The American College of Surgeons (ACS) Women in Surgery Committee (WiSC) is accepting nominations for the second annual Dr. Mary Edwards Walker Inspiring Women in Surgery Award, which will be presented at Clinical Congress 2017 in San Diego, CA. The award will be accorded in recognition of an individual’s significant contributions to the advancement of women in the field of surgery. Nominations are due April 30.

The award honors Dr. Mary Edwards Walker for the example she set for future generations as the first woman surgeon to serve as a U.S. Army physician and the only woman to ever receive the U.S. Armed Forces Medal of Honor for bravery.

Courtesy Library of Congress

The American College of Surgeons (ACS) Women in Surgery Committee (WiSC) is accepting nominations for the second annual Dr. Mary Edwards Walker Inspiring Women in Surgery Award, which will be presented at Clinical Congress 2017 in San Diego, CA. The award will be accorded in recognition of an individual’s significant contributions to the advancement of women in the field of surgery. Nominations are due April 30.

The award honors Dr. Mary Edwards Walker for the example she set for future generations as the first woman surgeon to serve as a U.S. Army physician and the only woman to ever receive the U.S. Armed Forces Medal of Honor for bravery.

Courtesy Library of Congress

The American College of Surgeons (ACS) Women in Surgery Committee (WiSC) is accepting nominations for the second annual Dr. Mary Edwards Walker Inspiring Women in Surgery Award, which will be presented at Clinical Congress 2017 in San Diego, CA. The award will be accorded in recognition of an individual’s significant contributions to the advancement of women in the field of surgery. Nominations are due April 30.

The award honors Dr. Mary Edwards Walker for the example she set for future generations as the first woman surgeon to serve as a U.S. Army physician and the only woman to ever receive the U.S. Armed Forces Medal of Honor for bravery.

Courtesy Library of Congress

Editor’s note: “Everything We Say and Do” is an informational series developed by the Society of Hospital Medicine’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experiences of care. Each article will focus on how the contributor applies one or more of the “key communication” tactics in practice to maintain provider accountability for “everything we say and do that affects our patients’ thoughts, feelings, and well-being.”

What I say and do

I empower all of my patients by giving them the opportunity to consider advance care planning.

Why I do it

Everyone deserves advance care planning, and every health care encounter, including a hospitalization, is an opportunity to better identify and document patients’ wishes for care should they become unable to express them. If we wait for patients to develop serious advanced illness before having advance care planning conversations, we risk depriving them of the care they would want in these situations. Additionally, we place a huge burden on family members who may struggle with excruciatingly difficult decisions in the absence of guidance about their loved one’s wishes.

How I do it

I start by identifying which components of advance care planning each patient needs, using a simple algorithm (see figure). All of my patients are queried about code status, and I give them the opportunity to better understand the value of having a healthcare proxy and advance directives, if they are not already in place.

To introduce the concept of a health care proxy and advance directives, I ask, “Have you ever thought about who you might choose to make medical decisions on your behalf if you became too sick to make those decisions yourself?” Then, finally, I share the following information, usually referring to the blank advance directives document they received in their admission packet: “There is a valuable way to put your wishes about specific care options in writing so others will know your wishes if you’re unable to communicate with them. Would you like to talk about that right now?” Again, this gives the patient control of the situation and an opportunity to decline the conversation if they are not interested or comfortable at that time.

It’s important to document the nature and outcome of these conversations. Keep in mind, advance care planning discussions need not occur at the time of admission. In fact, admission may be the worst time for some patients, further underscoring the importance of documentation so that subsequent providers can see whether advance care planning has been addressed during the hospital stay.

Note: For useful educational resources that address goals-of-care conversations in patients toward the end of life, the Center to Advance Palliative Care (www.capc.org) has a number of educational courses that address these important communication skills.
 

Dr. Rudolph is vice president of physician development and patient experience for Sound Physicians, Tacoma, Wash. and chair of the SHM Patient Experience Committee .

Reference

1. Moss, A.H., Ganjoo, J, Sharma S, et al. Utility of the “Surprise” Question to Identify Dialysis Patients with High Mortality. Clinical Journal of the American Society of Nephrology: CJASN. 2008;3(5):1379-84. doi:10.2215/CJN.00940208.




 

Editor’s note: “Everything We Say and Do” is an informational series developed by the Society of Hospital Medicine’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experiences of care. Each article will focus on how the contributor applies one or more of the “key communication” tactics in practice to maintain provider accountability for “everything we say and do that affects our patients’ thoughts, feelings, and well-being.”

What I say and do

I empower all of my patients by giving them the opportunity to consider advance care planning.

Why I do it

Everyone deserves advance care planning, and every health care encounter, including a hospitalization, is an opportunity to better identify and document patients’ wishes for care should they become unable to express them. If we wait for patients to develop serious advanced illness before having advance care planning conversations, we risk depriving them of the care they would want in these situations. Additionally, we place a huge burden on family members who may struggle with excruciatingly difficult decisions in the absence of guidance about their loved one’s wishes.

How I do it

I start by identifying which components of advance care planning each patient needs, using a simple algorithm (see figure). All of my patients are queried about code status, and I give them the opportunity to better understand the value of having a healthcare proxy and advance directives, if they are not already in place.

To introduce the concept of a health care proxy and advance directives, I ask, “Have you ever thought about who you might choose to make medical decisions on your behalf if you became too sick to make those decisions yourself?” Then, finally, I share the following information, usually referring to the blank advance directives document they received in their admission packet: “There is a valuable way to put your wishes about specific care options in writing so others will know your wishes if you’re unable to communicate with them. Would you like to talk about that right now?” Again, this gives the patient control of the situation and an opportunity to decline the conversation if they are not interested or comfortable at that time.

It’s important to document the nature and outcome of these conversations. Keep in mind, advance care planning discussions need not occur at the time of admission. In fact, admission may be the worst time for some patients, further underscoring the importance of documentation so that subsequent providers can see whether advance care planning has been addressed during the hospital stay.

Note: For useful educational resources that address goals-of-care conversations in patients toward the end of life, the Center to Advance Palliative Care (www.capc.org) has a number of educational courses that address these important communication skills.
 

Dr. Rudolph is vice president of physician development and patient experience for Sound Physicians, Tacoma, Wash. and chair of the SHM Patient Experience Committee .

Reference

1. Moss, A.H., Ganjoo, J, Sharma S, et al. Utility of the “Surprise” Question to Identify Dialysis Patients with High Mortality. Clinical Journal of the American Society of Nephrology: CJASN. 2008;3(5):1379-84. doi:10.2215/CJN.00940208.




 

Editor’s note: “Everything We Say and Do” is an informational series developed by the Society of Hospital Medicine’s Patient Experience Committee to provide readers with thoughtful and actionable communication tactics that have great potential to positively impact patients’ experiences of care. Each article will focus on how the contributor applies one or more of the “key communication” tactics in practice to maintain provider accountability for “everything we say and do that affects our patients’ thoughts, feelings, and well-being.”

What I say and do

I empower all of my patients by giving them the opportunity to consider advance care planning.

Why I do it

Everyone deserves advance care planning, and every health care encounter, including a hospitalization, is an opportunity to better identify and document patients’ wishes for care should they become unable to express them. If we wait for patients to develop serious advanced illness before having advance care planning conversations, we risk depriving them of the care they would want in these situations. Additionally, we place a huge burden on family members who may struggle with excruciatingly difficult decisions in the absence of guidance about their loved one’s wishes.

How I do it

I start by identifying which components of advance care planning each patient needs, using a simple algorithm (see figure). All of my patients are queried about code status, and I give them the opportunity to better understand the value of having a healthcare proxy and advance directives, if they are not already in place.

To introduce the concept of a health care proxy and advance directives, I ask, “Have you ever thought about who you might choose to make medical decisions on your behalf if you became too sick to make those decisions yourself?” Then, finally, I share the following information, usually referring to the blank advance directives document they received in their admission packet: “There is a valuable way to put your wishes about specific care options in writing so others will know your wishes if you’re unable to communicate with them. Would you like to talk about that right now?” Again, this gives the patient control of the situation and an opportunity to decline the conversation if they are not interested or comfortable at that time.

It’s important to document the nature and outcome of these conversations. Keep in mind, advance care planning discussions need not occur at the time of admission. In fact, admission may be the worst time for some patients, further underscoring the importance of documentation so that subsequent providers can see whether advance care planning has been addressed during the hospital stay.

Note: For useful educational resources that address goals-of-care conversations in patients toward the end of life, the Center to Advance Palliative Care (www.capc.org) has a number of educational courses that address these important communication skills.
 

Dr. Rudolph is vice president of physician development and patient experience for Sound Physicians, Tacoma, Wash. and chair of the SHM Patient Experience Committee .

Reference

1. Moss, A.H., Ganjoo, J, Sharma S, et al. Utility of the “Surprise” Question to Identify Dialysis Patients with High Mortality. Clinical Journal of the American Society of Nephrology: CJASN. 2008;3(5):1379-84. doi:10.2215/CJN.00940208.




 

I recently had the good fortune to read a commentary written by Dr. Peter Angelos in ACS Surgery News entitled, The Right Choice? Surgeons, confidence, and humility (2017, February, p. 11). The essay touches on the philosophy, psychology, and attitudes that surgeons adopt and express in their daily interactions with the public.

The article refers to “the balance between lack of confidence and overconfidence, and between thoughtful introspection and paralyzing fear of future complications.” This is a critically important struggle in the mind of the surgeon. I would like to propose an exercise to bolster self-esteem in the psyche of the surgeon, particularly in the formative stages of one’s career, without fostering false or pathological bravado.

Dr. Chuback is a vascular surgeon in private practice in Paramus, N.J.

I recently had the good fortune to read a commentary written by Dr. Peter Angelos in ACS Surgery News entitled, The Right Choice? Surgeons, confidence, and humility (2017, February, p. 11). The essay touches on the philosophy, psychology, and attitudes that surgeons adopt and express in their daily interactions with the public.

The article refers to “the balance between lack of confidence and overconfidence, and between thoughtful introspection and paralyzing fear of future complications.” This is a critically important struggle in the mind of the surgeon. I would like to propose an exercise to bolster self-esteem in the psyche of the surgeon, particularly in the formative stages of one’s career, without fostering false or pathological bravado.

Dr. Chuback is a vascular surgeon in private practice in Paramus, N.J.

I recently had the good fortune to read a commentary written by Dr. Peter Angelos in ACS Surgery News entitled, The Right Choice? Surgeons, confidence, and humility (2017, February, p. 11). The essay touches on the philosophy, psychology, and attitudes that surgeons adopt and express in their daily interactions with the public.

The article refers to “the balance between lack of confidence and overconfidence, and between thoughtful introspection and paralyzing fear of future complications.” This is a critically important struggle in the mind of the surgeon. I would like to propose an exercise to bolster self-esteem in the psyche of the surgeon, particularly in the formative stages of one’s career, without fostering false or pathological bravado.

Dr. Chuback is a vascular surgeon in private practice in Paramus, N.J.

Editor’s note: This new series highlights the professional pathways of quality improvement leaders. This month features the story of Kevin O’Leary, MD, MS, SFHM, chief of hospital medicine at Northwestern University Feinberg School of Medicine in Chicago.

Kevin O’Leary, MD, MS, SFHM, chose a career path in hospital medicine for the reasons that attract many to the specialty – a love of “a little bit of everything, clinically” and the opportunity to problem-solve a diverse range of professional challenges on a daily basis.

While he encourages anyone with an interest in QI to seek additional training opportunities, he says personal qualities – tenacity, curiosity, and a willingness to collaborate—are better predictors of success. For those wondering how to get started, “look for a niche, an unmet need that is valuable to your organization, and fill it,” he advised. “You don’t have to be an expert in that area, but you can become one.”

Making strong connections within the hospital system is essential. Reach out to the contacts you know, he said, and if they are not the ones to help you solve the problem, they often know who can.

“That’s key to quality improvement success, as well as career success,” he said. “Find a mentor. It might be someone who is more senior within the hospitalist group, in medicine, or even outside the hospital. Meet with them regularly and ask them for feedback on your ideas.”

Newcomers to QI should embrace opportunities to change care and not get discouraged when a project has unintended outcomes.

“Failure is when a team never gets to the point of implementing the intervention or when a team doesn’t know whether the intervention has actually changed results,” he said. “Learning why an intervention isn’t effective can be as valuable as implementing one that is. If every project is successful, it just means that you’re not taking enough risks.”

Dr. O’Leary spends about 25% of his professional time providing clinical care, and another 15% meeting his responsibilities as division chief. He uses the other protected time in his schedule to lead QI and teach QI skills in programs like Northwestern Medicine’s Academy for Quality and Safety Improvement (AQSI).

As a former faculty member in SHM’s Quality and Safety Educator’s Academy (QSEA), he has trained medical educators to develop curricula in quality improvement and patient safety. He says both AQSI and QSEA are especially effective because they encourage interaction, which is valuable to professionals at all levels looking to advance their skill in QI.

“Even in a teaching capacity,” he noted, “what I learned from other faculty and participants in QSEA was critical.”

Residents and junior hospitalists often have the impression that they lack the skills to lead quality initiatives, but Dr. O’Leary says medical school provides the nuts and bolts – analytical skills, statistical knowledge, critical thinking. He encouraged hospitalists to move ahead, even without formal QI training.

“If you have strong interpersonal skills – the willingness to make friends and build connections – you will be successful,” he said.

It’s also an excellent way to learn about the ins and outs of the hospital system and the work of other departments and specialties. Dr. O’Leary especially enjoys that aspect of his work, as well as the ability to address systemic issues that he values.

“I get the greatest fulfillment from the opportunity to be creative … and to implement projects that are important to me and help patients,” he said. “As long as the projects align with organizational goals, I can usually find the support we need to be successful.”

Claudia Stahl is a content manager for the Society of Hospital Medicine.

Editor’s note: This new series highlights the professional pathways of quality improvement leaders. This month features the story of Kevin O’Leary, MD, MS, SFHM, chief of hospital medicine at Northwestern University Feinberg School of Medicine in Chicago.

Kevin O’Leary, MD, MS, SFHM, chose a career path in hospital medicine for the reasons that attract many to the specialty – a love of “a little bit of everything, clinically” and the opportunity to problem-solve a diverse range of professional challenges on a daily basis.

While he encourages anyone with an interest in QI to seek additional training opportunities, he says personal qualities – tenacity, curiosity, and a willingness to collaborate—are better predictors of success. For those wondering how to get started, “look for a niche, an unmet need that is valuable to your organization, and fill it,” he advised. “You don’t have to be an expert in that area, but you can become one.”

Making strong connections within the hospital system is essential. Reach out to the contacts you know, he said, and if they are not the ones to help you solve the problem, they often know who can.

“That’s key to quality improvement success, as well as career success,” he said. “Find a mentor. It might be someone who is more senior within the hospitalist group, in medicine, or even outside the hospital. Meet with them regularly and ask them for feedback on your ideas.”

Newcomers to QI should embrace opportunities to change care and not get discouraged when a project has unintended outcomes.

“Failure is when a team never gets to the point of implementing the intervention or when a team doesn’t know whether the intervention has actually changed results,” he said. “Learning why an intervention isn’t effective can be as valuable as implementing one that is. If every project is successful, it just means that you’re not taking enough risks.”

Dr. O’Leary spends about 25% of his professional time providing clinical care, and another 15% meeting his responsibilities as division chief. He uses the other protected time in his schedule to lead QI and teach QI skills in programs like Northwestern Medicine’s Academy for Quality and Safety Improvement (AQSI).

As a former faculty member in SHM’s Quality and Safety Educator’s Academy (QSEA), he has trained medical educators to develop curricula in quality improvement and patient safety. He says both AQSI and QSEA are especially effective because they encourage interaction, which is valuable to professionals at all levels looking to advance their skill in QI.

“Even in a teaching capacity,” he noted, “what I learned from other faculty and participants in QSEA was critical.”

Residents and junior hospitalists often have the impression that they lack the skills to lead quality initiatives, but Dr. O’Leary says medical school provides the nuts and bolts – analytical skills, statistical knowledge, critical thinking. He encouraged hospitalists to move ahead, even without formal QI training.

“If you have strong interpersonal skills – the willingness to make friends and build connections – you will be successful,” he said.

It’s also an excellent way to learn about the ins and outs of the hospital system and the work of other departments and specialties. Dr. O’Leary especially enjoys that aspect of his work, as well as the ability to address systemic issues that he values.

“I get the greatest fulfillment from the opportunity to be creative … and to implement projects that are important to me and help patients,” he said. “As long as the projects align with organizational goals, I can usually find the support we need to be successful.”

Claudia Stahl is a content manager for the Society of Hospital Medicine.

Editor’s note: This new series highlights the professional pathways of quality improvement leaders. This month features the story of Kevin O’Leary, MD, MS, SFHM, chief of hospital medicine at Northwestern University Feinberg School of Medicine in Chicago.

Kevin O’Leary, MD, MS, SFHM, chose a career path in hospital medicine for the reasons that attract many to the specialty – a love of “a little bit of everything, clinically” and the opportunity to problem-solve a diverse range of professional challenges on a daily basis.

While he encourages anyone with an interest in QI to seek additional training opportunities, he says personal qualities – tenacity, curiosity, and a willingness to collaborate—are better predictors of success. For those wondering how to get started, “look for a niche, an unmet need that is valuable to your organization, and fill it,” he advised. “You don’t have to be an expert in that area, but you can become one.”

Making strong connections within the hospital system is essential. Reach out to the contacts you know, he said, and if they are not the ones to help you solve the problem, they often know who can.

“That’s key to quality improvement success, as well as career success,” he said. “Find a mentor. It might be someone who is more senior within the hospitalist group, in medicine, or even outside the hospital. Meet with them regularly and ask them for feedback on your ideas.”

Newcomers to QI should embrace opportunities to change care and not get discouraged when a project has unintended outcomes.

“Failure is when a team never gets to the point of implementing the intervention or when a team doesn’t know whether the intervention has actually changed results,” he said. “Learning why an intervention isn’t effective can be as valuable as implementing one that is. If every project is successful, it just means that you’re not taking enough risks.”

Dr. O’Leary spends about 25% of his professional time providing clinical care, and another 15% meeting his responsibilities as division chief. He uses the other protected time in his schedule to lead QI and teach QI skills in programs like Northwestern Medicine’s Academy for Quality and Safety Improvement (AQSI).

As a former faculty member in SHM’s Quality and Safety Educator’s Academy (QSEA), he has trained medical educators to develop curricula in quality improvement and patient safety. He says both AQSI and QSEA are especially effective because they encourage interaction, which is valuable to professionals at all levels looking to advance their skill in QI.

“Even in a teaching capacity,” he noted, “what I learned from other faculty and participants in QSEA was critical.”

Residents and junior hospitalists often have the impression that they lack the skills to lead quality initiatives, but Dr. O’Leary says medical school provides the nuts and bolts – analytical skills, statistical knowledge, critical thinking. He encouraged hospitalists to move ahead, even without formal QI training.

“If you have strong interpersonal skills – the willingness to make friends and build connections – you will be successful,” he said.

It’s also an excellent way to learn about the ins and outs of the hospital system and the work of other departments and specialties. Dr. O’Leary especially enjoys that aspect of his work, as well as the ability to address systemic issues that he values.

“I get the greatest fulfillment from the opportunity to be creative … and to implement projects that are important to me and help patients,” he said. “As long as the projects align with organizational goals, I can usually find the support we need to be successful.”

Claudia Stahl is a content manager for the Society of Hospital Medicine.

Washington – Marijuana abuse was independently associated with an eye-opening doubled risk of acute MI in a large, retrospective, age-matched cohort study, Ahmad Tarek Chami, MD, reported at the annual meeting of the American College of Cardiology.

The link was strongest by far in young adult marijuana abusers, with an adjusted 3.2-fold increased risk of MI in 25- to 29-year-olds with marijuana abuse noted in their medical records, compared with age-matched controls and a 4.56-fold greater risk among the 30- to 34-year-old cannabis abusers, according to Dr. Chami of Case Western Reserve University in Cleveland.

Bruce Jancin/Frontline Medical News

bjancin@frontlinemedcom.com

Washington – Marijuana abuse was independently associated with an eye-opening doubled risk of acute MI in a large, retrospective, age-matched cohort study, Ahmad Tarek Chami, MD, reported at the annual meeting of the American College of Cardiology.

The link was strongest by far in young adult marijuana abusers, with an adjusted 3.2-fold increased risk of MI in 25- to 29-year-olds with marijuana abuse noted in their medical records, compared with age-matched controls and a 4.56-fold greater risk among the 30- to 34-year-old cannabis abusers, according to Dr. Chami of Case Western Reserve University in Cleveland.

Bruce Jancin/Frontline Medical News

bjancin@frontlinemedcom.com

Washington – Marijuana abuse was independently associated with an eye-opening doubled risk of acute MI in a large, retrospective, age-matched cohort study, Ahmad Tarek Chami, MD, reported at the annual meeting of the American College of Cardiology.

The link was strongest by far in young adult marijuana abusers, with an adjusted 3.2-fold increased risk of MI in 25- to 29-year-olds with marijuana abuse noted in their medical records, compared with age-matched controls and a 4.56-fold greater risk among the 30- to 34-year-old cannabis abusers, according to Dr. Chami of Case Western Reserve University in Cleveland.

Bruce Jancin/Frontline Medical News

bjancin@frontlinemedcom.com

Sports and sports figures provide both a welcome relief from the stress of dealing with life and death in the ED and memorable ways of characterizing serious health care issues. When the Institute of Medicine issued its 2006 report “Hospital-Based Emergency Care: At the Breaking Point,” we thought that a quote about a popular restaurant by the late, great New York Yankees catcher Yogi Berra better described the severely overcrowded EDs and ambulance diversion: “Nobody goes there anymore—it’s too crowded.”

In late winter and early spring of this year, after vigorous attempts to repeal/revise the 2010 Affordable Care Act (ACA), a replacement bill was withdrawn immediately prior to a Congressional vote on March 24 due to a lack of support. Seven years earlier, when President Obama also seemed to have little chance of getting the ACA through Congress, we thought that there would be “many more balks before the president and Congress finally pitched a viable health care package to the nation.” Only a month later, however, with the ACA now the law, we suggested that our erroneous prediction was similar to that of “a father who convinces his son to leave for the parking lot during the bottom of the ninth inning of a 3-0 game only to hear the roar of the crowd from the exit ramp as the rookie batter hits a grand-slam home run to win the game.”

In June 2012, when the Supreme Court ruled on the constitutionality of the ACA, many reporters quickly read the Court’s rejection of the first two arguments defending the ACA, and rushed to report that it was dead, without considering that the government had “one more out to go…[the one] casting ACA as a tax—considered to be the weakest player in the lineup—[which] managed to score the winning run to uphold ACA. Game over. Final score: ACA wins 5 to 4.”

But with the 2017 baseball season finally underway, it is a recent football game that provides the perfect paradigm for emergency medicine (EM) and emergency physicians (EPs). The New England Patriots were slight favorites to win Super Bowl 51 over the Atlanta Falcons on February 5,and the first quarter ended with no score. But by halftime, Atlanta was leading 21-3. In 50 years of Super Bowls, no team had ever overcome more than a 10-point deficit to win the game, and with a little over 8 minutes left in the third quarter, the deficit had widened even further to 28-3. Then the Patriots began to turn things around. Though the Patriots never led during regulation play, and no Super Bowl had ever gone into overtime, the fourth quarter ended in a 28-28 tie, and the Patriots went on to win 34-28 in overtime.

Coming out of the locker room to play the second half of that game in front of over 111 million viewers must have been a daunting experience for the Patriots, but no more so than the experience depicted in EP/cinematographer Ryan McGarry’s award-winning documentary “Code Black,” in which he shows young EM residents walking through a packed waiting room to begin their shift, realizing that in the next 12 hours, they could never treat all of the ill patients waiting to be seen. But the young residents proceeded to treat one patient after another without ever giving up or losing their idealism, until in the end, they, too, had won the game against all odds.

Many patients arrive in EDs so ill that there is no reasonable expectation any intervention can save them, but we nevertheless try and sometimes succeed in doing the seemingly impossible. It is the type of medicine we have chosen to devote our careers to, and we are no less heroes than were the Patriots on February 5, 2017. Each time we go out to “play ball” in our overcrowded EDs, it is worth remembering another famous Yogi Berra quote: “It ain’t over till it’s over.” 

Sports and sports figures provide both a welcome relief from the stress of dealing with life and death in the ED and memorable ways of characterizing serious health care issues. When the Institute of Medicine issued its 2006 report “Hospital-Based Emergency Care: At the Breaking Point,” we thought that a quote about a popular restaurant by the late, great New York Yankees catcher Yogi Berra better described the severely overcrowded EDs and ambulance diversion: “Nobody goes there anymore—it’s too crowded.”

In late winter and early spring of this year, after vigorous attempts to repeal/revise the 2010 Affordable Care Act (ACA), a replacement bill was withdrawn immediately prior to a Congressional vote on March 24 due to a lack of support. Seven years earlier, when President Obama also seemed to have little chance of getting the ACA through Congress, we thought that there would be “many more balks before the president and Congress finally pitched a viable health care package to the nation.” Only a month later, however, with the ACA now the law, we suggested that our erroneous prediction was similar to that of “a father who convinces his son to leave for the parking lot during the bottom of the ninth inning of a 3-0 game only to hear the roar of the crowd from the exit ramp as the rookie batter hits a grand-slam home run to win the game.”

In June 2012, when the Supreme Court ruled on the constitutionality of the ACA, many reporters quickly read the Court’s rejection of the first two arguments defending the ACA, and rushed to report that it was dead, without considering that the government had “one more out to go…[the one] casting ACA as a tax—considered to be the weakest player in the lineup—[which] managed to score the winning run to uphold ACA. Game over. Final score: ACA wins 5 to 4.”

But with the 2017 baseball season finally underway, it is a recent football game that provides the perfect paradigm for emergency medicine (EM) and emergency physicians (EPs). The New England Patriots were slight favorites to win Super Bowl 51 over the Atlanta Falcons on February 5,and the first quarter ended with no score. But by halftime, Atlanta was leading 21-3. In 50 years of Super Bowls, no team had ever overcome more than a 10-point deficit to win the game, and with a little over 8 minutes left in the third quarter, the deficit had widened even further to 28-3. Then the Patriots began to turn things around. Though the Patriots never led during regulation play, and no Super Bowl had ever gone into overtime, the fourth quarter ended in a 28-28 tie, and the Patriots went on to win 34-28 in overtime.

Coming out of the locker room to play the second half of that game in front of over 111 million viewers must have been a daunting experience for the Patriots, but no more so than the experience depicted in EP/cinematographer Ryan McGarry’s award-winning documentary “Code Black,” in which he shows young EM residents walking through a packed waiting room to begin their shift, realizing that in the next 12 hours, they could never treat all of the ill patients waiting to be seen. But the young residents proceeded to treat one patient after another without ever giving up or losing their idealism, until in the end, they, too, had won the game against all odds.

Many patients arrive in EDs so ill that there is no reasonable expectation any intervention can save them, but we nevertheless try and sometimes succeed in doing the seemingly impossible. It is the type of medicine we have chosen to devote our careers to, and we are no less heroes than were the Patriots on February 5, 2017. Each time we go out to “play ball” in our overcrowded EDs, it is worth remembering another famous Yogi Berra quote: “It ain’t over till it’s over.” 

Sports and sports figures provide both a welcome relief from the stress of dealing with life and death in the ED and memorable ways of characterizing serious health care issues. When the Institute of Medicine issued its 2006 report “Hospital-Based Emergency Care: At the Breaking Point,” we thought that a quote about a popular restaurant by the late, great New York Yankees catcher Yogi Berra better described the severely overcrowded EDs and ambulance diversion: “Nobody goes there anymore—it’s too crowded.”

In late winter and early spring of this year, after vigorous attempts to repeal/revise the 2010 Affordable Care Act (ACA), a replacement bill was withdrawn immediately prior to a Congressional vote on March 24 due to a lack of support. Seven years earlier, when President Obama also seemed to have little chance of getting the ACA through Congress, we thought that there would be “many more balks before the president and Congress finally pitched a viable health care package to the nation.” Only a month later, however, with the ACA now the law, we suggested that our erroneous prediction was similar to that of “a father who convinces his son to leave for the parking lot during the bottom of the ninth inning of a 3-0 game only to hear the roar of the crowd from the exit ramp as the rookie batter hits a grand-slam home run to win the game.”

In June 2012, when the Supreme Court ruled on the constitutionality of the ACA, many reporters quickly read the Court’s rejection of the first two arguments defending the ACA, and rushed to report that it was dead, without considering that the government had “one more out to go…[the one] casting ACA as a tax—considered to be the weakest player in the lineup—[which] managed to score the winning run to uphold ACA. Game over. Final score: ACA wins 5 to 4.”

But with the 2017 baseball season finally underway, it is a recent football game that provides the perfect paradigm for emergency medicine (EM) and emergency physicians (EPs). The New England Patriots were slight favorites to win Super Bowl 51 over the Atlanta Falcons on February 5,and the first quarter ended with no score. But by halftime, Atlanta was leading 21-3. In 50 years of Super Bowls, no team had ever overcome more than a 10-point deficit to win the game, and with a little over 8 minutes left in the third quarter, the deficit had widened even further to 28-3. Then the Patriots began to turn things around. Though the Patriots never led during regulation play, and no Super Bowl had ever gone into overtime, the fourth quarter ended in a 28-28 tie, and the Patriots went on to win 34-28 in overtime.

Coming out of the locker room to play the second half of that game in front of over 111 million viewers must have been a daunting experience for the Patriots, but no more so than the experience depicted in EP/cinematographer Ryan McGarry’s award-winning documentary “Code Black,” in which he shows young EM residents walking through a packed waiting room to begin their shift, realizing that in the next 12 hours, they could never treat all of the ill patients waiting to be seen. But the young residents proceeded to treat one patient after another without ever giving up or losing their idealism, until in the end, they, too, had won the game against all odds.

Many patients arrive in EDs so ill that there is no reasonable expectation any intervention can save them, but we nevertheless try and sometimes succeed in doing the seemingly impossible. It is the type of medicine we have chosen to devote our careers to, and we are no less heroes than were the Patriots on February 5, 2017. Each time we go out to “play ball” in our overcrowded EDs, it is worth remembering another famous Yogi Berra quote: “It ain’t over till it’s over.” 

Headaches—pain or discomfort in the head, scalp, or neck—are a very common reason for ED visits.¹ In 2011, the World Health Organization estimated that 46.5% of the population in North and South America aged 18 to 65 years old experienced at least one headache within the previous year.¹

Migraine is a recurrent headache disorder that afflicts 18% of US women and 9% of US men,² resulting in at least 1.2 million visits to US EDs annually.¹ The economic cost resulting from migraine-related loss of productive time in the US workforce is more than $13 billion per year, most of which is in the form of reduced work productivity.³ Management and treatment for migraine headache in the ED commonly include intravenous (IV) or intramuscular (IM) medications, fluids, or oxygen. While ultimately effective, these methods require nursing care and additional time for posttreatment monitoring, both of which adversely affect patient flow.

In 2006, Mellick et al⁴ described the safety and effectiveness of paraspinous cervical nerve block (PCNB) to abort migraine headaches. Despite its demonstrated efficacy and safety, a decade later, PCNB is still rarely used. Friedman et al⁵ ranked peripheral nerve blocks as the fourth step in management suggestions for primary headache.

Case Reports of Headache Patients

We report on seven headache patients we treated in our ED with PCNB who had good-to-complete resolution of pain, suggesting that PCNB is efficacious and can potentially shorten the ED length of stay. This series of seven patients (six female, one male) was a convenience sample of primary headache patients who presented over a 10-month period and were safely and rapidly treated with PCNB (Table).

In each case, the PCNB procedure was explained to the patient and consent was obtained. Each patient was treated with a total of 3 cc of 0.5% bupivacaine with epinephrine injected into the posterior neck according to the method described by Mellick et al.⁴ Our seven patients achieved an average 5-point reduction in pain on a 10-point pain scale, with 0 = no pain and 10 = worse possible pain.

Other than the provision of medications, no nursing assistance was required. Only one of the patients required further treatment after the PCNB, and none had an adverse reaction. All of the patients reported that their headaches were similar in nature to past headaches. Based on their history and physical examination, none were diagnosed to be experiencing a secondary, more serious cause of headache, and none subsequently returned to our institution with a secondary type of headache.

The Paraspinal Cervical Nerve Block

Paraspinous cervical nerve block requires less time to administer and recovery is shorter than that from IM or IV opioids, sedatives, or neuroleptics. It is an easy technique to teach since it requires bilateral injections.

Technique

Prior to the procedure, cleanse the bilateral paravertebral zones surrounding C6 and C7 with chlorhexidine. Next, fill a 3 cc syringe using 0.5% bupivacaine with epinephrine.

Once the injection is complete, withdraw the needle completely, and compress and massage the injection site to facilitate anesthetic diffusion to surrounding tissues.

Indications

Paraspinous cervical nerve block is an appropriate treatment only for patients who are having a typical episode of chronic, recurring headaches, whose history and physical examination do not suggest the need for any further diagnostic work-up, and who, in the judgment of the treating clinician, require only pain relief.

Contraindications

A patient should not be considered for PCNB if he or she has a new-onset headache, fever, altered mental status, focal neurological deficits, meningismus, findings suggestive of meningitis, papilledema, increased intracranial pressure from a space-occupying lesion, recent head trauma with concern for intracranial hemorrhage, or suspicion of an alternate diagnosis.

Efficacy and Patient Response

Paraspinous cervical nerve block has been shown to decrease pain in patients who had failed standard migraine therapy and patients reported no complications. Of the seven patients in this case report, only one patient received opioids in the ED and none received prescriptions for opioids upon discharge for outpatient use.

Mellick and Mellick⁶ have postulated that pain may be modified due to the PCNB effect on the convergence of the trigeminal nerve with sensory fibers from the upper cervical roots. Since cervical innervation provides feeling to the head and upper neck, blocking this input can ameliorate pain.⁶

Summary

This series of seven patients provides further evidence of the effectiveness of PCNB in relieving headache symptoms for patients with recurrent, primary headaches when a secondary, more serious cause has been clinically excluded. Each of the seven patients had marked improvement of their pain and required only minimal nursing attention; moreover, all stated they would willingly undergo the procedure for future painful episodes.

Although there were no reported complications, this series is too small to demonstrate complete safety of the procedure. While this report is limited by a small sample size, it demonstrates that this is a quick, effective, and easily learned method of addressing a common ED complaint that obviates the need for parenteral medications and offers a potentially decreased patient length of stay.

Paraspinous cervical nerve block is a promising modality of treatment of ED patients who present with headache and migraine symptoms who do not respond to their outpatient “rescue” therapy. This procedure should be considered as an early treatment for migraine and other primary headaches unless contraindicated.

Headaches—pain or discomfort in the head, scalp, or neck—are a very common reason for ED visits.¹ In 2011, the World Health Organization estimated that 46.5% of the population in North and South America aged 18 to 65 years old experienced at least one headache within the previous year.¹

Migraine is a recurrent headache disorder that afflicts 18% of US women and 9% of US men,² resulting in at least 1.2 million visits to US EDs annually.¹ The economic cost resulting from migraine-related loss of productive time in the US workforce is more than $13 billion per year, most of which is in the form of reduced work productivity.³ Management and treatment for migraine headache in the ED commonly include intravenous (IV) or intramuscular (IM) medications, fluids, or oxygen. While ultimately effective, these methods require nursing care and additional time for posttreatment monitoring, both of which adversely affect patient flow.

In 2006, Mellick et al⁴ described the safety and effectiveness of paraspinous cervical nerve block (PCNB) to abort migraine headaches. Despite its demonstrated efficacy and safety, a decade later, PCNB is still rarely used. Friedman et al⁵ ranked peripheral nerve blocks as the fourth step in management suggestions for primary headache.

Case Reports of Headache Patients

We report on seven headache patients we treated in our ED with PCNB who had good-to-complete resolution of pain, suggesting that PCNB is efficacious and can potentially shorten the ED length of stay. This series of seven patients (six female, one male) was a convenience sample of primary headache patients who presented over a 10-month period and were safely and rapidly treated with PCNB (Table).

In each case, the PCNB procedure was explained to the patient and consent was obtained. Each patient was treated with a total of 3 cc of 0.5% bupivacaine with epinephrine injected into the posterior neck according to the method described by Mellick et al.⁴ Our seven patients achieved an average 5-point reduction in pain on a 10-point pain scale, with 0 = no pain and 10 = worse possible pain.

Other than the provision of medications, no nursing assistance was required. Only one of the patients required further treatment after the PCNB, and none had an adverse reaction. All of the patients reported that their headaches were similar in nature to past headaches. Based on their history and physical examination, none were diagnosed to be experiencing a secondary, more serious cause of headache, and none subsequently returned to our institution with a secondary type of headache.

The Paraspinal Cervical Nerve Block

Paraspinous cervical nerve block requires less time to administer and recovery is shorter than that from IM or IV opioids, sedatives, or neuroleptics. It is an easy technique to teach since it requires bilateral injections.

Technique

Prior to the procedure, cleanse the bilateral paravertebral zones surrounding C6 and C7 with chlorhexidine. Next, fill a 3 cc syringe using 0.5% bupivacaine with epinephrine.

Once the injection is complete, withdraw the needle completely, and compress and massage the injection site to facilitate anesthetic diffusion to surrounding tissues.

Indications

Paraspinous cervical nerve block is an appropriate treatment only for patients who are having a typical episode of chronic, recurring headaches, whose history and physical examination do not suggest the need for any further diagnostic work-up, and who, in the judgment of the treating clinician, require only pain relief.

Contraindications

A patient should not be considered for PCNB if he or she has a new-onset headache, fever, altered mental status, focal neurological deficits, meningismus, findings suggestive of meningitis, papilledema, increased intracranial pressure from a space-occupying lesion, recent head trauma with concern for intracranial hemorrhage, or suspicion of an alternate diagnosis.

Efficacy and Patient Response

Paraspinous cervical nerve block has been shown to decrease pain in patients who had failed standard migraine therapy and patients reported no complications. Of the seven patients in this case report, only one patient received opioids in the ED and none received prescriptions for opioids upon discharge for outpatient use.

Mellick and Mellick⁶ have postulated that pain may be modified due to the PCNB effect on the convergence of the trigeminal nerve with sensory fibers from the upper cervical roots. Since cervical innervation provides feeling to the head and upper neck, blocking this input can ameliorate pain.⁶

Summary

This series of seven patients provides further evidence of the effectiveness of PCNB in relieving headache symptoms for patients with recurrent, primary headaches when a secondary, more serious cause has been clinically excluded. Each of the seven patients had marked improvement of their pain and required only minimal nursing attention; moreover, all stated they would willingly undergo the procedure for future painful episodes.

Although there were no reported complications, this series is too small to demonstrate complete safety of the procedure. While this report is limited by a small sample size, it demonstrates that this is a quick, effective, and easily learned method of addressing a common ED complaint that obviates the need for parenteral medications and offers a potentially decreased patient length of stay.

Paraspinous cervical nerve block is a promising modality of treatment of ED patients who present with headache and migraine symptoms who do not respond to their outpatient “rescue” therapy. This procedure should be considered as an early treatment for migraine and other primary headaches unless contraindicated.

Headaches—pain or discomfort in the head, scalp, or neck—are a very common reason for ED visits.¹ In 2011, the World Health Organization estimated that 46.5% of the population in North and South America aged 18 to 65 years old experienced at least one headache within the previous year.¹

Migraine is a recurrent headache disorder that afflicts 18% of US women and 9% of US men,² resulting in at least 1.2 million visits to US EDs annually.¹ The economic cost resulting from migraine-related loss of productive time in the US workforce is more than $13 billion per year, most of which is in the form of reduced work productivity.³ Management and treatment for migraine headache in the ED commonly include intravenous (IV) or intramuscular (IM) medications, fluids, or oxygen. While ultimately effective, these methods require nursing care and additional time for posttreatment monitoring, both of which adversely affect patient flow.

In 2006, Mellick et al⁴ described the safety and effectiveness of paraspinous cervical nerve block (PCNB) to abort migraine headaches. Despite its demonstrated efficacy and safety, a decade later, PCNB is still rarely used. Friedman et al⁵ ranked peripheral nerve blocks as the fourth step in management suggestions for primary headache.

Case Reports of Headache Patients

We report on seven headache patients we treated in our ED with PCNB who had good-to-complete resolution of pain, suggesting that PCNB is efficacious and can potentially shorten the ED length of stay. This series of seven patients (six female, one male) was a convenience sample of primary headache patients who presented over a 10-month period and were safely and rapidly treated with PCNB (Table).

In each case, the PCNB procedure was explained to the patient and consent was obtained. Each patient was treated with a total of 3 cc of 0.5% bupivacaine with epinephrine injected into the posterior neck according to the method described by Mellick et al.⁴ Our seven patients achieved an average 5-point reduction in pain on a 10-point pain scale, with 0 = no pain and 10 = worse possible pain.

Other than the provision of medications, no nursing assistance was required. Only one of the patients required further treatment after the PCNB, and none had an adverse reaction. All of the patients reported that their headaches were similar in nature to past headaches. Based on their history and physical examination, none were diagnosed to be experiencing a secondary, more serious cause of headache, and none subsequently returned to our institution with a secondary type of headache.

The Paraspinal Cervical Nerve Block

Paraspinous cervical nerve block requires less time to administer and recovery is shorter than that from IM or IV opioids, sedatives, or neuroleptics. It is an easy technique to teach since it requires bilateral injections.

Technique

Prior to the procedure, cleanse the bilateral paravertebral zones surrounding C6 and C7 with chlorhexidine. Next, fill a 3 cc syringe using 0.5% bupivacaine with epinephrine.

Once the injection is complete, withdraw the needle completely, and compress and massage the injection site to facilitate anesthetic diffusion to surrounding tissues.

Indications

Paraspinous cervical nerve block is an appropriate treatment only for patients who are having a typical episode of chronic, recurring headaches, whose history and physical examination do not suggest the need for any further diagnostic work-up, and who, in the judgment of the treating clinician, require only pain relief.

Contraindications

A patient should not be considered for PCNB if he or she has a new-onset headache, fever, altered mental status, focal neurological deficits, meningismus, findings suggestive of meningitis, papilledema, increased intracranial pressure from a space-occupying lesion, recent head trauma with concern for intracranial hemorrhage, or suspicion of an alternate diagnosis.

Efficacy and Patient Response

Paraspinous cervical nerve block has been shown to decrease pain in patients who had failed standard migraine therapy and patients reported no complications. Of the seven patients in this case report, only one patient received opioids in the ED and none received prescriptions for opioids upon discharge for outpatient use.

Mellick and Mellick⁶ have postulated that pain may be modified due to the PCNB effect on the convergence of the trigeminal nerve with sensory fibers from the upper cervical roots. Since cervical innervation provides feeling to the head and upper neck, blocking this input can ameliorate pain.⁶

Summary

This series of seven patients provides further evidence of the effectiveness of PCNB in relieving headache symptoms for patients with recurrent, primary headaches when a secondary, more serious cause has been clinically excluded. Each of the seven patients had marked improvement of their pain and required only minimal nursing attention; moreover, all stated they would willingly undergo the procedure for future painful episodes.

Although there were no reported complications, this series is too small to demonstrate complete safety of the procedure. While this report is limited by a small sample size, it demonstrates that this is a quick, effective, and easily learned method of addressing a common ED complaint that obviates the need for parenteral medications and offers a potentially decreased patient length of stay.

Paraspinous cervical nerve block is a promising modality of treatment of ED patients who present with headache and migraine symptoms who do not respond to their outpatient “rescue” therapy. This procedure should be considered as an early treatment for migraine and other primary headaches unless contraindicated.

According to the Centers for Disease Control and Prevention, abdominal pain is the leading reason for ED visits in the United States, with approximately 10 million visits per year.¹ Though a large number of presentations are due to nontraumatic causes of abdominal pain, one etiology is among the most time-sensitive and critical diagnoses: acute colonic perforation.

Colonic perforations can be caused by diverticulitis, trauma, malignancy, ulcerative colitis, and other etiologies.² A rare, yet life-threatening cause of colonic perforation, of which only a few cases have been documented in the literature, is stercoral colonic perforation.²

Regardless of the etiology, the critical actions for any colonic perforation are quick recognition, medical stabilization, and surgical evaluation. This case report highlights the diagnosis and treatment of acute stercoral colonic perforation with peritonitis secondary to hypothyroidism.

Case

A 49-year-old woman with a medical history significant for hypothyroidism presented to the ED for evaluation of diffuse abdominal pain, nausea, and nonbilious, nonbloody vomiting that started in the early evening of presentation. The patient denied any previous pain or associated symptoms, and said she had a small, hard bowel movement 1 day prior to arrival. She began experiencing mild abdominal pain on the morning of presentation. Her symptoms acutely worsened at approximately 5:00 pm. She denied having any diarrhea, melena, or hematochezia. Her surgical history was significant for a cesarean delivery. She denied any history of small bowel obstruction. The patient admitted that she had stopped taking levothyroxine (150 mcg daily) prescribed for hypothyroidism approximately 1 month earlier, but had been restarted on it approximately 2 to 3 days prior to her presentation.

On physical examination, her vital signs were: heart rate, 156 beats/min; blood pressure, 134/84 mm Hg; respiratory rate, 20 breaths/min, and temperature, 97.4°F. The patient appeared ill and diaphoretic, writhing on the stretcher. Abdominal examination was significant for diminished bowel sounds, diffuse abdominal distension, rigidity, and tenderness with light palpation.

Laboratory evaluation showed an elevated lactic acid level of 7.7 mmol/L, a white blood cell count of 7,200 cells/mm³ (segment form, 69.5%), and the following abnormal blood chemistry results: creatinine, 2.08 mg/dL; aspartate aminotransferase, 176 U/L; alanine aminotransferase, 138 U/L; and thyroid-stimulating hormone (TSH), 225.3 mcIU/mL. Other laboratory results were within normal range. Her electrocardiogram showed sinus tachycardia with a rate of 154 beats/min, a QTc within normal limits, and no ST elevations or depressions.

An abdominopelvic computed tomography (CT) scan revealed free air, free fluid, and possibly stool within the abdomen and pelvis. The findings were consistent with a ruptured hollow viscus, possibly a sigmoid colonic perforation. The radiologist also noted hepatomegaly and significant hepatic steatosis. A surgeon was immediately notified and evaluated the patient in the ED. The working diagnosis was stercoral colonic perforation secondary to severe hypothyroidism, and the patient was taken emergently to the operating room for repair.

Intraoperatively, the patient underwent exploratory laparotomy, which revealed gross fecal contamination of the abdomen. The surgeon noted that there was fecal staining along the serosal surface of the small bowel and throughout the pelvis. There were also large, hard stool balls outside of the colon. The perforation was along the mesenteric surface of the sigmoid just above the rectosigmoid junction.

The abdomen was copiously irrigated, the perforated segment was resected, and a Hartmann colostomy was created. The diagnosis was stercoral sigmoid perforation with peritonitis, and the patient was transferred to the intensive care unit for antibiotic treatment and further medical care, including intravenous (IV) levothyroxine.

She was extubated uneventfully on postoperative day 2, and the acute renal failure improved with supportive care only. Her bowel function slowly returned without complication. She was switched to oral levothyroxine on postoperative day 3. On day 13, she was given strict instructions for continuation of her thyroid medication and close monitoring for postsurgical complications, and was discharged home with appropriate follow-up.

Discussion

Multiple contributing factors can lead to bowel perforation. In this case, severe hypothyroidism with constipation caused a colonic perforation. Our patient had severe constipation that increased intraluminal pressure, causing the bowel wall to become ischemic and subsequently perforate.³ Any disease that causes significant constipation or obstruction of transit could lead to the same catastrophic result.

According to Huang et al,⁴ as of 2002, fewer than 90 cases of general stercoral bowel perforation had been reported, with no clear age range. However, patients in their mid-50s to mid-60s appear to be the most commonly affected age group.⁴ Our patient was younger than this age group, making identification of the problem by age alone difficult.

Hypothyroidism

The incidence of hypothyroidism in iodine-replete communities varies between 1% to 2% of the general population.⁵ The condition is more common in older women, affecting approximately 10% of those over age 65 years. In the United States, the prevalence of biochemical hypothyroidism is 4.6%; however, clinically evident hypothyroidism is present in only 0.3%.⁶ Common causes for hypothyroidism are listed in the Table.^7,8

Myxedema Coma

Untreated, hypothyroidism can lead to potentially fatal conditions, such as myxedema coma, which is characterized by hypothermia, hypotension, bradycardia, respiratory depression, and altered mental status.⁷ Severe myxedema coma can result in cardiovascular collapse, and eventual death. Electrocardiography findings of severe hypothyroidism include bradycardia, low-voltage QRS, and widespread T-wave inversions.⁷ Our patient was tachycardic and did not have any acute findings to suggest myxedema coma.

Treatment for myxedema coma includes supportive care with ventilatory support and pressor support if necessary. Patients should be given IV hydrocortisone, 100 mg, to treat possible adrenal insufficiency and T₄, 4 mcg/kg by slow IV infusion.⁷ Caution should be taken if giving a patient T₃ due to the risk of dysrhythmias and myocardial infarction (MI).⁷ As our patient was not displaying myxedema coma, the surgeon elected not to start IV thyroid replacement to avoid exacerbating the patient’s tachycardia and possibly precipitating an MI intraoperatively.

Conclusion

Our case underscores the importance of promptly recognizing the signs and symptoms of stercoral colonic perforation in patients who present with nontraumatic abdominal pain accompanied by nausea and nonbilious, nonbloody vomiting. Although stercoral colonic perforation is a rare cause of nontraumatic abdominal pain, as with any type of colonic perforation, it constitutes a life-threatening medical emergency. As our case illustrates, prompt diagnosis through a thorough history taking, physical examination, and laboratory and imaging studies is critical to ensure medical stabilization and surgical management to reduce morbidity and mortality.

According to the Centers for Disease Control and Prevention, abdominal pain is the leading reason for ED visits in the United States, with approximately 10 million visits per year.¹ Though a large number of presentations are due to nontraumatic causes of abdominal pain, one etiology is among the most time-sensitive and critical diagnoses: acute colonic perforation.

Colonic perforations can be caused by diverticulitis, trauma, malignancy, ulcerative colitis, and other etiologies.² A rare, yet life-threatening cause of colonic perforation, of which only a few cases have been documented in the literature, is stercoral colonic perforation.²

Regardless of the etiology, the critical actions for any colonic perforation are quick recognition, medical stabilization, and surgical evaluation. This case report highlights the diagnosis and treatment of acute stercoral colonic perforation with peritonitis secondary to hypothyroidism.

Case

A 49-year-old woman with a medical history significant for hypothyroidism presented to the ED for evaluation of diffuse abdominal pain, nausea, and nonbilious, nonbloody vomiting that started in the early evening of presentation. The patient denied any previous pain or associated symptoms, and said she had a small, hard bowel movement 1 day prior to arrival. She began experiencing mild abdominal pain on the morning of presentation. Her symptoms acutely worsened at approximately 5:00 pm. She denied having any diarrhea, melena, or hematochezia. Her surgical history was significant for a cesarean delivery. She denied any history of small bowel obstruction. The patient admitted that she had stopped taking levothyroxine (150 mcg daily) prescribed for hypothyroidism approximately 1 month earlier, but had been restarted on it approximately 2 to 3 days prior to her presentation.

On physical examination, her vital signs were: heart rate, 156 beats/min; blood pressure, 134/84 mm Hg; respiratory rate, 20 breaths/min, and temperature, 97.4°F. The patient appeared ill and diaphoretic, writhing on the stretcher. Abdominal examination was significant for diminished bowel sounds, diffuse abdominal distension, rigidity, and tenderness with light palpation.

Laboratory evaluation showed an elevated lactic acid level of 7.7 mmol/L, a white blood cell count of 7,200 cells/mm³ (segment form, 69.5%), and the following abnormal blood chemistry results: creatinine, 2.08 mg/dL; aspartate aminotransferase, 176 U/L; alanine aminotransferase, 138 U/L; and thyroid-stimulating hormone (TSH), 225.3 mcIU/mL. Other laboratory results were within normal range. Her electrocardiogram showed sinus tachycardia with a rate of 154 beats/min, a QTc within normal limits, and no ST elevations or depressions.

An abdominopelvic computed tomography (CT) scan revealed free air, free fluid, and possibly stool within the abdomen and pelvis. The findings were consistent with a ruptured hollow viscus, possibly a sigmoid colonic perforation. The radiologist also noted hepatomegaly and significant hepatic steatosis. A surgeon was immediately notified and evaluated the patient in the ED. The working diagnosis was stercoral colonic perforation secondary to severe hypothyroidism, and the patient was taken emergently to the operating room for repair.

Intraoperatively, the patient underwent exploratory laparotomy, which revealed gross fecal contamination of the abdomen. The surgeon noted that there was fecal staining along the serosal surface of the small bowel and throughout the pelvis. There were also large, hard stool balls outside of the colon. The perforation was along the mesenteric surface of the sigmoid just above the rectosigmoid junction.

The abdomen was copiously irrigated, the perforated segment was resected, and a Hartmann colostomy was created. The diagnosis was stercoral sigmoid perforation with peritonitis, and the patient was transferred to the intensive care unit for antibiotic treatment and further medical care, including intravenous (IV) levothyroxine.

She was extubated uneventfully on postoperative day 2, and the acute renal failure improved with supportive care only. Her bowel function slowly returned without complication. She was switched to oral levothyroxine on postoperative day 3. On day 13, she was given strict instructions for continuation of her thyroid medication and close monitoring for postsurgical complications, and was discharged home with appropriate follow-up.

Discussion

Multiple contributing factors can lead to bowel perforation. In this case, severe hypothyroidism with constipation caused a colonic perforation. Our patient had severe constipation that increased intraluminal pressure, causing the bowel wall to become ischemic and subsequently perforate.³ Any disease that causes significant constipation or obstruction of transit could lead to the same catastrophic result.

According to Huang et al,⁴ as of 2002, fewer than 90 cases of general stercoral bowel perforation had been reported, with no clear age range. However, patients in their mid-50s to mid-60s appear to be the most commonly affected age group.⁴ Our patient was younger than this age group, making identification of the problem by age alone difficult.

Hypothyroidism

The incidence of hypothyroidism in iodine-replete communities varies between 1% to 2% of the general population.⁵ The condition is more common in older women, affecting approximately 10% of those over age 65 years. In the United States, the prevalence of biochemical hypothyroidism is 4.6%; however, clinically evident hypothyroidism is present in only 0.3%.⁶ Common causes for hypothyroidism are listed in the Table.^7,8

Myxedema Coma

Untreated, hypothyroidism can lead to potentially fatal conditions, such as myxedema coma, which is characterized by hypothermia, hypotension, bradycardia, respiratory depression, and altered mental status.⁷ Severe myxedema coma can result in cardiovascular collapse, and eventual death. Electrocardiography findings of severe hypothyroidism include bradycardia, low-voltage QRS, and widespread T-wave inversions.⁷ Our patient was tachycardic and did not have any acute findings to suggest myxedema coma.

Treatment for myxedema coma includes supportive care with ventilatory support and pressor support if necessary. Patients should be given IV hydrocortisone, 100 mg, to treat possible adrenal insufficiency and T₄, 4 mcg/kg by slow IV infusion.⁷ Caution should be taken if giving a patient T₃ due to the risk of dysrhythmias and myocardial infarction (MI).⁷ As our patient was not displaying myxedema coma, the surgeon elected not to start IV thyroid replacement to avoid exacerbating the patient’s tachycardia and possibly precipitating an MI intraoperatively.

Conclusion

Our case underscores the importance of promptly recognizing the signs and symptoms of stercoral colonic perforation in patients who present with nontraumatic abdominal pain accompanied by nausea and nonbilious, nonbloody vomiting. Although stercoral colonic perforation is a rare cause of nontraumatic abdominal pain, as with any type of colonic perforation, it constitutes a life-threatening medical emergency. As our case illustrates, prompt diagnosis through a thorough history taking, physical examination, and laboratory and imaging studies is critical to ensure medical stabilization and surgical management to reduce morbidity and mortality.

According to the Centers for Disease Control and Prevention, abdominal pain is the leading reason for ED visits in the United States, with approximately 10 million visits per year.¹ Though a large number of presentations are due to nontraumatic causes of abdominal pain, one etiology is among the most time-sensitive and critical diagnoses: acute colonic perforation.

Colonic perforations can be caused by diverticulitis, trauma, malignancy, ulcerative colitis, and other etiologies.² A rare, yet life-threatening cause of colonic perforation, of which only a few cases have been documented in the literature, is stercoral colonic perforation.²

Regardless of the etiology, the critical actions for any colonic perforation are quick recognition, medical stabilization, and surgical evaluation. This case report highlights the diagnosis and treatment of acute stercoral colonic perforation with peritonitis secondary to hypothyroidism.

Case

A 49-year-old woman with a medical history significant for hypothyroidism presented to the ED for evaluation of diffuse abdominal pain, nausea, and nonbilious, nonbloody vomiting that started in the early evening of presentation. The patient denied any previous pain or associated symptoms, and said she had a small, hard bowel movement 1 day prior to arrival. She began experiencing mild abdominal pain on the morning of presentation. Her symptoms acutely worsened at approximately 5:00 pm. She denied having any diarrhea, melena, or hematochezia. Her surgical history was significant for a cesarean delivery. She denied any history of small bowel obstruction. The patient admitted that she had stopped taking levothyroxine (150 mcg daily) prescribed for hypothyroidism approximately 1 month earlier, but had been restarted on it approximately 2 to 3 days prior to her presentation.

On physical examination, her vital signs were: heart rate, 156 beats/min; blood pressure, 134/84 mm Hg; respiratory rate, 20 breaths/min, and temperature, 97.4°F. The patient appeared ill and diaphoretic, writhing on the stretcher. Abdominal examination was significant for diminished bowel sounds, diffuse abdominal distension, rigidity, and tenderness with light palpation.

Laboratory evaluation showed an elevated lactic acid level of 7.7 mmol/L, a white blood cell count of 7,200 cells/mm³ (segment form, 69.5%), and the following abnormal blood chemistry results: creatinine, 2.08 mg/dL; aspartate aminotransferase, 176 U/L; alanine aminotransferase, 138 U/L; and thyroid-stimulating hormone (TSH), 225.3 mcIU/mL. Other laboratory results were within normal range. Her electrocardiogram showed sinus tachycardia with a rate of 154 beats/min, a QTc within normal limits, and no ST elevations or depressions.

An abdominopelvic computed tomography (CT) scan revealed free air, free fluid, and possibly stool within the abdomen and pelvis. The findings were consistent with a ruptured hollow viscus, possibly a sigmoid colonic perforation. The radiologist also noted hepatomegaly and significant hepatic steatosis. A surgeon was immediately notified and evaluated the patient in the ED. The working diagnosis was stercoral colonic perforation secondary to severe hypothyroidism, and the patient was taken emergently to the operating room for repair.

Intraoperatively, the patient underwent exploratory laparotomy, which revealed gross fecal contamination of the abdomen. The surgeon noted that there was fecal staining along the serosal surface of the small bowel and throughout the pelvis. There were also large, hard stool balls outside of the colon. The perforation was along the mesenteric surface of the sigmoid just above the rectosigmoid junction.

The abdomen was copiously irrigated, the perforated segment was resected, and a Hartmann colostomy was created. The diagnosis was stercoral sigmoid perforation with peritonitis, and the patient was transferred to the intensive care unit for antibiotic treatment and further medical care, including intravenous (IV) levothyroxine.

She was extubated uneventfully on postoperative day 2, and the acute renal failure improved with supportive care only. Her bowel function slowly returned without complication. She was switched to oral levothyroxine on postoperative day 3. On day 13, she was given strict instructions for continuation of her thyroid medication and close monitoring for postsurgical complications, and was discharged home with appropriate follow-up.

Discussion

Multiple contributing factors can lead to bowel perforation. In this case, severe hypothyroidism with constipation caused a colonic perforation. Our patient had severe constipation that increased intraluminal pressure, causing the bowel wall to become ischemic and subsequently perforate.³ Any disease that causes significant constipation or obstruction of transit could lead to the same catastrophic result.

According to Huang et al,⁴ as of 2002, fewer than 90 cases of general stercoral bowel perforation had been reported, with no clear age range. However, patients in their mid-50s to mid-60s appear to be the most commonly affected age group.⁴ Our patient was younger than this age group, making identification of the problem by age alone difficult.

Hypothyroidism

The incidence of hypothyroidism in iodine-replete communities varies between 1% to 2% of the general population.⁵ The condition is more common in older women, affecting approximately 10% of those over age 65 years. In the United States, the prevalence of biochemical hypothyroidism is 4.6%; however, clinically evident hypothyroidism is present in only 0.3%.⁶ Common causes for hypothyroidism are listed in the Table.^7,8

Myxedema Coma

Untreated, hypothyroidism can lead to potentially fatal conditions, such as myxedema coma, which is characterized by hypothermia, hypotension, bradycardia, respiratory depression, and altered mental status.⁷ Severe myxedema coma can result in cardiovascular collapse, and eventual death. Electrocardiography findings of severe hypothyroidism include bradycardia, low-voltage QRS, and widespread T-wave inversions.⁷ Our patient was tachycardic and did not have any acute findings to suggest myxedema coma.

Treatment for myxedema coma includes supportive care with ventilatory support and pressor support if necessary. Patients should be given IV hydrocortisone, 100 mg, to treat possible adrenal insufficiency and T₄, 4 mcg/kg by slow IV infusion.⁷ Caution should be taken if giving a patient T₃ due to the risk of dysrhythmias and myocardial infarction (MI).⁷ As our patient was not displaying myxedema coma, the surgeon elected not to start IV thyroid replacement to avoid exacerbating the patient’s tachycardia and possibly precipitating an MI intraoperatively.

Conclusion

Our case underscores the importance of promptly recognizing the signs and symptoms of stercoral colonic perforation in patients who present with nontraumatic abdominal pain accompanied by nausea and nonbilious, nonbloody vomiting. Although stercoral colonic perforation is a rare cause of nontraumatic abdominal pain, as with any type of colonic perforation, it constitutes a life-threatening medical emergency. As our case illustrates, prompt diagnosis through a thorough history taking, physical examination, and laboratory and imaging studies is critical to ensure medical stabilization and surgical management to reduce morbidity and mortality.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

Laboratory studies revealed leukocytosis with a left shift. Chest radiographs were negative for pneumonia. A magnetic resonance image (MRI) of the lumbar spine was obtained to evaluate for diskitis osteomyelitis. A radiograph of the pelvis was also obtained to evaluate the patient’s THAs, and a computed tomography scan (CT) of the abdomen and pelvis with contrast was obtained for further evaluation. Representative CT, radiographic, and MRI images are shown at left (Figures 1-3).

What is the suspected diagnosis?

Answer

The MRI of the lumbar spine demonstrated no evidence of diskitis osteomyelitis. However, T₂-weighted axial images showed enlarged heterogeneous bilateral psoas muscles with bright signal, indicating the presence of fluid (white arrows, Figure 4).

On the pelvic radiographs, both femoral heads appeared off-center within the acetabular cups (red arrows, Figure 5). This eccentric positioning indicated wear of the polyethylene in the THAs that normally occupies the space between the acetabular cup and the femoral head. In addition, focal lucency in the right acetabulum indicated breakdown of the bone, a condition referred to as osteolysis (white asterisk, Figure 5).

An abdominopelvic CT scan with contrast was performed and confirmed the findings of polyethylene wear and osteolysis. The CT scan also demonstrated large bilateral hip joint effusions (white arrows, Figure 6), decompressed along distended bilateral iliopsoas bursae (red asterisks, Figure 6), and communicating with the bilateral psoas muscle collections (red arrows, Figure 6).

Osteolysis With Iliopsoas Bursitis

Bursae are fluid-filled sacs lined by synovial tissue located throughout the body to reduce friction at sites of movement between muscles, bones, and tendons. Bursitis develops when these sacs become inflamed and/or infected and fill with fluid. The iliopsoas bursa lies between the anterior capsule of the hip and the psoas tendon, iliacus tendon, and muscle fibers.^1,2 This bursa frequently communicates with the hip joint.^3,4 Iliopsoas bursal distension has been reported following THA in the setting of polyethylene wear,⁵ and aseptic bursitis is a commonly seen incidental finding at the time of revision surgery.⁶

In this patient, long-standing polyethylene-induced synovitis had markedly expanded the hip joints and iliopsoas bursae, eventually resulting in superinfection, which accounted for the patient’s symptoms.

Treatment

Based on the imaging findings, interventional radiology services were contacted. The interventional radiologist drained the bilateral psoas abscesses. Cultures of the fluid were positive for both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S aureus (MSSA). The patient was admitted to the hospital for treatment of MRSA and MSSA with intravenous antibiotic therapy. He recovered from the infection and was discharged on hospital day 2, with instructions to follow up with an orthopedic surgeon to discuss eventual revision of the bilateral THAs.

Case

A 56-year-old woman presented to the ED with palpitations and lightheadedness, which began upon awakening that morning. The patient had a history of atrial fibrillation (AF), and believed this was the cause of her symptoms. Over the past 18 months, the patient had twice undergone successful cardioversion for AF with a rapid ventricular response (RVR); both cardioversions were performed by her cardiologist.

The patient denied experiencing any chest pain, shortness of breath, nausea, or vomiting. Her medical history was significant only for AF. Regarding her medication history, the patient had been prescribed metoprolol, but admitted that she frequently forgot to take it. She further stated that she was not taking aspirin or anticoagulation therapy for AF. She denied past or current alcohol consumption or tobacco use.

On physical examination, the patient’s vital signs were: heart rate (HR), 186 beats/min; blood pressure, 137/82 mm Hg; respiratory rate, 20 breaths/min, and temperature, afebrile. Oxygen saturation was 96% on room air. The head, eye, ears, nose, and throat examination was normal. Auscultation of the lungs revealed clear breath sounds bilaterally. On examination of the heart, the patient had an irregularly irregular rhythm that was tachycardic; no murmurs, rubs, or gallops were appreciated. The abdomen was soft and nontender. There was no edema or redness of the lower extremities.

The emergency physician (EP) placed the patient on a cardiac monitor and administered 2 L of oxygen via nasal cannula. An electrocardiogram (ECG), portable chest X-ray (CXR), and laboratory evaluation were ordered, and an intravenous (IV) line was established. The ECG revealed AF with RVR, without evidence of ischemia. The CXR was interpreted as normal. Laboratory studies, including complete blood count, basic metabolic profile, and serum troponin levels, were likewise within normal limits.

Based on the patient’s history and evaluation, the EP decided to cardiovert the patient rather than attempt rate control with IV medications. The patient consented to the cardioversion, based on the two previous successful cardioversions performed by her cardiologist. The EP gave the patient midazolam 2 mg IV and performed synchronized cardioversion at 200 joules. The patient converted to normal sinus rhythm with an HR of 86 beats/min. She was observed in the ED for 1 hour, given metoprolol 50 mg by mouth, and discharged home with instructions to follow up with her cardiologist the following week.

The next day, the patient suffered a large ischemic stroke in the distribution of the left middle cerebral artery, resulting in a dense right hemiparesis. The neurological deficit was significant, necessitating the patient’s placement in a nursing home.

The patient and her family sued the EP for malpractice for not anticoagulating the patient prior to and following cardioversion. A $3.3 million settlement was agreed upon prior to trial.

Discussion

Patients commonly present to the ED for complaints related to AF. In some cases, the EP is the first to diagnose the patient’s AF; in other cases, the patient has a history of AF and is presenting with a complication. The focus of this discussion is solely on the management of AF with RVR.

When managing a patient in AF with RVR, the EP must consider three issues: ventricular rate control (VRC), rhythm control, and anticoagulation. Selecting the best treatment strategy will depend on the patient’s hemodynamic stability, duration of her or his symptoms, local custom and preference, and the length of time the AF has been present.

Ventricular Rate Control and Cardioversion

For many stable patients, VRC is frequently the treatment of choice, with a goal HR of less than 100 beats/min. Intravenous diltiazem, esmolol, or metoprolol can be used to achieve VRC in patients in AF. Because these drugs only control ventricular rate and do not typically cardiovert, the risk of embolization is small.

Synchronized cardioversion has the benefit of providing both rate and rhythm control, but at the expense of the increased risk of arterial embolization. Some patients, including those with rheumatic heart disease, mitral stenosis, prosthetic heart valves, severe left ventricular dysfunction, or a history of thromboembolism, are at a constant high risk of developing a thromboembolism.¹

Risk-Benefit Ratio and Anticoagulation Therapy

To help determine the risk-benefit ratio in patients without the risk factors mentioned above, the EP should calculate the CHADS₂ (congestive heart failure [CHF], hypertension, age, diabetes mellitus [DM], prior stroke, transient ischemic attack [TIA], or thromboembolism [doubled]) score or CHA₂DS₂-VAS_C (CHF, hypertension, age 75 years or older [two scores], DM, previous stroke, TIA, or thromboembolism [doubled], vascular disease, age 65-74 years, sex [female]) score to help identify patients at risk for arterial embolic complications (Table).

For patients who have been in AF for less than 48 hours and who are at a very low-embolic risk (CHA₂DS₂-VAS_C score of 0), some experts suggest cardioversion without anticoagulation. However, other experts recommend anticoagulation prior to cardioversion—even in low-risk patients. Unfortunately, there is disagreement between professional organizations, with the American Heart Association/American College of Cardiology/Heart Rhythm Society stating that cardioversion may be performed with or without procedural anticoagulation,² while the 2016 European Society of Cardiology guidelines recommend immediate initiation of anticoagulants in all such patients scheduled for cardioversion.³

The reasoning in favor of anticoagulation prior to cardioversion is supported by an observational study by Airaksinen et al⁴ of 2,481 patients undergoing cardioversion for AF of less than 48 hours duration. This study demonstrated a definite thromboembolic event in 38 (0.7%) of the patients within 30 days (median of 2 days). The thromboembolic event was stroke in 31 of the 38 patients.⁴ Airaksinen et al⁴ found that age older than 60 years, female sex, heart failure (HF), and DM were the strongest predictors of embolization. The risk of stroke in patients without HF and those younger than age 60 years was only 0.2%.⁴

In a similar observational study by Hansen et al⁵ of 16,274 patients in AF undergoing cardioversion with and without anticoagulation therapy, the absence of post­cardio­version anticoagulation increased the risk of thromboembolism 2-fold—regardless of CHA₂DS₂-VAS_C scores.

Summary

While the management of AF with a duration of more than 48 hours should always include some type of anticoagulation therapy (pre- or postcardioversion, or both), the role of anticoagulation in low-risk patients with AF of less than 48 hours is not as clear. As this situation is not uncommon, the emergency medicine and cardiology physicians should consider developing a mutually agreed upon protocol on how best to manage these patients at their institution. When considering cardioversion without pre- or postanticoagulation in low-risk patients with AF, EPs should always involve the patient in the decision-making process.

Case

A 56-year-old woman presented to the ED with palpitations and lightheadedness, which began upon awakening that morning. The patient had a history of atrial fibrillation (AF), and believed this was the cause of her symptoms. Over the past 18 months, the patient had twice undergone successful cardioversion for AF with a rapid ventricular response (RVR); both cardioversions were performed by her cardiologist.

The patient denied experiencing any chest pain, shortness of breath, nausea, or vomiting. Her medical history was significant only for AF. Regarding her medication history, the patient had been prescribed metoprolol, but admitted that she frequently forgot to take it. She further stated that she was not taking aspirin or anticoagulation therapy for AF. She denied past or current alcohol consumption or tobacco use.

On physical examination, the patient’s vital signs were: heart rate (HR), 186 beats/min; blood pressure, 137/82 mm Hg; respiratory rate, 20 breaths/min, and temperature, afebrile. Oxygen saturation was 96% on room air. The head, eye, ears, nose, and throat examination was normal. Auscultation of the lungs revealed clear breath sounds bilaterally. On examination of the heart, the patient had an irregularly irregular rhythm that was tachycardic; no murmurs, rubs, or gallops were appreciated. The abdomen was soft and nontender. There was no edema or redness of the lower extremities.

The emergency physician (EP) placed the patient on a cardiac monitor and administered 2 L of oxygen via nasal cannula. An electrocardiogram (ECG), portable chest X-ray (CXR), and laboratory evaluation were ordered, and an intravenous (IV) line was established. The ECG revealed AF with RVR, without evidence of ischemia. The CXR was interpreted as normal. Laboratory studies, including complete blood count, basic metabolic profile, and serum troponin levels, were likewise within normal limits.

Based on the patient’s history and evaluation, the EP decided to cardiovert the patient rather than attempt rate control with IV medications. The patient consented to the cardioversion, based on the two previous successful cardioversions performed by her cardiologist. The EP gave the patient midazolam 2 mg IV and performed synchronized cardioversion at 200 joules. The patient converted to normal sinus rhythm with an HR of 86 beats/min. She was observed in the ED for 1 hour, given metoprolol 50 mg by mouth, and discharged home with instructions to follow up with her cardiologist the following week.

The next day, the patient suffered a large ischemic stroke in the distribution of the left middle cerebral artery, resulting in a dense right hemiparesis. The neurological deficit was significant, necessitating the patient’s placement in a nursing home.

The patient and her family sued the EP for malpractice for not anticoagulating the patient prior to and following cardioversion. A $3.3 million settlement was agreed upon prior to trial.

Discussion

Patients commonly present to the ED for complaints related to AF. In some cases, the EP is the first to diagnose the patient’s AF; in other cases, the patient has a history of AF and is presenting with a complication. The focus of this discussion is solely on the management of AF with RVR.

When managing a patient in AF with RVR, the EP must consider three issues: ventricular rate control (VRC), rhythm control, and anticoagulation. Selecting the best treatment strategy will depend on the patient’s hemodynamic stability, duration of her or his symptoms, local custom and preference, and the length of time the AF has been present.

Ventricular Rate Control and Cardioversion

For many stable patients, VRC is frequently the treatment of choice, with a goal HR of less than 100 beats/min. Intravenous diltiazem, esmolol, or metoprolol can be used to achieve VRC in patients in AF. Because these drugs only control ventricular rate and do not typically cardiovert, the risk of embolization is small.

Synchronized cardioversion has the benefit of providing both rate and rhythm control, but at the expense of the increased risk of arterial embolization. Some patients, including those with rheumatic heart disease, mitral stenosis, prosthetic heart valves, severe left ventricular dysfunction, or a history of thromboembolism, are at a constant high risk of developing a thromboembolism.¹

Risk-Benefit Ratio and Anticoagulation Therapy

To help determine the risk-benefit ratio in patients without the risk factors mentioned above, the EP should calculate the CHADS₂ (congestive heart failure [CHF], hypertension, age, diabetes mellitus [DM], prior stroke, transient ischemic attack [TIA], or thromboembolism [doubled]) score or CHA₂DS₂-VAS_C (CHF, hypertension, age 75 years or older [two scores], DM, previous stroke, TIA, or thromboembolism [doubled], vascular disease, age 65-74 years, sex [female]) score to help identify patients at risk for arterial embolic complications (Table).

For patients who have been in AF for less than 48 hours and who are at a very low-embolic risk (CHA₂DS₂-VAS_C score of 0), some experts suggest cardioversion without anticoagulation. However, other experts recommend anticoagulation prior to cardioversion—even in low-risk patients. Unfortunately, there is disagreement between professional organizations, with the American Heart Association/American College of Cardiology/Heart Rhythm Society stating that cardioversion may be performed with or without procedural anticoagulation,² while the 2016 European Society of Cardiology guidelines recommend immediate initiation of anticoagulants in all such patients scheduled for cardioversion.³

The reasoning in favor of anticoagulation prior to cardioversion is supported by an observational study by Airaksinen et al⁴ of 2,481 patients undergoing cardioversion for AF of less than 48 hours duration. This study demonstrated a definite thromboembolic event in 38 (0.7%) of the patients within 30 days (median of 2 days). The thromboembolic event was stroke in 31 of the 38 patients.⁴ Airaksinen et al⁴ found that age older than 60 years, female sex, heart failure (HF), and DM were the strongest predictors of embolization. The risk of stroke in patients without HF and those younger than age 60 years was only 0.2%.⁴

In a similar observational study by Hansen et al⁵ of 16,274 patients in AF undergoing cardioversion with and without anticoagulation therapy, the absence of post­cardio­version anticoagulation increased the risk of thromboembolism 2-fold—regardless of CHA₂DS₂-VAS_C scores.

Summary

While the management of AF with a duration of more than 48 hours should always include some type of anticoagulation therapy (pre- or postcardioversion, or both), the role of anticoagulation in low-risk patients with AF of less than 48 hours is not as clear. As this situation is not uncommon, the emergency medicine and cardiology physicians should consider developing a mutually agreed upon protocol on how best to manage these patients at their institution. When considering cardioversion without pre- or postanticoagulation in low-risk patients with AF, EPs should always involve the patient in the decision-making process.

Case

A 56-year-old woman presented to the ED with palpitations and lightheadedness, which began upon awakening that morning. The patient had a history of atrial fibrillation (AF), and believed this was the cause of her symptoms. Over the past 18 months, the patient had twice undergone successful cardioversion for AF with a rapid ventricular response (RVR); both cardioversions were performed by her cardiologist.

The patient denied experiencing any chest pain, shortness of breath, nausea, or vomiting. Her medical history was significant only for AF. Regarding her medication history, the patient had been prescribed metoprolol, but admitted that she frequently forgot to take it. She further stated that she was not taking aspirin or anticoagulation therapy for AF. She denied past or current alcohol consumption or tobacco use.

On physical examination, the patient’s vital signs were: heart rate (HR), 186 beats/min; blood pressure, 137/82 mm Hg; respiratory rate, 20 breaths/min, and temperature, afebrile. Oxygen saturation was 96% on room air. The head, eye, ears, nose, and throat examination was normal. Auscultation of the lungs revealed clear breath sounds bilaterally. On examination of the heart, the patient had an irregularly irregular rhythm that was tachycardic; no murmurs, rubs, or gallops were appreciated. The abdomen was soft and nontender. There was no edema or redness of the lower extremities.

The emergency physician (EP) placed the patient on a cardiac monitor and administered 2 L of oxygen via nasal cannula. An electrocardiogram (ECG), portable chest X-ray (CXR), and laboratory evaluation were ordered, and an intravenous (IV) line was established. The ECG revealed AF with RVR, without evidence of ischemia. The CXR was interpreted as normal. Laboratory studies, including complete blood count, basic metabolic profile, and serum troponin levels, were likewise within normal limits.

Based on the patient’s history and evaluation, the EP decided to cardiovert the patient rather than attempt rate control with IV medications. The patient consented to the cardioversion, based on the two previous successful cardioversions performed by her cardiologist. The EP gave the patient midazolam 2 mg IV and performed synchronized cardioversion at 200 joules. The patient converted to normal sinus rhythm with an HR of 86 beats/min. She was observed in the ED for 1 hour, given metoprolol 50 mg by mouth, and discharged home with instructions to follow up with her cardiologist the following week.

The next day, the patient suffered a large ischemic stroke in the distribution of the left middle cerebral artery, resulting in a dense right hemiparesis. The neurological deficit was significant, necessitating the patient’s placement in a nursing home.

The patient and her family sued the EP for malpractice for not anticoagulating the patient prior to and following cardioversion. A $3.3 million settlement was agreed upon prior to trial.

Discussion

Patients commonly present to the ED for complaints related to AF. In some cases, the EP is the first to diagnose the patient’s AF; in other cases, the patient has a history of AF and is presenting with a complication. The focus of this discussion is solely on the management of AF with RVR.

When managing a patient in AF with RVR, the EP must consider three issues: ventricular rate control (VRC), rhythm control, and anticoagulation. Selecting the best treatment strategy will depend on the patient’s hemodynamic stability, duration of her or his symptoms, local custom and preference, and the length of time the AF has been present.

Ventricular Rate Control and Cardioversion

For many stable patients, VRC is frequently the treatment of choice, with a goal HR of less than 100 beats/min. Intravenous diltiazem, esmolol, or metoprolol can be used to achieve VRC in patients in AF. Because these drugs only control ventricular rate and do not typically cardiovert, the risk of embolization is small.

Synchronized cardioversion has the benefit of providing both rate and rhythm control, but at the expense of the increased risk of arterial embolization. Some patients, including those with rheumatic heart disease, mitral stenosis, prosthetic heart valves, severe left ventricular dysfunction, or a history of thromboembolism, are at a constant high risk of developing a thromboembolism.¹

Risk-Benefit Ratio and Anticoagulation Therapy

To help determine the risk-benefit ratio in patients without the risk factors mentioned above, the EP should calculate the CHADS₂ (congestive heart failure [CHF], hypertension, age, diabetes mellitus [DM], prior stroke, transient ischemic attack [TIA], or thromboembolism [doubled]) score or CHA₂DS₂-VAS_C (CHF, hypertension, age 75 years or older [two scores], DM, previous stroke, TIA, or thromboembolism [doubled], vascular disease, age 65-74 years, sex [female]) score to help identify patients at risk for arterial embolic complications (Table).

For patients who have been in AF for less than 48 hours and who are at a very low-embolic risk (CHA₂DS₂-VAS_C score of 0), some experts suggest cardioversion without anticoagulation. However, other experts recommend anticoagulation prior to cardioversion—even in low-risk patients. Unfortunately, there is disagreement between professional organizations, with the American Heart Association/American College of Cardiology/Heart Rhythm Society stating that cardioversion may be performed with or without procedural anticoagulation,² while the 2016 European Society of Cardiology guidelines recommend immediate initiation of anticoagulants in all such patients scheduled for cardioversion.³

The reasoning in favor of anticoagulation prior to cardioversion is supported by an observational study by Airaksinen et al⁴ of 2,481 patients undergoing cardioversion for AF of less than 48 hours duration. This study demonstrated a definite thromboembolic event in 38 (0.7%) of the patients within 30 days (median of 2 days). The thromboembolic event was stroke in 31 of the 38 patients.⁴ Airaksinen et al⁴ found that age older than 60 years, female sex, heart failure (HF), and DM were the strongest predictors of embolization. The risk of stroke in patients without HF and those younger than age 60 years was only 0.2%.⁴

In a similar observational study by Hansen et al⁵ of 16,274 patients in AF undergoing cardioversion with and without anticoagulation therapy, the absence of post­cardio­version anticoagulation increased the risk of thromboembolism 2-fold—regardless of CHA₂DS₂-VAS_C scores.

Summary

While the management of AF with a duration of more than 48 hours should always include some type of anticoagulation therapy (pre- or postcardioversion, or both), the role of anticoagulation in low-risk patients with AF of less than 48 hours is not as clear. As this situation is not uncommon, the emergency medicine and cardiology physicians should consider developing a mutually agreed upon protocol on how best to manage these patients at their institution. When considering cardioversion without pre- or postanticoagulation in low-risk patients with AF, EPs should always involve the patient in the decision-making process.