The Pulse July 2008

The PULSE

Osteopathic Emergency Medicine Quarterly VOLUME XXXIII NO. 3

july 2008

Presidential Viewpoints Peter A. Bell, D.O., FACOEP

“What Do You Want: A Patchwork Quilt or a Well-Woven Blanket?"”

In looking at our American healthcare system today, it is clear that there is much to be fixed. As a patient I’m not satisfied with the cost, the quality I get for the money, and the service!

As a health care provider, I’m not satisfied with the reimbursement, the quality of care I’m expected to deliver (with diminishing resources), and the time I’m ‘allowed’ to spend with the patient. It seems like the system is slowly imploding for both the patient and the provider. This begs the question, what do I suggest we do?

First, do we really have a ‘system’?

What we have been calling a system is nothing more than successive ‘fixes’ to a public problem. In order for a country to grow, it needs people and an infrastructure.

Items like food, housing, education, and healthcare are essential components for people if we are to build a sustainable infrastructure. In our country, we continue to struggle with this concept. As a result, we have pieced together our fixes into a patchwork quilt called American healthcare. Its components are irregular, diverse, ragged, and sometimes too specific, but despite adherence at the edges, poorly connected.

For example, in an age of high technology, one would hope our communications would

bind the quilt together, but no! We now have to pursue Regional Health Information Organizations (RHIOs) so we can talk to each other. Redundancy and unnecessary testing reign supreme. We are deluged by paperwork as patients and providers. And to top it all off, the insurance companies and government spend more time trying not to pay, than solving the problem.

What we need is a Health Care Policy for the nation. What we have is a continuing debate fueled by politicians seeking office, special interest groups (including physicians) pursuing their own agendas, and health care expenditures last year exceeding $2.2 Trillion dollars (The federal budget is about $3 Trillion dollars, the federal deficit over $9 Trillion dollars).

We need to stop the rhetoric and seriously reconsider our priorities.

As a patient and a provider it may seem like I have competing interests. I would argue that it has made me sensitive to both sides of the debate. Here is what I propose: I want a new American Health Care System. I want a well-woven blanket, not another patch.

My system would address access. I would assure that sufficient numbers of primary care providers (doctors, PAs, NPs) were available to meet the current and future needs of the country. Everyone would have a “medical home” and all health care needs would be coordinated through this point of service 24/7 (and would provide medical care beyond the 9-5 paradigm). In

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addition, I would support an emergency medical system that functions for true emergencies. Entry into this emergency system would occur as the result of mandatory training of all patients, and breaking the current practice of ‘just go to the ER’. (We train kids in our schools on drug avoidance, safe sex, fire drills, etc.

Why not include proper use of the medical system?) All medical homes, ERs, and hospitals would have an integrated network of health care providers to choose from. No more shopping for a specialist, shipping patients out of the ER, or having a paucity of services.

A financial re-structuring would take place. Like our colleagues in New Zealand, the new system would be funded as a no-fault, all payers plan. Money would come from employers and the general tax base (if you read my previous articles, you can follow the money). It would pay for providers, facilities, and unexpected/adverse outcomes (formerly known as malpractice).

I would eliminate the National Practitioner Data Base and spend money on quality assurance. Negative trends would be met with education, re-training, assessment, and monitoring. A graduated physician is a terrible thing to waste! So lets not!

Primary care would be the focus with dollars reimbursed for preventative healthcare. Payment of services would be tied to behavior by both the physician (ex. documented the need to stop smoking, continued on page 4

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Editorial Drew Koch, D.O., FACOEP, Editor

National EMS Week: May 18-24, 2008 A C O E P joins with the American College of Emergency Physicians to salute thousands of EMS workers during National Emergency Services Week, May 18-24, 2008. The theme this year is: EMS: Your Life is Our Mission. By the time this article is read EMS week will be gone. If you did not recognize the hard working heroes during EMS week, please reflect now on how important these individuals are not only to the emergency departments throughout the country but to the individuals and communities that they serve.

It was not until I changed jobs last fall that I realized how important and vital the EMS personnel are to the emergency department and to the community. As an Emergency Medicine resident, I did an EMS rotation and rode with paramedics.

During my infancy as an EM attending, lectures to the paramedics and involvement with teaching ACLS were part of being an EM physician. As time went on and my employer no longer required board certified EM physicians to maintain the merit badge of ACLS; my interest in teaching ACLS waned and I became apathetic toward prehospital education. While serving an ACOEP’s EMS committee about 10 or so years ago, I was the only individual on the committee who was not actively

involved with EMS in their community and hospital. Fast forward to Fall 2007, I was told that part of my job responsibilities included “EMS”.

“EMS” meant that I was the hospital medical representation to the local EMS community, the Medical Director of the local EMS services, the county EMS Medical Director and a voting member of the Central New York Regional Emergency Medical Advisory Committee. This is quite different and challenging from being a medical command physician whose interactions with the prehospital providers was through the medical command radio, phone, and at the bedside when a patient was brought to the ED. Learning the prehospital jargon and acronyms is quite challenging. For the first 20 years of my EM career, there were EMTs and Paramedics. Now my vocabulary is filled with basic life support units that have EMT’s, EMT-D’s, CFR’s and CFR-D’s and advanced life support units that provide prehospital intermediate care, critical care and/or paramedic care. The responsibilities, abbreviations and location have changed for me, however, the dedication and commitment of all the hard working professionals who provide prehospital care have not changed.

This appreciation for the all the dedicated prehospital providers began six months ago.

What began as a public relations event between the hospital, the emergency department and one of the local ambulance companies has evolved into a positive working relationship between

emergency department and the local EMS community. The day started out with a photo shoot, an interview with the local media, and a tour of the county 911 center and culminated with a ride along with the ambulance crew. The adrenaline rush I experienced when the lights and sirens were activated on our first call does not compare to the professionalism and compassion that was exhibited by the crew during that call.

The outcome was grave for the patient but the crew was both professional and compassionate in their interaction with the family and the police investigators.

Two events that occurred earlier this year have reinforced in my mind and in the minds of two patients and their families whose lives have been given a second chance that these hard working dedicated EMS individuals are truly heroes. The first event involved a young graduate student who collapsed between classes and was fortunate that there was an AED available and that a passerby EMT used the AED to deliver a life saving shock. The second incident involved a call where an individual had called 911 because he felt ill and he was found unresponsive. CPR was started and he was delivered a life saving shock.

Both individuals are alive today and owe their existence to the actions of these highly trained and dedicated heroes of EMS. Even though EMS week has come and gone since this article was written, please take the time to reflect on the heroes of EMS who we take for granted on a given day and whose many lives in our communities that they have truly impacted.

Table of Contents Presidential Viewpoints, Peter A. Bell, D.O., FACOEP . . 1 Editorial, Drew Koch, D.O., FACOEP . . . . . . . . . . . . . . 3 Executive Director’s Desk . . . . . . . . . . . . . . . . . . . . . . . . 5 AOBEM Scientific Assembly Information . . . . . . . . . . . 7 Members in the News. . . . . . . . . . . . . . . . . . . . . . . . . . . 8 From the Pediatric Files . . . . . . . . . . . . . . . . . . . . . . . . 10 Guest Column, Thomas A. Brabson, D.O., FACOEP . . 14

Medical Update . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Student Case Competition . . . . . . . . . . . . . . . . . . . . . . 18 Guest Column, Wayne Jones, D.O., FACOEP . . . . . . . . 22 Medical Care Access Protection Act of 2007/S.243 . . . . 23 Perspective of a Young Physician . . . . . . . . . . . . . . . . . 27 Governmental Affairs . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Emergency Department Ethics . . . . . . . . . . . . . . . . . . . 29

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The Pulse – An Osteopathic Emergency Medicine Quarterly 142 E. Ontario St., Suite 1250 Chicago, IL 60611 312-587-3709 / 800-521-3709 Editorial Staff Drew A. Koch, D.O., FACOEP, Editor Wayne Jones, D.O., FACOEP, Asst. Editor Peter A. Bell, D.O., FACOEP Gary Bonfante, D.O., FACOEP Duane Siberski, D.O., FACOEP Janice Wachtler, Executive Director Communications Subcommittee Drew A. Koch, D.O., FACOEP, Chair Wayne Jones, D.O., FACOEP, Vice Chair Gary Bonfante, D.O., FACOEP, Advisor James Bonner, D.O., FACOEP, Advertising Bobby Johnson, Jr., D.O., FACOEP William Kokx, D.O., FACOEP Annette Mann, D.O., FACOEP The PULSE is a copyrighted quarterly publication distributed at no cost by the ACOEP to its Members, libraries of Colleges of Osteopathic Emergency, sponsors, and liaison agencies by the National Office of ACOEP. The Pulse and ACOEP accept no responsibility for statements made by contributors or advertisers.

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Presidential Viewpoints, continued from page 1 doing drugs, and start exercising etc), AND the patient (did they stop smoking, doing drugs, and start exercising?). Compensation for these services would increase substantially with a large decrease in reimbursement for procedures. This would level the playing field between primary and specialty care (Today we reward practitioners for doing expensive procedures disproportionate to our reimbursement for education and preventative care).

Gain sharing would be incorporated into the system at all levels and open to patients and providers. If someone finds a way to do something better, they are rewarded. If someone finds a way to save money AND improve quality or access, they get a piece of the savings. This approach of continuous improvement would only have positive incentives. Previous negative outcome plans would be replaced with reassessment of allocated resources (as to a Medical Home, ER, or hospital), education, and re-structuring.

Priority and limits of treatment, like those currently found in the United Kingdom and proposed in the original (1989) Oregon Health Plan would be adopted. We cannot afford to pay for everything. SIMPLE policies and CLEAR parameters would be established to guide the system in an effort to use limited resources wisely (Remember Mickey Mantle? He got a liver transplant then died of cancer one month later at the age of 65. Is that a wise use of limited resources?). Options for those who do not meet treatment criteria are available now. We need to realize and accept our mortal condition in order to bring about cultural change. We can do a lot with modern medicine, but we do not have unlimited resources and can not save

everyone. Pain control, comfort, and death with dignity are all available though our hospice programs. How many of us have said, “don’t intubate me just to leave me a vegetable post stroke in the ICU?” Let’s start applying what we believe to be best for us, to the advice we give patients and their families.

Implementation will be universal but not one system. While I am advocating for an integrated system of care, with one standard process, I do recognize ethic, regional, and environmental factors that can alter our delivery (and certainly the pathology). The pot of money will be centralized, but allocated according to defined regions of the country with similar needs per capita.

These will comprise systems. Motivation to use the funds expeditiously allows for innovation and best practices. Instead of using this as a core competency to eliminate other providers from the marketplace, we will share our successes to improve all regions.

The potential for centers of excellence is encouraged and will be rewarded.

So does this make a better condition for me as a patient? I think it addresses many concerns we all share. Would I as an emergency physician be happier knowing that I will see true emergencies, be paid for all the care I deliver, and not have to worry about malpractice? I believe so. The challenge in any ideal proposal is defining the terms such that everyone believes in the vision. It also requires a dash of optimism with a good dose of practicality. We are already spending more on health care per person than any other country in the world, and yet our outcomes are not comparable.

It is time for a change. Let us weave a new blanket to replace the worn out quilt.

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Executive Directors Desk Janice Wachtler

The topic of this column is raising “children.” Not necessarily biologic children but the parent/child relationship of organizations.

Organizational relationships are often much the same as familial relationships with one organization, normally the founding entity, giving birth to offspring (or children) as it grows and matures. Usually, an organization gains maturity in a field and pays its dues, and gives birth to another “generation” of organizations to help to build its progeny.

Child-organizations battle through youthful enthusiasm, perhaps hard-fought battles with peer groups, and lean on their parents and peer organizations for support as they establish themselves as adult participants in the familial unit.

These “children” organizations gain knowledge from the parent organization; they know what the parent organization knows. They learn from the people in the parent organization; they are what the parent organizations have taught them to be; their members directly reflect what they see the elder statesmen do.

Much like human families, child-organizations learn how to operate from watching and listening. If other child-organizations (or siblings) behave poorly they will try similar attention-getting mechanisms; whether they are successful or not, they will at least try. They will exert their muscles as they grow in stature and maturity; they will challenge the parent organization’s thinking and politics.

What parent organizations sometimes forget is that they too were “young” once.

They too have fought battles with “established” organizations, perhaps even their parental unit. What they cannot forget is that wherever their child-organization goes, they will bring the things they learned

Legacy from the parent-organization with them, as this has been the legacy that they have been handed, the example they watched as they matured. And, what all organizations forget is that these organizations, their “children” are the ones that will take a parent-organization to the next step. They are the chance that every parent seeks to have their children do better than they have done.

Right now, the ACOEP has two children: the Resident Chapter and Student Chapter. These organizations are nearly 20 years old being founded in 1990 and 1992, respectively. Over their first 10 years in existence, they were small organizations, often numbering in the 100-member range.

Since the late 1990’s as our residency programs began expanding and the Board of Directors waived dues in the Chapters, they have seen growth and an influx in interest and since 2004, the Presidents of both organizations have had seats on the Board of Directors of the ACOEP. Both “children” have had an allowance given to them to operate and both have had supporting organizations that have traditionally sponsored activities of the Chapters.

But both child-organizations have ebbed and flowed as the interests and abilities of officers have affected them. This has caused them to operate in fits and starts.

Recently, the bumps in the management of these organizations have smoothed out and the leadership has been more level and they have moved forward in a straighter and more directed fashion, with the Resident Chapter benefiting from a more linear transition from Student Officer to Resident Member to Resident Officer.

So we ask as a parent-organization, how do we best serve their needs? How do we best ensure their continued activity in the profession and the College? We look to the example that has been set for us by the AOA, our parent-organization. The AOA has been supportive of the ACOEP throughout the years. They have been there for us as we’ve matured and, for the most

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part, have watched from afar as we’ve aged and gone onto establish a well-functioning, financially-secure, mature organization.

If we were to take a snapshot of our ACOEP family, it will show a fairly dynamic group of physicians, who participate in the ACOEP’s family gatherings (CME Meetings), and support the family. This is the legacy we show our progeny, the Resident and Student Chapters. But we also show that while many attend our family only a handful stay on to wash the dishes, clean up the party favors, and begin planning for the next family reunion.

To pass on a legacy to our young physicians, we will need to have our members, both young and old, develop more of an interest in serving the family. We will need them to volunteer for and participate in committees of the ACOEP. We will need to incorporate their skills as mentors, teachers and lecturers into our CME programs and our residency programs. They will need to act as mentors to our next generation of physicians and become our new leaders in the College and profession.

Even though we would like 100% participation in our events and on our committees, we know that not everyone can participate in everything or want to be the leaders.

It takes interest in the family and the next generation to be part of the family and we need not only the front-line people but also those who are interested in maintaining the well being of the unit. These are the people who pay their dues, contribute to FOEM, and participate in the programs. These valued members must be on the forefront of the profession, as they are the ones who promote the specialty, the College and the Profession on a daily basis. They are the mentors; the practitioners; the trench doctors, and the face of osteopathic emergency medicine, and they must be members of the family.

As we move to a new tomorrow, we must remember that our children are the ones winning over the next generation of continued on page 26

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ACOEP Scientific Assembly Information ACOEP is proud to announce that online registration is now available for the 2008 Scientific Assembly, which will be held at Caesar’s Palace in Las Vegas on October 26 – 30. Please visit the ACOEP web site www.acoep.org to register for the conference and pay online, as well as book hotel reservations.

This is a special meeting for the ACOEP, as it is the first time the conference has been held independently of the AOA, as we move to meet the requests of emergency physicians to make the meeting more meaningful and cost effective.

Physicians who pre-register for the Scientific Assembly prior to September 15, 2008 will receive a discounted price of $425, a 20% savings from the regular price. Additionally, physicians reserving rooms at Caesar’s Palace on or before September 15 will enjoy a $219 per night room rate (plus tax); a substantial discount from the normal room rate.

The Scientific Assembly didactic sessions provide 23 hours of Category 1A credit; with an additional 10 hours of Category 1A credit available for attending the Case Presentation Competition and award presentation luncheons. 3 hours of Category 2B credit (Category 1A credit pending) will be provided for attending the Research Poster Presentations.

Committee Meeting Schedule Saturday, October 25 1:00 – 5:00 p.m.

Finance/Executive Sunday, October 26 9:00 – 11:00 a.m.

Emergency Medical Services Undergraduate Medical Education 11:30 a.m. – 1:30 p.m.

Communications Governmental Affairs Practice Management 2:00 – 4:00 p.m.

Member Services Pediatric Emergency Services Research 4:00 – 6:00 p.m.

Continuing Medical Education Program Directors

Tentative Agenda Monday, October 27 7:00 a.m. – 12:00 Noon Board of Directors Meeting (Executive Session: 7:00 – 10:00 a.m.)

(Open Session: 10:15 a.m. – 12:00 Noon) 7:00 a.m. – 2:00 p.m.

Case Presentation Competition 7:00 a.m. – 5:00 p.m.

Research Poster Competition 3:00 p.m.

Conference Registration Opens Exhibits Open 4:00 – 5:00 p.m.

Membership Meeting Registration 5:00 – 7:00 p.m.

Membership Meeting Tuesday, October 28 7:00 a.m. – 5:00 p.m.

Exhibits Open Resident Research Poster Presentation (on display) 8:00 a.m. – 1:00 p.m.

ACOEP Lectures 3:00 p.m. – 5:00 p.m.

ACOEP Lectures Wednesday, October 29 7:00 a.m. – 5:00 p.m.

Exhibits Open Resident Research Poster Presentation (on display) 7:30 – 11:30 a.m.

ACOEP Lectures 11:30 a.m. – 1:00 p.m.

FOEM-EMP Research Paper Presentations and Luncheon 1:00 p.m. – 5:00 p.m.

ACOEP Lectures 6:00 – 7:00 p.m.

Fellowship Ceremony 7:00 – 8:00 p.m.

Member Reception

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Thursday, October 30 6:30 – 7:30 a.m.

New Board Meeting 7:00 a.m. – 2:00 p.m.

Exhibits Open 7:30 – 11:30 a.m.

ACOEP Lectures 11:30 a.m. – 1:00 p.m.

Research Oral Abstract Presentation/ Competition Luncheon 1:00 p.m. – 5:00 p.m.

ACOEP Lectures Resident & Student Events Schedule Sunday, October 26 8:00 a.m. – 11:30 a.m.

Resident Jeopardy 8:00 a.m. – 6:00 p.m.

ACOEP Committee Meetings 9:00 a.m. – 12:00 Noon Student Lecture Series 11:30 a.m. – 1:00 p.m.

Resident Chapter Meeting & Luncheon 1:00 p.m. – 3:00 p.m.

Resident Ultrasound Course 2:00 p.m. – 4:00 p.m.

Student Residency Expo 3:00 p.m. – 5:00 p.m.

Resident Lecture Series 5:00 – 6:30 p.m.

Resident Chapter Reception Sponsored by ECI Monday, October 27 9:00 a.m. – 12:00 Noon Student Hands-On Clinic 2:00 p.m. – 4:00 p.m.

Student Membership Meeting 5:00 – 7:00 p.m.

ACOEP Membership Meeting 8:00 p.m.

Student Chapter New Board Meeting

Members in the News St. Barnabas Hospital, Emergency Medicine Department – Kudos go to the entire Staff of the Emergency Medicine Department at St. Barnabas Hospital in New York. The hospital’s Emergency Medicine Department was featured in three, one-hour segments of 911:The Bronx that aired on the Discovery Channel in late May. During these segments it showed emergency physicians handling the full gamut of emergency medicine encounters from the mundane to severe cases needing immediate medical intervention. Our congratulations go to their entire staff of physicians, nurses, and technicians. Bravo! We hear through the grapevine that the shows will air again in July/August and new segments may appear so watch your cable listings.

Peter A. Bell, D.O., FACOEP – On April 22nd, Dr. Bell was awarded the Columbus Osteopathic Association’s Advocacy Award. The Advocacy Award is granted annually to recognize long-term advocacy for community, patients, the osteopathic profession and student/ resident concerns.

New Fellows Announced At its meeting of March 27th, the Board of Directors of the ACOEP recognized the following physicians for Fellowship in the Association.

This prestigious award is based not only on physician membership, certification and service to the College, but on his or her individual service to the emergency medicine community. Based on this, the College annually reviews applications and is proud to announce the Fellows for 2008.

Fahim Shan Ahmed, D.O., West Islip, New York Dale Carrison, D.O., Las Vegas, Nevada Jack Chambers, D.O., Danielsville, Pennsylvania John Cunha, D.O., Lighthouse Point, Florida John DeSalvo, D.O., Tinley Park, Illinois

Julie Johns, D.O., Cave Creek, Arizona Sarah Minor, D.O., Hot Springs, Arkansas Michael Sheehy, D.O., Kingman, Arizona Matthew Wakeley, D.O., Mullica Hill, New Jersey John Zambito, D.O., Hartsdale, New York

We encourage physicians interested in seeking Fellowship in 2009 to check out our website to download the new application, the changes in the requirements for Fellowship and the new categories and revision in the qualifications for Fellowship are explained elsewhere in this edition of The Pulse. The deadline for application for Fellowship, Distinguished Fellow or Honorary Fellow categories is always March 1 and applications are taken the entire year, so don’t wait and apply at your leisure.

Important Dates for Board Certification / Recertification The AOBEM has supplied us with these dates in 2008 for anyone involved in the certification / recertification process during the calendar year of 2008. Please mark your calendars.

September 1

Application deadline for entry into the certification process of emergency medicine

September 14 -15

Part II Oral Examinations in Emergency Medicine, Philadelphia, Pennsylvania

November 1

Application deadline for CAQ Medical Toxicology

November 9 & 10

Part II Oral Examinations in Emergency Medicine, Chicago, Illinois

December 1

Submission of Part III (clinical) examination in emergency medicine

December 31

COLA 3 expires

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Ann M. Wittner “Shifts Gears” in Role at AOA Ann M. Wittner, AOA’s Associate Executive Director in charge of the Departments of Administration, Information Technology and Membership will leave the position she’s held for the past few years to become the Secretary to the Bureau of Conventions. Ms. Wittner was previously the Director of the Department of Administration and responsible for the administrative opera-tions, meeting arrangements for the AOA Board of Directors, House of Delegates and Convention Planning.

Ms. Wittner was also a key player in the establishment of the ACOEP assisting with the founding documents of our Association. She was made an Honorary Member of the ACOEP in 2004.

Ms. Wittner has been involved in the meeting industry in various capacities during her tenure with the AOA including being Vice Chair of the Convention Industry Council in 2001 and serves additional industry associations as a member of the Convene Magazine Advisory Council, the Membership Committee of the PCMA and the Holiday Showcase Committee of the Association Forum of Chicagoland.

We join the osteopathic profession in wishing Ms. Wittner well as she moves into her new position.

Updates on the ACOEP Web-based Database: In January, the ACOEP web-based database went LIVE on the ACOEP website offering members the opportunity to login and update their membership profiles online. We now invite you to begin using the other functionalities the database has to offer. Beginning July 1st, members will have the ability to register for events online and on August 1st, will have the ability to pay their dues and offer donations online.

If you have not already logged onto the site, we encourage you to go online and update your personal membership profile and become familiar with the database and the easy-to-use features it has to offer. To do so log onto our website (www.acoep.org) go into the “What’s New section” to the Temporary ACOEP Membership Log In section, click on “more” and use the temporary login with your “lastnameAOAnumber” (e.g. smith123456) and your password is “password.” If you have any questions regarding the database, please contact the ACOEP office (312) 587-3709 or email mandylundeen@acoep.org.

This database is an exciting step forward for ACOEP and we hope that each of you will find it to be a member-friendly resource.

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From the Pediatric Case Files...

Casey Miles, MD Anita W. Eisenhart, D.O., FACOEP, FACEP David Rosenberg. MD, FAAP, FCCM Roberto Murillo, MD, FAAP Pediatric Emergency Department Maricopa Integrated Health Systems Phoenix, Arizona

Purple Urine: A Presentation of Autoimmune Hemolytic Anemia in a 3-Year-Old Girl Introduction

The urine was dark brown with a purplish hue, again with few bacteria and the rest unable to be measured secondary to intensity of color. No RBC’s present and the color did not change with centrifuge. Since the patient had a 1 gm/dL drop in hemoglobin over 8 hours, a stool guaiac was performed (negative) as well as a CT scan of the chest, abdomen, and pelvis that showed no bleeding source, only a markedly distended bladder (figure 1).

Coombs was performed on previous and current blood samples. The initial study was weakly positive, and the most recent sample was direct coombs positive with complement present and negative for IgG. Haptoglobin was decreased at 10 mg/dL (normal=36-195 mg/dL). The antistreptolysin O (ASO) test was normal and the hepatitis panel was negative. Given the laboratory results, she was diagnosed with autoimmune hemolytic anemia (AIHA).

decreased activity, anorexia, and two membranes. She had mild tachypnea episodes of emesis described as non-bilious without retractions, and decreased breath Course Purple or brown urine in a child hasHospital a and non-bloody. sounds in the left base without wheeze or Initial management included a normal saline bolus of 20 ml/kg, and she was continued on 1.5 times maintenance IV fluids. A broad differential diagnosis, which includes;

The child was developmentally norcrackles.

Heart exam was remarkable for foley catheter was placed with good urine output. She was admitted to the general pediatric floor with serial CBC’s and metabolic panels ordered. Several serologies were sent, which included mycoplasma, Ebstein-Barr virus (EBV), coccidiomycosis (a prevalent infection mal, in the southwest), parvovirus, ANA, and anti-DNA; whichor weresurgical all negative. IgG sinus was low at tachycardia 337 mg/dL (normal=407-1509 a) hemolytic uremic syndrome (HUS) and had no other medical without any murmur. mg/dL). IgA and IgM were within normal limits. C3 complement was mildly decreased at 72 mg/dL (normal=79-152 mg/dL). C4 was normal. history. following a diarrhea or upper respiratory Her only recent medication was Abdominal exam was normal, with normal A pediatric hematology consult was obtained, and additional laboratory studies were ordered, including G6PD, Von Willebrand factor, and other clotting factors that were still pending at discharge. At 24 hours after initial presentation, she was started on illness, b) rhabdomyolysis from injury, illerythromycin ophthalmic ointment, which bowel sounds, and no hepatosplenomegaly methylprednisone 2 mg/kg every 6 hours.

Within 36 hours of initial presentation to the ED, her hemoglobin dropped to 5.6 gm/dL (figure 2). She was transferred to the ness, or metabolic/genetic disorders, c) foods the day nor Her skin pediatric was intensivediscontinued care unit (PICU) and received a totalprior of 150 mlto (10 presentaml/kg) packed red blood cells.masses.

After 96 hours, her steroids were was pale without changed to prednisone 2 mg/kg/day to complete at least a 2-week course before weaning. The duration of steroid taper was to be (beets, blackberries, fava beans, or food tion, and ibuprofen taken every six hours for jaundice and without petechiae. The rest of determined at follow up with the pediatric hematologist after repeat laboratory testing.

During her hospital course, she developed a urinary tract infection that was positive for >100,000 E. Coli and enterococcus, coloring) or drug (metronidazole, nitrofthe past two days.

There was no personal her exam was within normal limits. and she was treated with ceftriaxone and then discharged on amoxicillin. She was hospitalized a total of seven days. At discharge, her hemoglobin was stable at 9.7 gm/dL, and her reticulocyte count had increased to 9.7%. She was started on folic acid 1 mg/day at discharge. urnatoin, senna, or chlorquine) ingestion, or family history of hematologic or kidney The initial workup included a chest The patient presented to the ED for the 3 time on the 3 day after hospital discharge with watery diarrhea. Her vital signs were normal, she was afebrile,On and she appeared well exam.

Hemoglobin was stable gm/dL. At follow up, her hemoglobinwas was d) post-streptococcal glomerulonephridisease. review of onher clinic chart, herat 9.4 radiograph which normal, and a stable at 10.1 gm/dL, and urinalysis was clear, and without blood. tis, and e) intrinsic red blood cell (RBC) Figure 1. CT scan revealing distended bladder, catheterized urinalysis and culture. The membrane/enzyme defects or autoimmune urine was dark purple and the urinalyretention.

Figure 1. urinary CT scan revealing distended bladder, urinary retention. hemolytic anemia. sis reveled the following: specific gravity We present a case of a 3-year-old girl 1.023, dark red color, few bacteria, 0-2 with purple urine, consistent with the diaghyaline casts, 3-5 granular casts, protein, nosis of autoimmune hemolytic anemia. glucose and ketones were not measured Autoimmune hemolytic anemia (AIHA) is secondary to intense color. The laboratory a collection of disorders characterized by was contacted, and the urine was reviewed. premature red cell destruction secondary No RBC’s were present in the urine to autoantibodies that bind to a patient’s supernatant. A basic urine toxicological erythrocytes and lead to their destruction. screen was also negative.

Further laboratory tests included a Case hemoglobin six months prior to presenta- complete blood count (CBC) with white tion was 12.6 gm/dL, and her lead screen blood cell (WBC) of 9.8 gm/dL, hemoglobin A 3-year-old girl presented to the was <5 u/dL (normal).

9.3 gm/dL, hematocrit 26.1%, and platelets Emergency Department (ED) with diffuse On first presentation to the ED, her 244 K/uL, with normal red blood indices, abdominal pain and red-orange urine with vital signs included a heart rate of 146 including mean corpuscular volume 81 FL a strong odor, per her mother’s descrip- beats per minute, respiratory rate of 22 and RBC distribution width 12.3 K/uL, and tion. She had a history of conjunctivitis breaths per minute, oxygen saturation of no schistocytes or spherocytes. Reticulocyte six days prior, treated with erythromycin 97% on room air, blood pressure 104/71 count was low at 1.9%. Chemistries revealed ophthalmic ointment, and a 5-day history mmHg, and temperature 39.9oC. In a sodium of 133 mEq/L, potassium 4.0 of cough, congestion, and rhinorrhea. She general, she was well-developed and mEq/L, chloride 101 mEq/L, bicarbonate was seen two days prior in the ED and well-nourished, non-toxic appearing, and 22 mEq/L, blood urea nitrogen 18 mg/dL, diagnosed with an upper respiratory tract lying on the examination table in no dis- creatinine 0.4 mg/dL, glucose 137 mg/dL, infection. Since discharge from the ED, she tress. She had no scleral icterus, and her calcium 9.1 mg/dL, total bilirubin 3.3 developed a fever (T max: 40oC (104oF)), oropharynx was clear with moist mucous mg/dL with indirect bilirubin 2.7 mg/dL rd

10

rd

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Figure 2. Hemoglobin and Reticulocyte Trend

Figure 2. Hemoglobin and Reticulocyte Trend

Hemoglobin and Reticulocyte Trend 14

10 9

12

8

10

7 6

8

5

6

4

*

4

3 2

2

Reticulocyte Count (%)

Hemoglobin (gm/dL)

* Transfusion

1

0

5

0

28

24

1 16

7 13

3

3

11

10

91

83

75

63

55

47

40

33

31

23

14

8

0

6

m

on

th

s

pr

io

r

0

Tim e (hours) Hemoglobin

Reticulocyte Count

and direct bilirubin 0.2 mg/dL, elevated Glutamyl Transpeptidase (GGT) was normal Hospital Course aspartate aminotransferase (AST) 142 u/L, at 18 u/L. Creatine Phosphokinase (CPK) and normal alanine aminotransferase (ALT) was elevated at 306 u/L (normal=30-125 Initial management included a normal Discussion 16 u/L. Since the child was clinically stable, u/L), and LDH was also elevated at 9099 saline bolus of 20 ml/kg, and she was with only mild anemia with normal indices, u/L (normal=313-618 u/L). continued on 1.5 times maintenance IV Autoimmune hemolytic anemia (AIHA) has an annual incidence of 1 in 80,000 persons in the general population [1]. It affects and without hemolysis, we determined she fluids.

A foley the catheter withcells. When

The urine was dark brown with a children of all races and can present at any age. In all types of AIHA, the autoantibody decreases life ofwas the placed red blood may have ingested a dye that was intergood urine output.

She was admitted to the signs and purplish hue, again with few bacteria and the rate of hemolysis exceeds the ability of the bone marrow to replace the destroyed red cells, the patient develops fering with her laboratory tests, or that general pediatric floor with serial CBCâ&#x20AC;&#x2122;s and the rest unable to be measured secondary symptoms of anemia, including; tachycardia, weakness, shortness of breath, dizziness, systolic flow murmur, pallor, jaundice, and/or she was suffering a mild as hemolytic ordered. result Severalinseroloto intensity of color. No present andred metabolic dark urine.

AIHA from is classified either primary or secondary.

InRBCâ&#x20AC;&#x2122;s primary AIHA, blood cell panels autoantibodies hemolysis of the erythrocytes, but without evidence an underlying systemic illness. onlysent, onewhich manifestation of a broader systemic process. She was discharged home tooffolgiesiswere included mycoplasma, the color did not change withSecondary centrifuge.AIHA disease. low up the next day with her primary care Since the patient had a 1 gm/dL drop in Ebstein-Barr virus (EBV), coccidiomycosis Primary be subclassified based on specific characteristics of the autoantibodies.

Theseinautoantibody characteristics doctor and have allAIHA tests can repeated to see if hemoglobin (a prevalent infection the southwest), over 8 hours, a stool guaiac include: theclearing. type of antibody, its optimal temperature, fix complement the clinical the dye was parvovirus, ANA, andaffect anti-DNA; which and cause wasbinding performed (negative) asand wellthe as aability CT to intravascular hemoglobinemia, and anemia. is IgG intravascular, The child hemolysis returned to with the ED 8 hours scan hemoglobinuria, werehemolysis all negative. was low at the 337patient mg/ does not of the chest, abdomen, and pelvis Since that the develop organomegaly. later with persistent vomiting and no urine showed no bleeding source, only a markedly dL (normal=407-1509 mg/dL). IgA and The third subclassification of primary AIHA is cold agglutinin disease. It is relatively rare in children, but can occur after an output since catheterization in the ED. distended by were within limits. complebladder 1). infection with mycoplasma. It is characterized IgM (figure autoantibodies binding IgM erythrocyte I/I normal antigens at C3 colder temperatures, Her vital signs were essentially unchanged. ment was mildly decreased at 72 mg/dL

Coombs was performed on previous and complement fixation, leading to either complement-mediated intravascular hemolysis or immune-mediated extravascular clearance by Physicalmacrophages, exam was now significant for macrophages. current blood samples. The initial study (normal=79-152 mg/dL). C4 was normal. hepatic rather than splenic worsening pallor and a 2/6 systolic ejection was weakly positive, and the most recent A pediatric hematology consult was murmur. The patient had neither jaundice sample was direct coombs positive with obtained, and additional laboratory studnor hepatosplenomegaly. complement present and negative for IgG. ies were ordered, including G6PD, Von Table 1. Primary AIHA Types Classified Laboratory Characteristics, and Treatment Laboratory evaluation was repeated, and byHaptoglobin factor, and other clotting facwas decreased atPathophysiology, 10 mg/dL Willebrand Paroxysmal her hemoglobin had decreased toWarm 8.1 gm/dL reactive tors that were still pending at discharge. At (normal=36-195 mg/dL). The antistrep- cold Parameter AIHA hemoglobinuria Cold disease she was with a hematocrit of 22.7%. Her reticulo- tolysin O (ASO) afteragglutinin initial presentation, test was normal and the 24 hours Autoantibody isotype IgG Blood hepatitis panel IgG was negative. Given the started IgM cyte count remained low at 1.5%. on methylprednisone 2 mg/kg every Optimal thermal urea nitrogen, creatinine, direct and indirect laboratory results, she was diagnosed with 6 hours. reactivity Warm Cold36 hours of initial presentation bilirubin, and aspartate aminotransferase Within autoimmuneCold hemolytic anemia (AIHA).

Ability to fix (AST) were essentially unchanged.

Gamato the ED, her hemoglobin dropped to complement Positive DAT (Coombs) Erythrocyte autoantigen Type of hemolysis

Variable IgG, +/- C3 Rh, others Extravascular

Clinical Presentation

Organomegaly

Yes C3, +/- IgG P The PULSE JULY 2008 Intravascular Hemoglobinuria

Yes C3 I or i Both Organomegaly, hemoglobinuria

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complement fixation, leading to either complement-mediated intravascular hemolysis or immune-mediated extravascular clearance hepatic macrophages, rather than splenic macrophages.

Figure 3. Primary AIHA Types Classified

by Laboratory Characteristics, Pathophysiology and Treatment Table 1. Primary AIHA Types Classified

by Laboratory Characteristics, Pathophysiology, and Treatment

Parameter Autoantibody isotype Optimal thermal reactivity Ability to fix complement Positive DAT (Coombs) Erythrocyte autoantigen Type of hemolysis Clinical Presentation First-line therapy Secondary therapy

Warm AIHA IgG

reactive

Paroxysmal hemoglobinuria IgG

cold Cold agglutinin disease IgM

Warm

Cold

Cold

Variable IgG, +/- C3 Rh, others Extravascular

Yes C3, +/- IgG P Intravascular

Organomegaly Corticosteroids Splenectomy

Hemoglobinuria Avoidance of cold Corticosteroids

Yes C3 I or i Both Organomegaly, hemoglobinuria Avoidance of cold Plasmapheresis

5.6 gm/dL (figure 2). She was transferred to the pediatric intensive care unit (PICU) and received a total of 150 ml (10 ml/kg) packed red blood cells. After 96 hours, her steroids were changed to prednisone 2 mg/ kg/day to complete at least a 2-week course before weaning. The duration of steroid taper was to be determined at follow up with the pediatric hematologist after repeat laboratory testing.

During her hospital course, she developed a urinary tract infection that was positive for >100,000 E. Coli and enterococcus, and she was treated with ceftriaxone and then discharged on amoxicillin. She was hospitalized a total of seven days. At discharge, her hemoglobin was stable at 9.7 gm/dL, and her reticulocyte count had increased to 9.7%. She was started on folic acid 1 mg/day at discharge.

The patient presented to the ED for the 3rd time on the 3rd day after hospital discharge with watery diarrhea. Her vital signs were normal, she was afebrile, and she appeared well on exam. Hemoglobin was stable at 9.4 gm/dL. At follow up, her hemoglobin was stable at 10.1 gm/dL, and urinalysis was clear, and without blood.

develops signs and symptoms of anemia, including; tachycardia, weakness, shortness of breath, dizziness, systolic flow murmur, pallor, jaundice, and/or dark urine. AIHA is classified as either primary or secondary. In primary AIHA, red blood cell autoantibodies result in hemolysis of the erythrocytes, but without evidence of an underlying systemic illness. Secondary AIHA is only one manifestation of a broader systemic disease.

Primary AIHA can be subclassified based

on specific characteristics of the autoantibodies. These autoantibody characteristics include: the type of antibody, its optimal binding temperature, and the ability to fix complement affect the clinical and cause intravascular hemolysis with hemoglobinemia, hemoglobinuria, and anemia. Since the hemolysis is intravascular, the patient does not develop organomegaly.

The third subclassification of primary AIHA is cold agglutinin disease. It is

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Discussion Autoimmune hemolytic anemia (AIHA) has an annual incidence of 1 in 80,000 persons in the general population [1]. It affects children of all races and can present at any age. In all types of AIHA, the autoantibody decreases the life of the red blood cells. When the rate of hemolysis exceeds the ability of the bone marrow to replace the destroyed red cells, the patient

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relatively rare in children, but can occur after an infection with mycoplasma. It is characterized by IgM autoantibodies binding erythrocyte I/I antigens at colder temperatures, complement fixation, leading to either complement-mediated intravascular hemolysis or immune-mediated extravascular clearance by hepatic macrophages, rather than splenic macrophages.

Secondary AIHA is more like to present in adolescents with an underlying systemic illness, including: systemic autoimmune or inflammatory disorders (ie, systemic lupus erythematosus, Sjogren syndrome, scleroderma, rheumatoid arthritis, dermatomyositis, ulcerative colitis, and autoimmune thyroiditis) [5]; human immunodeficiency virus (HIV); Evans syndrome (AIHA and idiopathic thrombocytopenic purpura); autoimmune lymphoproliferative syndrome (ALPS); and malignancy (ie, Hodgkin disease, acute leukemia, and myelodysplasia).

Laboratory evaluation for autoimmune hemolytic anemia should include a CBC with differential and indices, reticulocyte count, peripheral blood smear, urinalysis, direct antiglobulin (DAT) or coombs test, comprehensive metabolic panel (CMP) with fractionated bilirubin, aspartate aminotransferase (AST) and alanine aminotransferase (ALT). If the Coombs test is positive, the laboratory should identify IgM or IgG type autoantibodies, and if complement is present.

The leukocyte and platelet count should be normal or elevated. Leukopenia or thrombocytopenia suggests the presence of bone marrow failure. RBC indices are often normal and the reticulocyte count is usually elevated. However, if the reticulocyte count is low, it may be secondary to a delayed bone marrow response to hemolysis, temporary suppression from infection, or an accelerated immune-mediated destruction of red blood precursors in the marrow.

The peripheral smear may show spherocytes (especially in warm reactive AIHA), teardrop cells, or schistocytes. In severe hemolysis, red blood cell precursors may be present. Urinalysis may be normal if the child has extravascular hemolysis. If intravascular hemolysis is present, hemoglobin is released into the plasma and cleared through the kidneys into the urine. Therefore, the urine dipstick will reveal the presence of

blood, but microscopic examination will be negative for red blood cells.

Direct antiglobulin (Direct Coombs) test is the most important and useful laboratory test to diagnosis AIHA because it detects the presence of antibodies (and isotype of antibody if present) and/or complement on the surface of the erythrocytes. If an antibody is present, it can be tested for thermal reactivity and specificity binding to erythrocyte antigens. If the DAT is negative, an antibody may still be present. The amount of IgG on the erythrocyte may be below the threshold for detection, or the antibodies may be IgM or IgA, which are not reactive with standard Coombs reagent. Consider contacting the laboratory for special testing for IgM and IgA antibodies. On chemistry studies, the total and indirect bilirubin, lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) are often elevated.

Serum haptoglobin should be low, since it binds to free plasma hemoglobin.

Initial management in the ED includes fluid resuscitation and the patient should be admitted to either the general pediatric floor or PICU, based on hemodynamic stability. Further treatment with corticosteroids, packed red blood cell transfusion, or avoidance of cold is dependent on the type of AIHA (table 1). IVIG is rarely effective in the treatment of AIHA in children. In patients with cold agglutinin disease, plasmapheresis is an option. IgM is a larger molecule than IgG, and is found mostly within the intravascular space loosely bound to erythrocytes.

Splenectomy is a treatment option for AIHA with IgG autoantibodies that result in splenic sequestration and splenomegaly.

Upon discharge, patients are often started on iron and/or folic acid supplements.

ence of spherocytes and schistocytes. It is also important to determine the type of AIHA to guide further management.

Our patient had primary AIHA. The autoantibody was direct coombs positive on serologic studies, with complement, and without the presence of IgG. These autoantibody characteristics are consistent with a diagnosis of paroxysmal cold hemoglobinuria. She was treated with corticosteroids, transfusion, and avoidance of cold.

References 1. Gehrs BC, Friedberg RC. Autoimmune hemolytic anemia. Am J Hematol 2002; 69:258.

2. Ware RE. Autoimmune Hemolytic Anemia in Children. UpToDate.com.

Updated Feb. 2008.

3. Habili B, Homberg JC, Schaison G, Salmon, C. Autoimmune hemolytic anemia in children. A review of 80 cases. Am J Med 1974; 56:61.

4. Gottsche B, Salama A, Mueller-Eckhardt C. Donath-Landsteirner autoimmune hemolytic anemia in children. A study of 22 cases. Vox Sang 1990; 58:281.

5. Engelfriet CP, Overbeeke MA, Borune von vem AE. Autoimmune hemolytic anemia. Semin Hematol 1992; 29:3.

Conclusion This case illustrates the rapid development of anemia from hemolysis and the need to utilize laboratory staff in assisting with the diagnosis of a hemolytic anemia.

If a urine specimen is dark and difficult to analyze with standard laboratory equipment, it should be reviewed manually by laboratory staff. If autoimmune hemolytic anemia is considered in the differential diagnosis, a peripheral blood smear should be reviewed by a pathologist for the pres-

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13

Guest Column Thomas A. Brabson, D.O., FACOEP President Elect

Preparing for the Future As I prepare for taking the Oath of Office as President of the American College of Osteopathic Emergency Physicians, I want to reach out to the College members to invite them to help me lead the ACOEP to the next level of excellence. I also want to inform you of some changes that will be instituted with the College and the Scientific Assembly.

Each President of the ACOEP brings certain aspirations and tasks that he or she hopes to accomplish during the two-year term in Office. One of the items that I hope to achieve is the growth of involvement in the College by all of our physician members, regardless of their member status.

From Student Member through Resident Member and up through Active and Life Members, I want to utilize our resources to increase the involvement of our members in College Committees and events. I ask you to communicate with me on how you want to become involved and share your expertise and talents with our College.

Currently, I ask those members who wish to be involved as Committee members to submit their current CV’s with a brief letter explaining what Committees they are interested in serving on. These can be sent electronically to either Jan Wachtler or Yvonne Treacy (janwachtler@acoep.org or yvonnetreacy@acoep.org), fax your information to 312-587-9951 or simply mail the information to the ACOEP. I will be making my appointments during the last quarter of the year and all appointments will take effect on January 1, 2009.

If you are not interested in becoming Committee members, the College is always looking for new inspectors to assist the Committee on Graduate Medical Education to evaluate our existing training programs or reviewing applications for new programs. To be an inspector, you will have to be certified in emergency medicine or any combined specialty or subspecialty of emergency medicine. It is helpful if you are

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currently or have been core faculty to a residency program (osteopathic or allopathic) and can travel, sometimes on as little as 12 weeks notice. New or junior inspectors, will be required to accompany experienced inspectors on one or two inspection visits and to attend an inspectors workshop that is incorporated into the Program Directors Workshop. The next inspectors workshop will take place during the 2009 Program Directors Workshop in Marco Island, Florida during the first week of February. If you are interested in taking advantage of this opportunity, you need to send your CV, noting your interest in becoming an inspector.

Beginning this fall, we will institute changes in the Fellowship process and you will see a more streamlined process to become a Fellow of the College. The rules for Fellowship now require physicians to attend 3 membership meetings over a 3½-year period. These requirements have now been streamlined to allow prospective Fellows to attend 2 membership meetings and 2 College-sponsored CME meetings over 5 years. Additionally, the criteria for service have been broadened and now include service to the Foundation, AOBEM, as well as the College. A new application is now up on the College’s website and is available through the ACOEP for all interested parties.

For those physicians who are currently Fellows of the College, there is now a mechanism in place to award a Distinguished Fellow status. Eligible physicians for this designation will have gone beyond the general criteria for Fellowship by being professionally active in recognized national, state or local emergency medicine organizations; involved in significant ongoing emergency medicine research endeavors; development of clinical training programs; emergency medicine service that has received national, state, or regional recognition, including excellence in teaching. To be considered

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for this prestigious award, physicians must be current Fellows of the ACOEP and must present a letter of nomination outlining the reason for this designation. All applications must be accompanied by a current curriculum vita. This can be a selfnominated award or physicians may be nominated by their peers. The ACOEP will contact the nominee to request a current curriculum vita for further consideration by the Fellowship and Nominations Committee.

Like the Fellowship, all applications/nominations must be received annually by March 1st for the Awards Ceremony at that year’s Scientific Assembly. Distinguished Fellows will utilize the acronym of FACOEP (Dist.) after their name.

Similarly, Honorary Members may qualify for Fellowship in the ACOEP if they have gone above and beyond in service to the specialty of emergency medicine or have made significant contribution to the development of a training program in emergency medicine. Any current Fellow or Distinguished Fellow of ACOEP may nominate an Honorary Member for Fellowship by outlining the person’s contributions to the profession and explaining why he/she should be granted this designation.

As advertised over this past year, the College will host its inaugural Scientific Assembly in the fall at Caesar’s Palace.

Members may register at a reduced rate of $425 through August 31st. This is a savings to members of $125 over last year’s registration costs. We encourage you to take advantage of this savings as well as savings on room rates. Please check our website for exact details. A schedule of events also appears in this issue of The Pulse.

I am looking forward to working with you all in the next few months prior to my inauguration and during my presidency as we work to make the ACOEP a better emergency medicine organization and building member confidence and participation.

Medical Update Steven J. Parrillo, D.O., FACOEP

Rheumatic Fever Acute rheumatic fever (ARF) is still around.

This disease causes chronic progressive damage to the heart and its valves. Until 1960, it was a leading cause of death in children and remains a common cause of structural heart disease. The association between sore throat and rheumatic fever made in 1880, while the connection with scarlet fever was made in the early 1900s. The Jones criteria were first formulated in 1944 to assist disease identification.

Modified in 1984, these criteria are still used. The introduction of antibiotics in the late 1940s allowed for the development of treatment and preventive strategies.

The dramatic decline in the incidence of rheumatic fever is thought to be due in large part to antibiotic treatment of streptococcal infection.

ARF is non-infectious sequelae of a group A streptococcal infection, usually of the upper respiratory tract. Only certain subtypes can elicit the inflammatory response. Most agree that genetic susceptibility also plays a role.

ARF involves the heart, joints, central nervous system, skin, and subcutaneous tissues. It is characterized by an exudative and proliferative inflammatory lesion of the connective tissue, especially that of the heart, joints, blood vessels, and subcutaneous tissue.

Disease prevalence in the US is a function of socioeconomic status, with higher frequency in areas of crowding. The US had experienced a resurgence of rheumatic fever in the last 2 decades with many of the reported cases involving persons in upper socioeconomic groups, possibly caused by of more virulent strains of group A streptococci. The overall incidence has been declining in developed nations but is still rampant in less developed ones.

The incidence is low in most parts of the country but is variable. There were 121 new cases in western Pennsylvania from 1994 to 2003. Consistent with earlier

reports, most patients were children and most had carditis.

Frequency of streptococcal infection and virulence of the bacterial strain determine the incidence of rheumatic fever in the population. As sequelae of beta-streptococcal exposure, ARF occurs during school years when streptococcal pharyngitis is most prevalent. Similarly, prevalence is higher in the colder months of the year when streptococcal pharyngitis is most likely to occur.

Morbidity from ARF is directly proportional to the rate of streptococcal infections.

Infections that are not treated adequately are most likely to cause the major findings noted in the Jones Criteria. Cardiac involvement is the major cause of long-term morbidity. Valvular vegetations (endocarditis) are the cause of mitral valve regurgitation, the end result being LV dilation and CHF. Myocarditis is present but not the cause of heart failure. Those with carditis as part of the initial episode are at greater risk of developing recurrences and of sustaining further cardiac injury. Those without carditis during the initial episode have a relatively low risk of developing carditis during recurrences, though such cases have been reported. Migratory polyarthritis occurs early in the disease course and is a common complaint for patients with rheumatic fever.

Joint involvement ranges from arthralgia without objective findings to overt arthritis with warmth, swelling, redness, and exquisite tenderness. The larger joints are involved most frequently, such as the knees, ankles, elbows, and wrists. An inverse relationship between severity of joint involvement and risk of carditis appears to exist.

In the U.S. attack rate is more a function of crowding than race, though the socioeconomic realities of those crowded conditions is no doubt is a factor. No gender predilection exists for diagnosis, but mitral valve prolapse and Sydenhamâ&#x20AC;&#x2122;s chorea occur more often in females than in males.

Although individuals of any age group

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may be affected, most cases are reported in persons aged 5-15 years. Rheumatic pericarditis and myocarditis are some of the cardiac emergencies in the first year of life.

ARF is associated with 2 distinct patterns of presentation. In the first type, presentation is sudden onset, beginning as polyarthritis 2-6 weeks after streptococcal pharyngitis and usually characterized by fever and toxicity. If the initial abnormality is mild carditis, ARF may be insidious or even subclinical.

Guidelines of diagnosis used by the American Heart Association include major and minor criteria (i.e., modified Jones criteria). In addition to evidence of a previous streptococcal infection, the diagnosis requires 2 major Jones criteria or 1 major plus 2 minor Jones criteria.

Major criteria o Carditis: May include cardiomegaly, new murmur, congestive heart failure, and pericarditis, with or without a rub and valvular disease. o Migratory polyarthritis: polyarticular, fleeting, involves the large joints. o Subcutaneous nodules (i.e., Aschoff bodies): These are edematous, fragmented collagen fibers that are firm and painless located on the extensor surfaces of the wrists, elbows, and knees. o Erythema marginatum: Rash is serpiginous and long lasting. o Chorea (also known as Sydenhamâ&#x20AC;&#x2122;s chorea and "St Vitus dance"): Consists of rapid, purposeless movements of the face and upper extremities. Onset may be delayed for several months and may cease when the patient is asleep.

Minor criteria o Clinical findings - arthralgia, fever and previous history of ARF o Laboratory findings - elevated acute phase reactants (e.g., erythrocyte sedimentation rate, C reactive protein), a prolonged PR interval, and evidence of antecedent group A streptococcal infections (i.e., posi-

15

tive throat culture or rapid streptococcal screen and an elevated or rising streptococcal antibody titer).

Specific confirmatory laboratory tests do not exist. However, several laboratory findings indicate rheumatic inflammation.

Some are part of the Jones minor criteria. Streptococcal antibody tests disclose preceding streptococcal infection.

Streptococci may be isolated on occasion via throat culture. Acute phase reactants (e.g., erythrocyte sedimentation rate [ESR], C-reactive protein [CRP] in serum) may be prolonged or elevated. Anemia is usually caused by suppression of erythropoiesis. PR interval prolongation is present in approximately 25% of all cases and is neither specific to nor diagnostic of ARF. Synovial fluid analysis may demonstrate an elevated white blood cell count with no crystals or organisms.

Echocardiography may be very helpful in establishing carditis. Chest film may show cardiomegaly or congestive heart failure, both signs of carditis.

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The emergency medicine physician's primary responsibilities are to suspect the diagnosis and to treat complications.

Antibiotics are a mainstay. Penicillin is the drug of choice and macrolides may be used in the penicillin-allergic. Most still believe that ARF usually is preventable if antibiotics are initiated within 9 days of the onset of streptococcal infection. It has been estimated that the number needed to treat to prevent one case of ARF is 100.

Medical therapy also involves steroids and salicylates both of which are useful in the control of pain and inflammation. Heart failure may require digitalis, fluid & sodium restriction, diuretics and oxygen. Prophylaxis against GABHS infections is indicated in patients who have had ARF. Most authorities suggest that prophylaxis be given for 5 years. For those who have rheumatic carditis, some authorities suggest life-long prophylaxis.

Phenobarbital and haloperidol may be helpful in controlling chorea.

It is worth noting that differences exist among nations in terms of diagnosing and

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treating GABHS pharyngitis. Most North American, French and Finnish guidelines consider diagnosis of strep essential (with either rapid antigen detection or with formal culture) and advise antibiotic therapy when strep is detected. Several European guidelines consider strep a self-limited disease and do not recommend antibiotics.

Whatâ&#x20AC;&#x2122;s new? Some authors have suggested that it may be time to revise the Jones criteria again. Possible changes include a lower threshold for fever, inclusion of arthralgia as a major (rather than minor) criterion, acceptance of monoarthritis instead of just polyarthritis and echocardiographic determination of carditis on all suspected cases.

Finally, a vaccine may be on the horizon. Phase I trials of a 6-valent and a 26-valent vaccine have shown promise.

Phase II trials should begin very soon.

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Student Case Competition Anne Newbold, MSIII University of New England College of Osteopathic Medicine Chief Complaint (8/15/07, 11:26a): Shortness of breath, chest pain, and lower abdominal pain History of Present Illness: Patient is a 48y/o female who presents to the Emergency Department with complaints of shortness of breath, chest pain, and lower abdominal pain. The onset of shortness of breath and chest pain began today, but the abdominal pain began 2 days ago and has been constant since. Ibuprofen alleviates some of the abdominal pain. Pain has a cramping quality that is located across the lower abdomen but does not radiate. Patient describes chest pain and shortness of breath as both being moderate in severity.

The patient is status post an endometrial biopsy on 8/2/07 for menorrhagia. One week after the procedure she used a tampon for watery discharge, which she states she always experiences. However, she states at that time the discharge was malodorous.

The tampon was inadvertently left in the vagina for 2 days and then removed by the patient.

The patient was then seen at the Emergency Department of a different hospital one-day prior with a chief complaint of lower abdominal pain and cramping that started in the morning. A transvaginal ultrasound showed a hyperemic enlarged right ovary with a dilated tube. She was treated for pelvic inflammatory disease with Ceftriaxone, Toradol (2 doses), and Morphine in triage. She was then sent home and treated as an outpatient. She was given a prescription for both Doxycycline and Percocet.

Currently she denies fever, but does admit to having chills. She states she had diarrhea and vomiting two nights ago that had resolved yesterday. However, she admits to vomiting a few times today but denies hematemesis. She admits to having a decreased appetite and is not tolerating food or liquids well. She denies constipation, jaundice, difficulty swallowing, heartburn,

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rectal bleeding, black or tarry stools, or hemorrhoids. She admits to having palpitations, but denies tachycardia, hypertension, and edema. She denies cough and wheezing. Her last normal menses started two days ago.

Past Medical and Surgical History: Past medical history is negative. Past surgical history is significant for an endometrial biopsy on 8/2/07 that showed polypoid proliferation of the endometrium with glandular and stromal breakdown. It also showed an endocervical polyp.

Medications and Allergies: Percocet (5/325mg 1-2 tabs p.o. every 4-6 hours prn pain), Doxycycline (100 mg p.o. twice a day for 14 days), and Ibuprofen (600mg 1 tab p.o. prn pain). Patient has no known drug allergies.

Review of Systems: Review of systems negative for HEENT, urinary, vascular, musculoskeletal, psychiatric and neurologic systems.

Physical Exam: General appearance: Patient is alert and oriented to person, place, and time. She is in severe distress.

Skin: Skin is pale, warm, and moist. No lesions noted.

HEENT: Unremarkable Thorax and Lungs: Thorax symmetric with good excursion. Upon auscultation the lungs have rales at the bases bilaterally. No wheezing or rhonchi. No chest wall tenderness upon palpation.

Cardiovascular: Normal S1 and S2 heart sounds present. No S3 or S4 heart sounds auscultated. No murmurs, rubs, or gallops.

Abdomen: Positive bowel sounds. There is generalized tenderness to palpation in left and right lower quadrants with guarding present. There is no rigidity or distention.

No hepatomegaly or splenomegaly is appreciated. No pulsitile masses are noted. There

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is no costovertebral angle tenderness.

Genitalia: Pelvic exam shows external genitalia without lesions. Vaginal and cervical mucosa are pink and without lesions.

Menstrual blood is noted on examination.

The bimanual exam shows an enlarged but non-tender uterus. No cervical or adnexal tenderness appreciated.

Extremities: Warm and without edema.

Negative Homanâ&#x20AC;&#x2122;s sign.

Peripheral Vascular: No edema in lower extremities bilaterally. Posterior tibial, femoral, and radial pulses strong and intact.

Vital Signs: Temperature:37.6°C Blood Pressure: 87/30 mmHg Respiratory Rate: 50 breaths per minute Heart Rate: 130 beats per minute 0xygen saturation: 81% (room air) Imaging: CT of the abdomen/pelvis: Infiltrate or atelectasis in both lung bases.

Free intraperitoneal air and intraperitoneal pelvic fluid. Inflammatory changes in the mesenteric fat. Cholelithiasis. Transvaginal ultrasound showed a large hyperemic right ovary. Evaluation of the right adnexa was limited secondary to overlying gas. Chest x-ray inconclusive.

EKG: Sinus Tachycardia Diagnostic Impression: Septic shock and peritonitis Plan of Disposition: The sepsis team was called for the patient. A re-examination at 12:04pm showed her blood pressure was 82/53 after receiving two liters of fluids IV. Additional IV fluids were then given.

Re-examination at 12:30pm showed she was still hypotensive after receiving additional fluids.

The patient was transferred to the Intensive Care Unit for continued care.

At 7:00pm the patient went to surgery for a pre-operative diagnosis of perforated viscous and septic shock. As the surgeons entered the abdomen, they encountered a large amount of greenish, thin fluid without odor. It seemed to be coming

from the right upper quadrant of the abdo- and was in a coma secondary to this. Two bowel perforation or in association with a men, and they thought it was most likely days later it was confirmed that she had pelvic malignancy [3]. In this patient, the from a perforated ulcer. However, after developed PRES, or posterior reversible formation of her TOA was likely secondary a thorough exploration they could not encephalopathy syndrome. to PID from a retained tampon. discover the source of the fluid. Finally, the PID arises from the spread of pathogens surgeons explored the uterus and ovaries Fortunately, this patient recovered from via the lumen of the reproductive organs. only to discover purulent discharge oozing the PRES with tight blood pressure control These pathogens then enter the pelvic from the right fallopian tube. The patient and eventually almost fully recovered from peritoneal cavity via the tubal ostea where then underwent a total abdominal hysterec- the multi-organ damage that she endured. infected surfaces agglutinate in immunotomy and bilateral salpingo-oophorectomy However, her road to recovery was not easy. compromised patients. An abscess forms as a result. 1100 mL of purulent fluid was She had to learn to speak again after the when bacteria, leukocytes, and fluids collect removed from the patient’s abdomen over- coma left her aphonic. She had to learn to within the enclosed space of the ostea. Since all. The post-operative diagnosis forLaboratory this and Ancillary Data: Data: Laboratory and Ancillary patient was a ruptured tubo-ovarian abscess WBC: 2.0 x 10 (3) critical Glucose: 122 mg/dL Bilirubin total: 2.0 mg/dL (TOA) and septic shock.

RBC: 4.16 X 10 (6) Urea nitrogen: 42 mg/dL Bilirubin direct: 0.77 mg/dL Hb: 12.3 g/dL Creatinine: 4.10 mg/dL AST: 273 intnl unit/L Her course in the ICU was unusual and Hct: 37.1% Sodium: 139 mmol/L ALT: 64 intnl unit/L interesting, requiring prolonged ventilaMCV: 89.1 fL Potassium: 3.4 mmol/L Alkaline phos: 56 intnl unit/L MCH: 29.5 pg/dL Chloride: 101 mmol/L Total protein: 5.2 g/dL tor support. She initially developed renal MCHC: 33.1 g/dL Carbon dioxide: 18 mmol/L Amylase: 54 intnl unit/L failure and global myocardial suppression RDW: 13.3% Lipase: 15 intnl unit/L Platelet: 293 x 10 (3)/ mcL Albumin: 2.4 g/dL secondary to the sepsis. She also had MPV: 7.9 fL Troponin-I: 0.03 ng/mL respiratory failure secondary to pulmonary Diff: neutrophils 5%, bands Brain natriuretic peptide (BNP): 41%, lymphocytes 19%, 909 pg/mL edema. The following day she developed monocytes 3%, eosinophils 5% HCG, urine: negative hyperthermia, ischemic toes and fingers, metamyelocytes 25%, myelocytes 2% and continued lactic acidosis. By the third PT: 12.7 d-dimer: 4.1 mcg/mL Lactic acid: 9.6 mmol/L day of her ICU admission, she had a severe INR: 1.3 fibrinogen: 1256 mg/dL CK: 2981 intnl unit/L PTT: 26.4 Urinalysis: negative CKMB: 90.10 ng/mL thrombocytopenia and a WBC count that Thrombin time: 14.5 sec CK index: 3.02 was climbing at alarming rates. She was Labs at 13:06: Labs at 14:14 becoming less alert and by the fourth day Repeat CBC (complete blood count) showed the Arterial Blood Gas (ABG): after admission she was in acute respiratory following abnormal values: pH: 7.16 WBC: 11.3 x 10 (3), with a differential of 39% pCO2: 45mmHg failure with severe adult respiratory distress neutrophils, 48% bands, 10% lymphocytes, 1% pO2: 45mmHg syndrome (ARDS). She also developed coneosinophils. The rest of the CBC was within HCO3: 15.7mmol/L normal limits.

CO2 total: 17 mmol/L gestive heart failure (CHF) and was started Base excess: -12.7 on hemodialysis for renal failure.

O2 sat: 68.3% Within 11 days of admission the patient was taken back to the operating roomImaging: for CT walk again and use her extremities since is noFree perfusion withinairthe an pelvic fluid. of the abdomen/pelvis: Infiltrate or atelectasis in both there lung bases. intraperitoneal andabscess, intraperitoneal Inflammatory changes in the mesenteric fat.from Cholelithiasis.

Transvaginal ultrasound showed a largeishyperemic right ovary. Evaluation drainage of pelvic fluid that was collecting. her muscles were atrophic lack of use. anaerobic environment created where of the right adnexa was limited secondary to overlying gas. Chest x-ray inconclusive.

She also had percutaneous placement of a Though her kidneys did not fully recover many anaerobes can grow. Abscess formaEKG: Sinus Tachycardia cholecystostomy secondary to cholecystitis from the overwhelming sepsis she endured, tion is considered one of the last lines of Impression: and peritonitis and elevated liver transaminases. ByDiagnostic the she was ableSeptic to shock continue dialysis treat- host defense, and if an infection reaches this end of her second week in the ICU, shePlan hadof Disposition: ments as an outpatient.

She left the hos- stage, it is considered severe and dangerous The sepsis team was called for the patient. A re-examination at 12:04pm showed her blood pressure was 82/53 after areceiving of fluids Additional IV fluids were then given.

Re-examination 12:30pm showed she was still hypotensive multi-organ failure and had developed pitaltwo77liters days afterIV.entering the Emergency due to the risk of atrupture.

If rupture does after receiving additional fluids. large pelvic hematoma.

Department doors, having survived an occur, it can be life threatening and is The patient was transferred to the Intensive Care Unit for continued care. At 7:00pm the patient went to surgery for aa pre-operative of perforated viscous andruptured septic shock.

As the surgeons entered the abdomen, they encountered a large amount of During the 3rd week in the ICUdiagnosis she initially undiagnosed tubo-ovarian surgical emergency because gram–negative greenish, thin fluid without odor. It seemed to be coming from the right upper quadrant of the abdomen, and they thought it was most developed ascending colitis, hypertension, abscess that almost took her life. endotoxic shock can develop rapidly likely from a perforated ulcer. However, after a thorough exploration they could not discover the source of the [4]. fluid. Finally, the discharge oozing these from thechains right fallopian tube. are The patient then and anemia of critical illness. She surgeons also explored the uterus and ovaries only to discover purulentUnfortunately, of events underwent a total abdominal hysterectomy and bilateral salpingo-oophorectomy as a result. 1100 mL of purulent fluid was removed tested positive for colonization of MRSA. Discussion: Tubo-ovarian abscesses happened toathis patient.

She suffered from the patient’s abdomen overall.

The post-operative diagnosiswhat for this patient was ruptured tubo-ovarian abscess (TOA) and Though her septic shock had resolved,septic she shock.

(TOAs) involve the ovaries and fallopian severe septic shock from a ruptured TOA Her course in the ICU was unusual and interesting, requiring prolonged ventilator support. She initially developed renal failure and was still suffering from multi-organ failure. tubes. suppression Most ofsecondary the time and subsequent pelvicedema. infec- The following global myocardial to thethey sepsis.develop She also had respiratory failure overwhelming secondary to pulmonary she developed hyperthermia, ischemic toesinflammatory and fingers, and continued lactic acidosis.

By the third day of her ICU admission, she Unfortunately, the final insult todayan as a complication of pelvic tion that was life threatening. had a severe thrombocytopenia and a WBC count that was climbing at alarming rates. She was becoming less alert and by the fourth already complicated medical illness came disease (PID), theyrespiratory can alsofailure be a with comPhysical examination of patients day after admission she wasbut in acute severe adult respiratory distress syndrome (ARDS).

She also developed heart failure (CHF) and was started on hemodialysis for renal failure. of having a TOA or PID should on hospital day 27 when she had a congestive new plication post-operatively.

Intra-abdominal suspected Within 11 days of admission the patient was taken back to the operating room for drainage of pelvic fluid that was collecting. She onset of seizures and delirium. A CTalso scanhad percutaneous processes, placement such as ofappendicitis or secondary diver- tofocus on bowel sounds,liver peritoneal findings, a cholecystostomy cholecystitis and elevated transaminases.

By the end of her second week in the ICU, she had multi-organ failure and had developed a large pelvic hematoma. of the head showed abnormal white matter ticulitis, can also lead to their development point of maximal pain, and palpation of During the 3rd week in the ICU she developed ascending colitis, hypertension, and anemia of critical illness. She also tested of low density with cortical involvement in for[1].

Additionally, been found masses Asuffering rectal from examination should positive colonization of MRSA. TOAs Though have her septic shock had resolved, she[5]. was still multi-organ failure.

Unfortunately, the final insult to an already complicated medical illness came on hospital day 27 when she had a new onset of both occipital and parietal regions. Three in patients with ovarian hyperstimulation be performed for the presence of blood, seizures and delirium. A CT scan of the head showed abnormal white matter of low density with cortical involvement in both occipital days later she developed an encephalopathy [2].

Secondarily, candeveloped result an from a tenderness, or otherto abnormaliand parietal regions.

Three days they later she encephalopathy and was masses, in a coma secondary this. Two days later it was confirmed that she had developed PRES, or posterior reversible encephalopathy syndrome.

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19

ties. Generally, wet mounts and cultures are obtained for gonorrhea and Chlamydia, especially if mucopurulent discharge is present [5]. Both a pelvic and bimanual exam should also be performed. A TOA will be a firm fixed mass and usually very tender [4].

However, bimanual pelvic exams performed by experienced ER doctors in the ED have been found to have poor inter-observer agreement for the evaluation of uterine size, uterine tenderness, adnexal tenderness or masses, and cervical motion tenderness [6]. Also, several studies have compared bimanual pelvic exam results to pelvic ultrasonography and laparotomy evaluations, showing accuracy of pelvic exams to be poor, especially when results are thought to be â&#x20AC;&#x153;normal.â&#x20AC;? [7, 8]. Since the reliability of pelvic exams is questionable, it should not be the sole criteria in which to diagnose TOA [6]. Case in point, this patient did not have a bimanual pelvic exam that pointed towards a diagnosis of TOA. There was no cervical motion tenderness, adnexal tenderness, or adnexal masses appreciated.

However, TOA could not be ruled out.

The work-up and diagnosis initially includes obtaining vital signs and assessing volume status. General appearance should be noted, as well as level of comfort. It was noted right away that this patient had abnormal vital signs (hypotension, tachycardia, poor oxygen saturations) and was in severe distress. She immediately received fluids to correct her hypotension [9].

Additionally, laboratory evaluation includes a urine pregnancy test, urinalysis, and testing for gonorrhea and Chlamydia.

Blood cell counts and chemistries should be obtained, along with coagulation studies, a chest x-ray, and an EKG. Urine

output should be monitored. Radiologic evaluation includes a pelvic ultrasound with Doppler flow analysis [9]. Ultrasonography is the test of choice to confirm or exclude a TOA [10]. It has been shown to have high sensitivity and specificity for evaluation of surgically confirmed pelvic masses and is routinely the standard of care for evaluating suspected pelvic and gynecologic pathology [9, 7]. Furthermore, diagnostic laparoscopy is the gold standard for confirming the diagnosis of TOA and PID [11]. This case upholds these guidelines for diagnosis. The patient had an inconclusive speculum and bimanual exam that did not necessarily suggest or rule out TOA. However, two different ultrasounds pointed to a lesion in the right ovary and fallopian tube, in which a TOA should have been considered in the differential diagnosis. Ultimately the exploratory surgery confirmed her diagnosis.

The differential diagnosis for nontraumatic pelvic pain in a non-pregnant adult, such as this patient, includes ovarian cysts (rupture, hemorrhage, torsion, and infection), adnexal torsion, salpingitis, PID, endometriosis, adenomyosis, leiomyosis, TOA, diverticular abscess, appendicitis, diverticulitis, incarcerated hernia [5].

The approach to treatment is to determine first if a true emergent condition exists that requires immediate treatment. Then treatment begins with IV fluids and potent broad-spectrum antibiotics. About 75% of women with TOAs respond to antimicrobial therapy alone [12]. Ampicillin (2g IV Q4h) plus gentamicin (standard doses) plus metronidazole (500mg PO or IV q 8h) is a widely used combination of antibiotics.

Single agent therapy includes of ticarcillin clavulanate (3.1 g IV q4h), piperacillin

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20

The PULSE JULY 2008

tazobactam (4g/0.5g IV q8h), or imipenem cilastatin (500mg IV q6h) [9]. However, initial outpatient treatment with antibiotics for TOA is unsafe because rupture and sepsis can occur unexpectedly, which still has a mortality rate of approximately 25% [9]. The majority of clinicians recommend at least 24 hours of direct inpatient observation for patients who have TOAs [13].

Unfortunately, this patient likely had a TOA when she was seen the previous day at another ER. The antibiotics that were prescribed to her at that time were not enough to treat her TOA, and she subsequently endured a very severe sepsis reaction that might have been prevented had she been initially treated as an inpatient.

Moreover, pain management is also one of the most important treatments in the patientâ&#x20AC;&#x2122;s care [5]. Patients with surgical conditions are easier to evaluate when their pain is somewhat controlled [9]. Correction of any other secondary medical derangements (i.e. anemia, hyperglycemia, hypoxia) should also be performed.

If medical therapy alone is not sufficient, drainage of the abscess is required [12].

Drainage using ultrasound guidance or laparoscopy are two ways to conservatively drain a TOA. A retrospective study of the use of transvaginal ultrasound-guided aspiration to drain TOAs found the treatment to be successful in 282 of 302 women (93%) [14]. Another study found that laparoscopic drainage was successful in 45 of 48 patients (94%) [15]. Surgical drainage is required if abscess is palpated in the midline, adherent to the vaginal wall, or distends in the upper one-third of the rectovaginal septum [16]. Fluid from the TOA should be sent for microbiologic evaluation and cytologic analysis should be considered.

In conclusion, TOAs are an important diagnosis for ER physicians to consider in patients presenting with pelvic and abdominal pain. They should be ruled out with ultrasonography in the ER. If a TOA is diagnosed, inpatient treatment is the standard of care. Unfortunately, the TOA in this patient was not diagnosed correctly the emergency department initially, and treatment as an outpatient for PID almost took her life.

References: 1. Jackson SL, Soper DE. Pelvic inflammatory disease in the postmenopausal woman.

Infect Dis Obstet Gynecol 1999; 7:248.

2. Govaerts I, Devreker F, Delbaere A, et al.

Short-term medical complications of 1500 oocyte retrievals for in vitro fertilization and embryo transfer. Eur J Obstet Gynecol Reprod Biol 1998; 77:239.

Obstet Gynecol Reprod Biol 2004; 114:203.

4. Berek JS. Gynecology. 14th edition.

Philadelphia, PA: Lippincott Williams & Wilkins; 2007.

5. Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine. 6th edition. New York, NY: McGraw Hill; 2004.

6. Close R, Sachs C, Dyne P: Reliability of 3. Protopapas AG, Diakomanolis ES, bimanual pelvic examinations performed Milingos SD, et al. Tubo-ovarian abscesses in emergency departments. West J Med 4/9/07 inACOEP/ThePulse_Location postmenopausal women: gynecological 175L240, 2001.11:30 AM Page 1 malignancy until proven otherwise? Eur j

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7. Carter J, Fowler J, Carson L: How accurate is the pelvic examination as compared to transvaginal sonography? J Reprod Med 39:32, 1994.

8. Andolf E, Jorgensen C: Prospective comparison of clinical ultrasound and operative examination of the female pelvis. J Ultrasound Med 7:617, 1988.

9. American College of Emergency Physicians: Clinical policy: Critical issues for the initial evaluation and management of patients presenting with a chief complaint of non-traumatic acute abdominal pain.

Ann Emerg Med 36:406, 2000.

10. Moir C, Robins RE. Role of ultrasound, gallium scanning, and computed tomography in the diagnosis of intra-abdominal abscess. Am J Surg 1982; 143:582.

11. McCormack WM: Pelvic inflammatory disease. New Engl J Med 330:115, 1994.

12. Reed SD, Landers DV, Sweet RL. Antibiotic treatment of tuboovarian abscesses: comparison of broad-spectrum B-lactam agents versus clindamycin-containing regimens. Am J Obstet Gynecol 1991: 164:1556-1562.

13. Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006; 55:1.

14. Gjelland K, Ekerhovd E, Granberg S. Transvaginal ultrasound-guided aspiration for the treatment of tubo-ovarian abscess: a study of 302 cases. Am J Obstet Gynecol 2005; 193:1323.

15. Henry-Suchet J, Soler A, Loffredo V. Laparoscopic treatment of tubo-ovarian abscesses. J Reprod Med 1984; 29:579.

16. Franklin EW, 3rd, Hevron JE Jr, Thompson JD. Management of the pelvic abscess. Clin Obstet Gynecol 1973; 16:66.

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21

Guest Column Wayne Jones, D.O., FACOEP

How Much Does Your Soul Weigh?

Though a changing concept, the idea of the soul has enlivened conversations since the time of the Greek philosophers. Being such an object of intrigue, the soul has changed and even accommodated different cultural beliefs and customs.

In its purest sense, the soul remains the intangible thing that is truly the person.

The Greeks referred to it only when envisioning death. This is best represented in the Iliad when Achilles reflects on the coming battle stating he will be “risking” his soul. Plainly, it was something owned and individual. Plato expanded on the concept of the soul to include those things felt to be distinctly human - our desires, our will and our reason. As humans we need all three to be unique and to be that which creates the “self ” (a term not spoken of for several more centuries).

In the Christian literature, the soul actually leaves the body at death. It is a defining moment where our essence becomes eternal in a place of continuous rest and vigilance. In fact, as Christians, you are taught that your soul actually belongs to God and with him is where your soul will reside upon death.

But if the soul were something to be lost then, should it contain “weight”? Well, in 1907 a Dr. Duncan MacDougall thought so. He conducted a series of “experiments” on patients who were terminal and placed them on specially constructed beds as to weigh them periodically to catch the loss of the soul weight at the moment of death.

There were only six patients in his study. At death their weights fluctuated, some with no change (no soul?) and others with significant weight change. He concluded that the soul weighed (on average) 21 grams. He would repeat this experiment using dogs.

The dogs were euthanised and weighed before and after death. He did not record any weight change. Since he knew that only humans were capable of maintaining a soul, this proved that it could only be the soul that accounted for immediate weight loss at the time of human death.

So why am I writing this article? Well,

22

who else, other than emergency physicians, witness more death than us? Can we return life by simply returning the soul to the body? I doubt it. But being the philosopher I am, I have my own theory of the soul.

Mine is much more like that of Plato.

I am taking a completely non-Christian approach in assuming the soul is not eternal in the same sense as a “living” soul but one of a gift or legacy. As we go through our lives we leave small pieces of ourselves everywhere we go and with everyone we encounter. Whether our actions are kind and caring or hurtful taints the “piece” we leave behind; but it is most certainly left.

Even casual interactions with people we will never meet again can change the person

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who experiences the interaction. A smile, a gift, the unexpected assistance that we leave with others also translates us to them.

Like a soldier in ancient Greece, as he risks his soul in battle, his courage and loyalty is transferred to his partners in battle who are then fortified by his soul.

We, as physicians, have a special place in life; that of an educator, healer and advocate. Our souls, though never diminished by our giving, continue to grow with each person, patient and student we touch. Our souls do have weight. And they will live eternally. So, how much does your soul weigh?

I would like to dedicate this to our graduating residents past and present.

Medical Care Access Protection Act of 2007/S.243 Jason J. Tanguay, D.O. Training in Health Policy Fellow, 2007-2008 Introduction Medical malpractice has taken center stage in the last several years as one of the most heated topics in health policy. According to the American Medical Association (AMA), untenable increases in malpractice liability insurance has forced physicians to either leave their practice or limit their scope of practice1. Indeed, their landmark 2004 editorial stated that 19 states were in an overt malpractice crisis and that 35 more were on the crux on one.

Such a crisis would compromise access to affordable quality care.

A sound health care liability system would ideally allow for expedient, just, and economical compensation for patients in the event of negligent injury, while also providing protection for physicians in the case of a suit. The current system, however, is not sound. Some physicians are reportedly being forced out of practice by the cost of the insurance designed to protect them.

On the patient’s side, only 17% of medical claims involve evidence of negligent care, and a mere 3% of victims of negligence filed2. In other words, too many patients file ‘frivolous’ suits and not nearly enough victims of negligence ever file. Who is really being protected by the current system?

Intent of the Bill The Medical Care Access Protection Act (MCAP/S.22) and its companion in the House of Representatives (H.R. 5) is a “bill to improve patient access to health care services and provide improved medical care by relieving the excessive burden the liability system places on the health care delivery system.” This bill would: 1) set a statute of limitations of three years (with exceptions) after the manifestation of injury; 2) require the court to impose sanctions for frivolous lawsuits; 3) limit non-economic damages to $250,000; 4) allow the court to restrict attorney contingency fees; 5) prescribe qualifications for expert witnesses; 6) require the court to reduce damages by the amount of collateral source benefits

received; 6) authorize punitive damages only where there is malicious intent, deliberate action, or compensatory damages are awarded; 7) prevent health care providers from being named in class-action law suits for the use of FDA approved products3.

These reforms assume that spending reductions would arise in two ways. First, a reduction in the size of a malpractice reward would translate into reduced premium cost for the practitioner (the so-called malpractice premium effect). Second, the volume of health care expenditure would decline as the practice of “defensive medicine” would decline (the so-called utilization effect).

The latter argument assumes much of medical utilization is based upon the fear of litigation and tort reform would mitigate this perceived threat. Lastly, though not a mechanism to reduce overall compensation to plaintiffs, reducing claim payouts by amounts given by collateral sources would obviously shrink payouts by insurance companies.

Supporters of the Medical Care Access Protection Act of 2007 include organized medical groups (American Medical Association, American Osteopathic Association), specialty physician groups (American College of Physicians, American College of Emergency Physicians), liability insurance groups (Physician Insurers Association of America), government agencies (Center for Medicare and Medicaid Studies, Department of Health and Human Services), most Congressional Republicans. They argue that federal tort reform will limit the growth of liability premiums for physicians and thereby ensure that physicians remain in practice, curb frivolous lawsuits, and reduce medical expenditure by limiting defensive medicine.

Opponents of the Medical Care Access Protection Act of 2007 include the American Association for Justice (formerly the American Trial Lawyers Association), advocates for state rights (National Governors Association, National Conference of State Legislators), and most congressional Democrats. The former group argues that

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reductions in rewards will essentially disenfranchise patients from proper compensation, reduce access to legal representation in the event of negligence, and prompt physicians to practice more cautious and diligent care to avoid medical errors. The latter group argues that liability insurance, like all other types of insurance, is really a state-controlled issue and should remain so.

History and Background Physicians purchase medical liability insurance to protect themselves and their patients in the untoward occurrence of negligence or unintentional injury. Such insurance provides indemnity in the event of a claim, and fund the three general types of malpractice damages—economic damages, non-economic damages, and punitive damages. Economic damages are funds paid to compensate claimants for past and future medical bills, future earnings, and property.

Such damages are considered objective and measurable. Non-economic damages are those designed to compensate for pain, suffering, emotional distress, loss of societal status, loss of enjoyment. In contrast to economic damages, these are largely subjective. Lastly, punitive damages are those awarded for willful or wanton misconduct that results in injury.

The rate of medical liability premium increase has been cited as the driving force in the malpractice crisis, though many groups do argue over what constitutes crisis. Nevertheless, premiums have increased at rates that have far exceeded physician salaries. During the 1980s national rates doubled in a two year period4. More recently, the Congressional Budget Office (CBO) reported a national average increase of 15% between 2000 and 2002; premium rate increases for obstetricians and gynecologists rose 22% and those of both general surgeons and internal medicine specialists 33% during the same period5,6,7. The Government Accountability Office (GAO) noted that rates of increase differed substan-

23

tially between states as well. For instance, premiums for general surgeons in Dade County, Florida increased by 75% between 1999 and 2002, whereas those for surgeons in Minnesota increased by 2% in the same period8. Such increases of geometric proportions are not sustainable in the long run and may preclude access to care if physicians are forced out of practice.

Why have premium rates increased in such dramatic and seemingly unpredictable ways? Several factors cause such rate variances. First, the GAO suggested that increases in reward size has accounted for the brunt of the increase in premium rates. In Mississippi, for instance, inflation adjusted payouts increased 142% between 1998 and 20019,10. Second, there has been a modest increase in the number of claims made11. Third, declines in the investment incomes of insurance carriers in times of slow markets—such as the period following 9/11—prompted premium rate increases to mitigate carrier losses. For example, between 2000 and 2002 the investment returns among the top 15 malpractice insurers fell by 1.6 percent, which accounted for approximately a 7.2 percent increase in premiums12. Fourth, the so-called “insurance cycle” contributed to marked variation in premium rates. Briefly, this cycle is caused by a discrepancy between a carrier’s claim forecasting, their premium revenue, and subsequent claim payouts. For instance, competition between insurance carriers in certain markets drove premiums to artificially low levels; later those companies could not cover their costs in response to claim payouts13,14,15.

In addition to the rise in liability insurance, physicians find themselves in a highly litigious environment that has affected their practice and encouraged “defensive medicine”—practices whereby the physician performs a test for fear of future litigation rather than true medical necessity. Current litigation rates suggest that 1 out of ever 7 physicians is sued annually, compared to the 1960s when approximately 1 in 7 were sued in their whole careers16. Despite beliefs that such practice increases health care cost, CBO estimates that defensive medicine may only slightly affect medical spending17.

This is curious, given that the total cost of

24

both private and governmental malpractice dollars amounts to only 2 percent of all health care spending18.

Tort reform has remained the central vehicle used to curb the liability crisis. The precedent for tort reform (and MCAP) was set in 1975 in California, with the Medical Insurance Compensation Reform Act (MICRA).

MICRA established a tort reform precedent in that it posited four major changes to the liability system. First, it imposed a cap of $250,000 on non-economic damages.

Second, it allowed juries to reduce awards by moneys dispersed by collateral sources.

Third, it allowed for periodic payouts of damages rather than one lump sum. Lastly, it limited contingency fees lawyers charge their clients19. Many of the provisions within the current MCAP bill were derived from MICRA, though the former aims to nationalize liability regulation. More recently, the Help Efficient Accessible Low Cost Timely Healthcare of 2003 (HEALTH Act 2003) proposed similar reforms to MICRA on the national level; it did fail as voting fell mostly along party lines, with Republicans in favor and Democrats opposed20.

The efficacy of non-economic damage caps (the most notorious aspect of the current MCAP bill) in the reduction of both total health care expenditure and liability costs is controversial. Proponents cite evidence that such caps in concert with reductions from collateral source benefits have reduced claim awards and ultimately medical malpractice premiums21,22. Indeed, a Rand analysis estimated that MICRA reduced claim magnitude by approximately 30 %, attorney fees by 60% and, unfortunately, net recovery by plaintiffs approximately 15%23. Analogously, the CBO estimated the caps proposed by the HEALTH Act of 2003 would lower malpractice premiums by 25%24,25. Opponents, however, argued this reduction is insignificant and such reforms would increase risks for patients. For instance, they argue a reduction in claims paid would essentially result in improper compensation for patients injured, and that malpractice will cease to be a deterrent for negligent medical care. Also, by reducing contingency fees, patients could effectively lose access to the necessary legal services to file a claim. Lastly, they argue such reform would not impact the cost of the health

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care system: malpractice costs in 2002 totaled $24 billion dollars (2% of total health expenditures), such a reduction only amounts to a 0.5% reduction in total health care costs, as well as a marginal translation into premium reduction26.

Another landmark set of reforms with less notoriety than MICRA occurred in Indiana. The Indiana Medical Malpractice Act, also passed in 1975, offered a broad liability reform consisting of three main provisions: a comprehensive cap on all damages, a mandated medical review board for any case heard in trial, and a state-run insurance fund to pay for claims in excess of $100,000—the Patient’s Compensation Fund (PCF). Despite the initial aim of the legislation, the reforms created several incentives that prompted unexpected utilization and results. First, only approximately 11% of claims utilized the medical review boards, most likely due to the slowness of the process27. Secondly, claims are much more likely to be settled expediently with many being in excess of the $100,000, thereby invoking the PCF28. Using the PCF requires payouts above this threshold and also implies an admittance of guilt on the physician’s part. This system led to three dramatic results: physicians’ liability costs were lower than the national average (and geographic neighbors); claim frequency and severity were no different than the national average; and rewards to patients significantly exceeded the national average29. If a no-fault system of medical liability involves the imposition of liability regardless of the defendant’s fault and places limits upon the damages paid, then Indiana essentially created a no-fault system inadvertently.

STAKEHOLDERS in opposition of MCAP American Association for Justice (formerly the American Trial Lawyers Association) The mission of the American Association for Justice is to promote a fair and effective justice system – and to support the work of attorneys in their efforts to ensure that any person who is injured by the misconduct or negligence of others can obtain justice in America’s courtrooms, even when taking on the most powerful interests. They argue that fear of lawsuits causes practitioners to exercise more caution and litigation will punish incompetent physicians30.

National Conference of tate Legislatures NCSL is a bipartisan organization that serves the legislators and staffs of the nation's 50 states, its commonwealths and territories.

NCSL is an effective and respected advocate for the interests of state governments before Congress and federal agencies. NCSL continues to oppose any federal preemption of state authority within the civil justice and tort law areas31.

National Governors Association (NGA) The NGA is a bipartisan organization of the nation's governors which promotes visionary state leadership and autonomy. Again, they argue malpractice reform should be a state issue32.

Stakeholders in support of MCAP American Medical Association The AMA is the largest association of doctors and medical students in the United States. They believe that excessive medical malpractice payments (in terms of payouts, settlements, and premiums) only function to increase the amount of revenue earned by lawyers, as plaintiffs only receive up to 40% of a settlement. They also argue that effective medical liability reform, based on the California MICRA model, is integral to health system reform33.

American Osteopathic Association The AOA is a member association representing more than 61,000 osteopathic physicians. The AOA supports comprehensive tort reform to ensure continued access to affordable, quality care.

Physician Insurers Association of America The PIAA is an organization of healthcare liability insurance entities. They support national tort reform34.

Recommendations MCAP should not be passed into law as it will not serve to protect patients’ access to affordable, high quality care. Instead, it would transfer the cost of malpractice from the physician and insurer to the patient. By imposing a non-economic cap on plaintiffs and, furthermore, by imposing sanctions upon patients for frivolous claims, victims

of negligence will have reducing access to representation. Moreover, an analysis of non-economic damage caps in California revealed that such caps are regressive, in as much as they serve to disproportionately reduce the award for the most serious injuries while they artificially inflate awards for the most trivial of injuries36. Also, MCAP overemphasizes the impact of rewards upon physician premium growth while underplaying—or altogether omitting—the role of the insurance carrier37. Since insurance companies often use current premium revenue to pay past claims, ideal legislation would provide incentives to curb this process or restructure their payment regimen. Sadly, however, national tort reform has been moved down the health agenda in a Democratic Congress.

Sound medical malpractice reform would engender an environment wherein victims of negligence receive fair, expedient, and economical payments for their injuries, while their physicians would be adequately protected from litigation. In other words, the “right” patients would file suit and be compensated. Physicians, moreover, would make fewer decisions based upon fear of litigation than evidence based medicine.

A no-fault system, I feel, could manifest such an environment. Lastly, reforms such as those in Indiana may be a transition step in a movement towards a national no-fault liability system.

References 1. Palmisano, D.J. 2004. Health care in crisis. Circulation. Vol.109: 2933-2935.

2. Saxton, Jim. 2005. Joint Economic Committee Research Report #109-2.

3. S.22 Available at http://thomas.loc.gov/ cgi-bin/bdquery/z?d108:s22:. Accessed on 11/30/07 4. Beider, P. and S. Hagen. 2004. Limiting tort liability for medical malpractice.

Congressional Budge Office Economic and Budget issue brief.

5. Viscus, W.K. and P.H. Born. 2005.

Damage caps, insurability, and the performance of medical malpractice insurance.

Journal Risk and Insurance. Vol. 72 (1): 23-43.

6. Beider, P. and S. Hagen. 2004. Limiting tort liability for medical malpractice.

Congressional Budge Office Economic and

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Budget issue brief.

7. Medical Malpractice Policy. Kaiser Foundation. Available at http://www.kaiseredu.org/topics_im.asp?id=226&imID= 1&parentID=59 Accessed on 11/30/07.

8. General Accounting Office, Medical malpractice insurance: multiple factors have contributed to increased premium rates, GAO-03-702.

June 2003.

9. General Accounting Office, Medical malpractice insurance: multiple factors have contributed to increased premium rates, GAO-03-702.

June 2003, p.27.

10. Mello, M.M. 2006. Understanding medical malpractice: a primer. http://www. rwjf.org/pr/product.jsp?id=15091 11. Mello, M.M. 2006. Understanding medical malpractice: a primer. http://www. rwjf.org/pr/product.jsp?id=15091 12. General Accounting Office, Medical malpractice insurance: multiple factors have contributed to increased premium rates, GAO-03-702. June 2003.

13. Medical Malpractice Policy. Kaiser Foundation. Available at http://www.kaiseredu.org/topics_im.asp?id=226&imID= 1&parentID=59 Accessed on 11/30/07.

14. Viscus, W.K. and P.H. Born. 2005.

Damage caps, insurability, and the performance of medical malpractice insurance.

Journal Risk and Insurance. Vol. 72 (1): 23-43.

15. Sage, W.M. 2004. The forgotten third: liability insurance and the medical malpractice crisis. Health Affairs. Vol 23 (4): 10-20.

16. Kereiakes, D.J. and J.T. Wilkerson.

2004. Circulation. Vol 109: 2939-2941.

17. Beider, P. and S. Hagen. 2004. Limiting tort liability for medical malpractice.

Congressional Budge Office Economic and Budget issue brief.

18. Beider, P. and S. Hagen. 2004. Limiting tort liability for medical malpractice.

Congressional Budge Office Economic and Budget issue brief.

19. Frech, H.E., W.G. Hamm, C.P. Wazzan.

2006. An economic assessment of damage caps in medical malpractice litigation imposed by state laws and the implications for federal policy and law. Health Matrix.

Vol 16: 693-722.

20. http://www.govtrack.us/congress/bill. xpd?bill=h108-5. Accessed 4/27/08.

21. Frech, H.E., W.G. Hamm, C.P. Wazzan.

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2006. An economic assessment of damage caps in medical malpractice litigation imposed by state laws and the implications for federal policy and law. Health Matrix.

Vol 16: 693-722.

22. Pace, N.M., D. Golinelli and L. Zakaras.

2004. Capping non-economic awards in medical malpractice trials: California jury verdicts under MICRA. Rand Institute for Civil Justice.

23. Pace, N.M., D. Golinelli and L. Zakaras.

2004. Capping non-economic awards in medical malpractice trials: California jury verdicts under MICRA. Rand Institute for Civil Justice.

24. Beider, P. and S. Hagen. 2004. Limiting tort liability for medical malpractice.

Congressional Budge Office Economic and Budget issue brief.

25. Frech, H.E., W.G. Hamm, C.P. Wazzan.

2006. An economic assessment of damage caps in medical malpractice litigation imposed by state laws and the implications for federal policy and law. Health Matrix.

Vol 16: 693-722.

26. Viscus, W.K. and P.H. Born. 2005.

Damage caps, insurability, and the performance of medical malpractice insurance.

Journal Risk and Insurance. Vol. 72 (1): 23-43.

27. Kinney, E.D. and W.P. Gronfein. 1991.

Indiana’s malpractice system: no-fault by

accident? Law & Contemp. Probs. Vol 54: 169-193.

28. Kinney, E.D. and W.P. Gronfein. 1991.

Indiana’s malpractice system: no-fault by accident? Law & Contemp. Probs. Vol 54: 169-193.

29. Kinney, E.D. and W.P. Gronfein. 1991.

Indiana’s malpractice system: no-fault by accident? Law & Contemp. Probs. Vol 54: 169-193.

30. http://www.justice.org/pressroom/ FACTS/health/index.aspx Accessed 4/20/08 31. http://www.ncsl.org/standcomm/sclaw/ medmaloverview.htm. Accessed 4/20/08 32. http://www.nga.org/portal/site/nga.

Accessed 4/20/08 33. http://www.ama-assn.org/ama/pub/category/7861.html. Accessed 4/20/08 34. http://www.osteopathic.org/index. cfm?PageID=gov_main. Accessed 4/20/08 35. http://www.piaa.us/government_relations/Issues/Legislative_Alert_122007. htm. Accessed 4/20/08 36. Studdert, D.M., Y.T. Yang, and M.M. Mello. 2004. Are damage caps regressive: A study of malpractice jury verdicts in California. Health Affairs. Vol 23: 54-67.

37. Sage, W.M. 2004. The forgotten third: liability insurance and the medical malpractice crisis. Health Affairs. Vol 23 (4): 10-20.

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Executive Director, cont'd from page 5 emergency physicians; they are our chance in a very competitive arena. How do we best serve them and their needs and insure our legacy in the profession?

I think is that we have them buy into the process. How, you ask? I believe that ACOEP committees have one, committed student and resident representative named to it. That each of these representatives is tasked with the responsibility for maintaining the College’s interests and reporting objectively back to their organizations.

Each organization must maintain a specific continuity of officers on its national board to ensure the smooth-running and continuous operation. Each organization is responsible for fund-raising and budget development within the ACOEP.

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Caesar’s Palace Las Vegas, Nevada October 26 –30, 2008

We must have them be a part of our family, a part of our parent-organization, and part of the osteopathic family, just as ACOEP must be. Together, we will assure a winning tomorrow and a legacy of a proud heritage formed so many years ago by our predecessors.

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Perspective of a Young Physician Brandon Lewis, D.O.

The Formation of a Young Physicians' Group If you haven’t been to an ACOEP meeting lately, you would be amazed at the growth of our College. Most remarkable to me is the strides that continue to be made by the resident and student chapters. Over the past few years these groups have grown in numbers and quality. Having previously served as President of both of these groups I am excited by the number of young physicians who are not just attending, but seeking leadership roles as well. However, after completing residency, most of these physicians will find themselves in a whole new world. Choosing a job, dealing with family changes, taking boards, planning a career, and finding a way to stay involved in ACOEP are all challenges that these young physicians will face.

It is at this stage in one’s career that a young physician could become overwhelmed by the important decisions to be made and may just abandon many worthwhile pursuits in an attempt to simplify things.

For others, having finished with the challenge of residency, a sense of complacency, or need for a little “coasting” may take hold.

Like beginning internship, a new emergency physician will be faced with many new challenges and may have difficulty adapting to new expectations. At this stage, more than ever, a physician needs support to find their niche; that special place that they want to be. For those who have shown an interest in leadership roles in medicine, this is the time when this interest needs to be fostered and encouraged. From the College’s perspective, it is imperative that young physicians who have shown the potential for leadership, and who are the future of the College, remain active and involved in college activities.

To meet these needs, other organizations in medicine have formed groups dedicated to the support of young physicians, which grow into large sections and provide a grooming ground for strong physicians and future leaders. With this in mind, President-elect Thomas Brabson and the

Board of Directors have encouraged the formation of a new committee dedicated to young physician issues. The first meeting of this group will be during our upcoming Fall Conference, October 26-30 at Caesar’s Palace in Las Vegas. The meeting is open to anyone wishing participate, we especially hope to have a large contingent of young physicians, those new to the practice of emergency medicine. We hope that our first meeting will be a productive one and will launch this new group on a path to success.

Like any new group, we will have a lot to accomplish at our first meeting. First of all, who exactly should be considered a young physician? While we want to be inclusive to all those interested, properly identifying a target group will help focus our goals and priorities. Second, in order to be successful, any group needs to have a clear mission and identified goals. Identifying the needs of

young physicians and creating solutions and ways of meeting these needs will be a huge challenge for this new group and we will depend heavily on input from those young physicians in attendance.

If you are a young physician who has needs or have experienced problems in the beginning of your career, please come and let your voice be heard. If you are young physician looking for a way to stay involved in the ACOEP, or to get involved for the first time, we hope to see you there.

If you are a “young at heart” physician, or otherwise have ideas that you think would be beneficial to young physicians, we welcome you attendance and input. Keep in mind, that schedules and meeting spaces have not been fully set, but please make up your mind now to find our meeting and participate in this new and worthy endeavor. Our success is dependent on your participation!!

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Governmental Affairs Yvonne Treacy

D.O. Day on the Hill April 24, 2008 was D.O. Day on the Hill and it dawned bright and sunny in our Nation’s Capital. This annual event first started in 2000 to provide osteopathic physicians with an opportunity to meet face to face with their national representatives.

This meeting is often the first encounter that doctors and professional staff of osteopathic organizations get to meet with the lawmakers and to become familiar with the important issues affecting Osteopathic medicine.

Our day started at 7 a.m. registration in the Renaissance Hotel, D.C. After an energizing breakfast, AOA’s Executive Director, John Crosby addressed the crowd with great excitement over the large number of physicians, professionals and students participating in this event. The group then learned about the events of the day from LeAnne Fox, Director Division of Washington Advocacy and Communications.

She reviewed informational packets for the

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event and providing instructions as to what is expected throughout the day of meetings.

The faces on the crowd were very unsure of themselves. For many, it was their first time in D.C. since their eight grade school trip.

Not knowing what to do and where to go.

Thankfully each school seemed to have a veteran to guide them.

We were sent in to groups and attended appointments that were arranged by the AOA. Senator Barack Obama as you can imagine was busy so his Aide, Lysette Alvarado met with us. Our purpose in meeting the Senators’ offices was to raise issues that needed to be addressed and to make our Senators and Representatives aware of the “Save Medicare Act of 2008” and to seek endorsement or cosponsorship of the act. This act will prevent a 10.6 percent cut in reimbursement scheduled for 2008 and an additional 5 percent cut in 2009. It also provides 0.5 percent positive update 2008 and 1.8 percent

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update in 2009. It extends important rural provisions (GPCI and Scarcity bonus) and Physicians Quality Reporting Initiative (PQRI).

In some cases the Representative may not have been in the office, but their Legislative Aide met with us and answered questions.

For my member of congress Danny Davis was unavailable, fortunately Charles Brown Jr. was there to representative him. It was important to ask our Representatives to sign the Dear Colleague Letter which at the time had 140 bi-partisan signers. This will call upon congress to act immediately to address the physicians pay cuts. Everybody in my group left feeling that they learned of both the federal and local legislative issues.

The day was long but very enjoyable.

Emergency Department Ethics Bernard Heilicser, D.O., MS, FACEP, FACOEP

What Would You Do? In this issue of The Pulse we will review the case of the 19 year-old female who was sexually assaulted by her estranged husband. The assailant subsequently sustained a self-inflicted GSW to the head. He was near death. The questions posed were: 1. Can lab for HIV, RPR, etc. be obtained without consent from the moribund assailant?

2. With the victim technically still married, can the wife consent for organ donation when the police are done with him.

This tragic case demonstrates how our options are sometimes not constrained by the legal system. Essentially, the potential source patient, the husband, can be tested regardless of the situation. The wife would certainly have the right to know her potential disease status, and the need for immediate drug intervention, if indicated.

Organ donation presents an interesting situation. The assailant’s wife is still the appropriate consent for him, even though separated. She should still be encouraged to offer the organs (perhaps his genitals to a pit bull). When she is approached, she could defer to another relative, i.e. mother or sibling, or still make an objective

September 12 – 13 Oral Board Review

Sheraton Four Points Hotel

Chicago, IL

10 Category 1A Credit October 26 – 30 Scientific Seminar

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CME Calendar

determination based on the altruism of the donation act.

This was a true case. The ethical dilemmas posed are theoretical, but do provide an interesting basis for discussion and thought.

If you have any cases in your practice that you would like to present or have reviewed in The Pulse, please fax them to us at 708-915-2743. Thank you.

2009 January 7 – 11 Emergency Medicine: An Intense Review

Westin River North

Chicago, IL

42 Category 1A Credits February 1-3 Program Directors Workshop

Hilton Marco Island Resort

Marco Island, FL April 14 – 18 Spring Seminar

Hyatt Regency Grand Cypress

Orlando, FL

2008

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