. The headache was much, much worse.”
An event and a process
Dr. Nowinski continued to insist he was “fine” and wrestled a few more matches in the following days before finally acknowledging something was wrong. He’d had his bell rung numerous times in football, but this was different. Even more worrisome, none of the doctors he consulted could give him any definitive answers. He finally found his way to Emerson Hospital, where Dr. Cantu was the chief of neurosurgery.
“I remember that day vividly,” said Dr. Cantu. “Chris was this big, strapping, handsome guy – a hell of an athlete whose star was rising. He didn’t realize that he’d suffered a series of concussions and that trying to push through them was the worst thing he could be doing.”
Concussions and their effects were misunderstood by many athletes, coaches, and even physicians back then. It was assumed that the quarter inch of bone surrounding the adult brain provided adequate protection from common sports impacts and that any aftereffects were temporary. A common treatment was smelling salts and a pat on the back as the athlete returned to action.
However, the brain floats inside the skull in a bath of cerebral fluid. Any significant impact causes it to slosh violently from side to side, damaging tissue, synapses, and cells resulting in inflammation that can manifest as confusion and brain fog.
“A concussion is actually not defined by a physical injury,” explained Dr. Nowinski, “but by a loss of brain function that is induced by trauma. Concussion is not just an event, but also a process.” It’s almost as if the person has suffered a small seizure.
Fortunately, most concussion symptoms resolve within 2 weeks, but in some cases, especially if there’s been additional head trauma, they can persist, causing anxiety, depression, anger, and/or sleep disorders. Known as postconcussion syndrome (PCS), this is what Dr. Nowinski was unknowingly suffering from when he consulted Dr. Cantu.
In fact, one night it an Indianapolis hotel, weeks after his initial concussion, he awoke to find himself on the floor and the room in shambles. His girlfriend was yelling his name and shaking him. She told him he’d been having a nightmare and had suddenly started screaming and tearing up the room. “I didn’t remember any of it,” he said.
Dr. Cantu eventually advised Dr. Nowinski against ever returning to the ring or any activity with the risk for head injury. Research shows that sustaining a single significant concussion increases the risk of subsequent more-severe brain injuries.
“My diagnosis could have sent Chris off the deep end because he could no longer do what he wanted to do with this life,” said Dr. Cantu. “But instead, he used it as a tool to find meaning for his life.”
Dr. Nowinski decided to use his experience as a teaching opportunity, not just for other athletes but also for sports organizations and the medical community.
His book, which focused on the NFL’s “tobacco-industry-like refusal to acknowledge the depths of the problem,” was published in 2006. A year later, Dr. Nowinski partnered with Dr. Cantu to found the Sports Legacy Institute, which eventually became the Concussion Legacy Foundation (CLF).
Cold calling for brain donations
Robert Stern, PhD, is another highly respected authority in the study of neurodegenerative disease. In 2007, he was directing the clinical core of Boston University’s Alzheimer’s Disease Center. After giving a lecture to a group of financial planners and elder-law attorneys one morning, he got a request for a private meeting from a fellow named Chris Nowinski.
“I’d never heard of him, but I agreed,” recalled Dr. Stern, a professor of neurology, neurosurgery, anatomy, and neurobiology at Boston University. “A few days later, this larger-than-life guy walked into our conference room at the BU School of Medicine, exuding a great deal of passion, intellect, and determination. He told me his story and then started talking about the long-term consequences of concussions in sports.”
Dr. Stern had seen patients with dementia pugilistica, the old-school term for CTE. These were mostly boxers with cognitive and behavioral impairment. “But I had not heard about football players,” he said. “I hadn’t put the two together. And as I was listening to Chris, I realized if what he was saying was true then it was not only a potentially huge public health issue, but it was also a potentially huge scientific issue in the field of neurodegenerative disease.”
Dr. Nowinski introduced Dr. Stern to Dr. Cantu, and together with Ann McKee, MD, professor of neurology and pathology at BU, they cofounded the Center for the Study of Traumatic Encephalopathy (CSTE) in 2008. It was the first center of its kind devoted to the study of CTE in the world.
One of Dr. Nowinski’s first jobs at the CSTE was soliciting and procuring brain donations. Since CTE is generally a progressive condition that can take decades to manifest, autopsy was the only way to detect it.
The brains of two former Pittsburgh Steelers, Mike Webster and Terry Long, had been examined after their untimely deaths. After immunostaining, investigators found both former NFL players had “protein misfolds” characteristic of CTE.
This finding drew a lot of public and scientific attention, given that Mr. Long died by suicide and Mr. Webster was homeless when he died of a heart attack. But more scientific evidence was needed to prove a causal link between the head trauma and CTE.
Dr. Nowinski scoured obituaries looking for potential brains to study. When he found one, he would cold call the family and try to convince them to donate it to science. The first brain he secured for the center belonged to John Grimsley, a former NFL linebacker who in 2008 died at age 45 of an accidental gunshot wound. Often, Dr. Nowinski would even be the courier, traveling to pick up the brain after it had been harvested.
Over the next 10 years, Dr. Nowinski and his research team secured 500 brain donations. The research that resulted was staggering. In the beginning only 45 cases of CTE had been identified in the world, but in the first 111 NFL players who were autopsied, 110 had the disorder.
Of the first 53 college football players autopsied, 48 had CTE. Although Dr. Nowinski’s initial focus was football, evidence of CTE was soon detected among athletes in boxing, hockey, soccer, and rugby, as well as in combat veterans. However, the National Football League and other governing sports bodies initially denied any connection between sport-related head trauma and CTE.
Cumulative damage
In 2017, after 7 years of study, Dr. Nowinski earned a PhD in neurology. As the scientific evidence continued to accumulate, two shifts occurred that Dr. Stern said represent Dr. Nowinski’s greatest contributions. First, concussion is now widely recognized as an acute brain injury with symptoms that need to be immediately diagnosed and addressed.
“This is a completely different story from where things were just 10 years ago,” said Dr. Stern, “and Chris played a central role, if not the central role, in raising awareness about that.”
All 50 states and the District of Columbia now have laws regarding sports-related concussion. And there are brain banks in Australia, Canada, New Zealand, Brazil, and the United Kingdom studying CTE. More than 2,500 athletes in a variety of sports, including NASCAR’s Dale Earnhardt Jr. and NFL hall of famer Nick Buoniconti, have publicly pledged to donate their brains to science after their deaths.
Second, said Dr. Stern, we now know that although concussions can contribute to CTE, they are not the sole cause. It’s repetitive subconcussive trauma, without symptoms of concussion, that do the most damage.
“These happen during every practice and in every game,” said Dr. Stern. In fact, it’s estimated that pro football players suffer thousands of subconcussive incidents over the course of their careers. So, a player doesn’t have to see stars or lose consciousness to suffer brain damage; small impacts can accumulate over time.
Understanding this point is crucial for making youth sports safer. “Chris has played a critical role in raising awareness here, too,” said Dr. Stern. “Allowing our kids to get hit in the head over and over can put them at greater risk for later problems, plus it just doesn’t make common sense.”
“The biggest misconception surrounding head trauma in sports,” said Dr. Nowinski, “is the belief among players, coaches, and even the medical and scientific communities that if you get hit in the head and don’t have any symptoms then you’re okay and there hasn’t been any damage. That couldn’t be further from the truth. We now know that people are suffering serious brain injuries due to the accumulated effect of subconcussive impacts, and we need to get the word out about that.”
A major initiative from the Concussion Legacy Foundation called “Stop Hitting Kids in the Head” has the goal of convincing every sport to eliminate repetitive head impacts in players under age 14 – the time when the skull and brain are still developing and most vulnerable – by 2026. In fact, Dr. Nowinski wrote that “there could be a lot of kids who are misdiagnosed and medicated for various behavioral or emotional problems that may actually be head injury–related.”
Starting in 2009, the NFL adopted a series of rule changes designed to better protect its players against repeated head trauma. Among them is a ban on spearing or leading with the helmet, penalties for hitting defenseless players, and more stringent return-to-play guidelines, including concussion protocols.
The NFL has also put more emphasis on flag football options for youngsters and, for the first time, showcased this alternative in the 2023 Pro Bowl. But Dr. Nowinski is pressuring the league to go further. “While acknowledging that the game causes CTE, the NFL still underwrites recruiting 5-year-olds to play tackle football,” he said. “In my opinion, that’s unethical, and it needs to be addressed.”
WWE one of the most responsive organizations
Dr. Nowinski said WWE has been one of the most responsive sports organizations for protecting athletes. A doctor is now ringside at every match as is an observer who knows the script, thereby allowing for instant medical intervention if something goes wrong. “Since everyone is trying to look like they have a concussion all the time, it takes a deep understanding of the business to recognize a real one,” he said.
But this hasn’t been the case with other sports. “I am eternally disappointed in the response of the professional sports industry to the knowledge of CTE and long-term concussion symptoms,” said Dr. Nowinski.
“For example, FIFA [international soccer’s governing body] still doesn’t allow doctors to evaluate [potentially concussed] players on the sidelines and put them back in the game with a free substitution [if they’re deemed okay]. Not giving players proper medical care for a brain injury is unethical,” he said. BU’s Center for the Study of Traumatic Encephalopathy diagnosed the first CTE case in soccer in 2012, and in 2015 Dr. Nowinski successfully lobbied U.S. Soccer to ban heading the ball before age 11.
“Unfortunately, many governing bodies have circled the wagons in denying their sport causes CTE,” he continued. “FIFA, World Rugby, the NHL, even the NCAA and International Olympic Committee refuse to acknowledge it and, therefore, aren’t taking any steps to prevent it. They see it as a threat to their business model. Hopefully, now that the NIH and CDC are aligned about the risks of head impact in sports, this will begin to change.”
Meanwhile, research is continuing. Scientists are getting closer to being able to diagnose CTE in living humans, with ongoing studies using PET scans, blood markers, and spinal fluid markers. In 2019, researchers identified tau proteins specific to CTE that they believe are distinct from those of Alzheimer’s and other neurodegenerative diseases. Next step would be developing a drug to slow the development of CTE once detected.
Nonetheless, athletes at all levels in impact sports still don’t fully appreciate the risks of repeated head trauma and especially subconcussive blows. “I talk to former NFL and college players every week,” said Dr. Stern. “Some tell me, ‘I love the sport, it gave me so much, and I would do it again, but I’m not letting my grandchildren play.’ But others say, ‘As long as they know the risks, they can make their own decision.’ “
Dr. Nowinski has a daughter who is 4 and a son who’s 2. Both play soccer but, thanks to dad, heading isn’t allowed in their age groups. If they continue playing sports, Dr. Nowinski said he’ll make sure they understand the risks and how to protect themselves. This is a conversation all parents should have with their kids at every level to make sure they play safe, he added.
Those in the medical community can also volunteer their time to explain head trauma to athletes, coaches, and school administrators to be sure they understand its seriousness and are doing everything to protect players.
As you watch this year’s Super Bowl, Dr. Nowinski and his team would like you to keep something in mind. Those young men on the field for your entertainment are receiving mild brain trauma repeatedly throughout the game.
Even if it’s not a huge hit that gets replayed and makes everyone gasp, even if no one gets ushered into the little sideline tent for a concussion screening, even if no one loses consciousness, brain damage is still occurring. Watch the heads of the players during every play and think about what’s going on inside their skulls regardless of how big and strong those helmets look.
A version of this article first appeared on Medscape.com.
Must-read acute care medicine articles from 2022
When 2022 began, we started seeing some light at the end of the COVID-19 tunnel. Vaccines were widely available, and even with new variants of the virus still occasionally emerging, the rates of severe morbidity and mortality appeared to be decreasing.
Expectedly, journals appeared to start moving more toward mainstream topics and publications rather than what seemed like a major focus on COVID-19 publications. The resulting literature was fantastic.
Several of those topics were discussed in a prior Emergency Medicine Viewpoint from this news organization, and many more of the research advances of 2022 will be discussed in the near future. However, in this Viewpoint, I would like to present my annual review of my three “must-read” articles of the past year.
As in past years, I am choosing reviews of the literature rather than original research articles (which, all too often, become outdated or debunked within a few years). I choose these articles in the hopes that readers will not simply settle for my brief reviews of the key points but instead will feel compelled to download and read the entire articles. These publications address common conditions and quandaries we face in the daily practice of emergency medicine and are practice-changing.
Myocardial dysfunction after cardiac arrest: Tips and pitfalls
The management of post–cardiac arrest patients remains a hot topic in the resuscitation literature as we continue to understand that the immediate post-arrest period is critical to patient outcome.
Ortuno and colleagues reviewed the current literature on post-arrest care and wrote an outstanding summary of how to optimally care for these patients. More specifically, they focused on post-arrest patients who demonstrate continued shock, or “post–cardiac arrest myocardial dysfunction” (PCAMD).
They propose three mechanisms for the pathogenesis of PCAMD: ischemia reperfusion phenomenon, systemic inflammatory response, and increased catecholamine release
I will skip through the details of the pathophysiology that they describe in the article, but I certainly do recommend that everyone review their descriptions.
Management of these patients begins with a good hemodynamic assessment, which includes clinical markers of perfusion (blood pressure, capillary refill), ECG, and point-of-care ultrasound (POCUS). If the initial assessment reveals an obvious cause of the cardiac arrest (e.g., massive pulmonary embolism, myocardial infarction, pericardial tamponade), then the underlying cause should be treated expeditiously.
In the absence of an obvious treatable cause of the shock, the fluid status and cardiac function should be addressed with POCUS. If the patient is hypovolemic, intravenous fluids should be administered. If the fluid status is adequate, POCUS should be used to estimate the patient’s ventricular function. If the ventricle appears to be hyperdynamic with good contractility, shock should be treated with norepinephrine. On the other hand, if the ventricle is hypodynamic, dobutamine should be substituted for norepinephrine or, more often, added to norepinephrine.
The above represents a simplified summary of the critical points, but the authors do delve into further detail and also discuss some other options for therapies, including steroids, coronary revascularization, extracorporeal membrane oxygenation, and so on. The review is very thoughtful, thorough, and definitely worth a full read.
Top myths of diagnosis and management of infectious diseases in hospital medicine
Most, if not all of us in medicine, have heard the saying that 50% of what we learn in medical school (or residency) will turn out to be wrong. I certainly believe in this concept and consequently, like many of you, I enjoy reading about myths and misconceptions that we have been taught. With that in mind, I have to say that I love this article because it seems to have been written specifically to address what I was taught!
This author group, consisting mostly of clinical PharmDs who are experts in antibiotic use, provide us with an evidence-based discussion of myths and pitfalls in how antibiotics are often used in current clinical practice. The authors review their top 10 myths involving the use of antibiotics in treating infections in the hospital setting. A few of these relate more to the inpatient setting, but here are my favorite emergency department (ED)–related myths that they address:
- “Antibiotics do no harm.” The authors address the risk-benefit of antibiotics based on assumed vs. confirmed infections, including a brief discussion of adverse drug effects.
- “Antibiotic durations of 7, 14, or 21 days are typically necessary.” The authors address appropriate duration of antibiotic use and the fact that unnecessarily long durations of use can lead to resistance. They also provide reassurance that some infections can be treated with quite short durations of antibiotics.
- “If one drug is good, two (or more!) is better.” The use of multiple antibiotics, often with overlapping bacterial coverage, is rampant in medicine and further increases the risk for adverse drug effects and resistance.
- “Oral antibiotics are not as good as intravenous antibiotics for hospitalized patients.” This is definitely a myth that I learned. I recall being taught by many senior physicians that anyone sick enough for admission should be treated with intravenous antibiotics. As it turns out, absorption and effectiveness of most oral antibiotics is just as good as intravenous antibiotics, and the oral formulations are often safer.
- “A history of a penicillin allergy means the patient can never receive a beta-lactam antibiotic.” This is a myth that was debunked quite a few years ago, but it seems that many clinicians still need a reminder.
The authors included five more myths that are worth the read. This is an article that needs to be disseminated among all hospital clinicians.
Guidelines for low-risk, recurrent abdominal pain in the emergency department
The Society for Academic Emergency Medicine (SAEM) recently initiated a program focused on creating evidence-based approaches to challenging chief complaints and presentations in the emergency department (ED). In 2021, they published an approach to managing patients with recurrent, low-risk chest pain in the ED. This past year, they published their second guideline, focused on the management of patients with low-risk, recurrent abdominal pain in the ED.
Recurrent low-risk abdominal pain is a common and vexing presentation to EDs around the world, and there is little prior published guidance. Do all of these patients need repeat imaging? How do we manage their pain? Are there nonabdominal conditions that should be considered?
Broder and colleagues did a fantastic review of the current literature and, on behalf of SAEM, have provided a rational approach to optimal management of these patients. The four major questions they addressed, with brief summaries of their recommendations, are:
- Should adult ED patients with low-risk, recurrent and previously undifferentiated abdominal pain receive a repeat CT abdomen-pelvis (CTAP) after a negative CTAP within the past 12 months? This is a typical question that we all ponder when managing these patients. Unfortunately, the writing group found insufficient evidence to definitively identify populations in whom CTAP was recommended vs could be safely withheld. It is a bit disappointing that there is no definite answer to the question. On the other hand, it is reassuring to know that the world’s best evidence essentially says that it is perfectly appropriate to use your own good clinical judgment.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain with a negative CTAP receive additional imaging with abdominal ultrasound? In this case, the writing group found enough evidence, though low-level, to suggest against routine ultrasound in the absence of concern specifically for pelvic or hepatobiliary pathology. Like most tests, ultrasound is best used when there are specific concerns rather than being used in an undifferentiated fashion.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive screening for depression/anxiety? The writing group found enough evidence, though low-level again, to suggest that screening for depression and/or anxiety be performed during the ED evaluation. This could lead to successful therapy for the abdominal pain.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive nonopioid and/or nonpharmacologic analgesics? The writing group found little evidence to suggest for or against these analgesics, but they made a consensus recommendation suggesting an opioid-minimizing strategy for pain control.
Although the final recommendations of the writing group were not definitive or based on the strongest level of evidence, I find it helpful to have this guidance, nevertheless, on behalf of a major national organization. I also find it helpful to know that even with the best evidence available, optimal patient care will often boil down to physician experience and gestalt. I should also add that the overall article is chock-full of pearls and helpful information that will further inform the readers’ decisions, and so the full version is definitely worth the read.
In summary
There you have it – my three favorite practice-changing articles of 2022. Although I have tried to provide key points here, the full discussions of those key points in the published articles will provide a great deal more education than I can offer in this brief write-up, and so I strongly encourage everyone to read the full versions. Please be sure to include in the comments section your own pick for favorite or must-read articles from the past year.
Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. She reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
When 2022 began, we started seeing some light at the end of the COVID-19 tunnel. Vaccines were widely available, and even with new variants of the virus still occasionally emerging, the rates of severe morbidity and mortality appeared to be decreasing.
Expectedly, journals appeared to start moving more toward mainstream topics and publications rather than what seemed like a major focus on COVID-19 publications. The resulting literature was fantastic.
Several of those topics were discussed in a prior Emergency Medicine Viewpoint from this news organization, and many more of the research advances of 2022 will be discussed in the near future. However, in this Viewpoint, I would like to present my annual review of my three “must-read” articles of the past year.
As in past years, I am choosing reviews of the literature rather than original research articles (which, all too often, become outdated or debunked within a few years). I choose these articles in the hopes that readers will not simply settle for my brief reviews of the key points but instead will feel compelled to download and read the entire articles. These publications address common conditions and quandaries we face in the daily practice of emergency medicine and are practice-changing.
Myocardial dysfunction after cardiac arrest: Tips and pitfalls
The management of post–cardiac arrest patients remains a hot topic in the resuscitation literature as we continue to understand that the immediate post-arrest period is critical to patient outcome.
Ortuno and colleagues reviewed the current literature on post-arrest care and wrote an outstanding summary of how to optimally care for these patients. More specifically, they focused on post-arrest patients who demonstrate continued shock, or “post–cardiac arrest myocardial dysfunction” (PCAMD).
They propose three mechanisms for the pathogenesis of PCAMD: ischemia reperfusion phenomenon, systemic inflammatory response, and increased catecholamine release
I will skip through the details of the pathophysiology that they describe in the article, but I certainly do recommend that everyone review their descriptions.
Management of these patients begins with a good hemodynamic assessment, which includes clinical markers of perfusion (blood pressure, capillary refill), ECG, and point-of-care ultrasound (POCUS). If the initial assessment reveals an obvious cause of the cardiac arrest (e.g., massive pulmonary embolism, myocardial infarction, pericardial tamponade), then the underlying cause should be treated expeditiously.
In the absence of an obvious treatable cause of the shock, the fluid status and cardiac function should be addressed with POCUS. If the patient is hypovolemic, intravenous fluids should be administered. If the fluid status is adequate, POCUS should be used to estimate the patient’s ventricular function. If the ventricle appears to be hyperdynamic with good contractility, shock should be treated with norepinephrine. On the other hand, if the ventricle is hypodynamic, dobutamine should be substituted for norepinephrine or, more often, added to norepinephrine.
The above represents a simplified summary of the critical points, but the authors do delve into further detail and also discuss some other options for therapies, including steroids, coronary revascularization, extracorporeal membrane oxygenation, and so on. The review is very thoughtful, thorough, and definitely worth a full read.
Top myths of diagnosis and management of infectious diseases in hospital medicine
Most, if not all of us in medicine, have heard the saying that 50% of what we learn in medical school (or residency) will turn out to be wrong. I certainly believe in this concept and consequently, like many of you, I enjoy reading about myths and misconceptions that we have been taught. With that in mind, I have to say that I love this article because it seems to have been written specifically to address what I was taught!
This author group, consisting mostly of clinical PharmDs who are experts in antibiotic use, provide us with an evidence-based discussion of myths and pitfalls in how antibiotics are often used in current clinical practice. The authors review their top 10 myths involving the use of antibiotics in treating infections in the hospital setting. A few of these relate more to the inpatient setting, but here are my favorite emergency department (ED)–related myths that they address:
- “Antibiotics do no harm.” The authors address the risk-benefit of antibiotics based on assumed vs. confirmed infections, including a brief discussion of adverse drug effects.
- “Antibiotic durations of 7, 14, or 21 days are typically necessary.” The authors address appropriate duration of antibiotic use and the fact that unnecessarily long durations of use can lead to resistance. They also provide reassurance that some infections can be treated with quite short durations of antibiotics.
- “If one drug is good, two (or more!) is better.” The use of multiple antibiotics, often with overlapping bacterial coverage, is rampant in medicine and further increases the risk for adverse drug effects and resistance.
- “Oral antibiotics are not as good as intravenous antibiotics for hospitalized patients.” This is definitely a myth that I learned. I recall being taught by many senior physicians that anyone sick enough for admission should be treated with intravenous antibiotics. As it turns out, absorption and effectiveness of most oral antibiotics is just as good as intravenous antibiotics, and the oral formulations are often safer.
- “A history of a penicillin allergy means the patient can never receive a beta-lactam antibiotic.” This is a myth that was debunked quite a few years ago, but it seems that many clinicians still need a reminder.
The authors included five more myths that are worth the read. This is an article that needs to be disseminated among all hospital clinicians.
Guidelines for low-risk, recurrent abdominal pain in the emergency department
The Society for Academic Emergency Medicine (SAEM) recently initiated a program focused on creating evidence-based approaches to challenging chief complaints and presentations in the emergency department (ED). In 2021, they published an approach to managing patients with recurrent, low-risk chest pain in the ED. This past year, they published their second guideline, focused on the management of patients with low-risk, recurrent abdominal pain in the ED.
Recurrent low-risk abdominal pain is a common and vexing presentation to EDs around the world, and there is little prior published guidance. Do all of these patients need repeat imaging? How do we manage their pain? Are there nonabdominal conditions that should be considered?
Broder and colleagues did a fantastic review of the current literature and, on behalf of SAEM, have provided a rational approach to optimal management of these patients. The four major questions they addressed, with brief summaries of their recommendations, are:
- Should adult ED patients with low-risk, recurrent and previously undifferentiated abdominal pain receive a repeat CT abdomen-pelvis (CTAP) after a negative CTAP within the past 12 months? This is a typical question that we all ponder when managing these patients. Unfortunately, the writing group found insufficient evidence to definitively identify populations in whom CTAP was recommended vs could be safely withheld. It is a bit disappointing that there is no definite answer to the question. On the other hand, it is reassuring to know that the world’s best evidence essentially says that it is perfectly appropriate to use your own good clinical judgment.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain with a negative CTAP receive additional imaging with abdominal ultrasound? In this case, the writing group found enough evidence, though low-level, to suggest against routine ultrasound in the absence of concern specifically for pelvic or hepatobiliary pathology. Like most tests, ultrasound is best used when there are specific concerns rather than being used in an undifferentiated fashion.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive screening for depression/anxiety? The writing group found enough evidence, though low-level again, to suggest that screening for depression and/or anxiety be performed during the ED evaluation. This could lead to successful therapy for the abdominal pain.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive nonopioid and/or nonpharmacologic analgesics? The writing group found little evidence to suggest for or against these analgesics, but they made a consensus recommendation suggesting an opioid-minimizing strategy for pain control.
Although the final recommendations of the writing group were not definitive or based on the strongest level of evidence, I find it helpful to have this guidance, nevertheless, on behalf of a major national organization. I also find it helpful to know that even with the best evidence available, optimal patient care will often boil down to physician experience and gestalt. I should also add that the overall article is chock-full of pearls and helpful information that will further inform the readers’ decisions, and so the full version is definitely worth the read.
In summary
There you have it – my three favorite practice-changing articles of 2022. Although I have tried to provide key points here, the full discussions of those key points in the published articles will provide a great deal more education than I can offer in this brief write-up, and so I strongly encourage everyone to read the full versions. Please be sure to include in the comments section your own pick for favorite or must-read articles from the past year.
Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. She reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
When 2022 began, we started seeing some light at the end of the COVID-19 tunnel. Vaccines were widely available, and even with new variants of the virus still occasionally emerging, the rates of severe morbidity and mortality appeared to be decreasing.
Expectedly, journals appeared to start moving more toward mainstream topics and publications rather than what seemed like a major focus on COVID-19 publications. The resulting literature was fantastic.
Several of those topics were discussed in a prior Emergency Medicine Viewpoint from this news organization, and many more of the research advances of 2022 will be discussed in the near future. However, in this Viewpoint, I would like to present my annual review of my three “must-read” articles of the past year.
As in past years, I am choosing reviews of the literature rather than original research articles (which, all too often, become outdated or debunked within a few years). I choose these articles in the hopes that readers will not simply settle for my brief reviews of the key points but instead will feel compelled to download and read the entire articles. These publications address common conditions and quandaries we face in the daily practice of emergency medicine and are practice-changing.
Myocardial dysfunction after cardiac arrest: Tips and pitfalls
The management of post–cardiac arrest patients remains a hot topic in the resuscitation literature as we continue to understand that the immediate post-arrest period is critical to patient outcome.
Ortuno and colleagues reviewed the current literature on post-arrest care and wrote an outstanding summary of how to optimally care for these patients. More specifically, they focused on post-arrest patients who demonstrate continued shock, or “post–cardiac arrest myocardial dysfunction” (PCAMD).
They propose three mechanisms for the pathogenesis of PCAMD: ischemia reperfusion phenomenon, systemic inflammatory response, and increased catecholamine release
I will skip through the details of the pathophysiology that they describe in the article, but I certainly do recommend that everyone review their descriptions.
Management of these patients begins with a good hemodynamic assessment, which includes clinical markers of perfusion (blood pressure, capillary refill), ECG, and point-of-care ultrasound (POCUS). If the initial assessment reveals an obvious cause of the cardiac arrest (e.g., massive pulmonary embolism, myocardial infarction, pericardial tamponade), then the underlying cause should be treated expeditiously.
In the absence of an obvious treatable cause of the shock, the fluid status and cardiac function should be addressed with POCUS. If the patient is hypovolemic, intravenous fluids should be administered. If the fluid status is adequate, POCUS should be used to estimate the patient’s ventricular function. If the ventricle appears to be hyperdynamic with good contractility, shock should be treated with norepinephrine. On the other hand, if the ventricle is hypodynamic, dobutamine should be substituted for norepinephrine or, more often, added to norepinephrine.
The above represents a simplified summary of the critical points, but the authors do delve into further detail and also discuss some other options for therapies, including steroids, coronary revascularization, extracorporeal membrane oxygenation, and so on. The review is very thoughtful, thorough, and definitely worth a full read.
Top myths of diagnosis and management of infectious diseases in hospital medicine
Most, if not all of us in medicine, have heard the saying that 50% of what we learn in medical school (or residency) will turn out to be wrong. I certainly believe in this concept and consequently, like many of you, I enjoy reading about myths and misconceptions that we have been taught. With that in mind, I have to say that I love this article because it seems to have been written specifically to address what I was taught!
This author group, consisting mostly of clinical PharmDs who are experts in antibiotic use, provide us with an evidence-based discussion of myths and pitfalls in how antibiotics are often used in current clinical practice. The authors review their top 10 myths involving the use of antibiotics in treating infections in the hospital setting. A few of these relate more to the inpatient setting, but here are my favorite emergency department (ED)–related myths that they address:
- “Antibiotics do no harm.” The authors address the risk-benefit of antibiotics based on assumed vs. confirmed infections, including a brief discussion of adverse drug effects.
- “Antibiotic durations of 7, 14, or 21 days are typically necessary.” The authors address appropriate duration of antibiotic use and the fact that unnecessarily long durations of use can lead to resistance. They also provide reassurance that some infections can be treated with quite short durations of antibiotics.
- “If one drug is good, two (or more!) is better.” The use of multiple antibiotics, often with overlapping bacterial coverage, is rampant in medicine and further increases the risk for adverse drug effects and resistance.
- “Oral antibiotics are not as good as intravenous antibiotics for hospitalized patients.” This is definitely a myth that I learned. I recall being taught by many senior physicians that anyone sick enough for admission should be treated with intravenous antibiotics. As it turns out, absorption and effectiveness of most oral antibiotics is just as good as intravenous antibiotics, and the oral formulations are often safer.
- “A history of a penicillin allergy means the patient can never receive a beta-lactam antibiotic.” This is a myth that was debunked quite a few years ago, but it seems that many clinicians still need a reminder.
The authors included five more myths that are worth the read. This is an article that needs to be disseminated among all hospital clinicians.
Guidelines for low-risk, recurrent abdominal pain in the emergency department
The Society for Academic Emergency Medicine (SAEM) recently initiated a program focused on creating evidence-based approaches to challenging chief complaints and presentations in the emergency department (ED). In 2021, they published an approach to managing patients with recurrent, low-risk chest pain in the ED. This past year, they published their second guideline, focused on the management of patients with low-risk, recurrent abdominal pain in the ED.
Recurrent low-risk abdominal pain is a common and vexing presentation to EDs around the world, and there is little prior published guidance. Do all of these patients need repeat imaging? How do we manage their pain? Are there nonabdominal conditions that should be considered?
Broder and colleagues did a fantastic review of the current literature and, on behalf of SAEM, have provided a rational approach to optimal management of these patients. The four major questions they addressed, with brief summaries of their recommendations, are:
- Should adult ED patients with low-risk, recurrent and previously undifferentiated abdominal pain receive a repeat CT abdomen-pelvis (CTAP) after a negative CTAP within the past 12 months? This is a typical question that we all ponder when managing these patients. Unfortunately, the writing group found insufficient evidence to definitively identify populations in whom CTAP was recommended vs could be safely withheld. It is a bit disappointing that there is no definite answer to the question. On the other hand, it is reassuring to know that the world’s best evidence essentially says that it is perfectly appropriate to use your own good clinical judgment.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain with a negative CTAP receive additional imaging with abdominal ultrasound? In this case, the writing group found enough evidence, though low-level, to suggest against routine ultrasound in the absence of concern specifically for pelvic or hepatobiliary pathology. Like most tests, ultrasound is best used when there are specific concerns rather than being used in an undifferentiated fashion.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive screening for depression/anxiety? The writing group found enough evidence, though low-level again, to suggest that screening for depression and/or anxiety be performed during the ED evaluation. This could lead to successful therapy for the abdominal pain.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive nonopioid and/or nonpharmacologic analgesics? The writing group found little evidence to suggest for or against these analgesics, but they made a consensus recommendation suggesting an opioid-minimizing strategy for pain control.
Although the final recommendations of the writing group were not definitive or based on the strongest level of evidence, I find it helpful to have this guidance, nevertheless, on behalf of a major national organization. I also find it helpful to know that even with the best evidence available, optimal patient care will often boil down to physician experience and gestalt. I should also add that the overall article is chock-full of pearls and helpful information that will further inform the readers’ decisions, and so the full version is definitely worth the read.
In summary
There you have it – my three favorite practice-changing articles of 2022. Although I have tried to provide key points here, the full discussions of those key points in the published articles will provide a great deal more education than I can offer in this brief write-up, and so I strongly encourage everyone to read the full versions. Please be sure to include in the comments section your own pick for favorite or must-read articles from the past year.
Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. She reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Doc never met patient who died from insect bite, but negligence suit moves forward; more
On-call specialist incurred a clear ‘duty of care,’ court rules
a state appeals court ruledThe appeals decision is the result of a case involving the late Dennis Blagden.
On July 26, 2017, Mr. Blagden arrived at the Graham Hospital ED, in Canton, Ill., complaining of neck pain and an insect bite that had resulted in a swollen elbow. His ED doctor, Matthew McMillin, MD, who worked for Coleman Medical Associates, ordered tests and prescribed an anti-inflammatory pain medication and a muscle relaxant.
Dr. McMillin consulted via telephone with Kenneth Krock, MD, an internal medicine specialist and pediatrician, who was on call that day and who enjoyed admitting privileges at Graham. (Krock was also an employee of Coleman Medical Associates, which provided clinical staffing for the hospital.)
Dr. Krock had final admitting authority in this instance. Court records show that Dr. McMillin and he agreed that the patient could be discharged from the ED, despite Krock’s differential diagnosis indicating a possible infection.
Three days later, now with “hypercapnic respiratory failure, sepsis, and an altered mental state,” Mr. Blagden was again seen at the Graham Hospital ED. Mr. Blagden underwent intubation by Dr. McMillin, his original ED doctor, and was airlifted to Methodist Medical Center, in Peoria, 30 miles away. There, an MRI showed that he’d developed a spinal epidural abscess. On Aug. 7, 2017, a little over a week after his admission to Methodist, Mr. Blagden died from complications of his infection.
In January 2019, Mr. Blagden’s wife, Judy, filed a suit against Dr. McMillin, his practice, and Graham Hospital, which is a part of Graham Health System. Her suit alleged medical negligence in the death of her husband.
About 6 months later, Mr.s Blagden amended her original complaint, adding a second count of medical negligence against Dr. Krock; his practice and employer, Coleman Medical Associates; and Graham Hospital. In her amended complaint, Mrs. Blagden alleged that although Krock hadn’t actually seen her husband Dennis, his consultation with Dr. McMillin was sufficient to establish a doctor-patient relationship and thus a legal duty of care. That duty, Mrs. Blagden further alleged, was breached when Dr. Krock failed both to rule out her husband’s “infectious process” and to admit him for proper follow-up monitoring.
In July 2021, after the case had been transferred from Peoria County to Fulton County, Dr. Krock cried foul. In a motion to the court for summary judgment – that is, a ruling prior to an actual trial – he and his practice put forth the following argument: As a mere on-call consultant that day in 2017, he had neither seen the patient nor established a relationship with him, thereby precluding his legal duty of care.
The trial court judge agreed and granted both Dr. Krock and Dr. Coleman the summary judgment they had sought.
Mrs. Blagden then appealed to the Appellate Court of Illinois, Fourth District, which is located in Springfield.
In its unanimous decision, the three-judge panel reversed the lower court’s ruling. Taking direct aim at Dr. Krock’s earlier motion, Justice Eugene Doherty, who wrote the panel’s opinion, said that state law had long established that “the special relationship giving rise to a duty of care may exist even in the absence of any meeting between the physician and the patient where the physician performs specific services for the benefit of the patient.”
As Justice Doherty explained, Dr. Krock’s status that day as both the on-call doctor and the one with final admitting authority undermined his argument for summary judgment. Also undermining it, Justice Doherty added, was the fact that the conversation between the two doctors that day in 2017 was a formal exchange “contemplated by hospital bylaws.”
“While public policy should encourage informal consultations between physicians,” the justice continued, “it must not ignore actual physician involvement in decisions that directly affect a patient’s care.”
Following the Fourth District decision, the suit against Dr. McMillin, Dr. Krock, and the other defendants has now been tossed back to the trial court for further proceedings. At press time, no trial date had been set.
Will this proposed damages cap help retain more physicians?
Fear of a doctor shortage, triggered in part by a recent history of large payouts, has prompted Iowa lawmakers to push for new state caps on medical malpractice awards, as a story in the Des Moines Register reports.
Currently, Iowa caps most noneconomic damages – including those for pain and suffering – at $250,000, which is among the lowest such caps in the nation.
Under existing Iowa law, however, the limit doesn’t apply in extraordinary cases – that is, those involving “substantial or permanent loss of body function, substantial disfigurement, or death.” It also isn’t applicable in cases in which a jury decides that a defendant acted with intentional malice.
Lawmakers and Iowa Gov. Kim Reynolds would like to change this.
Under a Senate bill that has now passed out of committee and is awaiting debate on the Senate floor, even plaintiffs involved in extreme cases would receive no more than $1 million to compensate for their pain, suffering, or emotional distress. (The bill also includes a 2.1% annual hike to compensate for inflation. A similar bill, which adds “loss of pregnancy” to the list of extreme cases, has advanced to the House floor.)
Supporters say the proposed cap would help to limit mega awards. In Johnson County in March 2022, for instance, a jury awarded $97.4 million to the parents of a young boy who sustained severe brain injuries during his delivery, causing the clinic that had been involved in the case to file for bankruptcy. This award was nearly three times the total payouts ($35 million) in the entire state of Iowa in all of 2021, a year in which there were 192 closed claims, including at least a dozen that resulted in payouts of $1 million or more.
Supporters also think the proposed cap will mitigate what they see as a looming doctor shortage, especially among ob.gyns. in eastern Iowa. “I just cannot overstate how much this is affecting our workforce, and that turns into effects for the women and the children, the babies, in our state,” Shannon Leveridge, MD, an obstetrician in Davenport said. “In order to keep these women and their babies safe, we need doctors.”
But critics of the bill, including some lawmakers and the trial bar, say it overreaches, even in the case of the $97.4 million award.
“They don’t want to talk about the actual damages that are caused by medical negligence,” explained a spokesman for the trial lawyers. “So, you don’t hear about the fact that, of the $50 million of economic damages ... most of that is going to go to the 24/7 care for this child for the rest of his life.”
A version of this article first appeared on Medscape.com.
On-call specialist incurred a clear ‘duty of care,’ court rules
a state appeals court ruledThe appeals decision is the result of a case involving the late Dennis Blagden.
On July 26, 2017, Mr. Blagden arrived at the Graham Hospital ED, in Canton, Ill., complaining of neck pain and an insect bite that had resulted in a swollen elbow. His ED doctor, Matthew McMillin, MD, who worked for Coleman Medical Associates, ordered tests and prescribed an anti-inflammatory pain medication and a muscle relaxant.
Dr. McMillin consulted via telephone with Kenneth Krock, MD, an internal medicine specialist and pediatrician, who was on call that day and who enjoyed admitting privileges at Graham. (Krock was also an employee of Coleman Medical Associates, which provided clinical staffing for the hospital.)
Dr. Krock had final admitting authority in this instance. Court records show that Dr. McMillin and he agreed that the patient could be discharged from the ED, despite Krock’s differential diagnosis indicating a possible infection.
Three days later, now with “hypercapnic respiratory failure, sepsis, and an altered mental state,” Mr. Blagden was again seen at the Graham Hospital ED. Mr. Blagden underwent intubation by Dr. McMillin, his original ED doctor, and was airlifted to Methodist Medical Center, in Peoria, 30 miles away. There, an MRI showed that he’d developed a spinal epidural abscess. On Aug. 7, 2017, a little over a week after his admission to Methodist, Mr. Blagden died from complications of his infection.
In January 2019, Mr. Blagden’s wife, Judy, filed a suit against Dr. McMillin, his practice, and Graham Hospital, which is a part of Graham Health System. Her suit alleged medical negligence in the death of her husband.
About 6 months later, Mr.s Blagden amended her original complaint, adding a second count of medical negligence against Dr. Krock; his practice and employer, Coleman Medical Associates; and Graham Hospital. In her amended complaint, Mrs. Blagden alleged that although Krock hadn’t actually seen her husband Dennis, his consultation with Dr. McMillin was sufficient to establish a doctor-patient relationship and thus a legal duty of care. That duty, Mrs. Blagden further alleged, was breached when Dr. Krock failed both to rule out her husband’s “infectious process” and to admit him for proper follow-up monitoring.
In July 2021, after the case had been transferred from Peoria County to Fulton County, Dr. Krock cried foul. In a motion to the court for summary judgment – that is, a ruling prior to an actual trial – he and his practice put forth the following argument: As a mere on-call consultant that day in 2017, he had neither seen the patient nor established a relationship with him, thereby precluding his legal duty of care.
The trial court judge agreed and granted both Dr. Krock and Dr. Coleman the summary judgment they had sought.
Mrs. Blagden then appealed to the Appellate Court of Illinois, Fourth District, which is located in Springfield.
In its unanimous decision, the three-judge panel reversed the lower court’s ruling. Taking direct aim at Dr. Krock’s earlier motion, Justice Eugene Doherty, who wrote the panel’s opinion, said that state law had long established that “the special relationship giving rise to a duty of care may exist even in the absence of any meeting between the physician and the patient where the physician performs specific services for the benefit of the patient.”
As Justice Doherty explained, Dr. Krock’s status that day as both the on-call doctor and the one with final admitting authority undermined his argument for summary judgment. Also undermining it, Justice Doherty added, was the fact that the conversation between the two doctors that day in 2017 was a formal exchange “contemplated by hospital bylaws.”
“While public policy should encourage informal consultations between physicians,” the justice continued, “it must not ignore actual physician involvement in decisions that directly affect a patient’s care.”
Following the Fourth District decision, the suit against Dr. McMillin, Dr. Krock, and the other defendants has now been tossed back to the trial court for further proceedings. At press time, no trial date had been set.
Will this proposed damages cap help retain more physicians?
Fear of a doctor shortage, triggered in part by a recent history of large payouts, has prompted Iowa lawmakers to push for new state caps on medical malpractice awards, as a story in the Des Moines Register reports.
Currently, Iowa caps most noneconomic damages – including those for pain and suffering – at $250,000, which is among the lowest such caps in the nation.
Under existing Iowa law, however, the limit doesn’t apply in extraordinary cases – that is, those involving “substantial or permanent loss of body function, substantial disfigurement, or death.” It also isn’t applicable in cases in which a jury decides that a defendant acted with intentional malice.
Lawmakers and Iowa Gov. Kim Reynolds would like to change this.
Under a Senate bill that has now passed out of committee and is awaiting debate on the Senate floor, even plaintiffs involved in extreme cases would receive no more than $1 million to compensate for their pain, suffering, or emotional distress. (The bill also includes a 2.1% annual hike to compensate for inflation. A similar bill, which adds “loss of pregnancy” to the list of extreme cases, has advanced to the House floor.)
Supporters say the proposed cap would help to limit mega awards. In Johnson County in March 2022, for instance, a jury awarded $97.4 million to the parents of a young boy who sustained severe brain injuries during his delivery, causing the clinic that had been involved in the case to file for bankruptcy. This award was nearly three times the total payouts ($35 million) in the entire state of Iowa in all of 2021, a year in which there were 192 closed claims, including at least a dozen that resulted in payouts of $1 million or more.
Supporters also think the proposed cap will mitigate what they see as a looming doctor shortage, especially among ob.gyns. in eastern Iowa. “I just cannot overstate how much this is affecting our workforce, and that turns into effects for the women and the children, the babies, in our state,” Shannon Leveridge, MD, an obstetrician in Davenport said. “In order to keep these women and their babies safe, we need doctors.”
But critics of the bill, including some lawmakers and the trial bar, say it overreaches, even in the case of the $97.4 million award.
“They don’t want to talk about the actual damages that are caused by medical negligence,” explained a spokesman for the trial lawyers. “So, you don’t hear about the fact that, of the $50 million of economic damages ... most of that is going to go to the 24/7 care for this child for the rest of his life.”
A version of this article first appeared on Medscape.com.
On-call specialist incurred a clear ‘duty of care,’ court rules
a state appeals court ruledThe appeals decision is the result of a case involving the late Dennis Blagden.
On July 26, 2017, Mr. Blagden arrived at the Graham Hospital ED, in Canton, Ill., complaining of neck pain and an insect bite that had resulted in a swollen elbow. His ED doctor, Matthew McMillin, MD, who worked for Coleman Medical Associates, ordered tests and prescribed an anti-inflammatory pain medication and a muscle relaxant.
Dr. McMillin consulted via telephone with Kenneth Krock, MD, an internal medicine specialist and pediatrician, who was on call that day and who enjoyed admitting privileges at Graham. (Krock was also an employee of Coleman Medical Associates, which provided clinical staffing for the hospital.)
Dr. Krock had final admitting authority in this instance. Court records show that Dr. McMillin and he agreed that the patient could be discharged from the ED, despite Krock’s differential diagnosis indicating a possible infection.
Three days later, now with “hypercapnic respiratory failure, sepsis, and an altered mental state,” Mr. Blagden was again seen at the Graham Hospital ED. Mr. Blagden underwent intubation by Dr. McMillin, his original ED doctor, and was airlifted to Methodist Medical Center, in Peoria, 30 miles away. There, an MRI showed that he’d developed a spinal epidural abscess. On Aug. 7, 2017, a little over a week after his admission to Methodist, Mr. Blagden died from complications of his infection.
In January 2019, Mr. Blagden’s wife, Judy, filed a suit against Dr. McMillin, his practice, and Graham Hospital, which is a part of Graham Health System. Her suit alleged medical negligence in the death of her husband.
About 6 months later, Mr.s Blagden amended her original complaint, adding a second count of medical negligence against Dr. Krock; his practice and employer, Coleman Medical Associates; and Graham Hospital. In her amended complaint, Mrs. Blagden alleged that although Krock hadn’t actually seen her husband Dennis, his consultation with Dr. McMillin was sufficient to establish a doctor-patient relationship and thus a legal duty of care. That duty, Mrs. Blagden further alleged, was breached when Dr. Krock failed both to rule out her husband’s “infectious process” and to admit him for proper follow-up monitoring.
In July 2021, after the case had been transferred from Peoria County to Fulton County, Dr. Krock cried foul. In a motion to the court for summary judgment – that is, a ruling prior to an actual trial – he and his practice put forth the following argument: As a mere on-call consultant that day in 2017, he had neither seen the patient nor established a relationship with him, thereby precluding his legal duty of care.
The trial court judge agreed and granted both Dr. Krock and Dr. Coleman the summary judgment they had sought.
Mrs. Blagden then appealed to the Appellate Court of Illinois, Fourth District, which is located in Springfield.
In its unanimous decision, the three-judge panel reversed the lower court’s ruling. Taking direct aim at Dr. Krock’s earlier motion, Justice Eugene Doherty, who wrote the panel’s opinion, said that state law had long established that “the special relationship giving rise to a duty of care may exist even in the absence of any meeting between the physician and the patient where the physician performs specific services for the benefit of the patient.”
As Justice Doherty explained, Dr. Krock’s status that day as both the on-call doctor and the one with final admitting authority undermined his argument for summary judgment. Also undermining it, Justice Doherty added, was the fact that the conversation between the two doctors that day in 2017 was a formal exchange “contemplated by hospital bylaws.”
“While public policy should encourage informal consultations between physicians,” the justice continued, “it must not ignore actual physician involvement in decisions that directly affect a patient’s care.”
Following the Fourth District decision, the suit against Dr. McMillin, Dr. Krock, and the other defendants has now been tossed back to the trial court for further proceedings. At press time, no trial date had been set.
Will this proposed damages cap help retain more physicians?
Fear of a doctor shortage, triggered in part by a recent history of large payouts, has prompted Iowa lawmakers to push for new state caps on medical malpractice awards, as a story in the Des Moines Register reports.
Currently, Iowa caps most noneconomic damages – including those for pain and suffering – at $250,000, which is among the lowest such caps in the nation.
Under existing Iowa law, however, the limit doesn’t apply in extraordinary cases – that is, those involving “substantial or permanent loss of body function, substantial disfigurement, or death.” It also isn’t applicable in cases in which a jury decides that a defendant acted with intentional malice.
Lawmakers and Iowa Gov. Kim Reynolds would like to change this.
Under a Senate bill that has now passed out of committee and is awaiting debate on the Senate floor, even plaintiffs involved in extreme cases would receive no more than $1 million to compensate for their pain, suffering, or emotional distress. (The bill also includes a 2.1% annual hike to compensate for inflation. A similar bill, which adds “loss of pregnancy” to the list of extreme cases, has advanced to the House floor.)
Supporters say the proposed cap would help to limit mega awards. In Johnson County in March 2022, for instance, a jury awarded $97.4 million to the parents of a young boy who sustained severe brain injuries during his delivery, causing the clinic that had been involved in the case to file for bankruptcy. This award was nearly three times the total payouts ($35 million) in the entire state of Iowa in all of 2021, a year in which there were 192 closed claims, including at least a dozen that resulted in payouts of $1 million or more.
Supporters also think the proposed cap will mitigate what they see as a looming doctor shortage, especially among ob.gyns. in eastern Iowa. “I just cannot overstate how much this is affecting our workforce, and that turns into effects for the women and the children, the babies, in our state,” Shannon Leveridge, MD, an obstetrician in Davenport said. “In order to keep these women and their babies safe, we need doctors.”
But critics of the bill, including some lawmakers and the trial bar, say it overreaches, even in the case of the $97.4 million award.
“They don’t want to talk about the actual damages that are caused by medical negligence,” explained a spokesman for the trial lawyers. “So, you don’t hear about the fact that, of the $50 million of economic damages ... most of that is going to go to the 24/7 care for this child for the rest of his life.”
A version of this article first appeared on Medscape.com.
A doctor intervenes in a fiery car crash
Emergencies happen anywhere, anytime, and sometimes physicians find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a Medscape series telling these stories.
I was coming off a 48-hour shift plus a day of doing outpatient sedation at Sparrow Hospital in Lansing. It was December and Michigan-cold.
I drove on the side of the road where I wasn’t really supposed to and got closer. An SUV had crashed into one of the big concrete structures under the bridge. I saw people running around but wasn’t able to spot EMS or any health care workers. From where I was, I could identify four kids who had already been extricated and one adult still in the driver’s seat. I estimated the kids’ ages were around 7, 5, 3, and an infant who was a few months old. I left my car and went to help.
I was able to peg the ages correctly because I’m a pediatric critical care physician. As a specialty, we’re not commonly known. We oversee patient care in intensive care units, except the patients are children. Part of the job is that we’re experts at triaging. We recognize what’s life-threatening and less so.
The kids were with some adults who kept them warm with blankets. I examined each of them. The infant was asleep but arousable and acting like a normal baby. The 3-year-old boy was vomiting and appeared very fatigued. The 5-year-old boy had a forehead laceration and was in and out of consciousness. The 7-year-old girl was screaming because of different injuries.
While all of the children were concerning to me, I identified one in particular: the 5-year-old boy. It was obvious he needed serious medical attention and fast. So, I kept that little guy in mind. The others had sustained significant injuries, but my best guess was they could get to a hospital and be stabilized.
That said, I’m a trauma instructor, and one of the things I always tell trainees is: Trauma is a black box. On the outside, it may seem like a patient doesn’t have a lot of injuries. But underneath, there might be something worse, like a brain injury. Or the chest might have taken a blunt impact affecting the heart. There may be internal bleeding somewhere in the belly. It’s really hard to tease out what exactly is going on without equipment and testing.
I didn’t even have a pulse oximeter or heart rate monitor. I pretty much just went by the appearance of the child: pulse, heart rate, awareness, things like that.
After the kids, I moved to look at the man in the car. The front end had already caught fire. I could see the driver – the kids’ father, I guessed – unconscious and hunched over. I was wondering, Why hasn’t this guy been extricated?
I approached the car on the front passenger side. And then I just had this feeling. I knew I needed to step back. Immediately.
I did. And a few seconds later, the whole car exploded in flames.
I believe God is in control of everything. I tried to get to that man. But the scene was unsafe. Later I learned that several people, including a young nurse at the scene, had tried to get to him as well.
When EMS came, I identified myself. Obviously, these people do very, very important work. But they may be more used to the 60-year-old heart attack, the 25-year-old gunshot wound, the occasional ill child. I thought that four kids – each with possible critical poly-traumatic injuries – posed a challenge to anyone.
I told them, “This is what I do on a daily basis, and this is the kid I’m worried about the most. The other kids are definitely worrisome, but I would prioritize getting this kid to the hospital first. Can I ride with you?” They agreed.
We got that boy and his older sister into the first ambulance (she was in a lot of pain, the result of a femur fracture). The two other kids rode in the second ambulance. The hospital where I had just left was 10 minutes away. I called the other pediatric critical care doctor there, my partner. He thought I was calling for a routine issue – no such luck. I said, “I’m with four kids who are level-1 traumas in two ambulances and I’m heading to the hospital right now, ETA 10 minutes.”
En route, I thought the little boy might lose consciousness at any moment. He needed a breathing tube, and I debated whether it should be done in the ambulance vs. waiting until we got to the emergency room. Based on my judgment and his vital signs, I elected to wait to have it done it in a more controlled environment. Had I felt like he was in immediate need of an airway, I would’ve attempted it. But those are the tough calls that you must make.
My partner had alerted the trauma and emergency medicine teams at the hospital. By the time we arrived, my partner was down in the ER with the trauma team and ER staff. Everyone was ready. Then it was like divide and conquer. He attended to one of the kids. The ER team and I were with the little guy I was really worried about. We had his breathing tube in within minutes. The trauma team attended to the other two.
All the kids were stabilized and then admitted to the pediatric intensive care unit. I’m happy to say that all of them did well in the end. Even the little guy I was worried about the most.
I must say this incident gave me perspective on what EMS goes through. The field medicine we do in the United States is still in its infancy in a lot of ways. One of the things I would love to see in the future is a mobile ICU. After a critical illness hits, sometimes you only have seconds, minutes, maybe hours if you’re lucky. The earlier you can get patients the treatment they need, the better the outcomes.
I like taking care of critically ill children and their families. It fits my personality. And it’s a wonderful cause. But you have to be ready for tragic cases like this one. Yes, the children came out alive, but the accident claimed a life in a horrible way. And there was nothing I could do about it.
Critical care takes an emotional, psychological, and physical toll. It’s a roller coaster: Some kids do well; some kids don’t do well. All I can do is hold myself accountable. I keep my emotions in check, whether the outcome is positive or negative. And I do my best.
Mohamed Hani Farhat, MD, is a pediatric critical care physician at the University of Michigan C.S. Mott Children’s Hospital in Ann Arbor and Sparrow Hospital in Lansing, Mich. Are you a physician with a dramatic medical story outside the clinic? Medscape would love to consider your story for Is There a Doctor in the House? Please email your contact information and a short summary of your story to access@webmd.net . A version of this article appeared on Medscape.com.
Emergencies happen anywhere, anytime, and sometimes physicians find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a Medscape series telling these stories.
I was coming off a 48-hour shift plus a day of doing outpatient sedation at Sparrow Hospital in Lansing. It was December and Michigan-cold.
I drove on the side of the road where I wasn’t really supposed to and got closer. An SUV had crashed into one of the big concrete structures under the bridge. I saw people running around but wasn’t able to spot EMS or any health care workers. From where I was, I could identify four kids who had already been extricated and one adult still in the driver’s seat. I estimated the kids’ ages were around 7, 5, 3, and an infant who was a few months old. I left my car and went to help.
I was able to peg the ages correctly because I’m a pediatric critical care physician. As a specialty, we’re not commonly known. We oversee patient care in intensive care units, except the patients are children. Part of the job is that we’re experts at triaging. We recognize what’s life-threatening and less so.
The kids were with some adults who kept them warm with blankets. I examined each of them. The infant was asleep but arousable and acting like a normal baby. The 3-year-old boy was vomiting and appeared very fatigued. The 5-year-old boy had a forehead laceration and was in and out of consciousness. The 7-year-old girl was screaming because of different injuries.
While all of the children were concerning to me, I identified one in particular: the 5-year-old boy. It was obvious he needed serious medical attention and fast. So, I kept that little guy in mind. The others had sustained significant injuries, but my best guess was they could get to a hospital and be stabilized.
That said, I’m a trauma instructor, and one of the things I always tell trainees is: Trauma is a black box. On the outside, it may seem like a patient doesn’t have a lot of injuries. But underneath, there might be something worse, like a brain injury. Or the chest might have taken a blunt impact affecting the heart. There may be internal bleeding somewhere in the belly. It’s really hard to tease out what exactly is going on without equipment and testing.
I didn’t even have a pulse oximeter or heart rate monitor. I pretty much just went by the appearance of the child: pulse, heart rate, awareness, things like that.
After the kids, I moved to look at the man in the car. The front end had already caught fire. I could see the driver – the kids’ father, I guessed – unconscious and hunched over. I was wondering, Why hasn’t this guy been extricated?
I approached the car on the front passenger side. And then I just had this feeling. I knew I needed to step back. Immediately.
I did. And a few seconds later, the whole car exploded in flames.
I believe God is in control of everything. I tried to get to that man. But the scene was unsafe. Later I learned that several people, including a young nurse at the scene, had tried to get to him as well.
When EMS came, I identified myself. Obviously, these people do very, very important work. But they may be more used to the 60-year-old heart attack, the 25-year-old gunshot wound, the occasional ill child. I thought that four kids – each with possible critical poly-traumatic injuries – posed a challenge to anyone.
I told them, “This is what I do on a daily basis, and this is the kid I’m worried about the most. The other kids are definitely worrisome, but I would prioritize getting this kid to the hospital first. Can I ride with you?” They agreed.
We got that boy and his older sister into the first ambulance (she was in a lot of pain, the result of a femur fracture). The two other kids rode in the second ambulance. The hospital where I had just left was 10 minutes away. I called the other pediatric critical care doctor there, my partner. He thought I was calling for a routine issue – no such luck. I said, “I’m with four kids who are level-1 traumas in two ambulances and I’m heading to the hospital right now, ETA 10 minutes.”
En route, I thought the little boy might lose consciousness at any moment. He needed a breathing tube, and I debated whether it should be done in the ambulance vs. waiting until we got to the emergency room. Based on my judgment and his vital signs, I elected to wait to have it done it in a more controlled environment. Had I felt like he was in immediate need of an airway, I would’ve attempted it. But those are the tough calls that you must make.
My partner had alerted the trauma and emergency medicine teams at the hospital. By the time we arrived, my partner was down in the ER with the trauma team and ER staff. Everyone was ready. Then it was like divide and conquer. He attended to one of the kids. The ER team and I were with the little guy I was really worried about. We had his breathing tube in within minutes. The trauma team attended to the other two.
All the kids were stabilized and then admitted to the pediatric intensive care unit. I’m happy to say that all of them did well in the end. Even the little guy I was worried about the most.
I must say this incident gave me perspective on what EMS goes through. The field medicine we do in the United States is still in its infancy in a lot of ways. One of the things I would love to see in the future is a mobile ICU. After a critical illness hits, sometimes you only have seconds, minutes, maybe hours if you’re lucky. The earlier you can get patients the treatment they need, the better the outcomes.
I like taking care of critically ill children and their families. It fits my personality. And it’s a wonderful cause. But you have to be ready for tragic cases like this one. Yes, the children came out alive, but the accident claimed a life in a horrible way. And there was nothing I could do about it.
Critical care takes an emotional, psychological, and physical toll. It’s a roller coaster: Some kids do well; some kids don’t do well. All I can do is hold myself accountable. I keep my emotions in check, whether the outcome is positive or negative. And I do my best.
Mohamed Hani Farhat, MD, is a pediatric critical care physician at the University of Michigan C.S. Mott Children’s Hospital in Ann Arbor and Sparrow Hospital in Lansing, Mich. Are you a physician with a dramatic medical story outside the clinic? Medscape would love to consider your story for Is There a Doctor in the House? Please email your contact information and a short summary of your story to access@webmd.net . A version of this article appeared on Medscape.com.
Emergencies happen anywhere, anytime, and sometimes physicians find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a Medscape series telling these stories.
I was coming off a 48-hour shift plus a day of doing outpatient sedation at Sparrow Hospital in Lansing. It was December and Michigan-cold.
I drove on the side of the road where I wasn’t really supposed to and got closer. An SUV had crashed into one of the big concrete structures under the bridge. I saw people running around but wasn’t able to spot EMS or any health care workers. From where I was, I could identify four kids who had already been extricated and one adult still in the driver’s seat. I estimated the kids’ ages were around 7, 5, 3, and an infant who was a few months old. I left my car and went to help.
I was able to peg the ages correctly because I’m a pediatric critical care physician. As a specialty, we’re not commonly known. We oversee patient care in intensive care units, except the patients are children. Part of the job is that we’re experts at triaging. We recognize what’s life-threatening and less so.
The kids were with some adults who kept them warm with blankets. I examined each of them. The infant was asleep but arousable and acting like a normal baby. The 3-year-old boy was vomiting and appeared very fatigued. The 5-year-old boy had a forehead laceration and was in and out of consciousness. The 7-year-old girl was screaming because of different injuries.
While all of the children were concerning to me, I identified one in particular: the 5-year-old boy. It was obvious he needed serious medical attention and fast. So, I kept that little guy in mind. The others had sustained significant injuries, but my best guess was they could get to a hospital and be stabilized.
That said, I’m a trauma instructor, and one of the things I always tell trainees is: Trauma is a black box. On the outside, it may seem like a patient doesn’t have a lot of injuries. But underneath, there might be something worse, like a brain injury. Or the chest might have taken a blunt impact affecting the heart. There may be internal bleeding somewhere in the belly. It’s really hard to tease out what exactly is going on without equipment and testing.
I didn’t even have a pulse oximeter or heart rate monitor. I pretty much just went by the appearance of the child: pulse, heart rate, awareness, things like that.
After the kids, I moved to look at the man in the car. The front end had already caught fire. I could see the driver – the kids’ father, I guessed – unconscious and hunched over. I was wondering, Why hasn’t this guy been extricated?
I approached the car on the front passenger side. And then I just had this feeling. I knew I needed to step back. Immediately.
I did. And a few seconds later, the whole car exploded in flames.
I believe God is in control of everything. I tried to get to that man. But the scene was unsafe. Later I learned that several people, including a young nurse at the scene, had tried to get to him as well.
When EMS came, I identified myself. Obviously, these people do very, very important work. But they may be more used to the 60-year-old heart attack, the 25-year-old gunshot wound, the occasional ill child. I thought that four kids – each with possible critical poly-traumatic injuries – posed a challenge to anyone.
I told them, “This is what I do on a daily basis, and this is the kid I’m worried about the most. The other kids are definitely worrisome, but I would prioritize getting this kid to the hospital first. Can I ride with you?” They agreed.
We got that boy and his older sister into the first ambulance (she was in a lot of pain, the result of a femur fracture). The two other kids rode in the second ambulance. The hospital where I had just left was 10 minutes away. I called the other pediatric critical care doctor there, my partner. He thought I was calling for a routine issue – no such luck. I said, “I’m with four kids who are level-1 traumas in two ambulances and I’m heading to the hospital right now, ETA 10 minutes.”
En route, I thought the little boy might lose consciousness at any moment. He needed a breathing tube, and I debated whether it should be done in the ambulance vs. waiting until we got to the emergency room. Based on my judgment and his vital signs, I elected to wait to have it done it in a more controlled environment. Had I felt like he was in immediate need of an airway, I would’ve attempted it. But those are the tough calls that you must make.
My partner had alerted the trauma and emergency medicine teams at the hospital. By the time we arrived, my partner was down in the ER with the trauma team and ER staff. Everyone was ready. Then it was like divide and conquer. He attended to one of the kids. The ER team and I were with the little guy I was really worried about. We had his breathing tube in within minutes. The trauma team attended to the other two.
All the kids were stabilized and then admitted to the pediatric intensive care unit. I’m happy to say that all of them did well in the end. Even the little guy I was worried about the most.
I must say this incident gave me perspective on what EMS goes through. The field medicine we do in the United States is still in its infancy in a lot of ways. One of the things I would love to see in the future is a mobile ICU. After a critical illness hits, sometimes you only have seconds, minutes, maybe hours if you’re lucky. The earlier you can get patients the treatment they need, the better the outcomes.
I like taking care of critically ill children and their families. It fits my personality. And it’s a wonderful cause. But you have to be ready for tragic cases like this one. Yes, the children came out alive, but the accident claimed a life in a horrible way. And there was nothing I could do about it.
Critical care takes an emotional, psychological, and physical toll. It’s a roller coaster: Some kids do well; some kids don’t do well. All I can do is hold myself accountable. I keep my emotions in check, whether the outcome is positive or negative. And I do my best.
Mohamed Hani Farhat, MD, is a pediatric critical care physician at the University of Michigan C.S. Mott Children’s Hospital in Ann Arbor and Sparrow Hospital in Lansing, Mich. Are you a physician with a dramatic medical story outside the clinic? Medscape would love to consider your story for Is There a Doctor in the House? Please email your contact information and a short summary of your story to access@webmd.net . A version of this article appeared on Medscape.com.
Infiltrating Wound Vacuum-Assisted Closure With Topical Amphotericin for Mucormycosis Infection of the Achilles Tendon
Vacuum-assisted closure (VAC) of wounds has become a foundational tool in the armamentarium of wound care specialists. Using a system consisting of a sponge, semi-occlusive barrier, and fluid collection device, VAC systems apply constant negative pressure resulting in macro and micro deformation to a wound, stabilization of the wound environment, and removal of inflammatory factors in wound fluid.1 These conditions allow for the removal of drainage and fluid from a wound bed, reduced edema and inflammation, reduced bacterial load, recruitment of healing factors, approximation of wound edges, and increased blood flow to the wound.2
In complex, infected wounds, a variation of negative pressure wound therapy (NPWT) via the instillation of topical antibiotics (instillation VAC) has been used.3 This variation has been advantageous even in soft tissue fungal infections. Early and aggressive treatment of such infections is critical to prevent dissemination, particularly in aggressive infections, such as mucormycosis.4 We present a case of a patient with a mucormycosis infection of his left Achilles tendon and overlying skin who was successfully treated with surgical debridement and wound care with instillation NPWT with topical amphotericin B.
Case Presentation
A 53-year-old man underwent left Achilles tendon reconstruction with allograft after a complete tear during exercise. He had no relevant medical history and was otherwise healthy, which he attributed to working out daily. About a week after the operation, he began having incisional breakdown, prompting presentation to an emergency department. There, he received IV antibiotics along with multiple debridements. After the wound failed to improve and intra-operative cultures grew mucormycosis, he was transferred to our facility for a higher level of care. On admission, he was immediately given IV amphotericin B and scheduled for repeat debridement.
After 1 prior debridement and 10 total days of IV amphotericin, a repeat debridement was performed. After the debridement, the installation VAC was applied to the patient’s left lower extremity wound with an instilling fluid of amphotericin B and the settings as follows: smart phase instill volume, 110 mL; soak time, 3.5 hours; target pressure, 125 mm Hg; intensity, low; and VAC therapy mode, continuous. After 5 days, the wound bed appeared clean without overt signs of infection. However, due to some toxicity to healthy surrounding soft tissue, the instillation VAC was discontinued and standard NPWT was started. The patient underwent 2 additional rounds of debridement with partial delayed closure. Four weeks after discontinuation of the instillation VAC, the wound appeared healthy and granulated so the patient underwent split-thickness skin grafting to the left posterior ankle. He subsequently completed a course of oral antifungal medication as an outpatient.
The patient was seen in the outpatient clinic for 14 months from the initial mucormycosis infection (Figure).
Discussion
Mucormycosis is an infection caused by fungi in the class Zygomycetes and of the order Mucorales that typically occurs in immunocompromised patients, especially those with diabetic ketoacidosis and neutropenia. Given that this patient had no relevant medical history and was otherwise healthy, he was at extremely low risk of this type of infection. In this patient’s case, the spores of this nonseptate hyphae wide-branching species were most likely introduced at the time of left Achilles tendon repair. Mucormycosis is progressive and can be fatal unless treated, with a mortality rate approaching 70%.5 The rarity and heterogeneity of mucormycosis make treatment variable.6 No prospective or randomized clinical trials exist in plastic surgery literature.
The use of wound VAC in combination with the instillation of amphotericin B to treat cutaneous mucormycosis is not well documented. Mucormycosis infections are traditionally addressed with surgical debridement and antifungal therapy, specifically IV amphotericin B.7,8 As previously noted, NPWT has become the gold standard in treating complex wounds.3 Additionally, wound VAC therapy with instillation has been noted in the literature as a reliable method to treat bacteria-infected wounds, providing a shorter treatment period and earlier wound closure.9 Instillation VAC therapy has proven particularly useful in complex, infected wounds, such as aggressive fungal infections.
Mucormycosis treatment is challenging particularly in the extremities as management must balance both mortality and limb salvage. In this case, the use of NPWT with wound VAC and intervals of instilling amphotericin B facilitated infection control in this lower extremity mucormycosis infection. The significant adverse effect profile of amphotericin B, particularly the nephrotoxicity, should be seriously considered when deciding the treatment regimen for patients affected by mucormycosis. Locally, topical amphotericin B has been reported to cause blistering, itchiness, redness, peeling, and dryness. However, topical preparations of amphotericin B are nontoxic unlike their IV counterpart, able to cross the physiological barriers of the skin while simultaneously targeting macrophages in the dermis and epidermis.10
Conclusions
Although the mainstay of treatment for systemic mucormycosis is radical debridement and IV amphotericin B, a more localized infection may benefit from an adjunct like an instillation wound VAC with topical amphotericin B, as presented in this case study. Swift treatment with wound VAC was beneficial in the overall recovery and tissue healing of this patient and may be beneficial in similar cases.
1. Normandin S, Safran T, Winocour S, et al. negative pressure wound therapy: mechanism of action and clinical applications. Semin Plast Surg. 2021;35(3):164-170. doi:10.1055/s-0041-1731792
2. Agarwal P, Kukrele R, Sharma D. Vacuum assisted closure (VAC)/negative pressure wound therapy (NPWT) for difficult wounds: a review. J Clin Orthop Trauma. 2019;10(5):845-848. doi:10.1016/j.jcot.2019.06.015
3. Gabriel A, Shores J, Bernstein B, et al. A clinical review of infected wound treatment with Vacuum Assisted Closure (V.A.C.) therapy: experience and case series. Int Wound J. 2009;6(suppl 2):1-25. doi:10.1111/j.1742-481X.2009.00628.x
4. Guégan S, Lanternier F, Rouzaud C, Dupin N, Lortholary O. Fungal skin and soft tissue infections. Curr Opin Infect Dis. 2016;29(2):124-130. doi:10.1097/QCO.0000000000000252
5. Ibrahim AS, Spellberg B, Walsh TJ, Kontoyiannis DP. Pathogenesis of mucormycosis. Clin Infect Dis. 2012;54(suppl 1):S16-S22. doi:10.1093/cid/cir865
6. Sipsas NV, Gamaletsou MN, Anastasopoulou A, Kontoyiannis DP. Therapy of mucormycosis. J Fungi (Basel). 2018;4(3):90. Published 2018 Jul 31. doi:10.3390/jof4030090
7. Spellberg B, Edwards J Jr, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005;18(3):556-569. doi:10.1128/CMR.18.3.556-569.2005
8. Losee JE, Selber J, Vega S, Hall C, Scott G, Serletti JM. Primary cutaneous mucormycosis: guide to surgical management. Ann Plast Surg. 2002;49(4):385-390. doi:10.1097/00000637-200210000-00009
9. Webb LX. New techniques in wound management: vacuum-assisted wound closure. J Am Acad Orthop Surg. 2002;10(5):303-311. doi:10.5435/00124635-200209000-00002
10. Varikuti S, Oghumu S, Saljoughian N, et al. Topical treatment with nanoliposomal Amphotericin B reduces early lesion growth but fails to induce cure in an experimental model of cutaneous leishmaniasis caused by Leishmania mexicana. Acta Trop. 2017;173:102-108. doi:10.1016/j.actatropica.2017.06.004
Vacuum-assisted closure (VAC) of wounds has become a foundational tool in the armamentarium of wound care specialists. Using a system consisting of a sponge, semi-occlusive barrier, and fluid collection device, VAC systems apply constant negative pressure resulting in macro and micro deformation to a wound, stabilization of the wound environment, and removal of inflammatory factors in wound fluid.1 These conditions allow for the removal of drainage and fluid from a wound bed, reduced edema and inflammation, reduced bacterial load, recruitment of healing factors, approximation of wound edges, and increased blood flow to the wound.2
In complex, infected wounds, a variation of negative pressure wound therapy (NPWT) via the instillation of topical antibiotics (instillation VAC) has been used.3 This variation has been advantageous even in soft tissue fungal infections. Early and aggressive treatment of such infections is critical to prevent dissemination, particularly in aggressive infections, such as mucormycosis.4 We present a case of a patient with a mucormycosis infection of his left Achilles tendon and overlying skin who was successfully treated with surgical debridement and wound care with instillation NPWT with topical amphotericin B.
Case Presentation
A 53-year-old man underwent left Achilles tendon reconstruction with allograft after a complete tear during exercise. He had no relevant medical history and was otherwise healthy, which he attributed to working out daily. About a week after the operation, he began having incisional breakdown, prompting presentation to an emergency department. There, he received IV antibiotics along with multiple debridements. After the wound failed to improve and intra-operative cultures grew mucormycosis, he was transferred to our facility for a higher level of care. On admission, he was immediately given IV amphotericin B and scheduled for repeat debridement.
After 1 prior debridement and 10 total days of IV amphotericin, a repeat debridement was performed. After the debridement, the installation VAC was applied to the patient’s left lower extremity wound with an instilling fluid of amphotericin B and the settings as follows: smart phase instill volume, 110 mL; soak time, 3.5 hours; target pressure, 125 mm Hg; intensity, low; and VAC therapy mode, continuous. After 5 days, the wound bed appeared clean without overt signs of infection. However, due to some toxicity to healthy surrounding soft tissue, the instillation VAC was discontinued and standard NPWT was started. The patient underwent 2 additional rounds of debridement with partial delayed closure. Four weeks after discontinuation of the instillation VAC, the wound appeared healthy and granulated so the patient underwent split-thickness skin grafting to the left posterior ankle. He subsequently completed a course of oral antifungal medication as an outpatient.
The patient was seen in the outpatient clinic for 14 months from the initial mucormycosis infection (Figure).
Discussion
Mucormycosis is an infection caused by fungi in the class Zygomycetes and of the order Mucorales that typically occurs in immunocompromised patients, especially those with diabetic ketoacidosis and neutropenia. Given that this patient had no relevant medical history and was otherwise healthy, he was at extremely low risk of this type of infection. In this patient’s case, the spores of this nonseptate hyphae wide-branching species were most likely introduced at the time of left Achilles tendon repair. Mucormycosis is progressive and can be fatal unless treated, with a mortality rate approaching 70%.5 The rarity and heterogeneity of mucormycosis make treatment variable.6 No prospective or randomized clinical trials exist in plastic surgery literature.
The use of wound VAC in combination with the instillation of amphotericin B to treat cutaneous mucormycosis is not well documented. Mucormycosis infections are traditionally addressed with surgical debridement and antifungal therapy, specifically IV amphotericin B.7,8 As previously noted, NPWT has become the gold standard in treating complex wounds.3 Additionally, wound VAC therapy with instillation has been noted in the literature as a reliable method to treat bacteria-infected wounds, providing a shorter treatment period and earlier wound closure.9 Instillation VAC therapy has proven particularly useful in complex, infected wounds, such as aggressive fungal infections.
Mucormycosis treatment is challenging particularly in the extremities as management must balance both mortality and limb salvage. In this case, the use of NPWT with wound VAC and intervals of instilling amphotericin B facilitated infection control in this lower extremity mucormycosis infection. The significant adverse effect profile of amphotericin B, particularly the nephrotoxicity, should be seriously considered when deciding the treatment regimen for patients affected by mucormycosis. Locally, topical amphotericin B has been reported to cause blistering, itchiness, redness, peeling, and dryness. However, topical preparations of amphotericin B are nontoxic unlike their IV counterpart, able to cross the physiological barriers of the skin while simultaneously targeting macrophages in the dermis and epidermis.10
Conclusions
Although the mainstay of treatment for systemic mucormycosis is radical debridement and IV amphotericin B, a more localized infection may benefit from an adjunct like an instillation wound VAC with topical amphotericin B, as presented in this case study. Swift treatment with wound VAC was beneficial in the overall recovery and tissue healing of this patient and may be beneficial in similar cases.
Vacuum-assisted closure (VAC) of wounds has become a foundational tool in the armamentarium of wound care specialists. Using a system consisting of a sponge, semi-occlusive barrier, and fluid collection device, VAC systems apply constant negative pressure resulting in macro and micro deformation to a wound, stabilization of the wound environment, and removal of inflammatory factors in wound fluid.1 These conditions allow for the removal of drainage and fluid from a wound bed, reduced edema and inflammation, reduced bacterial load, recruitment of healing factors, approximation of wound edges, and increased blood flow to the wound.2
In complex, infected wounds, a variation of negative pressure wound therapy (NPWT) via the instillation of topical antibiotics (instillation VAC) has been used.3 This variation has been advantageous even in soft tissue fungal infections. Early and aggressive treatment of such infections is critical to prevent dissemination, particularly in aggressive infections, such as mucormycosis.4 We present a case of a patient with a mucormycosis infection of his left Achilles tendon and overlying skin who was successfully treated with surgical debridement and wound care with instillation NPWT with topical amphotericin B.
Case Presentation
A 53-year-old man underwent left Achilles tendon reconstruction with allograft after a complete tear during exercise. He had no relevant medical history and was otherwise healthy, which he attributed to working out daily. About a week after the operation, he began having incisional breakdown, prompting presentation to an emergency department. There, he received IV antibiotics along with multiple debridements. After the wound failed to improve and intra-operative cultures grew mucormycosis, he was transferred to our facility for a higher level of care. On admission, he was immediately given IV amphotericin B and scheduled for repeat debridement.
After 1 prior debridement and 10 total days of IV amphotericin, a repeat debridement was performed. After the debridement, the installation VAC was applied to the patient’s left lower extremity wound with an instilling fluid of amphotericin B and the settings as follows: smart phase instill volume, 110 mL; soak time, 3.5 hours; target pressure, 125 mm Hg; intensity, low; and VAC therapy mode, continuous. After 5 days, the wound bed appeared clean without overt signs of infection. However, due to some toxicity to healthy surrounding soft tissue, the instillation VAC was discontinued and standard NPWT was started. The patient underwent 2 additional rounds of debridement with partial delayed closure. Four weeks after discontinuation of the instillation VAC, the wound appeared healthy and granulated so the patient underwent split-thickness skin grafting to the left posterior ankle. He subsequently completed a course of oral antifungal medication as an outpatient.
The patient was seen in the outpatient clinic for 14 months from the initial mucormycosis infection (Figure).
Discussion
Mucormycosis is an infection caused by fungi in the class Zygomycetes and of the order Mucorales that typically occurs in immunocompromised patients, especially those with diabetic ketoacidosis and neutropenia. Given that this patient had no relevant medical history and was otherwise healthy, he was at extremely low risk of this type of infection. In this patient’s case, the spores of this nonseptate hyphae wide-branching species were most likely introduced at the time of left Achilles tendon repair. Mucormycosis is progressive and can be fatal unless treated, with a mortality rate approaching 70%.5 The rarity and heterogeneity of mucormycosis make treatment variable.6 No prospective or randomized clinical trials exist in plastic surgery literature.
The use of wound VAC in combination with the instillation of amphotericin B to treat cutaneous mucormycosis is not well documented. Mucormycosis infections are traditionally addressed with surgical debridement and antifungal therapy, specifically IV amphotericin B.7,8 As previously noted, NPWT has become the gold standard in treating complex wounds.3 Additionally, wound VAC therapy with instillation has been noted in the literature as a reliable method to treat bacteria-infected wounds, providing a shorter treatment period and earlier wound closure.9 Instillation VAC therapy has proven particularly useful in complex, infected wounds, such as aggressive fungal infections.
Mucormycosis treatment is challenging particularly in the extremities as management must balance both mortality and limb salvage. In this case, the use of NPWT with wound VAC and intervals of instilling amphotericin B facilitated infection control in this lower extremity mucormycosis infection. The significant adverse effect profile of amphotericin B, particularly the nephrotoxicity, should be seriously considered when deciding the treatment regimen for patients affected by mucormycosis. Locally, topical amphotericin B has been reported to cause blistering, itchiness, redness, peeling, and dryness. However, topical preparations of amphotericin B are nontoxic unlike their IV counterpart, able to cross the physiological barriers of the skin while simultaneously targeting macrophages in the dermis and epidermis.10
Conclusions
Although the mainstay of treatment for systemic mucormycosis is radical debridement and IV amphotericin B, a more localized infection may benefit from an adjunct like an instillation wound VAC with topical amphotericin B, as presented in this case study. Swift treatment with wound VAC was beneficial in the overall recovery and tissue healing of this patient and may be beneficial in similar cases.
1. Normandin S, Safran T, Winocour S, et al. negative pressure wound therapy: mechanism of action and clinical applications. Semin Plast Surg. 2021;35(3):164-170. doi:10.1055/s-0041-1731792
2. Agarwal P, Kukrele R, Sharma D. Vacuum assisted closure (VAC)/negative pressure wound therapy (NPWT) for difficult wounds: a review. J Clin Orthop Trauma. 2019;10(5):845-848. doi:10.1016/j.jcot.2019.06.015
3. Gabriel A, Shores J, Bernstein B, et al. A clinical review of infected wound treatment with Vacuum Assisted Closure (V.A.C.) therapy: experience and case series. Int Wound J. 2009;6(suppl 2):1-25. doi:10.1111/j.1742-481X.2009.00628.x
4. Guégan S, Lanternier F, Rouzaud C, Dupin N, Lortholary O. Fungal skin and soft tissue infections. Curr Opin Infect Dis. 2016;29(2):124-130. doi:10.1097/QCO.0000000000000252
5. Ibrahim AS, Spellberg B, Walsh TJ, Kontoyiannis DP. Pathogenesis of mucormycosis. Clin Infect Dis. 2012;54(suppl 1):S16-S22. doi:10.1093/cid/cir865
6. Sipsas NV, Gamaletsou MN, Anastasopoulou A, Kontoyiannis DP. Therapy of mucormycosis. J Fungi (Basel). 2018;4(3):90. Published 2018 Jul 31. doi:10.3390/jof4030090
7. Spellberg B, Edwards J Jr, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005;18(3):556-569. doi:10.1128/CMR.18.3.556-569.2005
8. Losee JE, Selber J, Vega S, Hall C, Scott G, Serletti JM. Primary cutaneous mucormycosis: guide to surgical management. Ann Plast Surg. 2002;49(4):385-390. doi:10.1097/00000637-200210000-00009
9. Webb LX. New techniques in wound management: vacuum-assisted wound closure. J Am Acad Orthop Surg. 2002;10(5):303-311. doi:10.5435/00124635-200209000-00002
10. Varikuti S, Oghumu S, Saljoughian N, et al. Topical treatment with nanoliposomal Amphotericin B reduces early lesion growth but fails to induce cure in an experimental model of cutaneous leishmaniasis caused by Leishmania mexicana. Acta Trop. 2017;173:102-108. doi:10.1016/j.actatropica.2017.06.004
1. Normandin S, Safran T, Winocour S, et al. negative pressure wound therapy: mechanism of action and clinical applications. Semin Plast Surg. 2021;35(3):164-170. doi:10.1055/s-0041-1731792
2. Agarwal P, Kukrele R, Sharma D. Vacuum assisted closure (VAC)/negative pressure wound therapy (NPWT) for difficult wounds: a review. J Clin Orthop Trauma. 2019;10(5):845-848. doi:10.1016/j.jcot.2019.06.015
3. Gabriel A, Shores J, Bernstein B, et al. A clinical review of infected wound treatment with Vacuum Assisted Closure (V.A.C.) therapy: experience and case series. Int Wound J. 2009;6(suppl 2):1-25. doi:10.1111/j.1742-481X.2009.00628.x
4. Guégan S, Lanternier F, Rouzaud C, Dupin N, Lortholary O. Fungal skin and soft tissue infections. Curr Opin Infect Dis. 2016;29(2):124-130. doi:10.1097/QCO.0000000000000252
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6. Sipsas NV, Gamaletsou MN, Anastasopoulou A, Kontoyiannis DP. Therapy of mucormycosis. J Fungi (Basel). 2018;4(3):90. Published 2018 Jul 31. doi:10.3390/jof4030090
7. Spellberg B, Edwards J Jr, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev. 2005;18(3):556-569. doi:10.1128/CMR.18.3.556-569.2005
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Even one head injury boosts all-cause mortality risk
An analysis of more than 13,000 adult participants in the Atherosclerosis Risk in Communities (ARIC) study showed a dose-response pattern in which one head injury was linked to a 66% increased risk for all-cause mortality, and two or more head injuries were associated with twice the risk in comparison with no head injuries.
These findings underscore the importance of preventing head injuries and of swift clinical intervention once a head injury occurs, lead author Holly Elser, MD, PhD, department of neurology, Hospital of the University of Pennsylvania, Philadelphia, told this news organization.
“Clinicians should counsel patients who are at risk for falls about head injuries and ensure patients are promptly evaluated in the hospital setting if they do have a fall – especially with loss of consciousness or other symptoms, such as headache or dizziness,” Dr. Elser added.
The findings were published online in JAMA Neurology.
Consistent evidence
There is “pretty consistent evidence” that mortality rates are increased in the short term after head injury, predominantly among hospitalized patients, Dr. Elser noted.
“But there’s less evidence about the long-term mortality implications of head injuries and less evidence from adults living in the community,” she added.
The analysis included 13,037 participants in the ARIC study, an ongoing study involving adults aged 45-65 years who were recruited from four geographically and racially diverse U.S. communities. The mean age at baseline (1987-1989) was 54 years; 57.7% were women; and 27.9% were Black.
Study participants are followed at routine in-person visits and semiannually via telephone.
Data on head injuries came from hospital diagnostic codes and self-reports. These reports included information on the number of injuries and whether the injury required medical care and involved loss of consciousness.
During the 27-year follow-up, 18.4% of the study sample had at least one head injury. Injuries occurred more frequently among women, which may reflect the predominance of women in the study population, said Dr. Elser.
Overall, about 56% of participants died during the study period. The estimated median amount of survival time after head injury was 4.7 years.
The most common causes of death were neoplasm, cardiovascular disease, and neurologic disorders. Regarding specific neurologic causes of death, the researchers found that 62.2% of deaths were due to neurodegenerative disease among individuals with head injury, vs. 51.4% among those without head injury.
This, said Dr. Elser, raises the possibility of reverse causality. “If you have a neurodegenerative disorder like Alzheimer’s disease dementia or Parkinson’s disease that leads to difficulty walking, you may be more likely to fall and have a head injury. The head injury in turn may lead to increased mortality,” she noted.
However, she stressed that the data on cause-specific mortality are exploratory. “Our research motivates future studies that really examine this time-dependent relationship between neurodegenerative disease and head injuries,” Dr. Elser said.
Dose-dependent response
In the unadjusted analysis, the hazard ratio of mortality among individuals with head injury was 2.21 (95% confidence interval, 2.09-2.34) compared with those who did not have head injury.
The association remained significant with adjustment for sociodemographic factors (HR, 1.99; 95% CI, 1.88-2.11) and with additional adjustment for vascular risk factors (HR, 1.92; 95% CI, 1.81-2.03).
The findings also showed a dose-response pattern in the association of head injuries with mortality. Compared with participants who did not have head injury, the HR was 1.66 (95% CI, 1.56-1.77) for those with one head injury and 2.11 (95% CI, 1.89-2.37) for those with two or more head injuries.
“It’s not as though once you’ve had one head injury, you’ve accrued all the damage you possibly can. We see pretty clearly here that recurrent head injury further increased the rate of deaths from all causes,” said Dr. Elser.
Injury severity was determined from hospital diagnostic codes using established algorithms. Results showed that mortality rates were increased with even mild head injury.
Interestingly, the association between head injury and all-cause mortality was weaker among those whose injuries were self-reported. One possibility is that these injuries were less severe, Dr. Elser noted.
“If you have head injury that’s mild enough that you don’t need to go to the hospital, it’s probably going to confer less long-term health risks than one that’s severe enough that you needed to be examined in an acute care setting,” she said.
Results were similar by race and for sex. “Even though there were more women with head injuries, the rate of mortality associated with head injury doesn’t differ from the rate among men,” Dr. Elser reported.
However, the association was stronger among those younger than 54 years at baseline (HR, 2.26) compared with older individuals (HR, 2.0) in the model that adjusted for demographics and lifestyle factors.
This may be explained by the reference group (those without a head injury) – the mortality rate was in general higher for the older participants, said Dr. Elser. It could also be that younger adults are more likely to have severe head injuries from, for example, motor vehicle accidents or violence, she added.
These new findings underscore the importance of public health measures, such as seatbelt laws, to reduce head injuries, the investigators note.
They add that clinicians with patients at risk for head injuries may recommend steps to lessen the risk of falls, such as having access to durable medical equipment, and ensuring driver safety.
Shorter life span
Commenting for this news organization, Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology in Port St. Lucie and past president of the Florida Society of Neurology, said the large number of participants “adds validity” to the finding that individuals with head injury are likely to have a shorter life span than those who do not suffer head trauma – and that this “was not purely by chance or from other causes.”
However, patients may not have accurately reported head injuries, in which case the rate of injury in the self-report subgroup would not reflect the actual incidence, noted Dr. Conidi, who was not involved with the research.
“In my practice, most patients have little knowledge as to the signs and symptoms of concussion and traumatic brain injury. Most think there needs to be some form of loss of consciousness to have a head injury, which is of course not true,” he said.
Dr. Conidi added that the finding of a higher incidence of death from neurodegenerative disorders supports the generally accepted consensus view that about 30% of patients with traumatic brain injury experience progression of symptoms and are at risk for early dementia.
The ARIC study is supported by the National Heart, Lung, and Blood Institute. Dr. Elser and Dr. Conidi have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
An analysis of more than 13,000 adult participants in the Atherosclerosis Risk in Communities (ARIC) study showed a dose-response pattern in which one head injury was linked to a 66% increased risk for all-cause mortality, and two or more head injuries were associated with twice the risk in comparison with no head injuries.
These findings underscore the importance of preventing head injuries and of swift clinical intervention once a head injury occurs, lead author Holly Elser, MD, PhD, department of neurology, Hospital of the University of Pennsylvania, Philadelphia, told this news organization.
“Clinicians should counsel patients who are at risk for falls about head injuries and ensure patients are promptly evaluated in the hospital setting if they do have a fall – especially with loss of consciousness or other symptoms, such as headache or dizziness,” Dr. Elser added.
The findings were published online in JAMA Neurology.
Consistent evidence
There is “pretty consistent evidence” that mortality rates are increased in the short term after head injury, predominantly among hospitalized patients, Dr. Elser noted.
“But there’s less evidence about the long-term mortality implications of head injuries and less evidence from adults living in the community,” she added.
The analysis included 13,037 participants in the ARIC study, an ongoing study involving adults aged 45-65 years who were recruited from four geographically and racially diverse U.S. communities. The mean age at baseline (1987-1989) was 54 years; 57.7% were women; and 27.9% were Black.
Study participants are followed at routine in-person visits and semiannually via telephone.
Data on head injuries came from hospital diagnostic codes and self-reports. These reports included information on the number of injuries and whether the injury required medical care and involved loss of consciousness.
During the 27-year follow-up, 18.4% of the study sample had at least one head injury. Injuries occurred more frequently among women, which may reflect the predominance of women in the study population, said Dr. Elser.
Overall, about 56% of participants died during the study period. The estimated median amount of survival time after head injury was 4.7 years.
The most common causes of death were neoplasm, cardiovascular disease, and neurologic disorders. Regarding specific neurologic causes of death, the researchers found that 62.2% of deaths were due to neurodegenerative disease among individuals with head injury, vs. 51.4% among those without head injury.
This, said Dr. Elser, raises the possibility of reverse causality. “If you have a neurodegenerative disorder like Alzheimer’s disease dementia or Parkinson’s disease that leads to difficulty walking, you may be more likely to fall and have a head injury. The head injury in turn may lead to increased mortality,” she noted.
However, she stressed that the data on cause-specific mortality are exploratory. “Our research motivates future studies that really examine this time-dependent relationship between neurodegenerative disease and head injuries,” Dr. Elser said.
Dose-dependent response
In the unadjusted analysis, the hazard ratio of mortality among individuals with head injury was 2.21 (95% confidence interval, 2.09-2.34) compared with those who did not have head injury.
The association remained significant with adjustment for sociodemographic factors (HR, 1.99; 95% CI, 1.88-2.11) and with additional adjustment for vascular risk factors (HR, 1.92; 95% CI, 1.81-2.03).
The findings also showed a dose-response pattern in the association of head injuries with mortality. Compared with participants who did not have head injury, the HR was 1.66 (95% CI, 1.56-1.77) for those with one head injury and 2.11 (95% CI, 1.89-2.37) for those with two or more head injuries.
“It’s not as though once you’ve had one head injury, you’ve accrued all the damage you possibly can. We see pretty clearly here that recurrent head injury further increased the rate of deaths from all causes,” said Dr. Elser.
Injury severity was determined from hospital diagnostic codes using established algorithms. Results showed that mortality rates were increased with even mild head injury.
Interestingly, the association between head injury and all-cause mortality was weaker among those whose injuries were self-reported. One possibility is that these injuries were less severe, Dr. Elser noted.
“If you have head injury that’s mild enough that you don’t need to go to the hospital, it’s probably going to confer less long-term health risks than one that’s severe enough that you needed to be examined in an acute care setting,” she said.
Results were similar by race and for sex. “Even though there were more women with head injuries, the rate of mortality associated with head injury doesn’t differ from the rate among men,” Dr. Elser reported.
However, the association was stronger among those younger than 54 years at baseline (HR, 2.26) compared with older individuals (HR, 2.0) in the model that adjusted for demographics and lifestyle factors.
This may be explained by the reference group (those without a head injury) – the mortality rate was in general higher for the older participants, said Dr. Elser. It could also be that younger adults are more likely to have severe head injuries from, for example, motor vehicle accidents or violence, she added.
These new findings underscore the importance of public health measures, such as seatbelt laws, to reduce head injuries, the investigators note.
They add that clinicians with patients at risk for head injuries may recommend steps to lessen the risk of falls, such as having access to durable medical equipment, and ensuring driver safety.
Shorter life span
Commenting for this news organization, Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology in Port St. Lucie and past president of the Florida Society of Neurology, said the large number of participants “adds validity” to the finding that individuals with head injury are likely to have a shorter life span than those who do not suffer head trauma – and that this “was not purely by chance or from other causes.”
However, patients may not have accurately reported head injuries, in which case the rate of injury in the self-report subgroup would not reflect the actual incidence, noted Dr. Conidi, who was not involved with the research.
“In my practice, most patients have little knowledge as to the signs and symptoms of concussion and traumatic brain injury. Most think there needs to be some form of loss of consciousness to have a head injury, which is of course not true,” he said.
Dr. Conidi added that the finding of a higher incidence of death from neurodegenerative disorders supports the generally accepted consensus view that about 30% of patients with traumatic brain injury experience progression of symptoms and are at risk for early dementia.
The ARIC study is supported by the National Heart, Lung, and Blood Institute. Dr. Elser and Dr. Conidi have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
An analysis of more than 13,000 adult participants in the Atherosclerosis Risk in Communities (ARIC) study showed a dose-response pattern in which one head injury was linked to a 66% increased risk for all-cause mortality, and two or more head injuries were associated with twice the risk in comparison with no head injuries.
These findings underscore the importance of preventing head injuries and of swift clinical intervention once a head injury occurs, lead author Holly Elser, MD, PhD, department of neurology, Hospital of the University of Pennsylvania, Philadelphia, told this news organization.
“Clinicians should counsel patients who are at risk for falls about head injuries and ensure patients are promptly evaluated in the hospital setting if they do have a fall – especially with loss of consciousness or other symptoms, such as headache or dizziness,” Dr. Elser added.
The findings were published online in JAMA Neurology.
Consistent evidence
There is “pretty consistent evidence” that mortality rates are increased in the short term after head injury, predominantly among hospitalized patients, Dr. Elser noted.
“But there’s less evidence about the long-term mortality implications of head injuries and less evidence from adults living in the community,” she added.
The analysis included 13,037 participants in the ARIC study, an ongoing study involving adults aged 45-65 years who were recruited from four geographically and racially diverse U.S. communities. The mean age at baseline (1987-1989) was 54 years; 57.7% were women; and 27.9% were Black.
Study participants are followed at routine in-person visits and semiannually via telephone.
Data on head injuries came from hospital diagnostic codes and self-reports. These reports included information on the number of injuries and whether the injury required medical care and involved loss of consciousness.
During the 27-year follow-up, 18.4% of the study sample had at least one head injury. Injuries occurred more frequently among women, which may reflect the predominance of women in the study population, said Dr. Elser.
Overall, about 56% of participants died during the study period. The estimated median amount of survival time after head injury was 4.7 years.
The most common causes of death were neoplasm, cardiovascular disease, and neurologic disorders. Regarding specific neurologic causes of death, the researchers found that 62.2% of deaths were due to neurodegenerative disease among individuals with head injury, vs. 51.4% among those without head injury.
This, said Dr. Elser, raises the possibility of reverse causality. “If you have a neurodegenerative disorder like Alzheimer’s disease dementia or Parkinson’s disease that leads to difficulty walking, you may be more likely to fall and have a head injury. The head injury in turn may lead to increased mortality,” she noted.
However, she stressed that the data on cause-specific mortality are exploratory. “Our research motivates future studies that really examine this time-dependent relationship between neurodegenerative disease and head injuries,” Dr. Elser said.
Dose-dependent response
In the unadjusted analysis, the hazard ratio of mortality among individuals with head injury was 2.21 (95% confidence interval, 2.09-2.34) compared with those who did not have head injury.
The association remained significant with adjustment for sociodemographic factors (HR, 1.99; 95% CI, 1.88-2.11) and with additional adjustment for vascular risk factors (HR, 1.92; 95% CI, 1.81-2.03).
The findings also showed a dose-response pattern in the association of head injuries with mortality. Compared with participants who did not have head injury, the HR was 1.66 (95% CI, 1.56-1.77) for those with one head injury and 2.11 (95% CI, 1.89-2.37) for those with two or more head injuries.
“It’s not as though once you’ve had one head injury, you’ve accrued all the damage you possibly can. We see pretty clearly here that recurrent head injury further increased the rate of deaths from all causes,” said Dr. Elser.
Injury severity was determined from hospital diagnostic codes using established algorithms. Results showed that mortality rates were increased with even mild head injury.
Interestingly, the association between head injury and all-cause mortality was weaker among those whose injuries were self-reported. One possibility is that these injuries were less severe, Dr. Elser noted.
“If you have head injury that’s mild enough that you don’t need to go to the hospital, it’s probably going to confer less long-term health risks than one that’s severe enough that you needed to be examined in an acute care setting,” she said.
Results were similar by race and for sex. “Even though there were more women with head injuries, the rate of mortality associated with head injury doesn’t differ from the rate among men,” Dr. Elser reported.
However, the association was stronger among those younger than 54 years at baseline (HR, 2.26) compared with older individuals (HR, 2.0) in the model that adjusted for demographics and lifestyle factors.
This may be explained by the reference group (those without a head injury) – the mortality rate was in general higher for the older participants, said Dr. Elser. It could also be that younger adults are more likely to have severe head injuries from, for example, motor vehicle accidents or violence, she added.
These new findings underscore the importance of public health measures, such as seatbelt laws, to reduce head injuries, the investigators note.
They add that clinicians with patients at risk for head injuries may recommend steps to lessen the risk of falls, such as having access to durable medical equipment, and ensuring driver safety.
Shorter life span
Commenting for this news organization, Frank Conidi, MD, director of the Florida Center for Headache and Sports Neurology in Port St. Lucie and past president of the Florida Society of Neurology, said the large number of participants “adds validity” to the finding that individuals with head injury are likely to have a shorter life span than those who do not suffer head trauma – and that this “was not purely by chance or from other causes.”
However, patients may not have accurately reported head injuries, in which case the rate of injury in the self-report subgroup would not reflect the actual incidence, noted Dr. Conidi, who was not involved with the research.
“In my practice, most patients have little knowledge as to the signs and symptoms of concussion and traumatic brain injury. Most think there needs to be some form of loss of consciousness to have a head injury, which is of course not true,” he said.
Dr. Conidi added that the finding of a higher incidence of death from neurodegenerative disorders supports the generally accepted consensus view that about 30% of patients with traumatic brain injury experience progression of symptoms and are at risk for early dementia.
The ARIC study is supported by the National Heart, Lung, and Blood Institute. Dr. Elser and Dr. Conidi have reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM JAMA NEUROLOGY
Novel resuscitation for patients with nonshockable rhythms in cardiac arrest
This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr Robert Glatter, medical adviser for Medscape Emergency Medicine.
with a remarkable increase in neurologically intact survival. Welcome, gentlemen.Dr. Pepe, I’d like to start off by thanking you for taking time to join us to discuss this novel concept of head-up or what you now refer to as a neuroprotective cardiopulmonary resuscitation (CPR) bundle. Can you define what this entails and why it is referred to as a neuroprotective CPR bundle?
Paul E. Pepe, MD, MPH: CPR has been life saving for 60 years the way we’ve performed it, but probably only in a very small percentage of cases. That’s one of the problems. We have almost a thousand people a day who have sudden cardiac arrest out in the community alone and more in the hospital.
We know that early defibrillation and early CPR can contribute, but it’s still a small percentage of those. About 75%-85% of the cases that we go out to see will have nonshockable rhythms and flatlines. Some cases are what we call “pulseless electrical activity,” meaning that it looks like there is some kind of organized complex, but there is no pulse associated with it.
That’s why it’s a problem, because they don’t come back. Part of the reason why we see poor outcomes is not only that these cases tend to be people who, say, were in ventricular fibrillation and then just went on over time and were not witnessed or resuscitated or had a long response time. They basically either go into flatline or autoconvert into these bizarre rhythms.
The other issue is the way we perform CPR. CPR has been lifesaving, but it only generates about 20% and maybe 15% in some cases of normal blood flow, and particularly, cerebral perfusion pressure. We’ve looked at this nicely in the laboratory.
For example, during chest compressions, we’re hoping during the recoil phase to pull blood down and back into the right heart. The problem is that you’re not only setting a pressure rate up here to the arterial side but also, you’re setting back pressure wave on the venous side. Obviously, the arterial side always wins out, but it’s just not as efficient as it could be, at 20% or 30%.
What does this entail? It entails several independent mechanisms in terms of how they work, but they all do the same thing, which is they help to pull blood out of the brain and back into the right heart by basically manipulating intrathoracic pressure and creating more of a vacuum to get blood back there.
It’s so important that people do quality CPR. You have to have a good release and that helps us suck a little bit of blood and sucks the air in. As soon as the air rushes in, it neutralizes the pressure and there’s no more vacuum and nothing else is happening until the next squeeze.
What we have found is that we can cap the airway just for a second with a little pop-up valve. It acts like when you’re sucking a milkshake through a straw and it creates more of a vacuum in the chest. Just a little pop-up valve that pulls a little bit more blood out of the brain and the rest of the body and into the right heart.
We’ve shown in a human study that, for example, the systolic blood pressure almost doubles. It really goes from 40 mm Hg during standard CPR up to 80 mm Hg, and that would be sustained for 14-15 minutes. That was a nice little study that was done in Milwaukee a few years ago.
The other thing that happens is, if you add on something else, it’s like a toilet plunger. I think many people have seen it; it’s called “active compression-decompression.” It not only compresses, but it decompresses. Where it becomes even more effective is that if you had broken bones or stiff bones as you get older or whatever it may be, as you do the CPR, you’re still getting the push down and then you’re getting the pull out. It helps on several levels. More importantly, when you put the two together, they’re very synergistic.
We, have already done the clinical trial that is the proof of concept, and that was published in The Lancet about 10 years ago. In that study, we found that the combination of those two dramatically improved survival rates by 50%, with 1-year survival neurologically intact. That got us on the right track.
The interesting thing is that someone said, “Can we lift the head up a little bit?” We did a large amount of work in the laboratory over 10 years, fine tuning it. When do you first lift the head? How soon is too soon? It’s probably bad if you just go right to it.
We had to get the pump primed a little bit with these other things to get the flow going better, not only pulling blood out of the brain but now, you have a better flow this way. You have to prime at first for a couple of minutes, and we worked out the timing: Is it 3 or 4 minutes? It seems the timing is right at about 2 minutes, then you gradually elevate the head over about 2 minutes. We’re finding that seems to be the optimal way to do it. About 2 minutes of priming with those other two devices, the adjuncts, and then gradually elevate the head over 2 minutes.
When we do that in the laboratory, we’re getting normalized cerebral perfusion pressures. You’re normalizing the flow back again with that. We’re seeing profound differences in outcome as a result, even in these cases of the nonshockables.
Dr. Glatter: What you’re doing basically is resulting in an increase in cardiac output, essentially. That really is important, especially in these nonshockable rhythms, correct?
Dr. Pepe: Absolutely. As you’re doing this compression and you’re getting these intracranial pulse waves that are going up because they’re colliding up there. It could be even damaging in itself, but we’re seeing these intracranial raises. The intracranial pressure starts going up more and more over time. Also, peripherally in most people, you’re not getting good flow out there; then, your vasculature starts to relax. The arterials are starting to not get oxygen, so they don’t go out.
With this technique where we’re returning the pressure, we’re getting to 40% of normal now with the active compression-decompression CPR plus an impedance threshold device (ACD+ITD CPR) approach. Now, you add this, and you’re almost normalizing. In humans, even in these asystole patients, we’re seeing end-title CO2s which are generally in the 15-20 range with standard CPR are now up with ACD+ITD CPR in the 30%-40% range, where we’re getting through 30 or 40 end-tidal CO2s. Now, we’re seeing even the end-tidal CO2s moving up into the 40s and 50s. We know there’s a surrogate marker telling us that we are generating much better flows not only to the rest of the body, but most importantly, to the brain.
Dr. Glatter: Ryan, could you tell us about the approach in terms of on scene, what you’re doing and how you use the device itself? Maybe you could talk about the backpack that you developed with your fire department?
Ryan P. Quinn, BS, EMS: Our approach has always been to get to the patient quickly, like everybody’s approach on a cardiac arrest when you’re responding. We are an advanced life-support paramedic ambulance service through the fire department – we’re all cross-trained firefighter paramedics. Our first vehicle from the fire department is typically the ambulance. It’s smaller and a little quicker than the fire engine. Two paramedics are going to jump out with two backpacks. One has the automated compressive device (we use the Lucas), and the other one is the sequential patient lifting device, the EleGARD.
Our two paramedics are quick to the patient’s side, and once they make contact with the patient to verify pulseless cardiac arrest, they will unpack. One person will go right to compressions if there’s nobody on compressions already. Sometimes we have a first responder police officer with an automated external defibrillator (AED). We go right to the patient’s side, concentrate on compressions, and within 90 seconds to 2 minutes, we have our bags unpacked, we’ve got the devices turned on, patient lifted up, slid under the device, and we have a supraglottic airway that is placed within 15 seconds already premade with the ITD on top. We have a sealed airway that we can continue to compress with Dr. Pepe’s original discussion of building on what’s previously been shown to work.
Dr. Pepe: Let me make a comment about this. This is so important, what Ryan is saying, because it’s something we found during the study. It’s really a true pit-crew approach. You’re not only getting these materials, which you think you need a medical Sherpa for, but you don’t. They set it up and then when they open it up, it’s all laid out just exactly as you need it. It’s not just how fast you get there; it’s how fast you get this done.
When we look at all cases combined against high-performance systems that had some of the highest survival rates around, when we compare it to those, we found that overall, even if you looked at the ones that had over 20-minute responses, the odds ratios were still three to four times higher. It was impressive.
If you looked at it under 15 minutes, which is really reasonable for most systems that get there by the way, the average time that people start CPR in any system in these studies has been about 8 minutes if you actually start this thing, which takes about 2 minutes more for this new bundle of care with this triad, it’s almost 12-14 times higher in terms of the odds ratio. I’ve never seen anything like that where the higher end is over 100 in terms of your confidence intervals.
Ryan’s system did really well and is one of those with even higher levels of outcomes, mostly because they got it on quickly. It’s like the AED for nonshockables but better because you have a wider range of efficacy where it will work.
Dr. Glatter: When the elapsed time was less than 11 minutes, that seemed to be an inflection point in the study, is that correct? You saw that 11-fold higher incidence in terms of neurologically intact survival, is that correct?
Dr. Pepe: We picked that number because that was the median time to get it on board. Half the people were getting it within that time period. The fact that you have a larger window, we’re talking about 13- almost 14-fold improvements in outcome if it was under 15 minutes. It doesn’t matter about the 11 or the 12. It’s the faster you get it on board, the better off you are.
Dr. Glatter: What’s the next step in the process of doing trials and having implementation on a larger scale based on your Annals of Emergency Medicine study? Where do you go from here?
Dr. Pepe: I’ve come to find out there are many confounding variables. What was the quality of CPR? How did people ventilate? Did they give the breath and hold it? Did they give a large enough breath so that blood can go across the transpulmonary system? There are many confounding variables. That’s why I think, in the future, it’s going to be more of looking at things like propensity score matching because we know all the variables that change outcomes. I think that’s going to be a way for me.
The other thing is that we were looking at only 380 cases here. When this doubles up in numbers, as we accrue more cases around the country of people who are implementing this, these numbers I just quoted are going to go up much higher. Unwitnessed asystole is considered futile, and you just don’t get them back. To be able to get these folks back now, even if it’s a small percentage, and the fact that we know that we’re producing this better flow, is pretty striking.
I’m really impressed, and the main thing is to make sure people are educated about it. Number two is that they understand that it has to be done right. It cannot be done wrong or you’re not going to see the differences. Getting it done right is not only following the procedures, the sequence, and how you do it, but it also has to do with getting there quickly, including assigning the right people to put it on and having well-trained people who know what they’re doing.
Dr. Glatter: In general, the lay public obviously should not attempt this in the field lifting someone’s head up in the sense of trying to do chest compressions. I think that message is important that you just said. It’s not ready for prime time yet in any way. It has to be done right.
Dr. Pepe: Bystanders have to learn CPR – they will buy us time and we’ll have better outcomes when they do that. That’s number one. Number two is that as more and more systems adopt this, you’re going to see more people coming back. If you think about what we’re doing now, if we only get back 5% of these nonshockable vs. less than 1%, it’s 5% of 800 people a day because a thousand people a day die. Several dozens of lives can be saved on a daily basis, coming back neurologically intact. That’s the key thing.
Dr. Glatter: Ryan, can you comment about your experience in the field? Is there anything in terms of your current approach that you think would be ideal to change at this point?
Mr. Quinn: We’ve established that this is the approach that we want to take and we’re just fine tuning it to be more efficient. Using the choreography of which person is going to do which role, we have clearly defined roles and clearly defined command of the scene so we’re not missing anything. Training is extremely important.
Dr. Glatter: Paul, I want to ask you about your anecdotal experience of people waking up quickly and talking after elevating their heads and going through this process. Having people talk about it and waking up is really fascinating. Maybe you can comment further on this.
Dr. Pepe: That’s a great point that you bring up because a 40- to 50-year-old guy who got saved with this approach, when he came around, he said he was hearing what people were saying. When he came out of it, he found out he had been getting CPR for about 25 minutes because he had persistent recurring ventricular fibrillation. He said, “How could I have survived that that long?”
When we told him about the new approach, he added, “Well, that’s like neuroprotective.” He’s right, because in the laboratory, we showed it was neuroprotective and we’re also getting better flows back there. It goes along with everything else, and so we’ve adopted the name because it is.
These are really high-powered systems we are comparing against, and we have the same level of return of spontaneous circulation. The major difference was when you started talking about the neurointact survival. We don’t have enough numbers yet, but next go around, we’re going to look at cerebral performance category (CPC) – CPC1 vs. the CPC2 – which were both considered intact, but CPC1 is actually better. We’re seeing many more of those, anecdotally.
I also wanted to mention that people do bring this up and say, “Well, let’s do a trial.” As far as we’re concerned, the trial’s been done in terms of The Lancet study 10 years ago that showed that the active compression-decompression had tremendously better outcomes. We show in the laboratories that you augment that a little bit. These are all [Food and Drug Administration] approved. You can go out and buy it tomorrow and get it done. I have no conflicts of interest, by the way, with any of this.
To have this device that’s going to have the potential of saving so many more lives is really an exciting breakthrough. More importantly, we’re understanding more now about the physiology of CPR and why it works. It could work much better with the approaches that we’ve been developing over the last 20 years or so.
Dr. Glatter: Absolutely. I want to thank both of you gentlemen. It’s been really an incredible experience to learn more about an advance in resuscitation that could truly be lifesaving. Thank you again for taking time to join us.
Dr. Glatter is an attending physician in the department of emergency medicine, Lenox Hill Hospital, New York. Dr. Pepe is professor, department of management, policy, and community health, University of Texas Health Sciences Center, Houston. Mr. Quinn is EMS Chief, Edina (Minn.) Fire Department. No conflicts of interest were reported.
A version of this article first appeared Jan. 26 on Medscape.com.
This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr Robert Glatter, medical adviser for Medscape Emergency Medicine.
with a remarkable increase in neurologically intact survival. Welcome, gentlemen.Dr. Pepe, I’d like to start off by thanking you for taking time to join us to discuss this novel concept of head-up or what you now refer to as a neuroprotective cardiopulmonary resuscitation (CPR) bundle. Can you define what this entails and why it is referred to as a neuroprotective CPR bundle?
Paul E. Pepe, MD, MPH: CPR has been life saving for 60 years the way we’ve performed it, but probably only in a very small percentage of cases. That’s one of the problems. We have almost a thousand people a day who have sudden cardiac arrest out in the community alone and more in the hospital.
We know that early defibrillation and early CPR can contribute, but it’s still a small percentage of those. About 75%-85% of the cases that we go out to see will have nonshockable rhythms and flatlines. Some cases are what we call “pulseless electrical activity,” meaning that it looks like there is some kind of organized complex, but there is no pulse associated with it.
That’s why it’s a problem, because they don’t come back. Part of the reason why we see poor outcomes is not only that these cases tend to be people who, say, were in ventricular fibrillation and then just went on over time and were not witnessed or resuscitated or had a long response time. They basically either go into flatline or autoconvert into these bizarre rhythms.
The other issue is the way we perform CPR. CPR has been lifesaving, but it only generates about 20% and maybe 15% in some cases of normal blood flow, and particularly, cerebral perfusion pressure. We’ve looked at this nicely in the laboratory.
For example, during chest compressions, we’re hoping during the recoil phase to pull blood down and back into the right heart. The problem is that you’re not only setting a pressure rate up here to the arterial side but also, you’re setting back pressure wave on the venous side. Obviously, the arterial side always wins out, but it’s just not as efficient as it could be, at 20% or 30%.
What does this entail? It entails several independent mechanisms in terms of how they work, but they all do the same thing, which is they help to pull blood out of the brain and back into the right heart by basically manipulating intrathoracic pressure and creating more of a vacuum to get blood back there.
It’s so important that people do quality CPR. You have to have a good release and that helps us suck a little bit of blood and sucks the air in. As soon as the air rushes in, it neutralizes the pressure and there’s no more vacuum and nothing else is happening until the next squeeze.
What we have found is that we can cap the airway just for a second with a little pop-up valve. It acts like when you’re sucking a milkshake through a straw and it creates more of a vacuum in the chest. Just a little pop-up valve that pulls a little bit more blood out of the brain and the rest of the body and into the right heart.
We’ve shown in a human study that, for example, the systolic blood pressure almost doubles. It really goes from 40 mm Hg during standard CPR up to 80 mm Hg, and that would be sustained for 14-15 minutes. That was a nice little study that was done in Milwaukee a few years ago.
The other thing that happens is, if you add on something else, it’s like a toilet plunger. I think many people have seen it; it’s called “active compression-decompression.” It not only compresses, but it decompresses. Where it becomes even more effective is that if you had broken bones or stiff bones as you get older or whatever it may be, as you do the CPR, you’re still getting the push down and then you’re getting the pull out. It helps on several levels. More importantly, when you put the two together, they’re very synergistic.
We, have already done the clinical trial that is the proof of concept, and that was published in The Lancet about 10 years ago. In that study, we found that the combination of those two dramatically improved survival rates by 50%, with 1-year survival neurologically intact. That got us on the right track.
The interesting thing is that someone said, “Can we lift the head up a little bit?” We did a large amount of work in the laboratory over 10 years, fine tuning it. When do you first lift the head? How soon is too soon? It’s probably bad if you just go right to it.
We had to get the pump primed a little bit with these other things to get the flow going better, not only pulling blood out of the brain but now, you have a better flow this way. You have to prime at first for a couple of minutes, and we worked out the timing: Is it 3 or 4 minutes? It seems the timing is right at about 2 minutes, then you gradually elevate the head over about 2 minutes. We’re finding that seems to be the optimal way to do it. About 2 minutes of priming with those other two devices, the adjuncts, and then gradually elevate the head over 2 minutes.
When we do that in the laboratory, we’re getting normalized cerebral perfusion pressures. You’re normalizing the flow back again with that. We’re seeing profound differences in outcome as a result, even in these cases of the nonshockables.
Dr. Glatter: What you’re doing basically is resulting in an increase in cardiac output, essentially. That really is important, especially in these nonshockable rhythms, correct?
Dr. Pepe: Absolutely. As you’re doing this compression and you’re getting these intracranial pulse waves that are going up because they’re colliding up there. It could be even damaging in itself, but we’re seeing these intracranial raises. The intracranial pressure starts going up more and more over time. Also, peripherally in most people, you’re not getting good flow out there; then, your vasculature starts to relax. The arterials are starting to not get oxygen, so they don’t go out.
With this technique where we’re returning the pressure, we’re getting to 40% of normal now with the active compression-decompression CPR plus an impedance threshold device (ACD+ITD CPR) approach. Now, you add this, and you’re almost normalizing. In humans, even in these asystole patients, we’re seeing end-title CO2s which are generally in the 15-20 range with standard CPR are now up with ACD+ITD CPR in the 30%-40% range, where we’re getting through 30 or 40 end-tidal CO2s. Now, we’re seeing even the end-tidal CO2s moving up into the 40s and 50s. We know there’s a surrogate marker telling us that we are generating much better flows not only to the rest of the body, but most importantly, to the brain.
Dr. Glatter: Ryan, could you tell us about the approach in terms of on scene, what you’re doing and how you use the device itself? Maybe you could talk about the backpack that you developed with your fire department?
Ryan P. Quinn, BS, EMS: Our approach has always been to get to the patient quickly, like everybody’s approach on a cardiac arrest when you’re responding. We are an advanced life-support paramedic ambulance service through the fire department – we’re all cross-trained firefighter paramedics. Our first vehicle from the fire department is typically the ambulance. It’s smaller and a little quicker than the fire engine. Two paramedics are going to jump out with two backpacks. One has the automated compressive device (we use the Lucas), and the other one is the sequential patient lifting device, the EleGARD.
Our two paramedics are quick to the patient’s side, and once they make contact with the patient to verify pulseless cardiac arrest, they will unpack. One person will go right to compressions if there’s nobody on compressions already. Sometimes we have a first responder police officer with an automated external defibrillator (AED). We go right to the patient’s side, concentrate on compressions, and within 90 seconds to 2 minutes, we have our bags unpacked, we’ve got the devices turned on, patient lifted up, slid under the device, and we have a supraglottic airway that is placed within 15 seconds already premade with the ITD on top. We have a sealed airway that we can continue to compress with Dr. Pepe’s original discussion of building on what’s previously been shown to work.
Dr. Pepe: Let me make a comment about this. This is so important, what Ryan is saying, because it’s something we found during the study. It’s really a true pit-crew approach. You’re not only getting these materials, which you think you need a medical Sherpa for, but you don’t. They set it up and then when they open it up, it’s all laid out just exactly as you need it. It’s not just how fast you get there; it’s how fast you get this done.
When we look at all cases combined against high-performance systems that had some of the highest survival rates around, when we compare it to those, we found that overall, even if you looked at the ones that had over 20-minute responses, the odds ratios were still three to four times higher. It was impressive.
If you looked at it under 15 minutes, which is really reasonable for most systems that get there by the way, the average time that people start CPR in any system in these studies has been about 8 minutes if you actually start this thing, which takes about 2 minutes more for this new bundle of care with this triad, it’s almost 12-14 times higher in terms of the odds ratio. I’ve never seen anything like that where the higher end is over 100 in terms of your confidence intervals.
Ryan’s system did really well and is one of those with even higher levels of outcomes, mostly because they got it on quickly. It’s like the AED for nonshockables but better because you have a wider range of efficacy where it will work.
Dr. Glatter: When the elapsed time was less than 11 minutes, that seemed to be an inflection point in the study, is that correct? You saw that 11-fold higher incidence in terms of neurologically intact survival, is that correct?
Dr. Pepe: We picked that number because that was the median time to get it on board. Half the people were getting it within that time period. The fact that you have a larger window, we’re talking about 13- almost 14-fold improvements in outcome if it was under 15 minutes. It doesn’t matter about the 11 or the 12. It’s the faster you get it on board, the better off you are.
Dr. Glatter: What’s the next step in the process of doing trials and having implementation on a larger scale based on your Annals of Emergency Medicine study? Where do you go from here?
Dr. Pepe: I’ve come to find out there are many confounding variables. What was the quality of CPR? How did people ventilate? Did they give the breath and hold it? Did they give a large enough breath so that blood can go across the transpulmonary system? There are many confounding variables. That’s why I think, in the future, it’s going to be more of looking at things like propensity score matching because we know all the variables that change outcomes. I think that’s going to be a way for me.
The other thing is that we were looking at only 380 cases here. When this doubles up in numbers, as we accrue more cases around the country of people who are implementing this, these numbers I just quoted are going to go up much higher. Unwitnessed asystole is considered futile, and you just don’t get them back. To be able to get these folks back now, even if it’s a small percentage, and the fact that we know that we’re producing this better flow, is pretty striking.
I’m really impressed, and the main thing is to make sure people are educated about it. Number two is that they understand that it has to be done right. It cannot be done wrong or you’re not going to see the differences. Getting it done right is not only following the procedures, the sequence, and how you do it, but it also has to do with getting there quickly, including assigning the right people to put it on and having well-trained people who know what they’re doing.
Dr. Glatter: In general, the lay public obviously should not attempt this in the field lifting someone’s head up in the sense of trying to do chest compressions. I think that message is important that you just said. It’s not ready for prime time yet in any way. It has to be done right.
Dr. Pepe: Bystanders have to learn CPR – they will buy us time and we’ll have better outcomes when they do that. That’s number one. Number two is that as more and more systems adopt this, you’re going to see more people coming back. If you think about what we’re doing now, if we only get back 5% of these nonshockable vs. less than 1%, it’s 5% of 800 people a day because a thousand people a day die. Several dozens of lives can be saved on a daily basis, coming back neurologically intact. That’s the key thing.
Dr. Glatter: Ryan, can you comment about your experience in the field? Is there anything in terms of your current approach that you think would be ideal to change at this point?
Mr. Quinn: We’ve established that this is the approach that we want to take and we’re just fine tuning it to be more efficient. Using the choreography of which person is going to do which role, we have clearly defined roles and clearly defined command of the scene so we’re not missing anything. Training is extremely important.
Dr. Glatter: Paul, I want to ask you about your anecdotal experience of people waking up quickly and talking after elevating their heads and going through this process. Having people talk about it and waking up is really fascinating. Maybe you can comment further on this.
Dr. Pepe: That’s a great point that you bring up because a 40- to 50-year-old guy who got saved with this approach, when he came around, he said he was hearing what people were saying. When he came out of it, he found out he had been getting CPR for about 25 minutes because he had persistent recurring ventricular fibrillation. He said, “How could I have survived that that long?”
When we told him about the new approach, he added, “Well, that’s like neuroprotective.” He’s right, because in the laboratory, we showed it was neuroprotective and we’re also getting better flows back there. It goes along with everything else, and so we’ve adopted the name because it is.
These are really high-powered systems we are comparing against, and we have the same level of return of spontaneous circulation. The major difference was when you started talking about the neurointact survival. We don’t have enough numbers yet, but next go around, we’re going to look at cerebral performance category (CPC) – CPC1 vs. the CPC2 – which were both considered intact, but CPC1 is actually better. We’re seeing many more of those, anecdotally.
I also wanted to mention that people do bring this up and say, “Well, let’s do a trial.” As far as we’re concerned, the trial’s been done in terms of The Lancet study 10 years ago that showed that the active compression-decompression had tremendously better outcomes. We show in the laboratories that you augment that a little bit. These are all [Food and Drug Administration] approved. You can go out and buy it tomorrow and get it done. I have no conflicts of interest, by the way, with any of this.
To have this device that’s going to have the potential of saving so many more lives is really an exciting breakthrough. More importantly, we’re understanding more now about the physiology of CPR and why it works. It could work much better with the approaches that we’ve been developing over the last 20 years or so.
Dr. Glatter: Absolutely. I want to thank both of you gentlemen. It’s been really an incredible experience to learn more about an advance in resuscitation that could truly be lifesaving. Thank you again for taking time to join us.
Dr. Glatter is an attending physician in the department of emergency medicine, Lenox Hill Hospital, New York. Dr. Pepe is professor, department of management, policy, and community health, University of Texas Health Sciences Center, Houston. Mr. Quinn is EMS Chief, Edina (Minn.) Fire Department. No conflicts of interest were reported.
A version of this article first appeared Jan. 26 on Medscape.com.
This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr Robert Glatter, medical adviser for Medscape Emergency Medicine.
with a remarkable increase in neurologically intact survival. Welcome, gentlemen.Dr. Pepe, I’d like to start off by thanking you for taking time to join us to discuss this novel concept of head-up or what you now refer to as a neuroprotective cardiopulmonary resuscitation (CPR) bundle. Can you define what this entails and why it is referred to as a neuroprotective CPR bundle?
Paul E. Pepe, MD, MPH: CPR has been life saving for 60 years the way we’ve performed it, but probably only in a very small percentage of cases. That’s one of the problems. We have almost a thousand people a day who have sudden cardiac arrest out in the community alone and more in the hospital.
We know that early defibrillation and early CPR can contribute, but it’s still a small percentage of those. About 75%-85% of the cases that we go out to see will have nonshockable rhythms and flatlines. Some cases are what we call “pulseless electrical activity,” meaning that it looks like there is some kind of organized complex, but there is no pulse associated with it.
That’s why it’s a problem, because they don’t come back. Part of the reason why we see poor outcomes is not only that these cases tend to be people who, say, were in ventricular fibrillation and then just went on over time and were not witnessed or resuscitated or had a long response time. They basically either go into flatline or autoconvert into these bizarre rhythms.
The other issue is the way we perform CPR. CPR has been lifesaving, but it only generates about 20% and maybe 15% in some cases of normal blood flow, and particularly, cerebral perfusion pressure. We’ve looked at this nicely in the laboratory.
For example, during chest compressions, we’re hoping during the recoil phase to pull blood down and back into the right heart. The problem is that you’re not only setting a pressure rate up here to the arterial side but also, you’re setting back pressure wave on the venous side. Obviously, the arterial side always wins out, but it’s just not as efficient as it could be, at 20% or 30%.
What does this entail? It entails several independent mechanisms in terms of how they work, but they all do the same thing, which is they help to pull blood out of the brain and back into the right heart by basically manipulating intrathoracic pressure and creating more of a vacuum to get blood back there.
It’s so important that people do quality CPR. You have to have a good release and that helps us suck a little bit of blood and sucks the air in. As soon as the air rushes in, it neutralizes the pressure and there’s no more vacuum and nothing else is happening until the next squeeze.
What we have found is that we can cap the airway just for a second with a little pop-up valve. It acts like when you’re sucking a milkshake through a straw and it creates more of a vacuum in the chest. Just a little pop-up valve that pulls a little bit more blood out of the brain and the rest of the body and into the right heart.
We’ve shown in a human study that, for example, the systolic blood pressure almost doubles. It really goes from 40 mm Hg during standard CPR up to 80 mm Hg, and that would be sustained for 14-15 minutes. That was a nice little study that was done in Milwaukee a few years ago.
The other thing that happens is, if you add on something else, it’s like a toilet plunger. I think many people have seen it; it’s called “active compression-decompression.” It not only compresses, but it decompresses. Where it becomes even more effective is that if you had broken bones or stiff bones as you get older or whatever it may be, as you do the CPR, you’re still getting the push down and then you’re getting the pull out. It helps on several levels. More importantly, when you put the two together, they’re very synergistic.
We, have already done the clinical trial that is the proof of concept, and that was published in The Lancet about 10 years ago. In that study, we found that the combination of those two dramatically improved survival rates by 50%, with 1-year survival neurologically intact. That got us on the right track.
The interesting thing is that someone said, “Can we lift the head up a little bit?” We did a large amount of work in the laboratory over 10 years, fine tuning it. When do you first lift the head? How soon is too soon? It’s probably bad if you just go right to it.
We had to get the pump primed a little bit with these other things to get the flow going better, not only pulling blood out of the brain but now, you have a better flow this way. You have to prime at first for a couple of minutes, and we worked out the timing: Is it 3 or 4 minutes? It seems the timing is right at about 2 minutes, then you gradually elevate the head over about 2 minutes. We’re finding that seems to be the optimal way to do it. About 2 minutes of priming with those other two devices, the adjuncts, and then gradually elevate the head over 2 minutes.
When we do that in the laboratory, we’re getting normalized cerebral perfusion pressures. You’re normalizing the flow back again with that. We’re seeing profound differences in outcome as a result, even in these cases of the nonshockables.
Dr. Glatter: What you’re doing basically is resulting in an increase in cardiac output, essentially. That really is important, especially in these nonshockable rhythms, correct?
Dr. Pepe: Absolutely. As you’re doing this compression and you’re getting these intracranial pulse waves that are going up because they’re colliding up there. It could be even damaging in itself, but we’re seeing these intracranial raises. The intracranial pressure starts going up more and more over time. Also, peripherally in most people, you’re not getting good flow out there; then, your vasculature starts to relax. The arterials are starting to not get oxygen, so they don’t go out.
With this technique where we’re returning the pressure, we’re getting to 40% of normal now with the active compression-decompression CPR plus an impedance threshold device (ACD+ITD CPR) approach. Now, you add this, and you’re almost normalizing. In humans, even in these asystole patients, we’re seeing end-title CO2s which are generally in the 15-20 range with standard CPR are now up with ACD+ITD CPR in the 30%-40% range, where we’re getting through 30 or 40 end-tidal CO2s. Now, we’re seeing even the end-tidal CO2s moving up into the 40s and 50s. We know there’s a surrogate marker telling us that we are generating much better flows not only to the rest of the body, but most importantly, to the brain.
Dr. Glatter: Ryan, could you tell us about the approach in terms of on scene, what you’re doing and how you use the device itself? Maybe you could talk about the backpack that you developed with your fire department?
Ryan P. Quinn, BS, EMS: Our approach has always been to get to the patient quickly, like everybody’s approach on a cardiac arrest when you’re responding. We are an advanced life-support paramedic ambulance service through the fire department – we’re all cross-trained firefighter paramedics. Our first vehicle from the fire department is typically the ambulance. It’s smaller and a little quicker than the fire engine. Two paramedics are going to jump out with two backpacks. One has the automated compressive device (we use the Lucas), and the other one is the sequential patient lifting device, the EleGARD.
Our two paramedics are quick to the patient’s side, and once they make contact with the patient to verify pulseless cardiac arrest, they will unpack. One person will go right to compressions if there’s nobody on compressions already. Sometimes we have a first responder police officer with an automated external defibrillator (AED). We go right to the patient’s side, concentrate on compressions, and within 90 seconds to 2 minutes, we have our bags unpacked, we’ve got the devices turned on, patient lifted up, slid under the device, and we have a supraglottic airway that is placed within 15 seconds already premade with the ITD on top. We have a sealed airway that we can continue to compress with Dr. Pepe’s original discussion of building on what’s previously been shown to work.
Dr. Pepe: Let me make a comment about this. This is so important, what Ryan is saying, because it’s something we found during the study. It’s really a true pit-crew approach. You’re not only getting these materials, which you think you need a medical Sherpa for, but you don’t. They set it up and then when they open it up, it’s all laid out just exactly as you need it. It’s not just how fast you get there; it’s how fast you get this done.
When we look at all cases combined against high-performance systems that had some of the highest survival rates around, when we compare it to those, we found that overall, even if you looked at the ones that had over 20-minute responses, the odds ratios were still three to four times higher. It was impressive.
If you looked at it under 15 minutes, which is really reasonable for most systems that get there by the way, the average time that people start CPR in any system in these studies has been about 8 minutes if you actually start this thing, which takes about 2 minutes more for this new bundle of care with this triad, it’s almost 12-14 times higher in terms of the odds ratio. I’ve never seen anything like that where the higher end is over 100 in terms of your confidence intervals.
Ryan’s system did really well and is one of those with even higher levels of outcomes, mostly because they got it on quickly. It’s like the AED for nonshockables but better because you have a wider range of efficacy where it will work.
Dr. Glatter: When the elapsed time was less than 11 minutes, that seemed to be an inflection point in the study, is that correct? You saw that 11-fold higher incidence in terms of neurologically intact survival, is that correct?
Dr. Pepe: We picked that number because that was the median time to get it on board. Half the people were getting it within that time period. The fact that you have a larger window, we’re talking about 13- almost 14-fold improvements in outcome if it was under 15 minutes. It doesn’t matter about the 11 or the 12. It’s the faster you get it on board, the better off you are.
Dr. Glatter: What’s the next step in the process of doing trials and having implementation on a larger scale based on your Annals of Emergency Medicine study? Where do you go from here?
Dr. Pepe: I’ve come to find out there are many confounding variables. What was the quality of CPR? How did people ventilate? Did they give the breath and hold it? Did they give a large enough breath so that blood can go across the transpulmonary system? There are many confounding variables. That’s why I think, in the future, it’s going to be more of looking at things like propensity score matching because we know all the variables that change outcomes. I think that’s going to be a way for me.
The other thing is that we were looking at only 380 cases here. When this doubles up in numbers, as we accrue more cases around the country of people who are implementing this, these numbers I just quoted are going to go up much higher. Unwitnessed asystole is considered futile, and you just don’t get them back. To be able to get these folks back now, even if it’s a small percentage, and the fact that we know that we’re producing this better flow, is pretty striking.
I’m really impressed, and the main thing is to make sure people are educated about it. Number two is that they understand that it has to be done right. It cannot be done wrong or you’re not going to see the differences. Getting it done right is not only following the procedures, the sequence, and how you do it, but it also has to do with getting there quickly, including assigning the right people to put it on and having well-trained people who know what they’re doing.
Dr. Glatter: In general, the lay public obviously should not attempt this in the field lifting someone’s head up in the sense of trying to do chest compressions. I think that message is important that you just said. It’s not ready for prime time yet in any way. It has to be done right.
Dr. Pepe: Bystanders have to learn CPR – they will buy us time and we’ll have better outcomes when they do that. That’s number one. Number two is that as more and more systems adopt this, you’re going to see more people coming back. If you think about what we’re doing now, if we only get back 5% of these nonshockable vs. less than 1%, it’s 5% of 800 people a day because a thousand people a day die. Several dozens of lives can be saved on a daily basis, coming back neurologically intact. That’s the key thing.
Dr. Glatter: Ryan, can you comment about your experience in the field? Is there anything in terms of your current approach that you think would be ideal to change at this point?
Mr. Quinn: We’ve established that this is the approach that we want to take and we’re just fine tuning it to be more efficient. Using the choreography of which person is going to do which role, we have clearly defined roles and clearly defined command of the scene so we’re not missing anything. Training is extremely important.
Dr. Glatter: Paul, I want to ask you about your anecdotal experience of people waking up quickly and talking after elevating their heads and going through this process. Having people talk about it and waking up is really fascinating. Maybe you can comment further on this.
Dr. Pepe: That’s a great point that you bring up because a 40- to 50-year-old guy who got saved with this approach, when he came around, he said he was hearing what people were saying. When he came out of it, he found out he had been getting CPR for about 25 minutes because he had persistent recurring ventricular fibrillation. He said, “How could I have survived that that long?”
When we told him about the new approach, he added, “Well, that’s like neuroprotective.” He’s right, because in the laboratory, we showed it was neuroprotective and we’re also getting better flows back there. It goes along with everything else, and so we’ve adopted the name because it is.
These are really high-powered systems we are comparing against, and we have the same level of return of spontaneous circulation. The major difference was when you started talking about the neurointact survival. We don’t have enough numbers yet, but next go around, we’re going to look at cerebral performance category (CPC) – CPC1 vs. the CPC2 – which were both considered intact, but CPC1 is actually better. We’re seeing many more of those, anecdotally.
I also wanted to mention that people do bring this up and say, “Well, let’s do a trial.” As far as we’re concerned, the trial’s been done in terms of The Lancet study 10 years ago that showed that the active compression-decompression had tremendously better outcomes. We show in the laboratories that you augment that a little bit. These are all [Food and Drug Administration] approved. You can go out and buy it tomorrow and get it done. I have no conflicts of interest, by the way, with any of this.
To have this device that’s going to have the potential of saving so many more lives is really an exciting breakthrough. More importantly, we’re understanding more now about the physiology of CPR and why it works. It could work much better with the approaches that we’ve been developing over the last 20 years or so.
Dr. Glatter: Absolutely. I want to thank both of you gentlemen. It’s been really an incredible experience to learn more about an advance in resuscitation that could truly be lifesaving. Thank you again for taking time to join us.
Dr. Glatter is an attending physician in the department of emergency medicine, Lenox Hill Hospital, New York. Dr. Pepe is professor, department of management, policy, and community health, University of Texas Health Sciences Center, Houston. Mr. Quinn is EMS Chief, Edina (Minn.) Fire Department. No conflicts of interest were reported.
A version of this article first appeared Jan. 26 on Medscape.com.
Damar Hamlin’s cardiac arrest: Key lessons
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: 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: 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: 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.
A freak impalement by a model rocket has this doctor scrambling
North central Washington state is a lot of nothing other than fields. Every year, the Federal Aviation Administration closes the airspace in a remote part of the area for a model rocket competition, the National Association of Rocketry Annual Meet. It’s a 2-day event and a pretty big deal. People come from all over the country to be there.
When you were a kid, you probably saw those rockets that are 3 feet tall. You launch them up in the air, they have a little parachute that comes out and they come back down to the ground. Well, picture that on ultimate steroids. There are anywhere from 3-foot to almost 20-foot-long rockets at this thing. People show up with horse trailers full of rockets and components. I mean, it’s an obsession.
Some of these rockets are super sophisticated. They have different stages where the first stage burns out and the second takes over. They go up thousands of feet to the edge of the stratosphere. Most of them have GoPro cameras, so you get to see when the rocket reaches the top of its trajectory and the last engine burns out. As it starts to descend, a parachute deploys and it can drift back anywhere from pretty close to where you launched it to a couple miles away. Then you use your little GPS to find it.
Why not? I drove out there and parked my Jeep and was walking over to the competition when I noticed something off. A bigger commotion than there should have been.
Here’s what happened 2 minutes before I got there:
A 5-foot-long rocket, 2½ inches in diameter, had reached the top of its several thousand–foot trajectory and was ready to come back to Earth. But its parachute didn’t deploy. It turned itself point-down and literally shot back to earth like a rocket.
It had gone up pretty darn straight and came down just as straight – right into a circle of people sitting in lawn chairs.
It hit a middle-aged man. But you can’t imagine how. First of all, who knows how fast it was going. The point glanced off his forehead and ... how to describe the rest. The man was pretty heavy. So the rocket impaled him through the abdomen and stuck right into the ground. As in, the point entered the top of his belly just below chest level and came out the bottom of his belly. The rocket pinned him to the ground through his belly.
Well, this was not how I planned on spending my day. But my spectator time was over. There were a lot of people running around in circles where he was pinned, not really knowing what to do.
When I said I was an emergency physician, instantly 15 heads looked right at me for direction like, Oh my gosh, please take over! A lot of people were asking: “What can I do? What can I do?” I said: “Well, we don’t need to do CPR. What we really need to do is get this rocket out of the ground. We need to keep him still while we dig out the rocket and get him flat.”
People gently dug around the nose of the rocket. It was in about 6 or 8 inches, enough that we didn’t want to just yank on it (I still marvel at how fast it must have been traveling to both impale the man the way it did and also jam into the ground like that). We wanted to loosen it up and ease it out of the ground.
We managed to dig the nose out and get the guy on his back. Needless to say, he wasn’t particularly comfortable. He looked pretty ashen, like he was in pretty good trouble.
The festival had an EMS kit with some bandages in it, but not a whole lot else. There’s the old joke in emergency medicine: What can you do with duct tape, a Swiss army knife, and a paper clip? It’s like, what has anybody got that might work here?
What we really needed to do was keep both the rocket and the man from moving. We cut off his shirt and got his pants down so that I could better see where it entered and exited. Then we used a couple of clean T-shirts to stabilize the rocket so it didn’t move while he lay flat. It didn’t bleed all that much. And his belly wasn’t massively expanding like he was bleeding internally. I mean, he looked crappy. But so would I!
We were about an hour away from the closest EMS and only a couple people even had cell service out there. But we managed to get hold of EMS. It was also one of those 92-degree days with no shade for 50 miles in any direction.
There was a volunteer firefighter there to man the fire rig. He helped carry the guy into an air-conditioned trailer without moving him very much.
Basically, we stabilized him by keeping him super still and as comfortable as we could until EMS arrived. I rode with him about an hour and a half to the closest trauma center in Central Washington. He was conscious, which was lousy for him but reassuring for me. “You’re still talking to me,” I said. “I think you’re going to be okay.”
One of the take-home points from a medical point of view is never try to remove something sticking out of someone when you’re out in the field. If it’s pushing against something vital, you could do a lot of damage, and if it’s up against a blood vessel, that vessel’s going to bleed uncontrollably.
We got to the trauma center and they took him to the OR. By the grace of friendships, somebody got his wife to the hospital. She was calmer than I think I would have been if my spouse had been hit by a rocket.
The full diagnostic story: The rocket bouncing off his forehead gave him a small skull fracture and slight concussion. That was no big deal. But picture this: The rocket only went through his belly fat. It didn’t hit any of his abdominal organs! I still think this is absolutely amazing. If he had been leaning forward in his lawn chair even a few inches, the rocket would’ve gone through his head and that would’ve been all they wrote.
He stayed in the hospital for a couple of days. I never saw him again, but I received follow-up from the surgeon. And I read the paper the next day. Let me tell you, in Central Washington, this is pretty big news.
It wasn’t the way I’d planned my morning. But you just can’t predict that kind of thing. I don’t know, maybe spiritually or karma wise, I was meant to show up about 90 seconds after he’d been hit. The only emergency physician at the whole event, just by chance. My work blesses me with a certain skill set. I know when to really worry, how to go about keeping somebody safe until you can get them to the ED. It’s something I thank my stars for every single day.
As I said to the guy on the way to the hospital: “Well, it’s not your lucky day, but it sure as heck could have been a whole lot unluckier.”
Stephen Anderson, MD, is an emergency medicine physician in Auburn, Washington and is affiliated with MultiCare Auburn Medical Center.
A version of this article first appeared on Medscape.com.
North central Washington state is a lot of nothing other than fields. Every year, the Federal Aviation Administration closes the airspace in a remote part of the area for a model rocket competition, the National Association of Rocketry Annual Meet. It’s a 2-day event and a pretty big deal. People come from all over the country to be there.
When you were a kid, you probably saw those rockets that are 3 feet tall. You launch them up in the air, they have a little parachute that comes out and they come back down to the ground. Well, picture that on ultimate steroids. There are anywhere from 3-foot to almost 20-foot-long rockets at this thing. People show up with horse trailers full of rockets and components. I mean, it’s an obsession.
Some of these rockets are super sophisticated. They have different stages where the first stage burns out and the second takes over. They go up thousands of feet to the edge of the stratosphere. Most of them have GoPro cameras, so you get to see when the rocket reaches the top of its trajectory and the last engine burns out. As it starts to descend, a parachute deploys and it can drift back anywhere from pretty close to where you launched it to a couple miles away. Then you use your little GPS to find it.
Why not? I drove out there and parked my Jeep and was walking over to the competition when I noticed something off. A bigger commotion than there should have been.
Here’s what happened 2 minutes before I got there:
A 5-foot-long rocket, 2½ inches in diameter, had reached the top of its several thousand–foot trajectory and was ready to come back to Earth. But its parachute didn’t deploy. It turned itself point-down and literally shot back to earth like a rocket.
It had gone up pretty darn straight and came down just as straight – right into a circle of people sitting in lawn chairs.
It hit a middle-aged man. But you can’t imagine how. First of all, who knows how fast it was going. The point glanced off his forehead and ... how to describe the rest. The man was pretty heavy. So the rocket impaled him through the abdomen and stuck right into the ground. As in, the point entered the top of his belly just below chest level and came out the bottom of his belly. The rocket pinned him to the ground through his belly.
Well, this was not how I planned on spending my day. But my spectator time was over. There were a lot of people running around in circles where he was pinned, not really knowing what to do.
When I said I was an emergency physician, instantly 15 heads looked right at me for direction like, Oh my gosh, please take over! A lot of people were asking: “What can I do? What can I do?” I said: “Well, we don’t need to do CPR. What we really need to do is get this rocket out of the ground. We need to keep him still while we dig out the rocket and get him flat.”
People gently dug around the nose of the rocket. It was in about 6 or 8 inches, enough that we didn’t want to just yank on it (I still marvel at how fast it must have been traveling to both impale the man the way it did and also jam into the ground like that). We wanted to loosen it up and ease it out of the ground.
We managed to dig the nose out and get the guy on his back. Needless to say, he wasn’t particularly comfortable. He looked pretty ashen, like he was in pretty good trouble.
The festival had an EMS kit with some bandages in it, but not a whole lot else. There’s the old joke in emergency medicine: What can you do with duct tape, a Swiss army knife, and a paper clip? It’s like, what has anybody got that might work here?
What we really needed to do was keep both the rocket and the man from moving. We cut off his shirt and got his pants down so that I could better see where it entered and exited. Then we used a couple of clean T-shirts to stabilize the rocket so it didn’t move while he lay flat. It didn’t bleed all that much. And his belly wasn’t massively expanding like he was bleeding internally. I mean, he looked crappy. But so would I!
We were about an hour away from the closest EMS and only a couple people even had cell service out there. But we managed to get hold of EMS. It was also one of those 92-degree days with no shade for 50 miles in any direction.
There was a volunteer firefighter there to man the fire rig. He helped carry the guy into an air-conditioned trailer without moving him very much.
Basically, we stabilized him by keeping him super still and as comfortable as we could until EMS arrived. I rode with him about an hour and a half to the closest trauma center in Central Washington. He was conscious, which was lousy for him but reassuring for me. “You’re still talking to me,” I said. “I think you’re going to be okay.”
One of the take-home points from a medical point of view is never try to remove something sticking out of someone when you’re out in the field. If it’s pushing against something vital, you could do a lot of damage, and if it’s up against a blood vessel, that vessel’s going to bleed uncontrollably.
We got to the trauma center and they took him to the OR. By the grace of friendships, somebody got his wife to the hospital. She was calmer than I think I would have been if my spouse had been hit by a rocket.
The full diagnostic story: The rocket bouncing off his forehead gave him a small skull fracture and slight concussion. That was no big deal. But picture this: The rocket only went through his belly fat. It didn’t hit any of his abdominal organs! I still think this is absolutely amazing. If he had been leaning forward in his lawn chair even a few inches, the rocket would’ve gone through his head and that would’ve been all they wrote.
He stayed in the hospital for a couple of days. I never saw him again, but I received follow-up from the surgeon. And I read the paper the next day. Let me tell you, in Central Washington, this is pretty big news.
It wasn’t the way I’d planned my morning. But you just can’t predict that kind of thing. I don’t know, maybe spiritually or karma wise, I was meant to show up about 90 seconds after he’d been hit. The only emergency physician at the whole event, just by chance. My work blesses me with a certain skill set. I know when to really worry, how to go about keeping somebody safe until you can get them to the ED. It’s something I thank my stars for every single day.
As I said to the guy on the way to the hospital: “Well, it’s not your lucky day, but it sure as heck could have been a whole lot unluckier.”
Stephen Anderson, MD, is an emergency medicine physician in Auburn, Washington and is affiliated with MultiCare Auburn Medical Center.
A version of this article first appeared on Medscape.com.
North central Washington state is a lot of nothing other than fields. Every year, the Federal Aviation Administration closes the airspace in a remote part of the area for a model rocket competition, the National Association of Rocketry Annual Meet. It’s a 2-day event and a pretty big deal. People come from all over the country to be there.
When you were a kid, you probably saw those rockets that are 3 feet tall. You launch them up in the air, they have a little parachute that comes out and they come back down to the ground. Well, picture that on ultimate steroids. There are anywhere from 3-foot to almost 20-foot-long rockets at this thing. People show up with horse trailers full of rockets and components. I mean, it’s an obsession.
Some of these rockets are super sophisticated. They have different stages where the first stage burns out and the second takes over. They go up thousands of feet to the edge of the stratosphere. Most of them have GoPro cameras, so you get to see when the rocket reaches the top of its trajectory and the last engine burns out. As it starts to descend, a parachute deploys and it can drift back anywhere from pretty close to where you launched it to a couple miles away. Then you use your little GPS to find it.
Why not? I drove out there and parked my Jeep and was walking over to the competition when I noticed something off. A bigger commotion than there should have been.
Here’s what happened 2 minutes before I got there:
A 5-foot-long rocket, 2½ inches in diameter, had reached the top of its several thousand–foot trajectory and was ready to come back to Earth. But its parachute didn’t deploy. It turned itself point-down and literally shot back to earth like a rocket.
It had gone up pretty darn straight and came down just as straight – right into a circle of people sitting in lawn chairs.
It hit a middle-aged man. But you can’t imagine how. First of all, who knows how fast it was going. The point glanced off his forehead and ... how to describe the rest. The man was pretty heavy. So the rocket impaled him through the abdomen and stuck right into the ground. As in, the point entered the top of his belly just below chest level and came out the bottom of his belly. The rocket pinned him to the ground through his belly.
Well, this was not how I planned on spending my day. But my spectator time was over. There were a lot of people running around in circles where he was pinned, not really knowing what to do.
When I said I was an emergency physician, instantly 15 heads looked right at me for direction like, Oh my gosh, please take over! A lot of people were asking: “What can I do? What can I do?” I said: “Well, we don’t need to do CPR. What we really need to do is get this rocket out of the ground. We need to keep him still while we dig out the rocket and get him flat.”
People gently dug around the nose of the rocket. It was in about 6 or 8 inches, enough that we didn’t want to just yank on it (I still marvel at how fast it must have been traveling to both impale the man the way it did and also jam into the ground like that). We wanted to loosen it up and ease it out of the ground.
We managed to dig the nose out and get the guy on his back. Needless to say, he wasn’t particularly comfortable. He looked pretty ashen, like he was in pretty good trouble.
The festival had an EMS kit with some bandages in it, but not a whole lot else. There’s the old joke in emergency medicine: What can you do with duct tape, a Swiss army knife, and a paper clip? It’s like, what has anybody got that might work here?
What we really needed to do was keep both the rocket and the man from moving. We cut off his shirt and got his pants down so that I could better see where it entered and exited. Then we used a couple of clean T-shirts to stabilize the rocket so it didn’t move while he lay flat. It didn’t bleed all that much. And his belly wasn’t massively expanding like he was bleeding internally. I mean, he looked crappy. But so would I!
We were about an hour away from the closest EMS and only a couple people even had cell service out there. But we managed to get hold of EMS. It was also one of those 92-degree days with no shade for 50 miles in any direction.
There was a volunteer firefighter there to man the fire rig. He helped carry the guy into an air-conditioned trailer without moving him very much.
Basically, we stabilized him by keeping him super still and as comfortable as we could until EMS arrived. I rode with him about an hour and a half to the closest trauma center in Central Washington. He was conscious, which was lousy for him but reassuring for me. “You’re still talking to me,” I said. “I think you’re going to be okay.”
One of the take-home points from a medical point of view is never try to remove something sticking out of someone when you’re out in the field. If it’s pushing against something vital, you could do a lot of damage, and if it’s up against a blood vessel, that vessel’s going to bleed uncontrollably.
We got to the trauma center and they took him to the OR. By the grace of friendships, somebody got his wife to the hospital. She was calmer than I think I would have been if my spouse had been hit by a rocket.
The full diagnostic story: The rocket bouncing off his forehead gave him a small skull fracture and slight concussion. That was no big deal. But picture this: The rocket only went through his belly fat. It didn’t hit any of his abdominal organs! I still think this is absolutely amazing. If he had been leaning forward in his lawn chair even a few inches, the rocket would’ve gone through his head and that would’ve been all they wrote.
He stayed in the hospital for a couple of days. I never saw him again, but I received follow-up from the surgeon. And I read the paper the next day. Let me tell you, in Central Washington, this is pretty big news.
It wasn’t the way I’d planned my morning. But you just can’t predict that kind of thing. I don’t know, maybe spiritually or karma wise, I was meant to show up about 90 seconds after he’d been hit. The only emergency physician at the whole event, just by chance. My work blesses me with a certain skill set. I know when to really worry, how to go about keeping somebody safe until you can get them to the ED. It’s something I thank my stars for every single day.
As I said to the guy on the way to the hospital: “Well, it’s not your lucky day, but it sure as heck could have been a whole lot unluckier.”
Stephen Anderson, MD, is an emergency medicine physician in Auburn, Washington and is affiliated with MultiCare Auburn Medical Center.
A version of this article first appeared on Medscape.com.
Kids with concussions may benefit from early return to school
The timing for return to school after a concussion has been the subject of guidelines, but data on how the timing of school returns affects later symptom burdens are limited, Christopher G. Vaughan, PhD, of Children’s National Hospital, Rockville, Md., and colleagues wrote.
Examining how the timing of return to school (RTS) affects later symptoms is needed to inform early postinjury management, they said.
In the new study published in JAMA Network Open, the researchers identified 1,630 children and teens aged 5-18 years who were treated for concussions at nine Canadian pediatric EDs. The primary outcome was symptom burden at 14 days post concussion, based on the Post-Concussion Symptom Inventory (PCSI). Early RTS was defined as missing fewer than 3 days of school post concussion.
Overall, the mean number of missed school days was 3.74 (excluding weekends). When divided by age, the mean number of missed days was 2.61 for children aged 5-7 years, 3.26 for those aged 8-12 years, and 4.71 for those aged 13-18 years.
Slightly more than half (53.7%) of the participants had an early RTS of 2 missed days or fewer. Later RTS was most common in the oldest age group, followed by the middle and younger age groups.
The researchers used a propensity score–matched analysis to determine associations. At 14 days, an early RTS was associated with reduced symptoms among 8- to 12-year-olds and 13- to 18-year-olds, though not in the youngest patients aged 5-7 years. In addition, the researchers created quantiles based on initial symptom ratings.
For the youngest age group, the association between early RTS and reduced symptoms at day 14 was higher among those with lower initial symptoms.
For the two older groups, the association was higher for those with higher initial symptoms (based on the PCSI).
The findings that earlier RTS was associated with a lower symptom burden at day 14 for those with higher levels of symptoms at baseline was surprising, but the mechanisms of the timing and effect of RTS requires more study, the researchers wrote in their discussion.
The effect of early RTS on symptoms may be in part related to factors such as “the benefits of socialization, reduced stress from not missing too much school, maintaining or returning to a normal sleep-wake schedule, and returning to light to moderate physical activity (gym class and recreational activities),” the researchers noted.
Another study related to recovery and concussion recently appeared in Neurology. In that study, the authors found that those athletes who took a longer time to recover from a sports-related concussion could still return to play with additional time off, but the methods and populations differed from the current study, which focused on RTS rather than returning to play.
The current study findings were limited by several factors including the lack of randomization for RTS timing and a lack of data on the variety of potential supports and accommodations students received, the researchers noted.
However, the results were strengthened by the large size and diverse nature of the concussions, and the roughly equal representation of boys and girls, they said.
Although randomized trials are needed to determine the best timing for RTS, the current study suggests that RTS within 2 days of a concussion is associated with improved symptoms, “and may directly or indirectly promote faster recovery,” they concluded.
Early return remains feasible for most children and teens
“Return to school can be a complicated issue for children and teens with concussions,” said Caitlyn Mooney, MD, a pediatrician and specialist in sports medicine at the University of Texas Health Science Center, San Antonio, said in an interview. Although much research has focused on diagnosis and return to sport after a concussion, there has been less focus on returning to school and learning. Various issues post concussion can make schooling difficult, and students may experience trouble with vision, concentration, sleep, headaches, and more.
Despite this knowledge, studies that specifically address recommended school protocols are limited, Dr. Mooney said. “Additionally, all concussions are different; while some students will need minimal help to return and succeed in school, others may need individualized learning plans and accommodations for school.” A return to school ideally would be a team-based approach with input from the parent, patient, physician, and educators.
“The theory of cognitive rest stems from the idea that a concussion causes metabolic dysfunction in the brain, and that increasing the metabolic demands of the brain can result in symptoms and a delayed return to school,” said Dr. Mooney.
Evidence suggests that those who start resting early after a concussion improve more quickly, “but there has been ongoing discussion over the years of what is the correct balance of cognitive rest to returning to modified activity,” she said. “This has led to the current general recommendation of rest for 24-48 hours followed by a gradual return to school as tolerated.”
Although the current study is large, it is limited by the lack of randomization, Dr. Mooney noted, therefore conclusions cannot be made that the cause of the improved symptoms is a quicker return to school.
However, the results support data from previous studies, in that both of the older age groups showed less disease burden at 14 days after an earlier return to school, she said.
“With prolonged absences, adolescents get isolated at home away from friends, and they may have increased mood symptoms. Additionally, I have found a high number of my patients who do not go to school as quickly have more sleep disturbance, which seems to increase symptoms such as difficulty concentrating or headaches,” she said. “It seems like the students do benefit from a routine schedule even if they have to have some accommodations at school, especially older students who may have more stress about missing school and falling behind on schoolwork.”
The message for pediatricians is that return to school should be individualized, Dr. Mooney said.
Although the current study does not dictate the optimal return to school, the results support those of previous studies in showing that, after 1-2 days of rest, an early return does not harm children and teens and may improve symptoms in many cases, she said. “In my experience, sometimes schools find it easier to keep the student at home rather than manage rest or special accommodations,” but the current study suggests that delaying return to school may not be the right choice for many patients.
“I hope this study empowers clinicians to advocate for these students, that the right place for them is in the classroom even with rest, extra time, or other accommodations,” said Dr. Mooney.
“Each concussion should be evaluated and treated individually; there will likely be a few who may need to stay home for a longer period of time, but this study suggests that the majority of students will suffer no ill effects from returning to the normal routine after a 2-day rest,” she noted.
The study was supported by the Canadian Institutes for Health Research. Dr. Vaughan and several coauthors disclosed being authors of the Postconcussion Symptom Inventory outside of the current study. Dr. Mooney had no financial conflicts to disclose.
The timing for return to school after a concussion has been the subject of guidelines, but data on how the timing of school returns affects later symptom burdens are limited, Christopher G. Vaughan, PhD, of Children’s National Hospital, Rockville, Md., and colleagues wrote.
Examining how the timing of return to school (RTS) affects later symptoms is needed to inform early postinjury management, they said.
In the new study published in JAMA Network Open, the researchers identified 1,630 children and teens aged 5-18 years who were treated for concussions at nine Canadian pediatric EDs. The primary outcome was symptom burden at 14 days post concussion, based on the Post-Concussion Symptom Inventory (PCSI). Early RTS was defined as missing fewer than 3 days of school post concussion.
Overall, the mean number of missed school days was 3.74 (excluding weekends). When divided by age, the mean number of missed days was 2.61 for children aged 5-7 years, 3.26 for those aged 8-12 years, and 4.71 for those aged 13-18 years.
Slightly more than half (53.7%) of the participants had an early RTS of 2 missed days or fewer. Later RTS was most common in the oldest age group, followed by the middle and younger age groups.
The researchers used a propensity score–matched analysis to determine associations. At 14 days, an early RTS was associated with reduced symptoms among 8- to 12-year-olds and 13- to 18-year-olds, though not in the youngest patients aged 5-7 years. In addition, the researchers created quantiles based on initial symptom ratings.
For the youngest age group, the association between early RTS and reduced symptoms at day 14 was higher among those with lower initial symptoms.
For the two older groups, the association was higher for those with higher initial symptoms (based on the PCSI).
The findings that earlier RTS was associated with a lower symptom burden at day 14 for those with higher levels of symptoms at baseline was surprising, but the mechanisms of the timing and effect of RTS requires more study, the researchers wrote in their discussion.
The effect of early RTS on symptoms may be in part related to factors such as “the benefits of socialization, reduced stress from not missing too much school, maintaining or returning to a normal sleep-wake schedule, and returning to light to moderate physical activity (gym class and recreational activities),” the researchers noted.
Another study related to recovery and concussion recently appeared in Neurology. In that study, the authors found that those athletes who took a longer time to recover from a sports-related concussion could still return to play with additional time off, but the methods and populations differed from the current study, which focused on RTS rather than returning to play.
The current study findings were limited by several factors including the lack of randomization for RTS timing and a lack of data on the variety of potential supports and accommodations students received, the researchers noted.
However, the results were strengthened by the large size and diverse nature of the concussions, and the roughly equal representation of boys and girls, they said.
Although randomized trials are needed to determine the best timing for RTS, the current study suggests that RTS within 2 days of a concussion is associated with improved symptoms, “and may directly or indirectly promote faster recovery,” they concluded.
Early return remains feasible for most children and teens
“Return to school can be a complicated issue for children and teens with concussions,” said Caitlyn Mooney, MD, a pediatrician and specialist in sports medicine at the University of Texas Health Science Center, San Antonio, said in an interview. Although much research has focused on diagnosis and return to sport after a concussion, there has been less focus on returning to school and learning. Various issues post concussion can make schooling difficult, and students may experience trouble with vision, concentration, sleep, headaches, and more.
Despite this knowledge, studies that specifically address recommended school protocols are limited, Dr. Mooney said. “Additionally, all concussions are different; while some students will need minimal help to return and succeed in school, others may need individualized learning plans and accommodations for school.” A return to school ideally would be a team-based approach with input from the parent, patient, physician, and educators.
“The theory of cognitive rest stems from the idea that a concussion causes metabolic dysfunction in the brain, and that increasing the metabolic demands of the brain can result in symptoms and a delayed return to school,” said Dr. Mooney.
Evidence suggests that those who start resting early after a concussion improve more quickly, “but there has been ongoing discussion over the years of what is the correct balance of cognitive rest to returning to modified activity,” she said. “This has led to the current general recommendation of rest for 24-48 hours followed by a gradual return to school as tolerated.”
Although the current study is large, it is limited by the lack of randomization, Dr. Mooney noted, therefore conclusions cannot be made that the cause of the improved symptoms is a quicker return to school.
However, the results support data from previous studies, in that both of the older age groups showed less disease burden at 14 days after an earlier return to school, she said.
“With prolonged absences, adolescents get isolated at home away from friends, and they may have increased mood symptoms. Additionally, I have found a high number of my patients who do not go to school as quickly have more sleep disturbance, which seems to increase symptoms such as difficulty concentrating or headaches,” she said. “It seems like the students do benefit from a routine schedule even if they have to have some accommodations at school, especially older students who may have more stress about missing school and falling behind on schoolwork.”
The message for pediatricians is that return to school should be individualized, Dr. Mooney said.
Although the current study does not dictate the optimal return to school, the results support those of previous studies in showing that, after 1-2 days of rest, an early return does not harm children and teens and may improve symptoms in many cases, she said. “In my experience, sometimes schools find it easier to keep the student at home rather than manage rest or special accommodations,” but the current study suggests that delaying return to school may not be the right choice for many patients.
“I hope this study empowers clinicians to advocate for these students, that the right place for them is in the classroom even with rest, extra time, or other accommodations,” said Dr. Mooney.
“Each concussion should be evaluated and treated individually; there will likely be a few who may need to stay home for a longer period of time, but this study suggests that the majority of students will suffer no ill effects from returning to the normal routine after a 2-day rest,” she noted.
The study was supported by the Canadian Institutes for Health Research. Dr. Vaughan and several coauthors disclosed being authors of the Postconcussion Symptom Inventory outside of the current study. Dr. Mooney had no financial conflicts to disclose.
The timing for return to school after a concussion has been the subject of guidelines, but data on how the timing of school returns affects later symptom burdens are limited, Christopher G. Vaughan, PhD, of Children’s National Hospital, Rockville, Md., and colleagues wrote.
Examining how the timing of return to school (RTS) affects later symptoms is needed to inform early postinjury management, they said.
In the new study published in JAMA Network Open, the researchers identified 1,630 children and teens aged 5-18 years who were treated for concussions at nine Canadian pediatric EDs. The primary outcome was symptom burden at 14 days post concussion, based on the Post-Concussion Symptom Inventory (PCSI). Early RTS was defined as missing fewer than 3 days of school post concussion.
Overall, the mean number of missed school days was 3.74 (excluding weekends). When divided by age, the mean number of missed days was 2.61 for children aged 5-7 years, 3.26 for those aged 8-12 years, and 4.71 for those aged 13-18 years.
Slightly more than half (53.7%) of the participants had an early RTS of 2 missed days or fewer. Later RTS was most common in the oldest age group, followed by the middle and younger age groups.
The researchers used a propensity score–matched analysis to determine associations. At 14 days, an early RTS was associated with reduced symptoms among 8- to 12-year-olds and 13- to 18-year-olds, though not in the youngest patients aged 5-7 years. In addition, the researchers created quantiles based on initial symptom ratings.
For the youngest age group, the association between early RTS and reduced symptoms at day 14 was higher among those with lower initial symptoms.
For the two older groups, the association was higher for those with higher initial symptoms (based on the PCSI).
The findings that earlier RTS was associated with a lower symptom burden at day 14 for those with higher levels of symptoms at baseline was surprising, but the mechanisms of the timing and effect of RTS requires more study, the researchers wrote in their discussion.
The effect of early RTS on symptoms may be in part related to factors such as “the benefits of socialization, reduced stress from not missing too much school, maintaining or returning to a normal sleep-wake schedule, and returning to light to moderate physical activity (gym class and recreational activities),” the researchers noted.
Another study related to recovery and concussion recently appeared in Neurology. In that study, the authors found that those athletes who took a longer time to recover from a sports-related concussion could still return to play with additional time off, but the methods and populations differed from the current study, which focused on RTS rather than returning to play.
The current study findings were limited by several factors including the lack of randomization for RTS timing and a lack of data on the variety of potential supports and accommodations students received, the researchers noted.
However, the results were strengthened by the large size and diverse nature of the concussions, and the roughly equal representation of boys and girls, they said.
Although randomized trials are needed to determine the best timing for RTS, the current study suggests that RTS within 2 days of a concussion is associated with improved symptoms, “and may directly or indirectly promote faster recovery,” they concluded.
Early return remains feasible for most children and teens
“Return to school can be a complicated issue for children and teens with concussions,” said Caitlyn Mooney, MD, a pediatrician and specialist in sports medicine at the University of Texas Health Science Center, San Antonio, said in an interview. Although much research has focused on diagnosis and return to sport after a concussion, there has been less focus on returning to school and learning. Various issues post concussion can make schooling difficult, and students may experience trouble with vision, concentration, sleep, headaches, and more.
Despite this knowledge, studies that specifically address recommended school protocols are limited, Dr. Mooney said. “Additionally, all concussions are different; while some students will need minimal help to return and succeed in school, others may need individualized learning plans and accommodations for school.” A return to school ideally would be a team-based approach with input from the parent, patient, physician, and educators.
“The theory of cognitive rest stems from the idea that a concussion causes metabolic dysfunction in the brain, and that increasing the metabolic demands of the brain can result in symptoms and a delayed return to school,” said Dr. Mooney.
Evidence suggests that those who start resting early after a concussion improve more quickly, “but there has been ongoing discussion over the years of what is the correct balance of cognitive rest to returning to modified activity,” she said. “This has led to the current general recommendation of rest for 24-48 hours followed by a gradual return to school as tolerated.”
Although the current study is large, it is limited by the lack of randomization, Dr. Mooney noted, therefore conclusions cannot be made that the cause of the improved symptoms is a quicker return to school.
However, the results support data from previous studies, in that both of the older age groups showed less disease burden at 14 days after an earlier return to school, she said.
“With prolonged absences, adolescents get isolated at home away from friends, and they may have increased mood symptoms. Additionally, I have found a high number of my patients who do not go to school as quickly have more sleep disturbance, which seems to increase symptoms such as difficulty concentrating or headaches,” she said. “It seems like the students do benefit from a routine schedule even if they have to have some accommodations at school, especially older students who may have more stress about missing school and falling behind on schoolwork.”
The message for pediatricians is that return to school should be individualized, Dr. Mooney said.
Although the current study does not dictate the optimal return to school, the results support those of previous studies in showing that, after 1-2 days of rest, an early return does not harm children and teens and may improve symptoms in many cases, she said. “In my experience, sometimes schools find it easier to keep the student at home rather than manage rest or special accommodations,” but the current study suggests that delaying return to school may not be the right choice for many patients.
“I hope this study empowers clinicians to advocate for these students, that the right place for them is in the classroom even with rest, extra time, or other accommodations,” said Dr. Mooney.
“Each concussion should be evaluated and treated individually; there will likely be a few who may need to stay home for a longer period of time, but this study suggests that the majority of students will suffer no ill effects from returning to the normal routine after a 2-day rest,” she noted.
The study was supported by the Canadian Institutes for Health Research. Dr. Vaughan and several coauthors disclosed being authors of the Postconcussion Symptom Inventory outside of the current study. Dr. Mooney had no financial conflicts to disclose.
FROM JAMA NETWORK OPEN