The Pulse - October 2013

the

Pulse

October 2013

Osteopathic Emergency Medicine Quarterly

Presidential Viewpoints Gregory M. Christiansen DO, M.Ed, FACOEP-D

Something New

Do you remember what it was like being a kid when you got to try something new and different? Learning was exciting and led to further exploration. It was a chance to create an experience and wrestle with the questions of ‘how,’ ‘why’ and ‘what if ?’ The experience had an emotional component begging a response to the fact that now there is new information which had to be acknowledged, accepted or rejected. As the saying goes, “Your eyes cannot see what your mind does not know.” A person could no longer ignore what they did not know before. The question becomes how should this new information be handled?

This is precisely the experience a student had while working with me continued on page 4

Editor's Desk Page 5

Executive Director's Desk Page 6

ACOEP Brings You to The Edge Page 10

FOEM Foundation Focus Page 19

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The Pulse

VOLUME XXXVII

Editorial Committee Drew A. Koch, DO, FACOEP-D, Chair Timothy Cheslock, DO, FACOEP, Vice Chair Julia Alpin, DO Kenneth Argo David Bohorquez, DO Gregory Christiansen, DO, M.Ed., FACOEP-D Anthony Jennings, DO, FACOEP Wayne Jones, DO, FACOEP Peter J. Kaplan, Advertising Chair Andrew Little, DO Annette Mann, DO, FACOEP Matthew McCarthy, DO, FACOEP Mark A. Mitchell, DO, FACOEP Todd Thomas Danielle Turrin, DO Brian Thommen, Media & Technology Director Erin Sernoffsky, Communications Manager Thomas Baxter, Media & Technology Specialist The PULSE is a copyrighted quarterly publication distributed at no cost by the ACOEP to its Members, Colleges of Osteopathic Medicine, sponsors, exhibitors and liaison associations recognized by the national offices of the ACOEP. The PULSE and ACOEP accept no responsibility for the statements made by authors, contributors and/ or advertisers in this publication; nor do they accept responsibility for consequences or response to an advertisement. All articles and artwork remain the property of The PULSE and will not be returned.

Display and print advertisements are accepted by the publication through Norcom, Inc., Advertising/Production Department, PO Box 2566 Northbrook, IL 60065 ∙ 847-948-7762 or electronically at theteam@norcomdesign. com. Please contact Norcom for the specific rates and print specifications for both color and black and white print ads.

Deadlines for the submission of articles and advertisements are the first day of the month preceding the date of publication, i.e., December 1; March 1, June 1, and September 1. The ACOEP and the Editorial Board of The PULSE reserve the right to decline advertising and articles for any issue. ©ACOEP 2013 – All rights reserved.

Articles may not be reproduced without the expressed, written approval of the ACOEP and the author.

Pulse

the

Editorial Staff Drew A. Koch, DO, FACOEP-D, Editor Timothy Cheslock, DO, FACOEP, Assistant Editor Gregory Christiansen, DO, M.Ed., FACOEP-D Mark A. Mitchell, DO, FACOEP Erin Sernoffsky, Communication Manager Janice Wachtler, Executive Director

Osteopathic Emergency Medicine Quarterly

Table of Contents

Presidential Viewpoints...............................................................................................1 Gregory M. Christiansen, DO, M.Ed, FACOEP-D The Editors's Desk.......................................................................................................5 Drew A. Koch, DO, FACEOP-D Executive Director's Desk...........................................................................................6 Janice Wachtler, BAE, CBA What Would You Do?..................................................................................................7 Bernard Heilicser, DO, MS, FACEP, FACOEP A Season of Change....................................................................................................8 Mark A. Mitchell, DO, FACOEP, FACEP ACOEP Brings You to The Edge..............................................................................10 Donald Phillips, DO, FACOEP AOA Committee Appointments 2013-2014..........................................................13 Practice Management and You.................................................................................15 Jeremy Tucker, DO, FACOEP Keeping the Pace of Change....................................................................................16 Tim Cheslock, DO FACOEP AOBEM Update.........................................................................................................17 Donald Phillips, DO, FACOEP Important announcement regarding Part III of the AOBEM primary certification in Emergency Medicine.......................................................................17 Donald Phillips, DO, FACOEP FOEM Foundation Focus.........................................................................................19 Sherry D. Turner, DO, FACOEP Resident Wrap Up.......................................................................................................26 Megan McGrew Koenig, DO, MBA, MS Residency Spotlight.....................................................................................................27 Call to Meeting............................................................................................................29 Hypertriglyceridemia Induced Pancreatitis in a Type II Diabetic Presenting with DKA....................................................................................................................30 Ross Cohen, MS IV Upcoming Events.......................................................................................................34

the PULSE | October 2013

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Presidential Viewpoints

Gregory M. Christiansen, DO, M.Ed, FACOEP-D continued from page 1 one night in the emergency department. The prospect of observing the care of a multisystem trauma, cardiac arrest, or respiratory failure filled the student with anticipation and excitement. However, it was a simple case of back pain that made him wonder. The patient was a young black female who had been in a minor accident a week prior. Since then she had developed debilitating back pain. She was not able to carry her child and could not perform her daily activities. The student was perplexed because the patient had taken Motrin and tried hot backs without any relief, and was at her wits end and in tears because of the pain. I made my assessment and proceeded to manipulate her subluxations. With a couple of quick adjustments she had experienced the miracle of osteopathic manipulation and professed instant relief. She was able to return to her daily activities having been relieved of the pain.

The student looked at me with astonishment.

He asked if I was a DO. He was aware of osteopaths but he had never seen what a DO could do for a patient. He was envious of my skills and said he wished he had the ability to help similar patients. His allopathic training experience left him with a sense of lacking. Like me, he wanted to be the best doctor possible. He discovered there is a difference and it was absent in his training. His eyes lit up at the possibility of learning something new which could really make an impact in a patient’s well-being.

This vignette is in contrast to the recent failed negotiations between the ACGME and AOA in which they could not find common ground in their merger proposal.

The decision by the accrediting entities is mired in political discourse. It effectively denies allopathic physicians the opportunity to be the best doctors they can be because they are excluded from the opportunity to learn about osteopathic principles and practice. Likewise, osteopathic students will be denied training opportunities which could expand their skills.

From an outsider’s perspective, clearly both associations have much to learn from each other in order to become better organizations.

Now that both associations have learned there are better ways to serve our patients, will they have the impetus to improve the opportunities for our future doctors?

Honesty

is the first chapter

in the book of

wisdom

-Thomas Jefferson

the PULSE | October 2013

We Want to Hear from You! ER Physicians do incredible things every day and we want your stories! From Dr. Cheslock's views on expediency in the ED, to Dr. Tucker's information on practice management, we know that our members have thoughts to share. Send your story ideas to ThePulse@acoep.org, we would love to share your experience with our members.

We also encourage you to email ThePulse@acoep.org to share your thoughts on specific articles that you read here.

We want to keep the conversation rolling, whether you agree or disagree with a point of view represented in our articles, we want to highlight various perspectives from our diverse membership.

An ACOEP Member responds to the July article, ACOEP is not AOBEM – The Author has asked to remain anonymous.

In regard to the AOBEM answering to the public’s demands, I would say this: Board certification in emergency medicine means that we as a peer group have certain requirements that we ask are met by those seeking quality designation in emergency medicine. It has NOTHING to do with what a layperson expects he or she knows about emergency medicine. As such, I find their rationale not satisfying when it comes to them adding more and more stuff for us to do that we ALL know does not pertain to the measure of quality of an emergency room physician. I would propose that, if the public demands it, they can have their own “board” and we can chose to or not chose to be layperson board certified in emergency medicine. For example, a hospital can brag “our emergency medicine physicians are board certified, both by their peer consensus and by public consensus”, or they could brag, “Our emergency room physicians are board certified by their peer consensus”, or, of course, they could brag, “our emergency room physicians are not board certified”….certainly there will come a point where a designation of wisdom is choosing NOT to have jumped through the hoops.

Do you have a response to something you’ve read in The Pulse? We would love to hear from you! Email your thoughts to ThePulse@acoep.org

The Editor's Desk

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Drew A. Koch, DO, FACEOP-D

Memorandum of Understanding (MOU) in osteopathic medical schools and 4,770 graduates. This represents a 30% increase in enrollment and 50% increase in graduates since 2005. Over 6,000 osteopathic physicians are enrolled in DO post doctorate training programs for the year 2011-2012, and the number of osteopathic training spots is reported as greater than 12,000. The number of available osteopathic training slots to graduating osteopathic physicians appears less than the total number of DO’s enrolled in internship, residencies and fellowship currently.

It is hopeful that the AOA will continue to work with the ACGME to combine osteopathic and allopathic residency accreditation programs under a unified accreditation process and that DO graduates will continue to be able to match in either allopathic or osteopathic residencies and fellowships.

F

or almost two years the AOA and ACGME have been working together to develop a Memorandum of Understanding (MOU) to combine osteopathic and allopathic residency program accreditation processes under the umbrella of one agency. The AOA announced at its recent House of Delegates (HOD) meeting that it has not accepted the agreement.

Citing various inabilities of the agreement to protect osteopathic association concerns, like accreditation of COMS, osteopathic certification, OMM/OMT components in training, licensure and recognition of COMLEX, the House overwhelming supported the Board’s recommendation.

One can understand the HOD’s decision to maintain the identity and uniqueness of the osteopathic profession but what does this decision do for the future generations of osteopathic medical students and graduates?

The concern is where the osteopathic students, interns and residents will receive their clinical education.

One concern of the unification of osteopathic and allopathic accreditation process is the preservation of OMT or OMM. This is one modality of treatment that should separate the osteopathic physician from the allopathic physician.

Do osteopathic physicians who are trained in OMT actually practice OMT? If not is it acceptable to have an allopathic physician performing OMT? There are allopathic physicians who have undertaken OMT courses and workshops that are providing OMT. The training for OMT of these allopathic physicians is a fraction of the training that osteopathic students, interns and residents obtain during their training. In states where there is a separate Osteopathic and Allopathic Licensing Board, the osteopathic physicians are required to show proficiency in osteopathic medicine before one can be licensed in the state. Do these courses and

workshops provide adequate preparation, training and proficiency of OMT for allopathic physicians? The answer is, obviously, no but this is not discouraging allopathic physicians from attending these courses and providing OMT to patients.

Currently there is no mechanism in place that would prevent an allopathic physician from practicing OMT and insure that the physician is proficient in OMT in a private practice setting.

In a hospital setting or hospital based practice, criteria should be developed for allopathic physicians who request privileges in OMT: • Minimum education and training must be established • Proficiency in OMT techniques • Defining the techniques that the physician will employ • Proctoring by whom and for how long • Continuing education It can be argued that only osteopathic physicians perform OMT but that is not what is happening in the real world. Osteopathic physicians do not routinely incorporate OMT in their practice, especially those physicians who trained in allopathic residencies. Allopathic hospitals that have osteopathic physicians on staff do not always have OMT included as a privilege for osteopathic physicians.

Osteopathic physicians are losing their identity and OMT skills. Allopathic physicians are performing treatment modalities that were once considered unique to the osteopathic profession.

What was once considered unique to the osteopathic profession is now desirable to the allopathic profession-OMT. Should OMT be unique to osteopathic physicians or should it be the standard for all medical education and training?

The osteopathic profession has had the foresight to anticipate the shortage of physicians in the United States and has established 29 accredited osteopathic medical schools at 37 locations. Many of these locations are in underserved areas through the country. According to data from the American Association of Colleges of Osteopathic Medicine (AACOM) for academic year 20112012, there were over 26,650 students enrolled

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Executive Director's Desk Janice Wachtler, BAE, CBA

What Now? Prior to the July meetings of the AOA, allopathically accredited programs received a letter saying it was all in the hands of the AOA; AOA played everything close to the vest and said nothing. This has been AOA’s stance throughout to maintain confidentiality in the process.

We finally learned the outcome at the AOA’s House of Delegates and it seems that no memorandum has resulted from these negotiations. Blame seems to be coming from everywhere and aimed at the AOA. But the question remains is it totally AOA’s fault – I don’t think so. I think the outcome was known going in. The ACGME owned the sandbox and if osteopathic medicine was going to get in, they would play by their rules using their shovels and pails.

S

everal years ago, the osteopathic world was shocked with the news that beginning in 2015 certain allopathic institutions would only recognize allopathically trained and certified physicians as program directors. A scary thought for sure.

This was shortly followed by a statement from the Accreditation Council for Graduate Medical Education (ACGME) that only allopathically trained physicians (DO or MD) would be allowed entrance into allopathic fellowship programs. Then the coup-de-grace arrived shortly thereafter, there would only be one accreditor of graduate medical education in the United States and Canada, and that would be – you got it – ACGME. The specialty colleges and AOA rallied around the flag of osteopathic medicine and from there began a two-year negotiation between AOA and ACGME to develop a Memorandum of Understanding (MOU). In this negotiation, both groups pledged to work together toward a mutually agreeable system and negotiations would remain confidential. Throughout the negotiations AOA had non-negotiable items, including recognition of AACOM, COMLEX, osteopathic certification, as well as a few other important issues. Specialty colleges worked with allopathic Residency Review Committees (RRC) to ensure the osteopathic aspects and integrity of specialty training was maintained.

Most of all, we waited to see what would happen.

the PULSE | October 2013

So I guess the question is now where do we go from here?

As an educator, the accreditation processes for any system must be fair, based on overarching objectives, and most importantly, transparent. While I cannot speak to the ACGME’s problems, I can give an informed view of the osteopathic system, one in which I’ve worked for almost 35 years.

So while this may sound critical of the AOA, it is not. I’ve seen the system and processes change over this time, sometimes drastically, and the AOA should be proud of the system it has created – it’s done a good job and has created some fine physicians. But I believe it needs to make one more big change and that is to take accreditation out from under the aegis of the AOA and create a free-standing entity.

Why? Because that way it will be independent and transparent, something that must be done to keep the process clean and unencumbered by current processes.

Big steps need to be taken. First and most importantly, is teaching the public to know who osteopathic physicians are and how great osteopathic medicine is. It seems that after more than 120 years, Americans do not know the difference. The publishers from WestJEM, as well as the ACGME asked us what osteopathic emergency medicine is and how it differs from allopathic emergency medicine. To people in our field this is an easy question to answer, it is a practice by osteopathic physicians who are trained in systems paralleling that of allopathic training. The approach, philosophy

and techniques may different slightly, but not much. However, I think the bigger question should be how do we teach the American public about the best kept medical secret in America? How do we inform the public about the wonderful things osteopathic doctors are doing? I believe it begins with the education in our schools and residency programs. We need to produce programs and doctors dedicated to the practice and continue to have and carry the vision that was created so long ago.

In keeping with this ideology, education should be first and foremost. A non-political system of accreditation should be devised. One which incorporates physician and non-physician evaluators who make recommendations to an agency of professional educators (physician or non-physician) where accreditation should be objective-based and evaluated on evidence supporting the objectives.

The agency may report to the AOA, much like the AACOM and NBOME report to the AOA Board of Trustees, but an arms-length away from the association itself.

In today’s society, people are demanding accountability, and we have to be acutely aware of this in the preparation of tomorrow’s physician workforce. No profession can be a one-stop shop that takes its members from cradle to grave. We all need to be open and accountable, as well as transparent in our accreditation processes.

In conclusion, we know osteopathic medicine works; we know our training is equivalent, maybe it’s time to ensure our accreditation systems are equivalent before some agency in Washington develops a new accreditation and everyone loses.

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Ethics in Emergency Medicine

Bernarnd Heilicser, DO, M.S., FACEP, FACOEP

What Would You Do? Using the legally documented advance directive as a trump card is possible, but can be cruel. Approaching the dissenting friend/ family in a caring and compassionate manner is essential. Explaining to them that their loved one has requested not to have extraordinary treatment, or has appointed an agent to carry out this wish, is a start. Attempting to frame the situation that they should be an advocate for the patient, protecting them from us (because we can do it does not mean we should) and to honor their desires may help. Supporting this by explaining that certain treatment only prolongs the dying process, and provides no benefit or help to the patient may be persuasive.

I

n this issue of The Pulse we will review the article presented by our Executive Director, Jan Wachtler, in the July 2013 issue.

Jan so eloquently described the difficult decisions family members are confronted with when their loved one is dying. She described how a good friend was unable to allow for removal of a feeding tube and discontinuation of life-sustaining treatments, when her mother was in a vegetative state. Complicating this, the friend’s mother had a Living Will and requested no extraordinary measures to prolong her life.

and this is the primary decision, and should be explained to others.

End of life decisions are most difficult, as Jan tells us. Previous discussion and executing an advance directive can make a crisis situation into a calm decision.

Do you have something to add? Please share your thoughts by emailing ThePulse@acoep.org.

Or, if you have any cases that you would like to present or be reviewed in The Pulse, please email them to us. Thank you.

Putting all this in the context of a final act of love may provide emotional support for the caregiver.

Of course, if all else fails, ask the patient! We sometimes forget a really sick patient has decisionmaking capacity

How would you approach this type of situation in the emergency department with a patient in need of advanced life sustaining treatment, an advance directive declining this, and a family unable to abide?

Unfortunately, this situation is common. We are confronted with this dilemma in the middle of a chaotic department, with little time for philosophical deliberation, and “metrics� telling us to get moving.

Initially, ascertaining if an advance directive is present will provide a foundation for response.

A living will, or preferably, a power of attorney for health care document, should be honored.

If there is no contesting of this, there is no problem. But, when a caregiver or family member, who has devoted years of their life to taking care of the patient, is unable to let go, then what should we do?

the PULSE | October 2013

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The On-Deck Circle

Mark A. Mitchell, DO, FACOEP, FACEP, President-Elect

A Season of Change There will be many sideline coaches in the stands or watching on TV who will second guess the decision made on the field in the heat of the battle. These sideline coaches haven’t done the homework and preparation for the game, yet feel entitled to a strong opinion.

They also have nothing to lose in expressing their retrospective opinions. Doesn’t this sound familiar to those of us in emergency medicine?

We work diligently preparing for our EM career, we make decisions quickly in the heat of the battle, and yet others make judgments on our performance afterwards. It is much easier to be a Monday morning quarterback than it is during the game.

W

ith the fall season upon us change is in the air. The leaves will soon begin to change their colors and fall to the ground. Temperatures will drop and those above the Mason Dixon Line will be looking for sweaters and jackets, while those still in the Deep South are looking for a break from the unbearable heat. Many are glad to see the NCAA and NFL seasons off and running.

The NCAA and NFL teams have already begun this season with one thing in mind— winning. They have put much sweat and long days behind them only to take the field and give their best each and every play. The coaches study diligently each week preparing for the next opponent. Yet at the end of each contest someone wins and someone loses.

the PULSE | October 2013

The Emergency Department is a 24/7 operation that is subject to many second guesses by many different people. Many payers want us to deliver care quickly and cost effectively; however, if retrospectively the final diagnosis doesn’t appear “emergent or urgent” they don’t want to pay fairly for the work rendered. Many of our fellow medical staff physicians want us to have the crystal ball and be able to determine the exact etiology of the patient with vague abdominal or chest pain before accepting the admission or observation status.

These same physicians then keep the patients in the hospital for days before determining the etiology or feeling comfortable enough that they can send them home. So we understand what it is like to be second guessed after the play is over and the results of the call is known.

game plan, yet always be cognizant our plan will have to be modified and changed, sometimes at a moment’s notice. The game plan for us is relatively simple, yet also very complex— that is to put the interest of the patient first.

With the changes that are occurring in the “game” of healthcare we find ourselves in a great position. As changes take place between the outpatient and inpatient arenas, we are at the crossroads. As approximately 70% of all hospital admissions come from the Emergency Department (ED) and approximately 85% of all patients that present to the ED are discharged back to home care, we are right in the middle of this mix making critical decisions We make the most expensive decisions in healthcare today –the decision to admit a patient to the hospital. Therefore don’t underestimate the position we have in this game of healthcare.

So you can elect to sit on the sidelines and see how the game ends, pass judgment on each and every play, or you can elect to get involved and see what you can do to affect the outcome. “How?” you may ask. By becoming more informed on the issues at hand; by reaching out to your state and federal congress

" You must be the change you wish to see in the world."

With rapid paradigm shifts healthcare is currently undergoing we must stick to the

– Mahatma Gandhi

representatives; by looking for innovative ways to make your own ED a more efficient place by decreasing door to provider times, decreasing total length of stay, or making sure that you have access to medical records thereby possibly decreasing the ordering of unnecessary test.

Be an instrument of change; for the game we are playing has a far more important outcome than a football score.

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Check out the Student's and Resident's recently redesigned online publication

The new version of The Fast Track is more robust, with a combination of both anecdotal experiences, thought provoking articles, and peer reviewed research articles that will propel ACOEP to the next level in the student and resident publication arena.

Here are some articles featured in the Fall 2013 issue: • Wild Medicine • Lightning Injuries • Tricks of the Trade • Removing Ear Foreign Bodies • Fall Conference Interview Season Advice

You can view The Fast Track online by going to the Student Members page at:

www.acoepsc.org the PULSE | October 2013

SPRING SEMINAR

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ACOEP Brings You to The Edge ACOEP Presents

Janice Wachtler, BAE, CBA Executive Director

A

COEP is a dynamic association.

Through the years we’ve grown and evolved, adapting to the times and embracing change. It is this spirit of growth that inspired the name Emerge given to our Spring and Fall conferences—a name embracing a period of change, evolution, and maturation.

The journey of emergence has brought us to a precipice in emergency medicine, a place of unforeseen challenges and incredible opportunity. There is no roadmap as we journey into this uncharted territory; however as emergency physicians look to gain an edge, ACOEP will be a stalwart resource for its members.

It’s this unique point that inspires the new branding of all ACOEP conferences under one bold heading: The Edge. This is more than a name change and a new logo, The Edge is the inspiration and the foundation upon which our educational opportunities will be based.

To give you an to overcome new challenges, embrace the cutting edge of new technologies, opportunities and advancement, and journey together to the edge generating creative thoughts, solutions and lasting advancement.

This concept will be in the forefront as we plan conventions, find new topics and opportunities for our attendees. We hope it will be your outlook as you arrive, ready to give yourself an edge in learning the unknown, and broadening your horizons.

What’s in a brand? The branding of an event is more than simply marketing, or a name change. In the case of ACOEP’s conference our brand is the expression of what each individual ingredient brings to the whole. Didactic topics, new speakers, case presentations, hands-on training, innovative ideas, captivating debate, all are influenced by The Edge and all contribute to a whole greater than the sum of its parts.

A brand is a watchword, an objective and an inspiration.

the PULSE | October 2013

SCIENTIFIC ASSEMBLY

ACOEP Presents

INTENSE REVIEW ACOEP Presents ACOEP Presents

SPRING SEMINAR SPRING SEMINAR

ACOEP Presents ACOEP Presents

SCIENTIFIC ASSEMBLY SCIENTIFIC ASSEMBLY

ACOEP Presents ACOEP Presents

INTENSE REVIEW INTENSE REVIEW

‘14 ‘14 ‘14 ‘14 ‘14 ‘14 ‘14 ‘14 ‘14

ACOEP Presents

INTENSE REVIEW

‘14

Save the Date Intense Review 2014 The Westin River North Chicago, Illinois

January 16 - 20, 2014 Oral Board Review

January 14 & 15, 2014 REGISTER ONLINE TODAY! www.acoep.org/edge

ACOEP Presents

SPRING SEMINAR

ACOEP Presents

SCIENTIFIC ASSEMBLY

ACOEP Presents

INTENSE REVIEW

‘14 ‘14 ‘14

Save the Date Spring Seminar 2014 The Westin Kierland Resort & Spa Scottsdale, Arizona

April 22 - 26, 2014 For More Information Visit: www.acoep.org/edge

AOA Committee Appointments 2013-2014 ACOEP proudly congratulates its members who were appointed to an AOA Board, Bureaus, Councils or Committee for the upcoming service year.

John W. Becher, DO – Member, Board of Trustees; Chair, Department of Business Affairs; Chair, AOA Governance and Organizational Structure Darryl A. Beehler, DO – President’s Advisory Council Peter Allen Bell, DO – Bureau of Healthcare Facilities Accreditation; Bureau on OGME Development Gregory P. Bloxdorf, DO – Bureau on OGME Development Col. William Bograkos, DO – Bureau of Scientific Affairs and Public Health Thomas A. Brabson, DO, FACOEP – Chair, Bureau of Osteopathic Specialty Societies Joseph John Calabro, DO – Bureau on Osteopathic Education John Casey, DO, MA – Council of New Physicians Timothy Cheslock, DO – Council on Continuing Medical Education John Francis Dery, DO – Strategic Planning Committee of the Department of Business Affairs Charles A. Finch, DO – Bureau of Membership Robert A. George, DO – Appeal Committee of the Bureau of Healthcare Facilities Accreditation Douglas M. Hill, DO – Program and Training Review Council Joseph Kuchinski, DO – Bureau on Federal Health Programs Paul E. Lacasse, DO, MPH – Commission on Osteopathic College Accreditation Frederic B. Ludwin, DO – Bureau of Osteopathic Specialists Gary L. Moorman, DO – Bureau of Osteopathic Medical Educators Nicole Y. Ottens, DO – Council on Palliative Care Issue James D. Polk, DO - Commission on Osteopathic College Accreditation Donald J. Sefcik, DO, MBA – Bureau of Osteopathic Medical Educators Sonbol Shahid-Salles, DO – Member, Board of Trustees; Department of Business Affairs; Chair, Department of Professional Affairs; Board of Trustees/Chair; CIR Congress Gary L. Willyerd, DO – Council on Osteopathic Training Institutions; Council on Women, Men, and LGBTQ Health Issues

ACOEP Presents

SCIENTIFIC ASSEMBLY

ACOEP Presents

INTENSE REVIEW

‘14 ‘14

Save the Date Scientific Assembly 2014 Caesars Palace Las Vegas, Nevada

October 12 - 15, 2014 For More Information Visit: www.acoep.org/edge

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Practice Management and You Jeremy Tucker, DO, FACOEP Chair

T

he Practice Management Committee of ACOEP has a stated purpose to develop, maintain and publish policies to enhance or provide direction and information for medical professionals and the public on activities pertinent to emergency medicine practice. In keeping with this purpose, earlier this year, the Practice Management Committee surveyed ACOEP’s membership to find where to best focus its efforts to best meet member needs.

Previously, we have worked on policy development and have reviewed some ACEP policies as well. But it was clear from this survey the vast majority of the membership (83%) has never referenced an ACOEP policy.

This could reflect both the small number of approved policies available and the ease of navigating and accessing the policies.

The Committee received input from 110 physician-respondents, or about 2% of ACOEP’s members. An extremely small, but important sample. The majority, by a small

margin, of these physicians thought there was more value to “developing a tool kit” of information to operate or direct an emergency department than policy development.

The top five topics of interest to the respondents were, in order of preference: 1. Risk management/malpractice 2. Patient safety/error reduction 3. Emergency department process improvement/efficiency 4. Core measures 5. Patient satisfaction/customer relations The Committee will begin developing resources and information in these areas for easy access from the ACOEP website. While there may be some original contributions, many will be links to valuable information in these areas.

Such links may be to other professional society websites, like ACEP or AAEM, while still others may provide the reader with articles

or reference materials that are useful to developing standards and practices within your own hospital department.

Development of future policies will be posted on the front page of the ACOEP’s website and will allow the viewer to open the policy and comment on its usefulness or viability. There may also be a link to reference material in the development to show the viewer what the policy formulation was based on.

This period of public comment will last for a period of time (probably 30 – 45 days) before the policy is made and a final version is submitted for board approval. This will allow more members who may not have time for committee involvement to have some input or voice opinions or suggestions in the policy development process.

Finally, we’d like to thank all those who participated in the survey and look forward to your continued participation in this valuable asset to our College.

ACOEP Staffing Updates

Already 2013 has been a year of incredible changes! We have welcomed two new staff members as well as developed new departments to better accommodate our ever-growing membership. Below is an updated list of ACOEP staff along with their contact information. Feel free to call or email our staff with any questions, concerns, or needs that you may have.

Executive Executive Director Janice Wachtler, BAE, CBA 312.445.5705 janwachtler@acoep.org

FOEM Assistant Gina Schmidt 312.445.5701 gschmidt@acoep.org

Sr. Coordinator of Member Services Jaclyn Ronovsky 312.445.5702 jronovsky@acoep.org

Meetings and Conventions

Media and Technology

Development Director Stephanie Whitmer 312.445.5712 swhitmer@acoep.org

Manager of Meetings and Conventions Adam Levy 312.445.5710 alevy@acoep.org

Director of Media and Technology Brian Thommen 312.445.5703 bthommen@acoep.org

Executive Assistant Geri Phifer 312.445.5700 gphifer@acoep.org

Senior Meetings Coordinator Lorelei Crabb 312.445.5707 lcrabb@acoep.org

Communication Manager Erin Sernoffsky 312.445.5709 esernoffsky@acoep.org

Manager of Education Services Kristen Kennedy, M.Ed. 312.445.5708 kkennedy@acoep.org

Member Services

Media Technology Specialist Tom Baxter 312.445.5713 tbaxter@acoep.org

Director of Member Services Sonya Stephens 312.445.5704 sstephens@acoep.org

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Keeping the Pace of Change Tim Cheslock, DO FACOEP Vice Chair of the Publications Committee

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patient flow is important, especially while "While

the volume in the ED continues to grow, speed is not the end all be all measure of quality. "

his is my first article for The Pulse as the Vice Chair of the Publications Committee. I have written articles before as the Resident Chapter President but I’ll be the first to admit that I am not the most prolific author. So why would I accept this position? Maybe it was the challenge of something new, the desire to step outside of my comfort zone, or simply just to broaden my horizons and change things up a bit.

at levels higher than us who sit in cubicles, but never really have any patient contact, that think they can do our jobs better than we can—which may be a little jaded.

Change is something that we, as emergency physicians, see on a daily basis. It’s not so much in what we do, but often how we do it. The practice of medicine, and the evaluation and treatment of the conditions we are presented with, is something that we do very well. The constant change we often deal with on a daily, weekly or monthly basis is how we get from point A to point B. The process of flow, not only in the ED but in the hospital as well, seems to be a hot topic in almost every facility.

While patient flow is important, especially while the volume in the ED continues to grow, speed is not the end all be all measure of quality. The biggest issue with all of these endeavors is lack of physician buy in. The core members of the team, the physicians, are either excluded, ignored, or not sufficiently involved to make the process work. You can have buy in from everyone else—the nurses, the aides, the secretary. If your physicians do not buy in you are doomed to failure.

I have been a part of several different projects by well-intentioned staff on how we can do things faster, more efficient, and keep every patient's experience the best they have ever had. Does this sound familiar? Reams of data are presented on how quickly we room patients, have a provider at the bedside, total length of stay, etc. You know the drill. People

My most recent experience opened my eyes to the fact that we, the team leaders, need to be involved so that the real issues and problems affecting flow are addressed. It is often not a personnel issue, but an infrastructure issue, or EMR issue, or other issue that directly impacts the providers’ ability to perform efficiently. Without our input, resources and

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tasks are changed needlessly in an effort to “try something new” in order to hit the mark. We need to be at the table to add to and focus the discussion on the real needs. There is strength in numbers. Once I was able to get a larger group of my colleagues involved, our input could not be ignored and while the changes still have a way to go, at least we can say that our opinions have been.

Will this make it go away? Not even a chance, but we have the best shot at a successful outcome when we come out in force. That is the strength of our profession, not only in our individual places of work, but as a college as well. We as ACOEP can influence the discussion and help navigate the ever more complex healthcare system in this country. You are what makes this college strong and we need your continued, unwavering support to make it happen! I look forward to continuing to be a part of the solution, and hope I can count on each of you pledge the same. Only then can we harness the real strength of our numbers.

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AOBEM Update Donald Phillips, DO, FACOEP AOBEM Secretary

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reetings from AOBEM. We do not have many items to communicate at this time.

We have written a PROPOSED rule change that must first be approved by the AOA Bureau of Osteopathic Specialists (BOS). If this change is approved, all candidates entering the certification process on September 01, 2013 and thereafter will no longer have Part III. Candidates that are already in process must complete under the rules in place when they entered. Another way of stating this is that if you have not completed your certification, but have already taken Part I (written examination), you will still need to complete all three parts.

AOBEM will also have an information table at the EMERGE Scientific Assembly. Board members will be available intermittently. We especially want to help people through the process of OCC and especially Component 4.

We would ask that questions be informational only and not directed toward policy. Questions

related to policies, rules, etc should still be submitted in writing to allow the full board to discuss and issue a written response. This is to minimize the chance of conflicting answers and misunderstandings. In all appeals and discussions, written communication always is the final standard.

Currently, there are 567 candidates in process that will still have to complete Part III. Please be certain that the board is bound by this rule to ensure fairness and equity to candidates that entered the process at the same time (i.e. everyone has the same tasks).

If this change is approved, a letter will be sent directly to affected candidates notifying them that the requirement of Part III for them to become board certified is no longer in effect.

Important announcement regarding Part III of the AOBEM primary certification in Emergency Medicine.

Effective September 01, 2013, initial applicants for primary board certification in emergency medicine through AOBEM will no longer be required to complete the Part III (Clinical Examination).

Who will be affected by this change: Candidates who have not been credentialed to sit for Part I (Written Examination) prior to September 01, 2013.

Who is not affected by this change: Candidates who have already taken Part I or Part II prior to September 01, 2013.

1. C andidates who were credentialed to take Part I prior to September 01, 2013 but have had to reschedule or retake any part of the certification.

2. A ny candidate who has already submitted a Part III examination that is either not graded or is incomplete or has failed a prior Part III examination.

Any questions concerning this rule change must be submitted in writing (hard copy or email) to AOBEM.

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FOEM | BEACON

E M P H Y S I C I A N O P P O RT U N I T I E S

The NEW Mercy Health West Hospital Cincinnati, Ohio • 250 bed, state-of-the-art flagship, planning to serve approximately 55,000 patients per year.

• Rated a Top 15 Health Systems national winner for quality and the first recognized ACO in the region.

• A full complement of services including cardiovascular care, obstetrics, cancer treatment, women’s health, and orthopedics.

• Stable, cohesive, productivity-driven group, well represented at every level within the medical staff.

• Supported by University of Cincinnati Health for trauma and interventional stroke care, and Children’s Hospital of Cincinnati (one of the nation’s top 5).

• Experienced and highly productive mid-level providers and affiliated scribe company.

• Flexible scheduling and responsive leadership.

• Dedicated 64-slice CT scanner for ED and bedside ultrasound.

• Ample opportunities for leadership.

• Mixed shift lengths, with limited night responsibilities (2-3/mo.).

“It’s hard to draw up a better, community-based EM practice.”

— Kevin Meyer, MD

ED Medical Director, Mercy Health West Hospital

For more information about this and other EM physician opportunities contact Kim Rooney, (800) 726.3627 x3674; krooney@premierdocs.com

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FOEM | BEACON

masthead_Layout 1 4/18/13 10:24 AM Page 1

• A FOUNDATION DEDICATED TO RESEARCH IN OSTEOPATHIC EMERGENCY MEDICINE

Foundation Focus Sherry D. Turner, DO, FACOEP President

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s we at the Foundation prepare for the 2013 EMERGE Scientific Assembly in San Diego, it is hard to believe that Spring Seminar was already six months ago. It seems like just yesterday that we were raising funds at the Run for Research along the beautiful ocean-side path in Ft. Lauderdale, or watching the residents present their unique and interesting cases at the 2013 FOEM Case Competition sponsored by Premier Physician Services. Let’s take a moment to look back at Spring Seminar and share our experience with you.

finish line. What an enjoyable way to raise money for a good cause!

Overall, the event was enormously successful, bringing in over $9,000.00 to enable FOEM to improve patient care through quality research.

The funds were raised primarily by the pledge

forms each runner was given prior to the race, but FOEM had some help from corporate sponsors as well. Thank you so very much to the following companies that made the 2013 FOEM 5K “Run for Research” such a successful event. We couldn’t have done it without your support!

2013 FOEM Run for Research On Wednesday, April 3rd ACOEP members woke up bright and early and donned their FOEM 5K t-shirts as they gathered in the lobby. The sun had not yet come up, but spirits were high as colleagues and friends prepared to run alongside the ocean in an effort to raise money for FOEM. As the crowd moved outside, they were delighted to find a lit path made possible by FOEM board member, Peter Kaplan, who woke up even earlier than the rest to walk the route and drop glow sticks for everyone to follow. The runners were given glow sticks of their own and at 6:00 a.m. sharp, the race officially began. In just over 16 minutes, the first place runner came charging to the finish line – John Sillery, DO (16 minutes, 17 seconds). He was followed shortly after

by James Hansel DO (17 minutes, 13 seconds) and then by Andrew Miller, DO (19 minutes, 18 seconds). As the Florida sun rose gracefully over the palm trees, the rest of the runners trickled in and posed for photographs at the

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2013 Legacy Gala

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FOEM | BEACON

Monday, October 7, 2013 www.foem.org

VIP Reception 7:00 – 7:30 pm Dinner and Awards 7:30 –10:00 pm Hilton San Diego Bayfront Hotel San Diego, California

ACOEP Scientific Assembly Presenting Corporate Sponsor:

Friends:

Black Tie Optional | October the PULSEand 2013 For reservations complete information please contact: Stephanie Whitmer, Event Chair 312.587.1765 or swhitmer@foem.org

FOEM | BEACON 2013 FOEM Case Study Poster Competition Sponsored by

On the very same day as the 5K Run for Research, FOEM was able to showcase how the funds donated are used to fulfill our mission.

The 2013 Case Study Poster Competition is an annual event that allows residents to present unique and interesting cases that take place at their hospitals. This year, over 75 applications were submitted to the event that can only accommodate 25 presenters. However, FOEM asked those that could not be there to present to hang their posters so that others could learn from their experiences. It was such an engaging competition with so many interesting cases.

However, three cases rose above the rest and the following residents were given certificates, cash prizes, and tickets to the 2013 FOEM Legacy Gala. And now, without further ado, the winners of the 2013 Case Competition: 1st place: Justin McNamee, DO “A Lethal Secret: A Deadly Complication of IVDA” St. Joseph’s Regional Medical Center, Paterson, NJ 2nd place: Sonali Soral, DO “Radiographic Contrast Media-Induced Noncardiogenic Pulmonary Edema” McLaren-Macomb Hospital, Clinton Township, MI 3rd place: Ellen Kurkowski, DO “Pneumonia? Or Something More?”

UMDNJ-SOM Kennedy University Hospital, Stratford, NJ

— Winning Abstracts — Title: A Lethal Secret: A Deadly Complication of IVDA Authors: Justin McNamee DO PGY II and Nilesh Patel DO Department of Emergency Medicine St. Joseph’s Regional Medical Center, Paterson, NJ Case Report: 48 year old male with PMHx of Seizures presents to the ED with a 4 day history of shortness of breath. Patient states he was working on installing a new sink at home 4 days ago, when the sink fell onto his right chest and arm filled with water. He held the sink for approximately 20 minutes while his wife dumped the water. Patient recently saw his PMD for same complaint and was prescribed an albuterol inhaler without relief. He awoke this morning with worsening pleuritic chest

pain radiating to the center of his back. The pain was aggravated by supine position and unrelieved by movements or medications.

Patient’s spouse stated he has had intermittent low-grade fevers for the past four days. Patient denied nausea, vomiting, cough, abdominal pain, syncope, focal neurological deficits, or LE edema. He denied having similar symptoms in the past.

ED Course: Vitals; T:101°F, BP: 134/108, P: 146, RR: 24, 96% RA. Patient was in severe distress with continuous chest pain and SOB. Presenting complaint and physical exam were concerning for aortic dissection, so after bedside chest x-ray, patient was sent for emergent chest CT. His respiratory status continued to worsen and patient was placed on mechanical ventilation. Patient became hypotensive and was unresponsive to fluid boluses, so the patient was started on vasopressors. CXR revealed bilateral pleural effusions with scattered pulmonary nodules.

Despite a thorough initial history from the patient, on re-evaluation prior to intubation, the patient was questioned on his social history secondary to the concerning pattern on CXR. He reluctantly admitted to IVDA for the past 6 months, a secret he had kept from his family. Chest CT showed bilateral scattered cavitary pulmonary nodules consistent with septic pulmonary emboli presumably secondary to his IVDA. Patient was admitted to MICU on multiple vasopressors, broad-spectrum antibiotics, and sedatives with the diagnosis of Septic Shock secondary to Septic Pulmonary Emboli.

Introduction: Septic pulmonary emboli are a rare, but well recognized disease process.

It occurs with right-sided endocarditis or septic thrombophlebitis from dental, pelvic or tonsillar infections as well as infected central venous catheters. This uncommon pathological process generally presents with insidious onset of fevers, respiratory symptoms

and lung infiltrates. The diagnosis of septic pulmonary emboli is rarely made in the ED due to the nature of progression and the vague symptoms that accompany the disorder on initial presentation.

Septic pulmonary emboli is not a diagnosis exclusive to the adult population. Data has shown more cases in children due to physicians recognizing risk factors in the pediatric population. Risk factors in children include soft tissue infections, osteomyeltis, and intravenous catheters. An uncommon complication of pharyngitis in the United States has been linked to septic pulmonary emboli as an uncommon cause. Lemierre’s syndrome has been described for decades in the literature, but has rarely been recognized. There is a male predominance and usually affects the young, healthy individual with a primary HEENT infection being either pharyngitis, sinusitis, mastoiditis, or odontogenic infections. These infections lead to septic thrombophlebitis of the internal jugular vein, which subsequently leads to emboli formation and disseminated metastatic abscesses such as septic pulmonary emboli.

Pulmonary involvement has been noted in up to 97% of cases with pulmonary abscesses and empyema. The primary microbiological source of infection is different in Lemierre’s than other septic emboli. Fusobacterium, an anaerobic mircrobe, is the most common cause of Lemierre’s syndrome, whereas Staphylococcal species are the most common microbe of septic pulmonary emboli.

A study from, Chest 2005 described the initial presenting complaints for confirmed cases of septic pulmonary emboli. Fever was the most common symptom (93%) followed by dyspnea (36%), pleuritic chest pain (29%), sore throat (21%), cough (14%), and hemoptysis (7%). Most cases were not initially diagnosed in the ED with the median time to diagnosis being 3 days from time of admission. Due to the generality of symptoms, clinicians must be astute paying

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FOEM | BEACON particular attention to diagnostic imaging studies to make the diagnosis in the ED. According to Chest, all confirmed cases of septic pulmonary emboli had CXR abnormalities. All CXR were read as patchy infiltrates or nodules. Cavitations were seen in 23% of CXR and bilateral or unilateral effusions were noted in 54% of the x-rays. Chest CT scans are good follow-ups in toxic appearing patients or those with patchy infiltrates and possible cavitary lesions. A 2006 study from the Journal of Roentgenology states the most common CT finding in septic emboli are multiple nodules in various stages of cavitation.

Another clinical pearl that has been mentioned throughout the literature is to look for the “feeding vessel sign” on CT. A “feeding vessel” is a prominent central vessel within a nodule.

These vessels have been traced back to the left atrium on CT and the latest studies support pulmonary veins being the “feeding vessels.”

Septic pulmonary emboli are a rare and difficult diagnosis for an ED physician to make on admission due to the generality of symptoms. From symptom onset to diagnosis has a median time of 18 days, proving the difficulty of diagnosis for all clinicians. Eliciting a good history and discovering hidden risk factors for septic emboli may mean the difference between a hospital admission or morgue disposition.

Citations: 1. Kristensen , L. Hagelskjaer. “Human Necrobacillosis, with Emphasis on Lemierre’s Syndrome.” Oxford Journals.

31.2 (2000): 524-532. Web. 7 Jan. 2013.

2. Jorens, P.G. “Nonthrombotic Pulmonary Embolism.” European Respiratory Journal.

34.2 (2009): n. page.

3. Todd, Johnathan. “High-Resolution MDCT of Pulmonary Septic Embolism: Evaluation of the Feeding Vessel Sign.” American Journal of Roentgenology. 187.3 (2006): 623-629.

4. Cook, Rachel. “Septic Pulmonary Embolism.” Chest. 128.1 (2005): 162-166.

5. Hughes, Carolyn. “Septic Pulmonary Emboli Complicating Mastoiditis: Lemierre’s Syndrome Revisited.” Oxford Journals. 18.4 (1994): 633-635. Web. 7 Jan. 2013.

6. Jaffe, Richard. “Septic Pulmonary Emboli.”

Radiology. (1970): 527-532. Web. 7 Jan. 2013.

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Title: Radiographic Contrast MediaInduced Noncardiogenic Pulmonary Edema Author: Sonali Soral, DO McLaren Macomb Emergency Medicine Resident Introduction: Acute pulmonary edema after intravascular administration of contrast medium is an extremely rare complication. This adverse reaction is generally ascribed to the effects of contrast-induced volume overload in patients with compromised cardiac status.

In cardiogenic pulmonary edema, a high pulmonary capillary pressure is responsible for the abnormal movement of excess fluid into the alveoli. In contrast, noncardiogenic pulmonary edema is caused by various disorders in which factors other than elevated pulmonary capillary pressure are responsible for protein and fluid accumulation in the alveoli. The following case report describes a patient with noncardiogenic pulmonary edema induced by contrast material in which the edema may have been due to the toxic effect of the contrast material on the pulmonary capillary membrane.

It is essential to distinguish this rare reaction from cardiogenic pulmonary edema caused by intravenous contrast as well as from the more typical bronchospastic anaphylactoid reaction in order to avoid delay in starting appropriate therapy and prevent detrimental sequelae that could occur with misdiagnosis Case Report: A 60-year-old Caucasian woman presents to the ED with a chief complaint of intermittent left lower quadrant abdominal cramping for the last two weeks and sudden onset of heavy vaginal bleeding beginning one hour ago. She denies fever, nausea/ vomiting, chest pain, shortness of breath, diarrhea, hematochezia, melena, dysuria or any prior history of her current symptoms.

Past medical history is significant for diverticulitis, hypertension, type 2 diabetes, hypothyroidism, iron-deficiency anemia and resolved Hodgkin’s lymphoma. Surgical history is significant for hysterectomy 27 years ago. The patient’s allergies include penicillin and tetracycline, and her social history is unremarkable. The patient states that due to her history of diverticulitis diagnosed via colonoscopy 6 months earlier, her gastroenterologist prescribed her ciprofloxacin prophylactically, which she has been taking with no relief of her abdominal pain. Physical exam was remarkable for moderate left lower quadrant abdominal tenderness only. There was no rebound, rigidity or guarding noted. Initial vital signs revealed blood pressure 151/83, pulse 104, respiratory rate 18, oral temperature 98.2F, and pulse ox of 94% on room air. The

patient was placed on IVF and was given a 500cc bolus of 0.9NS followed by a steady infusion at 100cc/hr. Laboratory testing was performed, including CBC, electrolytes, glucose, BUN, Creatine, PT, PTT and INR and all were unremarkable. Urinalysis revealed a small urinary tract infection. CT Abdomen/Pelvis with oral /IV contrast was then obtained to evaluate for possible vaginal-colonic fistula.

Shortly after the administration of intravenous dye, the patient complained of dyspnea, became cyanotic and began to produce copious amounts of pink frothy sputum. Diffuse inspiratory and expiratory rales were heard throughout all lung fields.

She had no rash, itching, wheeze, urticaria or angioedema. The patient relayed that she had no history of cardiopulmonary disease and was unsure if she had received radiographic contrast media in the past.

On arrival in the resuscitation room, she was pale, cyanosed, and breathless, but with a warm periphery. She was tachycardic and hypertensive with heart rate of 136 and blood pressure of 213/101. She had good air entry on auscultation but there were still widespread rales throughout both lung fields. Pulse oximetry showed her oxygen saturation to be 76% on room air, and she was immediately administered supplemental oxygen. Preparations were made for urgent intubation and ventilation, and respiratory therapy was called to bedside. The patient was immediately treated with furosemide, nitroglycerin, diphenhydramine, methylprednisolone and a duoneb updraft. BiPAP was administered with rapid resolution of symptoms and the patient’s pulse ox increased to 100%.

EKG was performed and was unchanged from the patient’s prior reading of sinus tachycardia. A chest film was obtained and revealed vascular and interstitial prominence with a normal cardiac silhouette. CT results were available at this time and showed inflammatory changes consistent with the patient’s history of diverticulitis in the left lower quadrant with involvement of the superior vagina, consistent with a vaginalcolonic fistula. Edema and inflammatory change of the bilateral lung bases was also present. Cardiac enzymes were obtained and were normal and BNP value was within normal limits with a value of 57.

Upon stabilizing the patient, she was then admitted to the intensive care unit with care to be received from the internal medicine, cardiology and surgery departments. One week into her hospitalization, she developed multifactorial acute tubular necrosis due to her blood loss, chronic anemia, underlying

FOEM | BEACON diabetic nephropathy, and possibly ARBinduced interstitial nephritis, with a rise in her creatinine on day seven to 5.0 and ended up being dialyzed. Cardiology evaluation supported the patient’s claim of no cardiac history and her echocardiogram performed during her stay revealed a normal EF of 60%. She did suffer from repeat episodes of fluid overload, hypoxia and respiratory distress throughout her stay which was attributed to adverse effects from her tubular necrosis; however the initial episode in the ER appears to be unrelated and attributed directly to the intravenous contrast.

Discussion: Under normal conditions, fluid flows from the capillary system to the interstitial space and returns to the systemic circulation through the pulmonary lymphatic system. When capillary fluid efflux into the interstitial space exceeds the lymphatic absorption, pulmonary edema occurs. Cardiogenic shock primarily results from increased pulmonary hydrostatic pressure, which causes plasma ultrafiltrate to cross the pulmonary capillary membrane into the interstitium. In contrast, noncardiogenic pulmonary edema, or NCPE, is characterized by diffuse alveolar damage and most often results from a rise in microvascular permeability with fluid lost from the circulation. This leads to accumulation of protein-rich fluid in the alveolar air sacs.

Acute pulmonary edema is among the rarest reactions to radiographic contrast media. The pathogenesis is unclear, but it has been shown that contrast material can have direct chemotoxic effects on pulmonary endothelial cells, with secondary capillary leakage. Edema could be caused by mediator release and complement activation resulting in endothelial damage or as the result of a direct irritant effect of the drug on the lungs.

The pulmonary capillary endothelial junctions are widened by toxic damage of the alveolarcapillary membrane, which is very thin and disrupts immediately, resulting in alveolar flooding. Water and proteins move freely from the intravascular to the interstitial space.

Thus, the concentration of protein is almost identical in these two compartments. This fluid accumulation in the alveolar space ultimately results in the formation of hyaline membranes that are derived from fibrin and protein, leading to decreased diffusing capacity, hypoxemia and shortness of breath. Oxygenation is further hampered by decreased surfactant production secondary to cellular damage. Ultimately, alveolar collapse results, producing decreased pulmonary compliance, increased work of breathing, respiratory distress and eventually respiratory failure. The natural evolution of the disease process is resolution of the neutrophilic

inflammation and proliferation of other cells, leading to either architectural restoration of lung tissue or the development of interstitial fibrosis and chronic pulmonary dysfunction or death.

NCPE is a clinical syndrome characterized by simultaneous presence of severe hypoxemia, bilateral alveolar infiltrates on chest x-ray and no evidence of left atrial hypertension or congestive heart failure. Clinically, patients are usually young and have no history of cardiac or pulmonary disease. In cardiogenic pulmonary edema, usually due to failure of the left side of the heart, clinical examination reveals low flow state (cool periphery), S3 gallop, cardiomegaly, JVD and wet crackles. NCPE is usually high flow state (warm periphery), with bounding pulses, no gallop, no JVD and with dry crackles.

EKG and cardiac enzymes are usually normal.

On chest x-ray, alveolar fluid accumulation is evidenced by patchy or peripheral distribution of edema, and air bronchograms are frequently seen. There is no hemodynamic data to suggest a cardiogenic etiology, with pulmonary capillary wedge pressure of less than 18 mmHg. The ratio of pulmonary edema fluid protein to plasma protein concentration is 0.7 or above.

Measurement of plasma BNP has also been used to distinguish heart failure (high BNP) from lung disease (normal or mildly elevated BNP) as a cause of dyspnea with a high degree of accuracy even in patients with both lung and heart disease.

The patient in the aforementioned case had normal left ventricular function and a low likelihood of coronary artery disease as determined by normal echocardiogram results.

It therefore seems likely that acute lung injury was the cause of her symptoms and she experienced a non-cardiac form of acute pulmonary edema. Other findings consistent with a cardiogenic source, such as peripheral edema, JVD and ventricular gallop, were not present. Furthermore, the absence of urticaria and angioedema does not support the diagnosis of anaphylaxis.

Treatment for NCPE is largely supportive and aimed at ensuring adequate ventilation and oxygenation. The primary emergency treatment is oxygen with BiPAP, or invasive ventilation with peep, together with optimizing fluid balance to maximize patient outcomes.

Although the pulmonary edema is not due to fluid overload, elevation in circulating blood volume and subsequent intravascular pressure can result in worsening of alveolar fluid collection and deoxygenation. Fluid restriction should occur, but not to the degree to produce hypotension or decrease perfusion to end organs, and left ventricular preload should be maintained. Judicious use of small amounts

of diuretics can produce small reductions in intravascular volume but significant reductions in extracellular alveolar edema, enhancing ventilatory function and oxygenation. It is important to distinguish this rare reaction from cardiogenic pulmonary edema caused by the osmotic load of IV contrast which draws fluid into the circulation and affects patients with pre-existing cardiovascular compromise.

Studies have shown that treating the patient for anaphylaxis is not beneficial. However, treatment of severe NCPE includes high doses of glucocorticoids secondary to their anti-inflammatory properties. Overall, clinical management involves primarily supportive measures to maintain cellular and metabolic function while waiting for the acute lung injury to resolve.

In patients having an adverse reaction to radiographic contrast media, the risk for recurrence on future exposure has been estimated to range from 16% to 35%. Unlike the more frequently seen anaphylactoid reactions, pretreatment with the usual doses of prednisone and diphenhydramine appears to be ineffective at preventing recurrences. Patients who give a history of acute respiratory distress after receiving radiographic contrast media should be approached with extreme caution before reexposure is considered.

Conclusion: Although adverse reactions to radiographic contrast media have occurred in 1% to 4.7% of procedures, there are only seven reports of noncardiogenic pulmonary edema.

The underlying mechanisms leading to such reactions have not been evidenced yet, as patients are rarely properly investigated. The cardiopulmonary pathophysiology which exists in these patients is well understood, however the pathogenesis of the abnormal pulmonarycapillary permeability remains obscure. All things considered, acute pulmonary edema after administration of radiographic contrast media is life-threatening or fatal if not treated correctly. Treatment must be directed toward diuresis and the maintenance of adequate gas exchange. In conclusion, this case serves to remind us that although severe life-threatening adverse effects associated with radiographic contrast medium are rare, we should still have a high index of suspicion for this problem in any patient experiencing acute dyspnea after a radiologic procedure with contrast media.

Prompt adequate management is essential if the patient’s life is to be saved.

References: 1. Borish, L., Matloff, S. M., Findlay, S. R. (July 1984). Radiographic contrast mediainduced noncardiogenic pulmonary edema: Case report and review of the literature

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FOEM | BEACON [Electronic version]. Journal of Allergy and Clinical Immunology, 74(1): 104-107.

2. Bouachour, G., Varache, N., Szapiro, N., et al. (August 1991). Noncardiogenic Pulmonary Edema Resulting from Intravascular Administration of Contrast Material [Electronic version]. American Journal of Roentgenology, 157: 255-256.

3. Givertz, M. M. (2010, February 5).

Noncardiogenic pulmonary edema.

UpToDate. Retrieved February 20, 2012, from http://www.uptodate.com/contents/ noncardiogenic-pulmonary-edema.

4. Goldsmith, S. R., Steinberg, P. (1995) Noncardiogenic pulmonary edema induced by nonionic low-osmolality radiographic contrast media [Electronic version]. Journal of Allergy and Clinical Immunology, 96: 698699.

5. Hsu, H., Lin, C. M., Tsai, C. Y., et al.

(2005). Acute Non-cardiogenic Pulmonary Edema Associated with the Radiographic Contrast Medium Ioversol [Electronic version]. Tzu Chi Medical Journal, 17(4): 273-277.

6. Kakouros, N. S., Kakouros, S. N. (2003).

Non-Cardiogenic Pulmonary Edema [Electronic version]. Hellenic Journal of Cardiology, 44: 385-391.

7. Kozlowski, C., Kollef, M. H. (1992) Noncardiogenic pulmonary edema associated with intravenous radiocontrast administration [Electronic version]. Chest, 102: 620-621.

8. Malins, A. F. (May 1979). Pulmonary edema following radiological investigation of patients with peripheral occlusive vascular disease: Adverse reaction to contrast media [Electronic version].

American Heart Journal, 97(5): 676-677.

9. Paul, R., Grizelda, G. (March 2002). Fatal non-cardiogenic pulmonary oedema after intravenous non-ionic radiographic contrast [Electronic version]. The Lancet, 359: 1037-1038.

10. Perina, D. G. (2003). Noncardiogenic pulmonary edema [Electronic version].

Emergency Medicine Clinics of North America, 21: 385-393.

Title:

neumonia? Or Something P More?

Authors: Ellen Kurkowski, DO and Andrew Caravello DO University of Medicine and

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Dentistry of New Jersey-School of Osteopathic Medicine Kennedy University Hospital Acute chest syndrome (ACS) is not an uncommon sequela of patients with sickle cell disease and must be considered in any patient who presents with chest pain or shortness of breath. ACS is the most frequent cause of morbidity and hospitalization in this patient population.2 However, it is far less common in patients with hemoglobin SC as compared to patients with hemoglobin SS, but still remains an important complication to consider in these patients.

A 27 year old male presents to the emergency department with EMS from his home for evaluation of unresponsiveness. Per the EMS, his grandmother, who dialed 911, found the patient unresponsive at home. The patient was found next to an empty bottle of Percocet.

Prior to arrival in the emergency department, the patient received two mg of intranasal Narcan from the medics and did become more responsive. The patient arrived in the emergency department moaning. He was also tachycardic, diaphoretic, pale, and had icteric sclera. The patient was unable to provide a complete history.

The patient’s grandmother arrived in the emergency department and stated that her grandson was in an altercation a few days prior and subsequently received Percocet from the emergency department for his pain. She states that around 4:30am she awoke to her grandson coughing. She denied any knowledge of her grandson having a history of suicidal or homicidal ideations. She stated that her grandson had sickle cell disease, but denied any recent exacerbations. She denied any knowledge of recent infections or recent complaints by her grandson, other than pain from his altercation.

The patient’s past medical history was significant for sickle cell disease with a hemoglobin SC mutation. The patient had never undergone a surgical procedure. He did have a history of tobacco use, but had quit within the last year. The patient did not use illicit drugs or alcohol. His family history was significant for sickle cell disease in multiple family members. The only medicine that the patient was prescribed was Percocet from an ED visit 3 days prior to arrival. He did not have any allergies to medications.

On physical exam, the patient arrived with a blood pressure of 127/97, a pulse rate of 172, a respiratory rate of 24 breaths a minute with a pulse oximetry of 92% on room air.

His temperature was 99.1 degrees Fahrenheit (temporal). His blood glucose upon arrival

was 158. He was awake, but could only moan.

He was atraumatic and normocephalic with 2mm reactive pupils bilaterally. His sclera were icteric, but he did not have any discharge or conjunctival changes. His ears were normal to inspection with intact tympanic membranes.

His neck was supple without meningeal signs, adenopathy, or JVD. His cervical spine was non-tender to palpation. On his lung exam, he was tachypneic and had diminished breath sounds on the right side. His left lung sounds were clear to auscultation. His heart sounds were positive for S1S2 and he was tachycardic.

On abdominal exam, his abdomen was soft, non-tender, non-distended, and without signs of ecchymosis or trauma. He had normal bowel sounds. His rectal exam showed yellowish brown soft stool that was hemocult negative.

He did not have tenderness to palpation of his back. His was moving all extremities equally and he did not have clubbing, cyanosis, or edema.

His GCS score was 10. He was diaphoretic. The patient was intubated shortly after arrival in the emergency department for airway protection.

His post intubation vitals were a blood pressure of 133/59, a heart rate of 154, a respiratory rate of 18 with a pulse ox of 100% on an FiO2 of 100% on the ventilator. The patient was started on both Versed and fentanyl drips for sedation. An EKG obtained at this time showed sinus tachycardia at 167 with rightward axis and nonspecific ST segment changes.

Labs obtained in the emergency department showed the following: The ABG on PRVC 100/16/5/500 showed a pH of 7.35, pCO2 of 37, paO2 of 136, bicarb of 20, and a 99% saturation with base deficit of -4.8. WBC was 24.7, hemoglobin of 6.7 with a hematocrit of 19.6, and platelets of 27. He had 84.2 percent neutrophils and bands of 6. His retic count was 5.5 and IRF of 0.72. Sodium was 139, potassium was 3.6, chloride of 102, bicarb was 22, BUN was 22, creatinine was 1.22. His glucose was 144, calcium of 8.7, phosphorus was 4.0, and magnesium was 2.2. His anion gap was 15. His total bilirubin was 6.2, direct bilirubin was 3.2, indirect bilirubin was 3.0. Total protein of 7.5, albumin of 4.4, alkaline phosphatase was 327, ALT of 80, AST was 165, and GGTP was 43.

The PT was 16.8, aPTT was 29.2, and INR of 1.4. His ammonia was 21 and lactate was 9.2.

His LDH was 1823, fibrinogen was 387, and d-dimer was >20. His influenza A and B was negative. His total CK was 1461 with a CK-MB of 2.5 and troponin of 0.24. His BNP was 710. The urinalysis was clear with a specific gravity of 1.020. The pH was 6.0, negative for leukocyte esterase, nitrites, or glucose. Protein was 30, ketones were 15, urobilinogen was 0.2, small amount of bilirubin, trace blood, RBC were 0-1, WBC were 0-1, and a few bacteria.

His UDS was positive for opiates, while his acetaminophen level was <10, salicylate level

FOEM | BEACON was 11.3, and alcohol level was 11.

The patientâ&#x20AC;&#x2122;s post-intubation chest x-ray showed extensive patchy right lung consolidation and patchy consolidation in the left lower lobe. The ETT was 3cm above the carina and the tip of the gastric tube was at the entrance of the stomach. A CT scan of the brain without contrast did not show evidence of acute intracranial hemorrhage and did not have any midline shift or hydrocephalus. A CTA of the chest (PE protocol) did not show filling defects suspicious for pulmonary embolism. It did show a large consolidation in the right upper, middle, and lower lobes along with a consolidation of the left lower lobe. It also commented that there was splenomegaly.

The patient had been typed and screened with his initial lab draw. Four units of pRBC and one unit of platelets were ordered for transfusion. Upon return from CT, the patientâ&#x20AC;&#x2122;s vitals were a blood pressure of 98/54, heart rate of 135, respiratory rate of 26 with a pulse oximetry of 100% on the ventilator. At this time, consent was obtained to gain central IV access on the patient from his grandmother.

A triple lumen catheter was placed in the right femoral vein of the patient under sterile conditions. Also, an 8.5f cordis was placed in the left femoral vein of the patient. The blood transfusions were started after obtaining consent from his grandmother. The patient also received Vancomycin, Levaquin, and Zosyn for antibiotic coverage. The patient continued to become unstable and he was started on Levophed for blood pressure support. A call was placed to the hematologist/oncologist who recommended a complete blood exchange. At this time, the patient was diagnosed with acute chest syndrome. A complete blood exchange

could not be performed in our system, so the patient was transferred to a tertiary facility and underwent complete blood exchange. The patient is doing better. He is still intubated, but his oxygen requirement has improved as have his x-ray findings.

Acute chest syndrome is a pneumonia like illness that develops in sickle cell patients.

Typically, it presents with pleuritic chest pain, fever, rales on pulmonary examination, and a pulmonary infiltrate seen on chest x-ray.2 Patients may develop ACS secondary to vaso-occlusion of the pulmonary vasculature leading to ischemia and potentially infarcts of the lungs. Other causes are associated with viral infections, mycoplasma, fat embolism, and hypoventilation-atelectasis secondary to rib infarctions.2 The incidence for ACS is inversely proportionate to the age of the patient, with most patients presenting with their first episode between two and four years of age and the lowest incidence at greater than 20 years of age.2 The treatment of ACS consists of antibiotics and potentially antivirals.1 All patients with ACS should be considered for a total blood exchange.

3. Vichinsky, Elliott P., et al. Causes and Outcomes of the Acute Chest Syndrome in Sickle Cell Disease. The New England Journal of Medicine 2000; 342: 1855-65 5. Hsu, H., Lin, C. M., Tsai, C. Y., et al.

(2005). Acute Non-cardiogenic Pulmonary Edema Associated with the Radiographic Contrast Medium loversol [Electronic version]. Tzu Chi Medical Journal, 17(4): 273-277.

6. Kakouros, N. S., Kakouros, S. N. (2003).

Non-Cardiogenic Pulmonary Edema [Electronic version]. Hellenic Journal of Cardiology, 44: 385-391.

7. Kozlowski, C., Kolle[, M. H. (1992) Noncardiogenic pulmonary edema associated with intravenous radiocontrast administration [Electronic version]. Chest, 102: 620-621.

8. Malins, A. F. (May 1979). Pulmonary edema following radiological investigation of patients with peripheral occlusive vascular disease: Adverse reaction to contrast media [Electronic version].

American Heart Journal, 97(5): 676-677.

References: 1. Poulter, Elana Y., et al. Acute Chest Syndrome Is Associated With History of Asthma in Hemoglobin SC Disease.

Pediatric Blood Cancer 2011; 57: 289-293

9. Paul, R., Grizelda, G. (March 2002). Fatal non-cardiogenic pulmonary oedema after intravenous non-ionic radiographic contrast [Electronic version]. The Lancet, 359: 1037-1038.

2. O Castro, DJ Brabilla, et al. The acute chest syndrome in sickle cell disease: incidence and risk factors. The Cooperative Study of Sickle Cell Disease. Blood1994; 84-2 (July 15): 643-649

10. Perina, D. G. (2003). Noncardiogenic pulmonary edema [Electronic version].

Emergency Medicine Clinics of North America, 21: 385-393.

View back issues and read current articles from your laptop, desktop, tablet or mobile device.

www.acoep.org/pulse the PULSE | October 2013

25

26

Resident Wrap Up

Megan McGrew Koenig DO, MBA, MS President

On behalf of the Resident Chapter, I would like to thank the membership at large for allowing us the incredible opportunity of representing them at the national level as well as ACOEP for the amazing support they continue to provide us from year to year.

With an entire team effort, we have been able to accomplish many great things this year to further the growth of the Resident Chapter. From research competitions and resources, to a new membership guide and creative conference planning, we have all been hard at work creating a product we can be proud of.

Sadly, it is that time of year when we have to say goodbye to several great residents who will be moving on to the next steps in their lives. Justin Arnold, Kimberly Irvin, Kade Rasmussen and Aimee Washington have all been involved throughout all of their residencies and several were even involved throughout all of medical school. Their dedication to ACOEPâ&#x20AC;&#x2122;s students and residents is to be commended.

Despite the loss of such great teammates, we are looking forward to welcoming in a set of new faces at our annual elections on Saturday, October 5th. It is always refreshing to have new opinions and ideas to simulate even greater ideas for ACOEP. Thank you again to the ACOEP membership and Board of Directors for the incredible support you provide to our chapter, we are lucky to be a part of such a great network of emergency medicine physicians nationwide.

Sincerely,

Megan (McGrew) Koenig, DO, MBA, MS ACOEP Resident Chapter President ACOEP Board of Directors Midwestern University Chief Resident

the PULSE | October 2013

27

Residency Spotlight Program: Freeman Health System Address: 1102 W. 32nd St. City/State/Zip: Joplin, MO 64804 Hospital Information: Type (Community, rural, urban): Community Trauma Level: II Number of Hospital Beds: 450 (West & East Campus) 67 (Neosho Campus) Number of ED Beds: 41 bed (27 of those beds are in private rooms) EM Program Information: Phone: 417-347-6612 Website: www.freemanhealth.com Total Number of EM Residents: 9 Residents to Attending Ratio Working Clinically: 1:1 typically Accepts Medical Student Rotations? Yes EM Program Curriculum: PGY 1: PGY 2: PGY 3: PGY 4: REQUIRED ROTATIONS A. Emergency Medicine (24 G. Trauma (1 Month) Months) * B. C ritical Care (2 Months) H. A dministration / Research (1 Month) C. G eneral Medicine (2 I. Female Reproductive Med Months) (1 Month) D. Surgical Subspecialty (2 J. S elective Months (6 Months) Months) E. Orthopedics ( 1 Month) K. Elective Months (2 Months) F. Pediatrics (2 Months) L. Vacation / Selective Time EM Program Application Information: Dates applications are accepted: August – December Prefers COMLEX Scores of: Each individual is assessed on a case by case basis.

Interview Dates: Rolling – highly encourage a rotation at our site.

Number of Letters of Recommendations and who can write the letters: 3 – preceptors, program directors, professional references, etc.

Program: Ohio Valley Medical Center Address: 2000 Eoff Street City/State/Zip: Wheeling, WV 26003

Hospital Information: Type (Community, rural, urban): Community Trauma Level: OVMC is level 2 and our affiliate East Ohio Regional Hospital is level 3 Number of Hospital Beds: OVMC 250 EORH 200 Number of ED Beds: OVMC 17 beds; 31,000 visits EORH 14 bed; 26,000 visits EM Program Information: Phone: 304-234-8177 Website: www.ovmc-eorh.com Total Number of EM Residents: 16 EM and 4 IM/EM Residents to Attending Ratio Working Clinically: Accepts Medical Student Rotations? yes EM Program Curriculum: PGY 1: 4 PGY 2: 4 PGY 3: 4 PGY 4: 4 IM/EM has 1 PGY-4, 1 PGY-3, and 2 PGY-2.

EM Program Application Information: Dates applications are accepted: August-December Prefers COMLEX Scores of: 465/80 Interview Dates: September 26-December 12 Number of Letters of Recommendations and who can write the letters: Any DO, but preferably an EM physician SLOR

Program: Albert Einstein Medical Center Address: 5501 Old York Road City/State/Zip: Philadelphia, PA 19141 Hospital Information Type: Urban Trauma Level: Level 1 Regional Resource Trauma Center ED Visits/Year: 100,000 Number of Hospital Beds: 509 Hospital Beds Number of ED Beds: 70 ED Beds EM Program Information Website: www.einstein.edu/education/emergency-medicine/ Number of Positions: 60 Residents Residents to Attending Ratio Working Clinically: 2.5 Residents: 1 Attending Working Clinically Accepts Medical Student Rotations: Yes, through VSAS EM Program Application Information: Dates applications are accepted: Mid-July to December 30 Recommendations: Two EM SLORS required Scores: Comlex and/or USMLES accepted

the PULSE | October 2013

28

Residency Spotlight (continued) Program: McLaren Oakland Address: 50 North Perry Street City/State/Zip: Pontiac, MI 48342 Hospital Information: Type (Community, rural, urban): Community Trauma Level: ACS Level 2 Trauma Center Number of Hospital Beds: 308 Number of ED Beds: 22 EM Program Information: Phone: (248) 338-5392 Website: www.mclaren.org/oakland/ResidenciesOakland.aspx Total Number of EM Residents: 16 Total Number of EM/IM Residents: 8 Total Number of EM/FM Residents: 10 Residents to Attending Ratio Working Clinically: 1 or 2:1 Accepts Medical Student Rotations? Yes EM Program Curriculum: Curriculum for OGME 1 Year of Emergency Medicine: • Four (4) months of emergency medicine • One (1) month of pediatric emergency medicine at Children’s Hospital of Michigan • One (1) month of female reproductive medicine • One (1) month of general internal medicine • One (1) month of cardiology • One (1) month of clinical care • One (1) month of orthopedics • One (1) month of general surgery • One (1) month of surgical subspecialty including but not limited to:

- Ophthalmology

- ENT

- Urology

- Hand surgery

- Plastic surgery

- Anesthesiology Curriculum for OGME 2, 3 & 4 Years of Emergency Medicine In the final three (3) years of training to be compliant with the basic standards the following must be completed in addition to what was scheduled during the OGME 1 year: • Twenty-two (22) months of emergency medicine with a minimum of four (4) months per year • One (1) month of critical care • One (1) month of pediatric intensive care rotation at William Beaumont Hospital Royal Oak or Hurley Medical Center • One (1) month of trauma at Hurley Medical Center • One (1) of emergency medical services • One (1) month of administrative related activities, e.g.,

- Research

the PULSE | October 2013

- Medical legal

- Quality assurance, etc.

• Six (6) months of minimum of selected rotations, selected by and at the discretion of the program director. Currently these are:

1. Pulmonary medicine

2. Radiology

3. Neurology

4. Toxicology (Wayne State University/ Detroit Recovery Hospital)

5. Surgical Subspecialty

6. Medical sub specialty • Three (3) months minimum of elective rotation.

• Vacations and selective times shall be scheduled at the discretion of the program director.

• OGME 2 year-all rotations at McLaren Oakland.

• OGME 3 & 4 year- All out of hospital rotations are completed. The specific year of completion depends on the availability of the rotation at the hospital where it is offered.

EM Program Application Information: Dates applications are accepted: July 1-October 1 Prefers COMLEX Scores of: not published Interview Dates: Variable by appointment three Wednesdays/ month from September 4-December 1 Number of Letters of Recommendations and who can write the letters: Three letters of recommendation required. Physician Preceptors, Program Directors, or Medical School Professors.

29

Committed Physicians Interested in Serving on College Committees The annual appointment for physicians seeking committee positions on ACOEP Committees will begin during the last quarter of 2013. Physicians seeking appointment to any committee should send his or her CV with a letter naming the committee they would like to be appointed to and why. All applications must be received by December 1st and will be assigned based on availability. Terms are 3 years beginning January 1 and ending on December 31st.

Committees are open to any physician and we encourage interested physicians to sit in on meetings of Committees that you are interested in being appointed to.

Appointees must attend 66% of all meetings, conference calls and must participate in the activities of the Committee. Failure to do so will cause the appointee to be removed from the committee.

Send your information to: Jan Wachtler, Executive Director, ACOEP, 142 E. Ontario St., Suite 1500, Chicago, IL 60611

Call to Meeting At the request of the Secretary, John C. Prestosh, DO, FACOEP, a meeting of the membership of the American College of Osteopathic Emergency Physicians has been arranged for October 6, 2013 at 5:00 p.m. at the Hilton San Diego Bayfront Hotel in San Diego, California. This event will be followed immediately by the Welcome Reception for the Collegeâ&#x20AC;&#x2122;s 2013 Scientific Assembly.

Voting for Board Members will once again take place online and will be available to Active, Fellow, Distinguished, Retired and Life Membership between August 7th and 4:30 p.m. on October 6th. Please watch for voting keys that will be emailed to any eligible members on August 6th.

the PULSE | October 2013

30

Student Case Competition

Winning Case by Ross Cohen, MS IV

Hypertriglyceridemia Induced Pancreatitis in a Type II Diabetic Presenting with DKA Ross Cohen, MS IV University of Medicine and Dentistry of New Jersey School of Osteopathic Medicine (UMDNJ-SOM) Lehigh Valley Health Network, Allentown, PA

Chief Complaint: Abdominal Pain, vomiting, weakness x2 days History of Present Illness: A 66 y/o Caucasian male with a history of type 2 diabetes mellitus presented to the Lehigh Valley Health Network Hospital ED, with a two day history of abdominal pain, nausea and vomiting. The patient stated that his abdominal pain began suddenly yesterday, was a constant 7/10 dull pain, was located diffusely across the upper abdomen and was associated with persistent vomiting. He had vomited a brown colored liquid at least five times. Due to his nausea, he had not been able to keep any food or liquid down and had not taken any of his medications for the last two days. He had never experienced similar symptoms in the past. The patient denied fever, chest pain, shortness of breath, urinary or bowel symptoms.

Past Medical History: The patient was an obese male with a past medical history of diabetes mellitus type two, peripheral vascular disease, hypertension and hyperlipidemia.

Past Surgical History: Surgical history is significant for a cholecystectomy 15 years ago.

Social History: The patient has a 20 pack year smoking history. He Denied alcohol and illicit drug use.

Medications:

the PULSE | October 2013

• Crestor 10 mg PO qday • Lovaza 1g four capsules PO qday • Metformin 500 mg PO q12hr • Aspirin 81 mg PO qday • Diovan 160 mg PO qday • HumaLOG 1 unit/kg/day 15 minutes before meal • Lantus 0.2 unit/kg once daily Allergies: The patient reported no known drug, food or environmental allergies.

Review of Systems: • Gen: + weakness, + fatigue, - dizziness, - weight loss, - fever/chills • HEENT: - blurred vision, -tinnitus or hearing loss, -difficulty swallowing or speaking • CV/ Resp: - chest tightness, - shortness of breath, - dyspnea on exertion, - orthopnea, - cough, - palpitations, -diaphoresis • Abd: +nausea and vomiting x 5 over the past 2 days, + abdominal pain, -constipation/ diarrhea • GU: - hematuria, -dysuria, -frequency or urgency, -flank pain • Ext: - edema, - calf tenderness, - muscle cramps • Skin: -rash, -bruising or petechiae, -purpura

Physical Examination: • Vital Signs: Temp (max)- 99.2, Pulse105, BP- 116/66, RR 25, Pulse Ox 95% RA • General: The patient is a 66 year old obese male in moderate distress. He is awake and alert and oriented to person, place, and time.

• Head: Normocephalic and atraumatic.

• Eyes: Pupils are equal, round, and reactive to light. Extra-ocular muscles are intact.

Sclera and conjunctiva are normal.

• ENT: External ears are normal, tympanic membranes are intact bilaterally and there is no drainage from the ears. There are no nasal polyps, septal deviation, epistaxis or rhinorrhea.

• Mucus membranes are dry. There is no pharyngeal exudate or edema.

• Neck: Supple with normal range of motion.

No meningeal signs are appreciated.

Cervical spine is non-tender to palpation.

No thyromegaly, jugular venous distention, carotid bruits, tracheal deviation or cervical lymphadenopathy.

• Respiratory: Lung sounds are clear to auscultation bilaterally. No abnormal lung sounds appreciated. No chest wall deformity or tenderness is noted. No respiratory distress or accessory muscle usage.

31 • Cardiovascular: Tachycardic at 105 bpm, regular rhythm. Normal S1 and S2, no murmurs, no rubs, no S3 or S4 present.

• Abdomen: Soft, mild tenderness to palpation diffusely, distended with dullness to percussion. Normal bowel sounds auscultated in all 4 quadrants. No masses, no peritoneal signs.

• Back: No costovertebral angle tenderness, no tenderness to palpation.

• Extremities: Normal range of motion, no cyanosis, clubbing or edema.

• Neurologic: GCS 15. No focal motor or sensory deficits. Cranial nerves are intact.

No cerebellar deficits, nystagmus, clonus or asterixis. Normal deep tendon reflexes, absent Babinski sign. Speech normal, gait normal.

• Skin: Warm, dry, and intact. Normal color.

pH

7.31 L

Pc02

34 wnl

pO2

100 wnl

• Lipase: 1480 H • Liver Function Tests: AST 45; ALT 14 wnl • Lactate: wnl • U/A: wnl • Hemocult: Negative • Cardiac Enzymes: Troponin: <.04 ng/ mL * *specimen cleared of lipemia by ultracentrifugation • Coagulation Profile: PT and INR wnl Ancillary Testing: • HgA1c: >12H

• Lymphatic: No cervical, axillary, or inguinal adenopathy.

• Lipid Testing Lipid Levels

Results

• Psychiatric: Normal affect. No suicidal or homicidal ideation.

Triglyceride

3670 H

Cholesterol

670 H

HDL

15 L

NHDL

655 H

Laboratory Data: • CBC CBC

Results

Hemoglobin

14.2 wnl

Hematocrit

41.4 wnl

WBC

8.4 wnl

Platelet

226 wnl

Radiologic Data: • 12 lead EKG: showed sinus tachycardia • CT abdomen w oral and IV contrast: was performed showing acute pancreatitis.

• CMP CMP

Results

Sodium

130 L

Potassium

5.8 H

Chloride

83 L

CO2

19 L

BUN

25 wnl

Creatinine

1.07 wnl

Glucose

363 H

Results

Acetone

Moderate wnl

Beta Hydroxybuturate

8.16 H

• Blood Venous Gas BVG

Results

Treatment of Patient and Disposition: Due to the availability and timing of laboratory data, the patient was initially thought to solely have DKA. Labs revealed an elevated glucose, positive ketones and an anion gap metabolic acidosis consistent with DKA. Aggressive IV hydration and Insulin therapy (10 units Insulin IV followed by Insulin drip (.05-.1 U/kg/hr)) was initiated.

Acute Pancreatitis was later discovered in ED with the additional data of a lipase of 1480 and a CT scan showing acute pancreatitis.

Conventional treatment of acute pancreatitis included aggressive fluid resuscitation, electrolyte correction, prevention of vomiting with antiemetics, analgesia, NPO precautions and NG suction as needed.

The cause of the patient’s pancreatitis was also discovered in the ED. Clues to the cause were initially revealed upon reviewing cardiac enzymes. The footnote stated that the lab specimen was cleared of lipemia by ultracentrifugation. This prompted the ordering of a lipid panel which revealed an elevated triglyceride level of 3670.

With the source of his pancreatitis now known, the patient remained on the Insulin drip that was started initially for his DKA. The ultimate goal of the Insulin therapy was to decrease his serum triglycerides to < 500 mg/ dL. Care was then transferred to the ICU. Follow Up: Two days after his initial presentation to the ED, a chart review revealed that the patient was still on the Insulin drip. His Lipase had decreased from 3670 to 979. Orders were written to keep the patient NPO and continue Insulin infusion until the triglycerides were below 500 and his anion gap had been closed.

Upon discharge the patient would be started on fenofibrate therapy at 600 mg PO qDay.

• Blood Ketone Levels Ketone Levels

to acute pancreatitis. The pancreatitis was found to be caused by hypertriglyceridemia.

Thus, the patient was ultimately diagnosed with DKA secondary to hypertriglyceridemia induced pancreatitis. The arrival at this complex conclusion was only possible through a stepwise, organized diagnostic approach to the initial complaint. The details will be further discussed below.

Diagnostic Impression: The patient’s physical exam and laboratory data initially suggested a diagnosis of diabetic ketoacidosis. It was later discovered in the ED that this finding was in fact secondary

Discussion: Although hypertriglyceridemia is the third leading cause of acute pancreatitis, its diagnosis in this case was delayed due to its atypical presentation (3). Accounting for anywhere between 1-38% of all cases of acute pancreatitis, the diagnosis of the underlying cause of pancreatitis is imperative for proper

the PULSE | October 2013

32

Student Case Competition

Winning Case by Ross Cohen, MS IV management, treatment and prevention (4).

Hypertriglyceridemia is diagnosed at serum triglyceride levels > 1000 mg/dL (4). Primary causes of hypertriglyceridemia include genetic disorders of lipid metabolism, most commonly diagnosed in children (3). Secondary causes include diabetes mellitus, DKA and obesity (8).

As seen in this case, our patient’s risk factors included all of the above secondary causes.

Ancillary testing of our patient revealed a HgA1C of >12. Other secondary causes include alcohol, hypothyroidism, estrogen hormone supplementation, medications and pregnancy (10).

Pathogenesis of HTG induced pancreatitis In order to better understand the pathophysiology behind hypertriglyceridemia induced pancreatitis, a discussion of lipid metabolism is necessary (3). Free fatty acids, the building blocks of triglycerides, are volatile molecules. When combined with glycerol, a more stable molecule is formed called a triglyceride (10). Triglycerides can enter the blood from either the diet or by synthesis from the liver. Since they are insoluble molecules, once in the blood they are packaged as soluble lipoproteins. These lipoproteins are called chylomicrons if they came from the diet, or VLDLs if synthesized from the liver (10).

Lipoprotein lipase is an enzyme that interacts with these lipoproteins in peripheral tissue. It is here that the lipoproteins are broken back down into triglycerides to store in muscle or fat tissue as future energy stores (10). Essentially, the blood triglyceride level is then a balance of the synthesis and catabolism of their lipoproteins.

Hypertriglyceridemia is diagnosed at a serum triglyceride level > 1000 mg/dL (5). At high triglyceride levels, chylomicron levels specifically remain elevated and the serum becomes full of fat (5). Chylomicrons are the largest of the lipoproteins and can obstruct capillaries leading to ischemia and academia (10). In the case of hypertriglyceridemia induced pancreatitis, this local damage occurs in the pancreas and can expose triglycerides to pancreatic lipases. These lipases hydrolyze trigylcerides to free fatty acids which are volatile molecules. This creates an inflammatory response and ultimately leads to acute pancreatitis (5).

Clinical Presentation, Work-Up & Differential Diagnosis In this specific case, the patient’s hypertriglyceridemia induced acute pancreatitis was not readily apparent upon presentation to the ED. The presentation of abdominal pain, weakness and vomiting in a 66 y/o obese type two diabetic male created a vast differential diagnosis. With a broad differential including cardiac, metabolic and biliary/bowel disease processes, an IV line was established and labs

the PULSE | October 2013

were ordered to rule in/out these diseases.

The patient’s cardiac workup was negative.

Although both his troponin level and CBC were within normal limits, the lab results were marked with a unique phrase “specimen cleared of lipemia by ultracentrifugation.”

His metabolic workup revealed an elevated blood glucose at 363 with an anion gap metabolic acidosis (AG 23, BVG pH 7.31). In addition, his blood ketone levels were positive for BHB at 81.6. It seemed his diagnosis was clear, he had belly pain and had not taken his medications for the last two days and was therefore in DKA. We began treating him with aggressive IV hydration and Insulin.

The patient’s biliary labs returned shortly after showing an elevated Lipase of 1480. CT scan confirmed a diagnosis of acute pancreatitis.

His diagnosis was now complicated because in addition to his DKA, the patient also had data supporting the diagnosis of acute pancreatitis; a history of abdominal pain, nausea, vomiting and an elevated lipase level. The cause of his pancreatitis was still elusive, however his cardiac workup reminded us that he had lipemia. This prompted ordering a triglyceride level which was remarkably elevated at 3670. Thus, his pancreatitis was caused by hypertriglyceridemia.

The complications of his pancreatitis resulted in DKA. Treatment Treatment for patients with HTG induced acute pancreatitis includes both short term and long term goals (4). Acutely, management is aimed at controlling the symptoms of acute pancreatitis as well as well as lowering triglyceride levels. Conventional treatment of acute pancreatitis is indicated and includes aggressive fluid resuscitation, electrolyte correction, prevention of vomiting with antiemetics, analgesia, NPO precautions and NG suction as needed (4).

The other acute management goal is to reduce serum triglyceride levels to <500 mg/ dL (8). This can be accomplished by either apheresis or Insulin. Decisions regarding the specific modality are dependant on the patient’s blood sugar and are outlined in figure one below.

Since our patient had an elevated glucose, Insulin therapy was indicated (8). Although it is well known that Insulin can decrease blood glucose, it can also decrease serum triglyceride levels. Insulin enhances lipoprotein lipase activity which accelerates chylomicron metabolism (4). Thus, this clears the body of the volatile triglycerides. Interestingly, our intial treatment of DKA was actually treating his hyperlipidemia as well. An IV infusion of regular insulin in 5% dextrose is given at a rate of .1 to .3 u/kg/hr to maintain glucose between

150 and 200 mg/dL. Finger stick glucose levels are to be monitored q 4hr and triglyceride levels are to be monitored q 12 to 24 hr with adjustment of insulin dosage as needed (8). The IV insulin should be discontinued when serum triglyceride levels are <500 mg/dL, which can take up to 3-4 days.

The long term treatment goals are aimed at maintaining low triglyceride levels to decrease the recurrence of pancreatitis (4). This includes oral antihyperlipidemic agents such as Gemofibrozil dosed at 600mg BID. Other efforts to reduce triglycerides include dietary fat restrictions or even periodic apheresis (10).

Closing: Although the classic presentation and management of acute pancreatitis is seemingly straightforward, this case study reminds us of a few key tips to remember while in the ED. First, the presentation of pancreatitis is sometimes elusive, and may be masked by overlying conditions, such as DKA in this case.

In addition, this case teaches us the importance of maintaining a broad differential with regards to the causes of pancreatitis as this will dictate the management of our patients in the ED, as well as future treatment goals to prevent recurrences.

References 1 Alagozlu H, Cindoruk M, Unal S. Tamoxifeninduced severe hypertriglyceridaemia and acute pancreatitis. Clin Drug Investig 2006; 26:297.

2

hang CC, Hsieh YY, Tsai HD, et al. Acute C pancreatitis in pregnancy. Zhonghua Yi Xue Za Zhi (Taipei) 1998; 61:85.

3

F redrickson DS. An international classification of hyperlipidemias and hyperlipoproteinemias. Ann Intern Med 1971; 75:471.

4

ortson MR, Freedman SN, Webster PD F 3rd. Clinical assessment of hyperlipidemic pancreatitis. Am J Gastroenterol 1995; 90:2134.

5

oldenberg NM, Wang P, Glueck CJ. G An observational study of severe hypertriglyceridemia, hypertriglyceridemic acute pancreatitis, and failure of triglyceridelowering therapy when estrogens are given to women with and without familial hypertriglyceridemia. Clin Chim Acta 2003; 332:11.

6

aber PS, Wilson JS, Apte MV, et al.

H Lipid intolerance does not account for susceptibility to alcoholic and gallstone

33 pancreatitis.

106:742.

Gastroenterology

1994;

7

avel RJ. Familial dysbetalipoproteinemia.

H New aspects of pathogenesis and diagnosis.

Med Clin North Am 1982; 66:441.

8

air S, Yadav D, Pitchumoni CS. N Association of diabetic ketoacidosis and acute pancreatitis: observations in 100 consecutive episodes of DKA. Am J Gastroenterol 2000; 95:2795.

9

hitfield JB, Hensley WJ, Bryden D, W Gallagher H. Some laboratory correlates of drinking habits. Ann Clin Biochem 1978; 15:297.

10

’Brien T, Dinneen SF, O’Brien PC, O Palumbo PJ. Hyperlipidemia in patients with primary and secondary hypothyroidism. Mayo Clin Proc 1993; 68:860.

Figure 1 FOEM 1087 (4M_EmerSyst)NewLogo_Layout 1 9/12/13 9:43 AM Page 1

EM Residency Program Director

It is always

wise to look ahead, but

difficult to look further than

you can

see

-Winston Churchill

Physician owned and operated, 4M Emergency Systems has over 15 years of experience management and staffing emergency departments and urgent care centers. We are now looking for qualified physicians at the following locations: Cleveland, Ohio: 4M Emergency Systems has an excellent opportunity for a BC Osteopathic Emergency Medicine Practitioner to join the UH Regional Hospital EM Residency Program, as the Program Director. Candidates are expected to demonstrate aptitude with both clinical leadership and medical education leadership experiences. Prior administrative experience in Emergency Medicine residency leadership roles is required. Candidates must have completed an accredited osteopathic emergency medicine training program and must be ABOEM board certified.

Outstanding compensation and benefits program including an incentive plan, stipend, paid health plan, 401K, malpractice, life & long/short-term disability and much more. For more information about this position, contact Erin Waggoner, 4M Emergency Systems, telephone 888-758-3999; or email ewaggoner@4mdocs.com.

STOP by our booth #14 at ACOEP’s Scientific Assembly in San Diego!

October 2013 Pulse Ad Quarter Page - Color

Norcom Inc. 847-948-7762 theteam@norcomdesign.com

the PULSE | October 2013

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Attention Members!

Please be Aware of these Upcoming Events!

Pre-Conference OMT Workshop:

â&#x20AC;&#x153;Counterstrain to the Lower Half of the Bodyâ&#x20AC;?

December 5, 2013 8 hours category 1-A credit anticipated, pending approval of the AOA CCME Hyatt Regency, Indianapolis, IN Sponsor: Indiana Academy of Osteopathy

Contact: IAO, (317) 926-3009 or (800) 942-501 or www.inosteo.org

32nd Annual Winter Update: December 6 - 8, 2013

25 hours category 1-A credit anticipated, pending approval of the AOA CCME Hyatt Regency, Indianapolis, IN

Sponsor: Indiana Osteopathic Association

Contact: IOA, (317) 926-3009 or (800) 942-0501 or www.inosteo.org

Do you know of events and meetings that our members should know about? Let us know at ThePulse@ACOEP.org!

the PULSE | October 2013

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the PULSE | October 2013

Presorted Standard U.S. Postage

PAID

Chicago, IL Permit No. 2177

142 E. Ontario Street Suite 1500 Chicago, Illinios 60611

What you love is important.

Start there.

It’s really that simple. Do you love feeling energized by the people you work with?

Do you love being part of a group that takes care of each other like family? Do you love feeling like you own the future? We do.

At EMP, our approach to creating the best EM careers for physicians is different than any other group. That’s because we own our company. EMP is 100 % owned and operated by EMP physicians who focus on two key values: Servant’s heart and Owner’s mind. We’re in the driver’s seat.

Visit emp.com/jobs

or call Ann Benson at 800-828-0898. abenson@emp.com

Visit us at booth 915

Opportunities from New York to Hawaii.

AZ, CA, CT, HI, IL, MI, NH, NV, NY, NC, OH, OK, PA, RI, TX, WV