Trauma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Among professional football players, the concussion burden during years of active play is associated with post-career high blood pressure, a new study suggests.

Among more than 4,000 participants, 37% had hypertension at a median of 24 years post career and reported a median concussion symptom score (CSS) of 23 on a scale of 0 to 130.

“We have long seen an incompletely explained link between football participation and later-life cardiovascular disease,” Aaron L. Baggish, MD, of Massachusetts Hospital and Harvard Medical School, Boston, told this news organization.

“This study tested [whether] concussion burden during years of active play would be a determinant of later-life hypertension, the most common cause of cardiovascular disease, and indeed found this relationship to be a strong one.”

The study was published online in Circulation.
 

Link to cognitive decline?

Dr. Baggish and colleagues recruited former professional American-style football (ASF) players to participate in a survey administered by the Football Players Health Study at Harvard University.

Concussion burden was quantified with respect to the occurrence and severity of common concussion symptoms – e.g., headaches, nausea, dizziness, confusion, loss of consciousness (LOC), disorientation, and feeling unsteady on one’s feet – over years of active participation.

Prevalent hypertension was determined either by the participants’ previously receiving from a clinician a recommendation for medication for “high blood pressure” or by the participants’ taking such medication at the time of survey completion. Diabetes status was determined by the participants’ receiving a prior recommendation for or prescription for “diabetes or high blood sugar” medication.

Of 15,070 invited to participate in the study, 4,168 did so. The mean age of the participants was 51.8 years; 39.4% were Black; the mean body mass index was 31.3; and 33.9% were linemen. Participants played for a mean of 6.9 seasons and were surveyed at a median 24.1 years post ASF career completion. The median CSS was 23.

A total of 1,542 participants (37.3%) had hypertension, and 8.8% had diabetes.

After adjustment for established hypertension risk factors, including smoking, race, diabetes, age, and BMI, there was a graded association between CSS category and odds of later-life hypertension and between high CSS exposure and prevalent hypertension.

Results persisted when LOC, a single highly specific severe concussion symptom, was used in isolation as a surrogate for CSS, the investigators noted.

“These results suggest that repetitive early-life brain injury may have later-life implications for cardiovascular health,” they wrote. They also noted that hypertension has been shown to independently increase the risk of cognitive decline.

While premature cognitive decline among ASF players is generally attributed to chronic traumatic encephalopathy, “data from the current study raise the possibility that some element of cognitive decline among former ASF players may be attributable to hypertension,” which is potentially treatable.

“Future studies clarifying associations and causal pathways between brain injury, hypertension, and brain health are warranted,” they concluded.

Dr. Baggish added, “We hope that clinicians will now understand that head injury is an independent risk factor for high blood pressure and will screen vulnerable populations accordingly, as this may lead to better recognition of previously underdiagnosed hypertension with subsequent opportunities for intervention.”
 

Close monitoring

Commenting on the study, Jonathan Kim, MD, chair-elect of the American College of Cardiology’s Sports–Cardiology Section and chief of sports cardiology at Emory University in Atlanta, said, “They clearly show an independent association, which is not causality but is a new finding that requires more research. To me, it really emphasizes that cardiovascular risk is the most important health consequence that we should be worried about in retired NFL [National Football League] players.

“There are multifactorial reasons – not just repetitive head trauma – why this athletic population is at risk for the development of high blood pressure, even among college players,” he said.

Dr. Kim’s team has shown in studies conducted in collaboration with Dr. Baggish and others that collegiate football players who gain weight and develop increased systolic blood pressure are at risk of developing a “pathologic” cardiovascular phenotype.

Other research from this group showed links between nonsteroidal anti-inflammatory drug use among high school and collegiate ASF players and increased cardiovascular risk, as well as ASF-associated hypertension and ventricular-arterial coupling. 

The suggestion that late-life hypertension could play a role in premature cognitive decline among ASF players “warrants further study,” Dr. Kim said, “because we do know that hypertension in the general population can be associated with cognitive decline. So that’s an important future direction.”

He concluded: “It’s a matter of focusing on cardiac prevention.” After their careers, players should be counseled on the importance of losing weight and adopting heart-healthy habits. In addition to some of the traditional concerns that might lead to closer follow-up of these patients, “having a lot of concussions in the history could potentially be another risk factor that should warrant close monitoring of blood pressure and, of course, treatment if necessary.”

The study was supported by Harvard Catalyst/the Harvard Clinical and Translational Science Center and the NFL Players Association. Dr. Baggish and several coauthors have received funding from the NFL Players Association.

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

Among professional football players, the concussion burden during years of active play is associated with post-career high blood pressure, a new study suggests.

Among more than 4,000 participants, 37% had hypertension at a median of 24 years post career and reported a median concussion symptom score (CSS) of 23 on a scale of 0 to 130.

“We have long seen an incompletely explained link between football participation and later-life cardiovascular disease,” Aaron L. Baggish, MD, of Massachusetts Hospital and Harvard Medical School, Boston, told this news organization.

“This study tested [whether] concussion burden during years of active play would be a determinant of later-life hypertension, the most common cause of cardiovascular disease, and indeed found this relationship to be a strong one.”

The study was published online in Circulation.
 

Link to cognitive decline?

Dr. Baggish and colleagues recruited former professional American-style football (ASF) players to participate in a survey administered by the Football Players Health Study at Harvard University.

Concussion burden was quantified with respect to the occurrence and severity of common concussion symptoms – e.g., headaches, nausea, dizziness, confusion, loss of consciousness (LOC), disorientation, and feeling unsteady on one’s feet – over years of active participation.

Prevalent hypertension was determined either by the participants’ previously receiving from a clinician a recommendation for medication for “high blood pressure” or by the participants’ taking such medication at the time of survey completion. Diabetes status was determined by the participants’ receiving a prior recommendation for or prescription for “diabetes or high blood sugar” medication.

Of 15,070 invited to participate in the study, 4,168 did so. The mean age of the participants was 51.8 years; 39.4% were Black; the mean body mass index was 31.3; and 33.9% were linemen. Participants played for a mean of 6.9 seasons and were surveyed at a median 24.1 years post ASF career completion. The median CSS was 23.

A total of 1,542 participants (37.3%) had hypertension, and 8.8% had diabetes.

After adjustment for established hypertension risk factors, including smoking, race, diabetes, age, and BMI, there was a graded association between CSS category and odds of later-life hypertension and between high CSS exposure and prevalent hypertension.

Results persisted when LOC, a single highly specific severe concussion symptom, was used in isolation as a surrogate for CSS, the investigators noted.

“These results suggest that repetitive early-life brain injury may have later-life implications for cardiovascular health,” they wrote. They also noted that hypertension has been shown to independently increase the risk of cognitive decline.

While premature cognitive decline among ASF players is generally attributed to chronic traumatic encephalopathy, “data from the current study raise the possibility that some element of cognitive decline among former ASF players may be attributable to hypertension,” which is potentially treatable.

“Future studies clarifying associations and causal pathways between brain injury, hypertension, and brain health are warranted,” they concluded.

Dr. Baggish added, “We hope that clinicians will now understand that head injury is an independent risk factor for high blood pressure and will screen vulnerable populations accordingly, as this may lead to better recognition of previously underdiagnosed hypertension with subsequent opportunities for intervention.”
 

Close monitoring

Commenting on the study, Jonathan Kim, MD, chair-elect of the American College of Cardiology’s Sports–Cardiology Section and chief of sports cardiology at Emory University in Atlanta, said, “They clearly show an independent association, which is not causality but is a new finding that requires more research. To me, it really emphasizes that cardiovascular risk is the most important health consequence that we should be worried about in retired NFL [National Football League] players.

“There are multifactorial reasons – not just repetitive head trauma – why this athletic population is at risk for the development of high blood pressure, even among college players,” he said.

Dr. Kim’s team has shown in studies conducted in collaboration with Dr. Baggish and others that collegiate football players who gain weight and develop increased systolic blood pressure are at risk of developing a “pathologic” cardiovascular phenotype.

Other research from this group showed links between nonsteroidal anti-inflammatory drug use among high school and collegiate ASF players and increased cardiovascular risk, as well as ASF-associated hypertension and ventricular-arterial coupling. 

The suggestion that late-life hypertension could play a role in premature cognitive decline among ASF players “warrants further study,” Dr. Kim said, “because we do know that hypertension in the general population can be associated with cognitive decline. So that’s an important future direction.”

He concluded: “It’s a matter of focusing on cardiac prevention.” After their careers, players should be counseled on the importance of losing weight and adopting heart-healthy habits. In addition to some of the traditional concerns that might lead to closer follow-up of these patients, “having a lot of concussions in the history could potentially be another risk factor that should warrant close monitoring of blood pressure and, of course, treatment if necessary.”

The study was supported by Harvard Catalyst/the Harvard Clinical and Translational Science Center and the NFL Players Association. Dr. Baggish and several coauthors have received funding from the NFL Players Association.

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

Among professional football players, the concussion burden during years of active play is associated with post-career high blood pressure, a new study suggests.

Among more than 4,000 participants, 37% had hypertension at a median of 24 years post career and reported a median concussion symptom score (CSS) of 23 on a scale of 0 to 130.

“We have long seen an incompletely explained link between football participation and later-life cardiovascular disease,” Aaron L. Baggish, MD, of Massachusetts Hospital and Harvard Medical School, Boston, told this news organization.

“This study tested [whether] concussion burden during years of active play would be a determinant of later-life hypertension, the most common cause of cardiovascular disease, and indeed found this relationship to be a strong one.”

The study was published online in Circulation.
 

Link to cognitive decline?

Dr. Baggish and colleagues recruited former professional American-style football (ASF) players to participate in a survey administered by the Football Players Health Study at Harvard University.

Concussion burden was quantified with respect to the occurrence and severity of common concussion symptoms – e.g., headaches, nausea, dizziness, confusion, loss of consciousness (LOC), disorientation, and feeling unsteady on one’s feet – over years of active participation.

Prevalent hypertension was determined either by the participants’ previously receiving from a clinician a recommendation for medication for “high blood pressure” or by the participants’ taking such medication at the time of survey completion. Diabetes status was determined by the participants’ receiving a prior recommendation for or prescription for “diabetes or high blood sugar” medication.

Of 15,070 invited to participate in the study, 4,168 did so. The mean age of the participants was 51.8 years; 39.4% were Black; the mean body mass index was 31.3; and 33.9% were linemen. Participants played for a mean of 6.9 seasons and were surveyed at a median 24.1 years post ASF career completion. The median CSS was 23.

A total of 1,542 participants (37.3%) had hypertension, and 8.8% had diabetes.

After adjustment for established hypertension risk factors, including smoking, race, diabetes, age, and BMI, there was a graded association between CSS category and odds of later-life hypertension and between high CSS exposure and prevalent hypertension.

Results persisted when LOC, a single highly specific severe concussion symptom, was used in isolation as a surrogate for CSS, the investigators noted.

“These results suggest that repetitive early-life brain injury may have later-life implications for cardiovascular health,” they wrote. They also noted that hypertension has been shown to independently increase the risk of cognitive decline.

While premature cognitive decline among ASF players is generally attributed to chronic traumatic encephalopathy, “data from the current study raise the possibility that some element of cognitive decline among former ASF players may be attributable to hypertension,” which is potentially treatable.

“Future studies clarifying associations and causal pathways between brain injury, hypertension, and brain health are warranted,” they concluded.

Dr. Baggish added, “We hope that clinicians will now understand that head injury is an independent risk factor for high blood pressure and will screen vulnerable populations accordingly, as this may lead to better recognition of previously underdiagnosed hypertension with subsequent opportunities for intervention.”
 

Close monitoring

Commenting on the study, Jonathan Kim, MD, chair-elect of the American College of Cardiology’s Sports–Cardiology Section and chief of sports cardiology at Emory University in Atlanta, said, “They clearly show an independent association, which is not causality but is a new finding that requires more research. To me, it really emphasizes that cardiovascular risk is the most important health consequence that we should be worried about in retired NFL [National Football League] players.

“There are multifactorial reasons – not just repetitive head trauma – why this athletic population is at risk for the development of high blood pressure, even among college players,” he said.

Dr. Kim’s team has shown in studies conducted in collaboration with Dr. Baggish and others that collegiate football players who gain weight and develop increased systolic blood pressure are at risk of developing a “pathologic” cardiovascular phenotype.

Other research from this group showed links between nonsteroidal anti-inflammatory drug use among high school and collegiate ASF players and increased cardiovascular risk, as well as ASF-associated hypertension and ventricular-arterial coupling. 

The suggestion that late-life hypertension could play a role in premature cognitive decline among ASF players “warrants further study,” Dr. Kim said, “because we do know that hypertension in the general population can be associated with cognitive decline. So that’s an important future direction.”

He concluded: “It’s a matter of focusing on cardiac prevention.” After their careers, players should be counseled on the importance of losing weight and adopting heart-healthy habits. In addition to some of the traditional concerns that might lead to closer follow-up of these patients, “having a lot of concussions in the history could potentially be another risk factor that should warrant close monitoring of blood pressure and, of course, treatment if necessary.”

The study was supported by Harvard Catalyst/the Harvard Clinical and Translational Science Center and the NFL Players Association. Dr. Baggish and several coauthors have received funding from the NFL Players Association.

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

Some time ago I was invited to join a bipartisan congressional task force on valley fever, also known as coccidioidomycosis. A large and diverse crowd attended the task force’s first meeting in Bakersfield, Calif. – a meeting for everyone: the medical profession, the public, it even included veterinarians.

The whole thing was a resounding success. Francis Collins was there, the just-retired director of the NIH. Tom Frieden, then-director of the Centers for Disease Control and Prevention was there, as were several congresspeople and also my college roommate, a retired Navy medical corps captain. I was enjoying it.

Afterward, we had a banquet dinner at a restaurant in downtown Bakersfield. One of the people there was a woman I knew well – her husband was a physician friend. The restaurant served steak and salmon, and this woman made the mistake of ordering the steak.

Not long after the entrees were served, I heard a commotion at the table just behind me. I turned around and saw that woman in distress. A piece of steak had wedged in her trachea and she couldn’t breathe.

Almost immediately, the chef showed up. I don’t know how he got there. The chef at this restaurant was a big guy. I mean, probably 6 feet, 5 inches tall and 275 pounds. He tried the Heimlich maneuver. It didn’t work.

At that point, I jumped up. I thought, “Well, maybe I know how to do this better than him.” Probably not, actually. I tried and couldn’t make it work either. So I knew we were going to have to do something.

Paul Krogstad, my friend and research partner who is a pediatric infectious disease physician, stepped up and tried to put his finger in her throat and dig it out. He couldn’t get it. The patient had lost consciousness.

So, I’m thinking, okay, there’s really only one choice. You have to get an airway surgically.

I said, “We have to put her down on the floor.” And then I said, “Knife!”

I was looking at the steak knives on the table and they weren’t to my liking for doing a procedure. My college roommate – the retired Navy man – whipped out this very good pocketknife.

So, there we were, I had Paul Krogstad holding her head, and CDC Director Tom Frieden taking her pulse, which she still had. I took the knife and did a cricothyroidotomy. I had never done this in my life.

While I was making the incision, somebody gave Paul a ballpoint pen and he broke it into pieces to make a tracheostomy tube. Once I’d made the little incision, I put the tube in. She wasn’t breathing, but she still had a pulse.

I leaned forward and blew into the tube and inflated her lungs. I could see her lungs balloon up. It was a nice feeling, because I knew I was clearly in the right place.

I can’t quite explain it, but while I was doing this, I was enormously calm and totally focused. I knew there was a crowd of people around me, all looking at me, but I wasn’t conscious of that.

It was really just the four of us: Paul and Tom and me and our patient. Those were the only people that I was really cognizant of. Paul and Tom were not panic stricken at all. I remember somebody shouting, “We have to start CPR!” and Frieden said, “No. We don’t.”

Moments later, she woke up, sat up, coughed, and shot the piece of steak across the room.

She was breathing on her own, but we still taped that tube into place. Somebody had already summoned an ambulance; they were there not very long after we completed this procedure. I got in the ambulance with her and we rode over to the emergency room at Mercy Truxtun.

She was stable and doing okay. I sat with her until a thoracic surgeon showed up. He checked out the situation and decided we didn’t need that tube and took it out. I didn’t want to take that out until I had a surgeon there who could do a formal tracheostomy.

They kept her in the hospital for 3 or 4 days. Now, this woman had always had difficulties swallowing, so steak may not have been the best choice. She still had trouble swallowing afterward but recovered.

I’ve known her and her husband a long time, so it was certainly rewarding to be able to provide this service. Years later, though, when her husband died, I spoke at his funeral. When she was speaking to the gathering, she said, “And oh, by the way, Royce, thanks for saving my life.”

That surprised me. I didn’t think we were going to go there.

I’d never tried to practice medicine “at the roadside” before. But that’s part of the career.

Royce Johnson, MD, is the chief of the division of infectious disease among other leadership positions at Kern Medical in Bakersfield, Calif., and the medical director of the Valley Fever Institute.

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

Some time ago I was invited to join a bipartisan congressional task force on valley fever, also known as coccidioidomycosis. A large and diverse crowd attended the task force’s first meeting in Bakersfield, Calif. – a meeting for everyone: the medical profession, the public, it even included veterinarians.

The whole thing was a resounding success. Francis Collins was there, the just-retired director of the NIH. Tom Frieden, then-director of the Centers for Disease Control and Prevention was there, as were several congresspeople and also my college roommate, a retired Navy medical corps captain. I was enjoying it.

Afterward, we had a banquet dinner at a restaurant in downtown Bakersfield. One of the people there was a woman I knew well – her husband was a physician friend. The restaurant served steak and salmon, and this woman made the mistake of ordering the steak.

Not long after the entrees were served, I heard a commotion at the table just behind me. I turned around and saw that woman in distress. A piece of steak had wedged in her trachea and she couldn’t breathe.

Almost immediately, the chef showed up. I don’t know how he got there. The chef at this restaurant was a big guy. I mean, probably 6 feet, 5 inches tall and 275 pounds. He tried the Heimlich maneuver. It didn’t work.

At that point, I jumped up. I thought, “Well, maybe I know how to do this better than him.” Probably not, actually. I tried and couldn’t make it work either. So I knew we were going to have to do something.

Paul Krogstad, my friend and research partner who is a pediatric infectious disease physician, stepped up and tried to put his finger in her throat and dig it out. He couldn’t get it. The patient had lost consciousness.

So, I’m thinking, okay, there’s really only one choice. You have to get an airway surgically.

I said, “We have to put her down on the floor.” And then I said, “Knife!”

I was looking at the steak knives on the table and they weren’t to my liking for doing a procedure. My college roommate – the retired Navy man – whipped out this very good pocketknife.

So, there we were, I had Paul Krogstad holding her head, and CDC Director Tom Frieden taking her pulse, which she still had. I took the knife and did a cricothyroidotomy. I had never done this in my life.

While I was making the incision, somebody gave Paul a ballpoint pen and he broke it into pieces to make a tracheostomy tube. Once I’d made the little incision, I put the tube in. She wasn’t breathing, but she still had a pulse.

I leaned forward and blew into the tube and inflated her lungs. I could see her lungs balloon up. It was a nice feeling, because I knew I was clearly in the right place.

I can’t quite explain it, but while I was doing this, I was enormously calm and totally focused. I knew there was a crowd of people around me, all looking at me, but I wasn’t conscious of that.

It was really just the four of us: Paul and Tom and me and our patient. Those were the only people that I was really cognizant of. Paul and Tom were not panic stricken at all. I remember somebody shouting, “We have to start CPR!” and Frieden said, “No. We don’t.”

Moments later, she woke up, sat up, coughed, and shot the piece of steak across the room.

She was breathing on her own, but we still taped that tube into place. Somebody had already summoned an ambulance; they were there not very long after we completed this procedure. I got in the ambulance with her and we rode over to the emergency room at Mercy Truxtun.

She was stable and doing okay. I sat with her until a thoracic surgeon showed up. He checked out the situation and decided we didn’t need that tube and took it out. I didn’t want to take that out until I had a surgeon there who could do a formal tracheostomy.

They kept her in the hospital for 3 or 4 days. Now, this woman had always had difficulties swallowing, so steak may not have been the best choice. She still had trouble swallowing afterward but recovered.

I’ve known her and her husband a long time, so it was certainly rewarding to be able to provide this service. Years later, though, when her husband died, I spoke at his funeral. When she was speaking to the gathering, she said, “And oh, by the way, Royce, thanks for saving my life.”

That surprised me. I didn’t think we were going to go there.

I’d never tried to practice medicine “at the roadside” before. But that’s part of the career.

Royce Johnson, MD, is the chief of the division of infectious disease among other leadership positions at Kern Medical in Bakersfield, Calif., and the medical director of the Valley Fever Institute.

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

Some time ago I was invited to join a bipartisan congressional task force on valley fever, also known as coccidioidomycosis. A large and diverse crowd attended the task force’s first meeting in Bakersfield, Calif. – a meeting for everyone: the medical profession, the public, it even included veterinarians.

The whole thing was a resounding success. Francis Collins was there, the just-retired director of the NIH. Tom Frieden, then-director of the Centers for Disease Control and Prevention was there, as were several congresspeople and also my college roommate, a retired Navy medical corps captain. I was enjoying it.

Afterward, we had a banquet dinner at a restaurant in downtown Bakersfield. One of the people there was a woman I knew well – her husband was a physician friend. The restaurant served steak and salmon, and this woman made the mistake of ordering the steak.

Not long after the entrees were served, I heard a commotion at the table just behind me. I turned around and saw that woman in distress. A piece of steak had wedged in her trachea and she couldn’t breathe.

Almost immediately, the chef showed up. I don’t know how he got there. The chef at this restaurant was a big guy. I mean, probably 6 feet, 5 inches tall and 275 pounds. He tried the Heimlich maneuver. It didn’t work.

At that point, I jumped up. I thought, “Well, maybe I know how to do this better than him.” Probably not, actually. I tried and couldn’t make it work either. So I knew we were going to have to do something.

Paul Krogstad, my friend and research partner who is a pediatric infectious disease physician, stepped up and tried to put his finger in her throat and dig it out. He couldn’t get it. The patient had lost consciousness.

So, I’m thinking, okay, there’s really only one choice. You have to get an airway surgically.

I said, “We have to put her down on the floor.” And then I said, “Knife!”

I was looking at the steak knives on the table and they weren’t to my liking for doing a procedure. My college roommate – the retired Navy man – whipped out this very good pocketknife.

So, there we were, I had Paul Krogstad holding her head, and CDC Director Tom Frieden taking her pulse, which she still had. I took the knife and did a cricothyroidotomy. I had never done this in my life.

While I was making the incision, somebody gave Paul a ballpoint pen and he broke it into pieces to make a tracheostomy tube. Once I’d made the little incision, I put the tube in. She wasn’t breathing, but she still had a pulse.

I leaned forward and blew into the tube and inflated her lungs. I could see her lungs balloon up. It was a nice feeling, because I knew I was clearly in the right place.

I can’t quite explain it, but while I was doing this, I was enormously calm and totally focused. I knew there was a crowd of people around me, all looking at me, but I wasn’t conscious of that.

It was really just the four of us: Paul and Tom and me and our patient. Those were the only people that I was really cognizant of. Paul and Tom were not panic stricken at all. I remember somebody shouting, “We have to start CPR!” and Frieden said, “No. We don’t.”

Moments later, she woke up, sat up, coughed, and shot the piece of steak across the room.

She was breathing on her own, but we still taped that tube into place. Somebody had already summoned an ambulance; they were there not very long after we completed this procedure. I got in the ambulance with her and we rode over to the emergency room at Mercy Truxtun.

She was stable and doing okay. I sat with her until a thoracic surgeon showed up. He checked out the situation and decided we didn’t need that tube and took it out. I didn’t want to take that out until I had a surgeon there who could do a formal tracheostomy.

They kept her in the hospital for 3 or 4 days. Now, this woman had always had difficulties swallowing, so steak may not have been the best choice. She still had trouble swallowing afterward but recovered.

I’ve known her and her husband a long time, so it was certainly rewarding to be able to provide this service. Years later, though, when her husband died, I spoke at his funeral. When she was speaking to the gathering, she said, “And oh, by the way, Royce, thanks for saving my life.”

That surprised me. I didn’t think we were going to go there.

I’d never tried to practice medicine “at the roadside” before. But that’s part of the career.

Royce Johnson, MD, is the chief of the division of infectious disease among other leadership positions at Kern Medical in Bakersfield, Calif., and the medical director of the Valley Fever Institute.

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. For the first time, the National Institutes of Health (NIH) acknowledged there was a causal link between repeated blows to the head and chronic traumatic encephalopathy (CTE).

“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. For the first time, the National Institutes of Health (NIH) acknowledged there was a causal link between repeated blows to the head and chronic traumatic encephalopathy (CTE).

“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. For the first time, the National Institutes of Health (NIH) acknowledged there was a causal link between repeated blows to the head and chronic traumatic encephalopathy (CTE).

“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.

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. This past year brought some outstanding publications related to emergency medicine that are practice changers.

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. This past year brought some outstanding publications related to emergency medicine that are practice changers.

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. This past year brought some outstanding publications related to emergency medicine that are practice changers.

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.

On-call specialist incurred a clear ‘duty of care,’ court rules

An Illinois doctor who consulted with a patient’s treating physician but never actually saw the patient himself can’t escape a medical malpractice claim, a state appeals court ruled late in January.

The 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

An Illinois doctor who consulted with a patient’s treating physician but never actually saw the patient himself can’t escape a medical malpractice claim, a state appeals court ruled late in January.

The 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

An Illinois doctor who consulted with a patient’s treating physician but never actually saw the patient himself can’t escape a medical malpractice claim, a state appeals court ruled late in January.

The 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.

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. The roads were fine – no snow – but I noticed an unusual amount of traffic on the freeway. Then I saw smoke coming from an overpass up ahead.

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 [email protected] . 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. The roads were fine – no snow – but I noticed an unusual amount of traffic on the freeway. Then I saw smoke coming from an overpass up ahead.

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 [email protected] . 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. The roads were fine – no snow – but I noticed an unusual amount of traffic on the freeway. Then I saw smoke coming from an overpass up ahead.

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 [email protected] . A version of this article appeared on Medscape.com.

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.

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.

Sustaining even a single head injury has been linked to a significantly increased risk of all-cause mortality in new research.

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.

Sustaining even a single head injury has been linked to a significantly increased risk of all-cause mortality in new research.

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.

Sustaining even a single head injury has been linked to a significantly increased risk of all-cause mortality in new research.

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.

This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr Robert Glatter, medical adviser for Medscape Emergency Medicine. Today, we have Dr. Paul Pepe, an emergency physician and highly recognized expert in EMS, critical care, and resuscitation, along with Ryan Quinn, EMS chief for Edina Fire Department in Edina, Minn., joining us to discuss a significant advance in resuscitation for patients with nonshockable rhythms in cardiac arrest 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. Today, we have Dr. Paul Pepe, an emergency physician and highly recognized expert in EMS, critical care, and resuscitation, along with Ryan Quinn, EMS chief for Edina Fire Department in Edina, Minn., joining us to discuss a significant advance in resuscitation for patients with nonshockable rhythms in cardiac arrest 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. Today, we have Dr. Paul Pepe, an emergency physician and highly recognized expert in EMS, critical care, and resuscitation, along with Ryan Quinn, EMS chief for Edina Fire Department in Edina, Minn., joining us to discuss a significant advance in resuscitation for patients with nonshockable rhythms in cardiac arrest 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.