Northeast Florida Medicine - Spring 2013 - Diseases of the Stomach by Duval County Medical Society

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RefeRRing Physician Office 4500 San Pablo Road, Jacksonville, FL 32224 904.953.2583 | MCJRPO@mayo.edu 2 Vol. 64, No. 1 2013 Northeast Florida Medicine

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Use of state-of-the art imaging techniques, including high resolution endoscopy with narrow band imaging, confocal laser endomicroscopy and other advanced systems.

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Esophagectomy using conventional and laparoscopic minimally invasive techniques.

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NCI-designated comprehensive cancer center with numerous clinical trials evaluating novel tests and treatments for esophageal cancer and other gastrointestinal malignancies. www . DCMS online . org

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Inside this issue of

VOLUME 64, NUMBER 1 Stomach Diseases, Spring 2013 EDITOR IN CHIEF Raed Assar, MD (Chair) MANAGING EDITOR Leora Legacy and Laura Townsend ASSOCIATE EDITORS Laura Armas-Kolostroubis, MD Abubakr Bajwa, MD Kim Barbel-Johnson, MD Ruple Galani, MD Kathy Harris (Alliance) Sunil Joshi, MD (Vice Chair) James Joyce, MD Daniel Kantor, MD Neel Karnani, MD Mobeen Rathore, MD James St. George, MD

EXECUTIVE VICE PRESIDENT Bryan Campbell DCMS FOUNDATION BOARD OF DIRECTORS Ashley B. Norse, MD, President Eli N. Lerner, MD, President-Elect Neel G. Karnani, MD, Vice President Mobeen Rathore, MD, Vice President Daniel Kantor, MD, Vice President Raed Assar, MD, Secretary Sunil Joshi, MD, Treasurer Malcolm Foster, Jr., MD, Im. Past President Cynthia Anderson, MD Elizabeth Burns, MD Paul Chappano, MD Rui Fernandes, MD Ruple J. Galani, MD E. Rawson Griffin, MD Mark L. Hudak, MD TraChella Johnson Foy, MD James J. Joyce, MD Harry M. Koslowski, MD Stephen E. Mandia, MD Jesse P. McRae, MD Jason D. Meier, MD Nathan P. Newman, MD Alexander Pogrebniak, MD James St. George, MD Nathan P. Newman, MD Sanjay Swami, MD David L. Wood, MD Bouali Amoli, DMD, MD, Resident LT George Salgado, MC, USN, Resident Amit Grover, MD, Resident Monique Gray, MD, Resident Northeast Florida Medicine is published by the DCMS Foundation, Jacksonville, Florida, on behalf of the County Medical Societies of Duval, Clay, Nassau, Putnam, and St. Johns. Except for official announcements from the County Medical Societies, no material or advertisements published in NEFM are to be seen as representing the policy or views of the DCMS Foundation or its colleague Medical Societies. All advertising is subject to acceptance by the Editor in Chief. Address correspondence and advertising to: 555 Bishopgate Lane, Jacksonville, FL 32204 (904-355-6561), or email: ltownsend@dcmsonline.org.

www . DCMS online . org

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Northeast Florida Medicine

Features

Diseases of the Stomach

Upper Gastrointestinal Bleeding: Variceal and Non Variceal Hemorrhage

Ziad T. Awad, MD, FACS, Guest Editor

Camille McGaw, MD; Sujai Jalaj, MD, Paul Sievert, MD and James S. Scolapio, MD

Managing Complications of Peptic Ulcer Disease

Andrea McNab, MD; Reginald Griffin, MD and Ziad T. Awad, MD

Current Management and Future Strategies of Gastric Cancer

Ziad T. Awad, MD

Management of Gastroparesis

Gastroparesis

Prevention of Medical Errors: Root Causes and Strategies to Avoid Errors (CME)

Joes M. Nieto, DO

Bijo K. John, MD; Ann J. Lee, MD; Paul Sievert, MD and James S. Scolapio, MD

Vicki-lynne Gloger, BA, MSSM

Special Articles

Dr. Eli Lerner Inaugurated as 126th DCMS President and Awards Presented During the 160th DCMS Annual Meeting

Departments

From the Editor’s Desk From the President’s Desk Young Physician Leader Award From the EVP's Desk Residents' Corner Patient Page Trends in Public Health

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From the Editor’s Desk

Policy Impact of Deaths from Prescription Pain Meds Misuse and Abuse

A recent report by the CDC indicated that deaths from accidental prescription overdose have exceeded those caused by car accidents with 75% of these deaths caused by abuse and misuse of prescription pain killers. The American Society of Interventional Pain Physicians reported that Americans consume over 80% of the painkillers produced in the world. Every 19 minutes, a person dies from an accidental prescription drug overdose in the US. Florida had the highest sold scripts per person and was number 6 in the nation in related deaths per 100,000 (www.cdc.gov). The figures are alarming and are likely to lead to major public health actions. A year has passed since the Northeast Florida Medicine Journal (NEFMJ) addiction issue, which was guest edited by Dr. Raymond Pomm. The NEFMJ presented great articles on the subject and suggested solutions. Since then, the CDC published shocking reports and policy statements. Again, Florida physicians find themselves in the line of fire in a major public health issue. All prudent physicians agree that all patients deserve adequate pain control. With that said, it is still difficult to justify the utilization statistics above and the deadly consequences. The causes of this problem exceed the capacity of this editorial. However, the solutions recommended by leading health entities focus the attention on physicians. Policy documents mention lack of adequate prescription drug monitoring programs (PDMP) to properly identify and address improper patient use of painkillers; lack of adequate laws to address pill mills and doctor shopping; suggest professional licensing boards take more action against inappropriate prescribing; and lack of access to substance abuse treatment. As to patient responsibility, patients are told to use prescription painkillers only as directed by a health care provider and to make sure they are the only ones to use their prescription painkillers (no selling or sharing with others). Clinical data sharing among health care professionals, facilities and managed care organizations, e.g. Health Information Exchanges and health plan monitoring programs will continue to increase. All of the above affects physicians and their information and practice. Physicians are also asked to follow guidelines for responsible painkiller prescribing, including screening and monitoring for substance abuse and mental health problems; prescribe painkillers only when other treatments have not been effective for pain; prescribe only the quantity of painkillers needed based on the expected length of pain; use patient-provider agreements combined with urine drug tests for people using prescription painkillers long term; talk with patients about safely using, storing and disposing of prescription painkillers; and use PDMPs to identify patients who are improperly using prescription painkillers. Raed Assar, MD, MBA Editor-in-Chief Northeast Florida Medicine

The causes are truly multi-factorial to levels of contention that might rival that of the gun control arguments with one major difference. Although the impact in terms of loss of life and poor financial outcomes could be more significant; there is lack of the critical incident syndrome that plagues some of the national discussions. Deaths from overdoses are sporadic and do not involve a large number of innocent victims such as in a school shooting. However, this situation could become more problematic to the medical community. With major health care cost drivers such as obesity and diabetes affecting the future of healthcare in this country, physicians need to put some wins on the board in their favor. It is unlikely to identify other major statistic that can be more readily and directly traced back to them in the form of physicians’ prescriptions. The public is not likely to sympathize with the physicians’ position on this issue at the expense of the patients. Whether appropriate or not, the public is likely to assign more responsibility on physicians rather than patients. Regardless of the level of sensational publicity, this issue requires the immediate attention of the medical community. At any point, these statistics can be brought up to present the physicians as part of the problem rather than part of the solution. The medical community has a tremendous opportunity to lead an effort to decipher the data and determine the best course of action before others dictate solutions that might not necessarily produce the best results. Will this issue rise to a high enough priority to garnish the attention of the medical community in 2013? Yes, the medical community has to be proactive in the shaping of a public health policy on this issue before it is thought of as part of the problem. Physicians have to identify their part in this process, understand the patients’ actions and responsibilities, consider the psychosocial issues of abuse and addiction, provide active monitoring and management, and lead the national effort to address this issue. Dr. Raed Assar is Aetna’s Medical Director for North Florida. Articles or opinions provided by Dr. Assar do not necessarily reflect the views of Aetna.

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From the President’s Desk

DCMS: Illustrious History But Current Challenges Duval County Medical Society (DCMS) is the oldest organized medical society in Florida, originating in 1853. (See Florida’s Pioneer Medical Society: A History of the Duval County Medical Society & Medicine in Northeast Florida for a complete history). The Society has a long history of activity in public health and helping doctors in their practice of medicine. From the work during the 1877 yellow fever outbreak, to our current engagement with accountable care organizations (ACOs) and the electronic health record (EHR), the Society stands on the leading edge of issues important in the practice of medicine in Duval County. The DCMS will take that leading role in preparing its members for ACOs, starting with a major symposium to be held in the spring focused on ACOs and Patient Protection and Accountable Care Act (PPACA). We are entering a brave new world of medical care dominated by dictates from ACOs, generation gaps among our colleagues who have varying goals and expectations, and the challenge of EHRs. All of these affect our entire membership. None of us will remain untouched from the changes brought about by the PPACA, and physicians, as well as their patients, are ill-prepared for what is coming. “Obamacare” will alter the fabric of our daily work and we must adjust to it. ACOs will be the new model of patient care as small group and solo practices close. Physicians will be working for these organizations, many of which will be hospital-based. Physicians for the first time will be collecting a paycheck rather than billing a patient or an insurance company for services. The ACOs will be in charge financially, and it is in our best interest to find a way to be among the administrators of these programs. We need to do this to maintain a “seat at the table” in order to be adequately compensated for our services.

Eli Lerner, MD 2013 DCMS President

Meeting these challenges and solving these problems requires a local organization to look after our best interests and those of our patients. DCMS is that group. The Society is hosting meetings to address practice patterns and how to practice effective medicine within an ACO. Other meetings are being held to help young physicians understand the business aspects of their practice, the need for investments and also how to prepare eventually for retirement. It is the goal of these gatherings to help members be in more control of their practice lives, happier in their profession and hopefully, more involved in organized medicine.

For several years we have been actively engaged in studying the EHR. DCMS had a major meeting that served as a primer of EHRs with speakers nationally recognized who live in our state. They explained the basis of what health records should be able to do. A second series of meetings focused on products which experts felt would be of help. However, there were still no answers as we came closer to mandatory EHR nationally. We still have more questions than answers. Our DCMS Health Information Technology Committee is trying to find us answers and has been deeply involved with a regional program to bring us connectivity. Generational gaps are a very difficult problem. We span at least four distinct generations. The things that interest me have little or no relevance to our younger members, yet we all realize that we have to stay united to maintain our professional ideals and practices. These generations have been studied, and we will try to encourage all members to stay active. I am committed to exploring various approaches to our broad based membership. I will move forward with committees and groups through our Internet presence for those among us who wish to be active but who, for one reason or another, cannot physically attend meetings. We will develop a cyber-presence for the DCMS to more deeply involve members and imbue a pride of involvement and activity within them. Our patients are the most important people in this whole changing face of health care. It is no longer enough to care for their physical and emotional needs. We must now become their guides through this brave new medical world in which we find ourselves. It will become more of our mission as physicians and the future of our profession may very well rest with how we answer these questions and how we defend patients’ accessibility to the care that they need. We will have to help them navigate those murky waters. I pray that we will all work together to navigate the seas of changing health care that form our future, creating a better work environment for us, our colleagues and our patients. I believe that we can and will go forward and make Duval County an even greater medical workplace than it is today. Get aboard and help DCMS navigate the health care typhoons facing us in the future.

www . DCMS online . org

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Become a Partner in Medicine. The Duval County Medical Society’s Partners in Medicine program offers several different options for getting involved with the DCMS and its members including: advertising in our quarterly journal (Northeast Florida Medicine), advertising in the DCMS Membership Directory, exhibiting at our annual meeting and/or supporting an educational or general membership meeting! Take a look at who is already a Partner in Medicine. PIM LEVELS INCLUDE: Physician Level – $10,000

Fellowship Level – $5,000 Resident Level – $2,500

Partner Level – $1,000

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Philip H. Gilbert Invited Editorial

Physicians Need To Retain Their Leadership in the Community Sunil Joshi, MD 2012 Philip H. Gilbert Young Physician Leadership Award Recipient Physicians have always been viewed as the ultimate leaders and providers of healthcare in the community. This has been true for hundreds of years and remains partially true today. Unfortunately, in the current healthcare environment, the lines of authority have blurred and now include physician extenders, pharmacists, health insurance companies, government agencies, hospital administrators and even the President of the United States. As physicians, we must differentiate ourselves from the others by leading the discussion and direction of healthcare in our communities. In order to do this successfully, however, the public must see doctors as trustworthy and altruistic professional leaders who are looking out for the best interests of people in their own localities. To be effective, we must understand that much like medicine itself, leadership is an art that evolves over time and takes many forms. A physician can be a leader without being a government official or a CEO of a hospital or the chairman of a department. For instance, we can be involved in the countless number of not-for-profit organizations that help to raise awareness and direct effective programs that educate the public about common chronic health conditions. These groups are in need of engaged physicians to sit on advisory boards or to be chairman of committees and/or special events programs. Our experience and extensive fund of medical knowledge are invaluable and can be used to impact hundreds of residents in a meaningful way. Many physicians have young children involved in multiple after school activities. These doctors have an opportunity to lead by volunteering to sit on the Parent Teacher Association (PTA), or to help with the school band, sporting events, field trips or any school program. This is not only a way to promote the caring nature of the profession, but it is also extremely satisfying personally. The Duval County Medical Society (DCMS) provides its members with multiple opportunities to educate the public through a relationship with the Florida Times Union. The “Doctors on-call” section which is published on most Wednesdays, allows the physicians in town to inform the public about complicated medical matters in the appropriate way as opposed to learning it from a website blog or uninformed news reports. The DCMS has also become the “go to” source of medical information for local television and radio media outlets. These are certainly opportunities where physicians can lead the discussion about important health related topics. Immediate Past President, Dr. Ashley Booth Norse presents Dr. Sunil Joshi with the 2012 Philip H. Organized medicine also provides physicians with an opportunity to make Gilbert Young Physician Leadership Award. a difference. Many of us complain about the direction of healthcare in this country, but so few of us take the time to affect change. Simply paying annual dues to the AMA, FMA and DCMS are all extremely helpful at promoting our cause, but taking the time to attend a political fundraiser or author a resolution to the FMA or speak to our elected leaders in Tallahassee and Washington make much more of a meaningful impact. One of the problems that has led to physicians losing their positions as the leaders in healthcare is their lack of involvement. This must change, and that starts with each of us taking an extra step. In conclusion, I do not believe that people are born leaders. When given an opportunity, we as physicians can do great things. Whether it is volunteering at our children’s schools, advising not-for-profit health organizations, or disseminating appropriate information about medical conditions through the media, we can all begin the process of being health care leaders in a relatively short time and on our schedules. Once the momentum of the effort builds, leading becomes second nature. Remember, leading is not a right that we are born with. “Leaders are made not born,” and when given the appropriate opportunity, they can affect change in a positive way for themselves and their communities. Let’s start today!

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From the EVP’s Desk Welcome to the first issue of 2013. The focus of the Duval County Medical Society in 2013 is you, the member. So, to help kick that off, we have a number of member benefits that I would like to share with you. Income Protection Insurance DCMS Members enjoy between 25% and 40% reduction on Income Protection Insurance through Mass Mutual, and between 10% - 40% on Long Term Care Insurance. To learn more, contact Nathan Rogero atnrogero@financialguide.com and include “DCMS Benefit” in the email.

Bryan Campbell DCMS Executive Vice President

Medical Malpractice Insurance FPIC is now The Doctors Company, but the same great rates and benefits, including the Tribute Plan, are still in place for DCMS Members to take advantage of. To learn more, contact Shelly Hakes at SHakes@thedoctors.com and include “DCMS Benefit” in the email.

HIPAA Compliant Payment Processing Is your payment processing HIPAA compliant? Does your system encrypt confidential data before it hits the internet? WorldPay is a global leader in secure payment processing. Make the switch to WorldPay and receive a $50 credit towards your 2014 DCMS dues. To learn more, contact Scott King at Scott.King@WorldPay.us and include “DCMS Benefit” in the email. Boat Club Membership DCMS isn’t just looking out for your practice, we’re looking to save you money in your free time, as well. If you love boating, this is the benefit for you. Jax Boat Club is offering three free months of boat club membership to DCMS Members. That’s a savings of up to $1,200. To learn more, contact Marc Ball at Marc@jaxboatclub.com and include “DCMS Benefit” in the email. Continuing Education for your Staff We are pleased to announce the newest edition to our DCMS Membership Benefit Package. The Florida State College of Jacksonville is partnering with DCMS to create continuing education programs for DCMS Members and their staff. These courses range from Microsoft Office to Customer Service, with special rates for DCMS Members and their staff only.

To help us get started, we need your feedback. Please take the short survey below (or go to www.surveymonkey.com/s/XBXJLTR to fill out online) and fax your response to 904.353.5848. 1. Are you interested in you or your employees attending business, professional, or computer classes offered by Florida State College at Jacksonville at a discounted rate and sponsored by the Duval County Medical Society? q Yes q No 2. How often would you like the Duval County Medical Society to sponsor the College to offer a class in business, professional, or computer education to you or your employees? q Every Other Week q Monthly q Every Other Month q Quarterly 3. Which days of the week are most convenient for your schedule or your employees’ schedules to attend a class offered by the College? q Monday q Tuesday q Wednesday q Thursday q Friday q Saturday

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4. What time of day would you prefer a class be held? q 8 AM – 5 PM (M – F) q 6 PM – 8 PM (M – F) q 12 PM – 5 PM (M - F) q 8 AM – 12 PM (M – S) 5. Would you prefer a one-day class (8 AM – 5 PM) or the class held over a few sessions (example: four two-hour classes one day per week)? 6. Please review the sample FSCJ course offerings below and choose the top 5 classes that you believe would be most beneficial for you or your employees. q Basic Health Insurance q Business Etiquette q Business Writing q Essential Leadership Skills q Excel 2010 Basic q Excel 2010 Intermediate q Excel 2010 Advanced q Exceptional Customer Service q Fundamentals of Finance q I’m Okay, You’re Difficult

q q q q q q q q

Microsoft Office Suite QuickBooks Pro Social Media in the Business Environment Stress Management The Essence of Supevision Thinking Critically about Ethical Issues Windows 7 Basic Word 2010 Basic

7. Please list any additional course topics that you would like to have offered by the College. 8. Please provide your name and email address.

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Residents’ Corner: St. Vincent’s Family Medicine Residency Program Editor’s Note: In an effort to connect more Duval County Medical Society members with residents, in each 2012 issue there will be a “Residents’ Corner” with information about a residency program in the area, details about research being done and/or a list of achievements/accomplishments of the program’s residents. This “Residents’ Corner” features the University of Florida's Oral & Maxillofacial Surgery Residency Program.

Overview of the Program

The St. Vincent’s Family Medicine Residency Program was developed in 1972 and has expanded with time; now accepting 10 residents per year for the three-year program. The residency is dually accredited by the Allopathic and Osteopathic Boards. Osteopathic physician graduates are eligible for both the ABFM and the AOBFP board certification. The Program has successfully graduated 285 board certified family physicians who work throughout the country in a variety of practices since its inception. The Family Medicine Residency Program is staffed by full-time faculty physicians dedicated to resident education, which includes Family Medicine, Pediatrics, and OB/GYN. In addition to being fully unopposed the program has affiliations with Ascension Health, St. Vincent’s Medical Center, Wolfson Children’s Hospital, FSU and the University of South Florida for additional training. The residency program is housed in a 30,000 square foot building containing 34 examination rooms and 4 minor surgical rooms, which makes it possible for over 33,000 office visits per year. The program is fully equipped with ultrasound machine, laboratory, and EMR. The building is located across the street from the main hospital which houses 528 beds, including ICUs and the Family Birthing Center. Residents have participated in over 499 obstetrical deliveries yearly.

Resident Research

• Jacqueline Wells, MD (PGY3), Natasha Hunter, MD (PGY3), Monique Gray-Jefferson, MD (PGY2), Elizabeth Marquez, MD (PGY 2), Stacey Quinn, DO (PGY1) - We are working to understand why breast feeding rates have been declining and to help improve those rates in our clinic patients through education. We hope to be able to extrapolate that data to be used in the hospital for all patients. • Mandy Franklin, MD (PGY3) – Is working to assist with establishing the medical home by improving our specialist referral process. • Monique Gray-Jefferson, MD (PGY2) – Working to increase completion of HPV vaccination rates in our clinic by identifying the loop holes that all patients to fall through and fixing them. • Benjamin O’Connell, DO (PGY2) – As part of our Medical Home Project, he is working to decrease our pediatric asthma emergency room rates and those lost to follow-up. We hope to accomplish this by increasing asthma control checks at least every 6 months and ensuring each patient has an updated Asthma Action Control Plan at each visit.

Residency Outreach

• Each year residents participate in the many mission trips to Haiti to assist in Pediatric or Gynecological care, conducting more than 1000 pediatric exams and several free surgeries. • Many of the clinic’s uninsured and underinsured patients have benefited from the advanced technology of the DaVinci Robotic surgeries conducted by one of our part time Ob/Gyn physicians, Dr. William Cody and senior residents. • Each year our residents participate in the Special Olympics, conducting more than 300 hundred physical exams to help Olympiad hopefuls play safe. • We have recently added a rural health site to our curriculum in Crescent City through the local AHEC organization. • Many of the residents and faculty volunteer to assist with the Mobile Health Unit, which is a group of physicians, nurses and staff who travel to underserved communities and provide free medical care in the surrounding counties.

Residency Achievements

• Danielle Carter, MD (PGY3) – Recently received the award for FAFP Scholar of the Year. She has also been inducted as the FAFP Resident Director and accepted to Ob/Gyn Fellowship at Mayo Clinic in Rochester.

• Robert Raspa, MD – Recently inaugurated as the FAFP President. On the national level, he is also the Chair of the Subcommittee on Graduate Curriculum for the Commission on Education for the AAFP. • Drs. John Waidner and Helena Karnani, and Caroline Daniels LPN BSSA, have completed an 18 month program with the Florida Pediatric Medical Home Project and were presented with a recognition award. The project involved 16 Pediatric and Family Medicine practices from the State of Florida who conducted research, attended learning sessions, and implemented core measures that furthered the establishment of a Pediatric Medical Home within their practices. At St Vincent’s Family Medicine center we have developed an asthma registry for pediatric patients with asthma and used it to ensure patients get needed F/U appointments and flu shots. We have also implemented screening programs for Autism and developmental delays in children. • “The Sapphire Awards and Symposium is Florida’s only statewide event that recognizes organizations, programs and individuals that have demonstrated excellence and innovation in community health. Since its inception, 45 individuals and/or health-focused non-profits have been honored and over $2.4 million has been awarded in recognition of their achievements”. This year the Sapphire Award Program Honoree is St. Vincent’s HealthCare Foundation, Mobile Health Outreach Ministry in Jacksonville, Florida. Much of the care rendered by the MHU could not be possible without the St. Vincent’s Family Practice Residency Program residents.

Monique Gray-Jefferson, MD is a resident at St. Vincent’s Family Medicine Residency Program and will attain completion in 2014. She plans to stay in Jacksonville, Florida to continue her medical career. www . DCMS online . org

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Patient Page* - Peptic Ulcer Disease

Peptic Ulcer Disease (Information adapted from “Managing Complications of Peptic Ulcer Disease” by Andrea McNab, MD; Reginald Griffin, MD; and Ziad T. Awad, MD, FACS in Northeast Florida Medicine, Vol. 64, No. 1, Spring 2013)

Overview

Definition

“an ulcer of the upper digestive tract, usually in the stomach or duodenum, (beginning of lower intestine) where the mucous membrane is exposed to gastric secretions.” (Stedman’s Medical Dictionary)

• Peptic ulcer disease (PUD) and its complications are a significant cause of illness and death worldwide. • Complications are on the rise in older patients because of increased use of non-steroidal anti-inflammatory drugs (NSAIDS), but it is declining in younger patients. • In the past, a PUD diagnosis generally meant an operation was necessary. Today, the condition is mostly treated medically and operations are not indicated for uncomplicated disease.

Main Causes

• Helicobacter pylori – bacteria in stomach responsible for up to 85% of the changes to the gastric mucosa seen in peptic ulcers. • Aspirin and NSAIDs (non-steroid anti-inflammatory drugs, ie. Advil®, motrin, ibuprofen or naproxen) – alone or in combination with H. pylori • Smoking also increases recurrence, impairs ulcer healing, and increases chances of surgical intervention.

Symptoms

• Nausea • Vomiting • Bloating • Weight loss • Gastroesophageal reflux • Intermittent abdominal pain sometimes related to eating.

Common Complications • Bleeding • Perforation • Obstruction

Management of PUD

Non-surgical treatment and preventive measures are used now rather than surgery. Increasing use of PPI ( proton pump inhibitor ie. Prilosec OTC®), antibiotics, and reduction in causal factors have decreased need for elective surgery. However, PUD complications are still very frequent. With the continuing development of endoscopic and laparoscopic therapies, operations are becoming less invasive.

Further Reading • Milosavljevic T, Kostic-Milosavljevic M, Jovanovic I. Complications of peptic ulcer disease. Dig Dis. 2011;29(5):491-3. • NIH consensus conference. Helicobacter pylori in peptic ulcer disease. NIH consensus development panel on Helicobacter pylori in peptic ulcer disease. JAMA. 1994;272(1):65-9. • Kato I, Nomura AM, Stemmermann GN. A prospective study of gastric duodenal ulcer and its relation to smoking, alcohol, and diet. Am J of Epidem. 1992;135(5):521-530.

*Copy and distribute to patients or go to dcsmsonline.org to download. 12 Vol. 64, No. 1 2013 Northeast Florida Medicine

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Diseases of the Stomach Ziad T. Awad, MD, FACS It is my pleasure to be the Guest Editor for the spring edition of the Northeast Florida Medicine journal. The stomach has many diseases; functional, infectious, inflammatory, ulcerative and neoplastic. I chose four topics to focus on for this issue. They are management of upper gastrointestinal bleeding, complications of peptic ulcer disease, gastric cancer and gastroparesis. While other diseases of the stomach are more common, in my opinion, they are easier to manage, and pose less of a problem for the physician and health care system. In “Upper Gastrointestinal Bleeding: Variceal and Non Variceal Hemorrhage” by Camille, McGaw, MD; Sujai Jalaj, MD, Paul Sievert, MD and James S. Scolapio, MD, the focus is on upper gastrointestinal bleeding (UGIB). The aim of the article is “to review the evaluation and intervention for variceal bleeing as well as non-variceal bleeding.” In “Managing Complications of Peptic Ulcer Disease,” by Andrea McNab, MD; Reginald Griffin, MD and myself, the article highlights peptic ulcer disease (PUD) and its complications that are a significant cause of morbidity and mortality worldwide. Most operations are being performed for emergent complications of PUD. This article is also the basis for the Patient Page in the issue. Physicians may copy this page and place it in their office waiting rooms for patient education on the topic.

Ziad T. Awad, MD, FACS Guest Editor, Spring 2013

Of particular interest to me is gastric cancer, so I authored “Current Management and Future Strategies of Gastric Cancer.” Although the overall prognosis for this cancer has gradually improved over the past decades, the outcome of advanced this stomach disease still remains poor with currently available treatments.

I asked two colleagues to independently write about gastroparesis since it a difficult problem to manage and poses a significant burden to the health care system. It causes prolonged hospitalization, recurrent hospital admissions, and unpredictable success with available treatment options. Jose Nieto, DO, wrote “Management of Gastroparesis”. He discusses management of this disease such as dietary changes, nutritional supplementation, psychological intervention, anti-emetic and prokeinetic medications, gastric electrical stimulation as well as endoscopic and surgical procedures. Bijo K. John, MD; Ann J. Lee, MD, Paul Sievert, MD and James S. Scolapion, MD authored, “Gastroparesis”. This article provides an update on gastroparesis, focusing on clinical features, diagnostic evaluation and management. Diseases of the stomach are many and varied. All cause great discomfort and many are difficult to not only diagnosis but treat successfully. Gastrointestinal bleeding, peptic ulcers, gastric cancer and gastroparesis are among those stomach diseases that challenge physicians and threaten the long term health of patients. I trust this issue gives the journal readership not only helpful information but some direction on how to handle these illnesses

2013 Northeast Florida Medicine Schedule Spring: Diseases of the Stomach Summer: Preventive Medicine Fall: Pediatric and Adult Congenital Heart Disease Winter: Sleep Health

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This Issue’s Focus: Gastric Disease

Upper Gastrointestinal Bleeding: Variceal and Non Variceal Hemorrhage Camille McGaw, MD, Sujai Jalaj, MD, Paul Sievert, MD and James S. Scolapio, MD Abstract: Upper gastrointestinal bleeding (UGIB) is defined as hemorrhage originating proximal to the ligament of Treitz. UGIB continues to be a common cause of hospitalization with substantial mortality throughout the world. UGIB can be divided into two categories: variceal and nonvariceal bleeding. In both instances, initial therapy is geared towards resuscitation. Pharmacologic therapy is initiated prior to endoscopic therapy which is the definitive intervention. Endoscopy is recommended within 12 hours for variceal hemorrhage and within 24 hours for non-variceal hemorrhage. The aim of this article is to review the evaluation and intervention for variceal bleeding as well as non-variceal bleeding (with a focus on peptic ulcer disease.)

Introduction: Variceal Hemorrhage An acute UGIB in the setting of liver cirrhosis raises the concern for an acute variceal hemorrhage. A major cause of cirrhosis-related morbidity and mortality is the development of variceal hemorrhage, a direct consequence of portal hypertension. Nearly 50% of all patients with cirrhosis have varices at the time of diagnosis.1 The incidence of variceal hemorrhage occurs at an estimated yearly rate of 5-15% in cirrhotic patients and is influenced primarily by the size of varices.2 This section reviews the natural history of varices as well as the current approach to management of acute variceal hemorrhage, and the prevention of initial and recurrent variceal hemorrhage. Natural History of Varices — Varices and variceal hemorrhage are complications of cirrhosis that result most directly from portal hypertension. Portal hypertension results from physiologic changes causing an increase in both portal vascular resistance and portal blood flow. These physiologic changes lead to the formation of gastroesophageal varices (GEV), which serve as collaterals between the portal and systemic venous systems. As portal pressure increases, varices grow in size and their vessel wall thins, resulting in increased wall tension and eventual rupture. Portal hypertension exists when the portal pressure is greater than 5 mmHg. Portal hypertension can be measured by determining the hepatic venous pressure gradient (HVPG). HVPG is calculated with a balloon catheter by measuring the free hepatic vein pressure (FHVP) and the wedged hepatic venous pressure (WHVP) as follows:

HVPG = WHVP - FHVP

HVPG greater than 10 mmHg predisposes to the development of varices, while a HVPG greater than 20 mmHG is a poor prognostic factor during a variceal bleed.3 14 Vol. 64, No. 1 2013 Northeast Florida Medicine

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Initial Management — Initial therapy for acute variceal hemorrhage is resuscitation in an emergency room or intensive care unit. Blood volume restitution should be undertaken promptly but with caution, with the goals of maintaining hemodynamic stability and hemoglobin levels around 7-8 g/ dL.3,4 Overtransfusion or volume overexpansion can lead to further increase in portal pressure and consequently precipitate variceal rebleeding. There should also be a low clinical threshold for endotracheal intubation in order to protect the airway, as the risk of aspiration is high in the presence of encephalopathy, hematemesis, and during emergent endoscopy. Pharmacologic Therapy — Although endoscopy is the definitive therapy, pharmacologic advances have led to the development of drugs that can minimize the extent of bleeding from varices by inducing splanchnic vasoconstriction and thereby reducing portal pressure. Octreotide, a somatostatin analogue, has splanchnic vasoconstrictive effects and is the only drug of its class available for use in the United States. Octreotide is administered with a loading dose IV bolus of 50 μg followed by a continuous infusion of 50 μg/hour. Octreotide is generally well tolerated and should be used for up to five days.5 Octreotide use in combination with urgent endoscopy has been shown to improve hemostasis and reduce the rate of early rebleeding compared to endoscopy alone. However, rates of mortality and other adverse events remain unchanged.6 Antibiotic Prophylaxis — Bacterial infections are a common and severe complication among cirrhotic patients presenting with an UGIB irrespective of cause (variceal or non-variceal). About 20% of cirrhotic patients with an UGIB have a bacterial infection upon presentation, and nearly 50% acquire nosocomial infections during hospitalization.7 Short-term antibiotics should always be administered to cirrhotic patients with UGIB whether ascites is present or not. Norfloxacin is a reasonable choice of antibiotic and can be administered at a dose of 400mg orally twice a daily for seven days. In high-risk patients (multiple co-morbidities and Child-Pugh Class B or C), IV ceftriaxone at 1g/day may be a better choice.3 Endoscopic Therapy — Endoscopic evaluation should occur within the first 12 hours of a patient presenting with an acute variceal bleed. Endoscopic treatments are successful in controlling bleeding in 80% to 90% of cases.8 Endoscopic variceal ligation (EVL), also known as variceal banding, is the current endoscopic standard of care. Banding occludes www . DCMS online . org

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variceal blood flow and leads to ischemia and necrosis of the mucosa and submucosa. Both the elastic bands and necrotic tissue slough off over a period of 2 to 3 weeks, leaving shallow ulcerations called esophageal band ulcers. Salvage Therapy — As mentioned earlier, endoscopic treatments are successful in controlling bleeding in 80% to 90% of cases. In the 10% to 20% of cases in which endoscopy is not successful in controlling bleeding, transjugular intrahepatic portosystemic shunt (TIPS) is the preferred rescue therapy. Decision to proceed to TIPS should be made in select group of patients because mortality rates after TIPS remain high at 30% to 50%, although this measure is likely inflated due to the selection bias inherent in this severely ill patient cohort.9 TIPS is contraindicated in the presence of the following conditions: pulmonary hypertension, hepatopulmonary syndrome, advanced congestive heart failure, current or previous hepatic encephalopathy, active systemic infection (sepsis or hepatic abscess), polycystic liver disease and patients with Child-Pugh class C cirrhosis. Balloon tamponade is another potential salvage intervention. Balloon tamponade should be considered only after all pharmacologic and endoscopic interventions have been exhausted, and when definitive treatment, such as TIPS, is anticipated within 24 hours. It is highly important to remember that balloon tamponade is a transient and temporizing measure to control bleeding. Patients should be intubated before placement of balloon tamponade. Prophylaxis Against Variceal Bleeding — Prophylaxis against variceal bleeding falls into three categories: primary, pre-primary, and secondary prophylaxis. Primary prophylaxis aims to prevent variceal hemorrhage in patients with known varices but who do not have a history of variceal bleeding. Pre-primary prophylaxis refers to measures that aim to prevent the development of varices. Measures aimed at preventing hemorrhage in patients with history of variceal hemorrhage are referred to as secondary prophylaxis. Non-selective β blockers are the pharmacologic agent of choice as they have been shown to lower risk of variceal bleeding. Non-selective β blockers act through β1 and β2 adrenoreceptors to reduce portal blood flow. β blockers should be adjusted to the maximum tolerated dose or to maintain a resting heart rate of 55 to 60 beats per minute.3,4 Once a patient is diagnosed with cirrhosis, screening for varices with endoscopy is performed to check for presence and grade of varices. The stage of cirrhosis guides the frequency of screening endoscopy after the initial diagnosis. Patients with compensated cirrhosis are recommended to undergo screening endoscopy every two years while those with decompensated cirrhosis undergo endoscopic screening annually. Address Correspondence to: James S. Scolapio, MD, Professor of Medicine, Chief, Division of Gastroenterology, University of Florida, 4555 Emerson Street, Suite 300, Jacksonville, FL 32207. Phone: 904-633-0089. Email: james.scolapio@jax.ufl.edu. www . DCMS online . org

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After esophageal varices are diagnosed on endoscopy, it is important to determine size of the varices. Variceal size is classified as small, medium or large. In patients with no endoscopic evidence of varices, a large randomized controlled trial showed that there was no protective benefit in patients given non-selective β blockers in prevention of variceal development.3 When small varices are found, non-selective beta blockers may be used for the prevention of first variceal hemorrhage in patients who have an increased risk of hemorrhage as supported by presence of Child-Pugh class B/C disease or visualized red wale marks on endoscopy.4 Evidence for efficacy of prophylaxis for low-risk patients with small varices is mixed. Patients with medium/large varices that have not bled, β blocker is the preferred method of treatment for the prevention of first variceal hemorrhage. Among patients with medium/large varices, β blockers reduced the rate of bleeding by more than half.4 Prevention of variceal bleed may also be achieved by obliteration of varices with EVL. If β blockers are contraindicated or not tolerated due to side effects, obliteration of varices using EVL can be considered. After obliteration, endoscopic surveillance is scheduled in 1 to 3 months and every 6 to 12 months thereafter. EVL may be used as primary prophylaxis, but current data does not clearly favor endoscopic therapy over β blocker therapy. Optimal treatment for secondary prophylaxis is a combination of non-selective β blocker therapy and EVL. In patients who have a recurrence of variceal hemorrhage despite combined treatment with pharmacologic and endoscopic therapy, TIPS should be considered to allow for decompression of the portal system. Liver transplantation provides the only definitive treatment for rebleeding because it addresses the underlying pathophysiology. Patients who are transplant candidates should be referred to a transplant center for evaluation. Gastric Varices — Thus far, we have focused our attention on esophageal varices, yet portal hypertension leads to pathologies at other sites such as gastric varices. Gastric varices occur in approximately one-fifth of cirrhotic patients and account for less than 10% of cases of acute variceal bleeding.10 The lower rate of bleeding of gastric varices is due to primarily two mechanisms. First, gastric varices are perfused by the short and posterior gastric veins, which have lower luminal pressures. Secondly, gastric varices are often decompressed by spontaneous gastrorenal shunts. Gastric varices are classified into two major categories on the basis of location: gastroesophageal varices (GOV) as well as isolated gastric varices (IGV). GOV are simply an extension of esophageal varices into the stomach. GOV is further divided into two groups: GOV1 and GOV2. GOV1 comprises varices that extend below the GE junction along the lesser curvature of the stomach. GOV2 describes varices that extend toward the fundus of the stomach.

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Figure 1 Forest Classification of Peptic Ulcers in UGIB27 Ba

C (Used with permission)

Forest classification can be summarized as grade: (Aa) Arterial hemorrhage (“splurting”). (Ab) Diffuse hemorrhage (“oozing”). (Ba) Non-bleeding visible vessel. (Bb) Adherent clot. (Bc) Flat pigmented spot. (C) Ulcer without recent stigmata of bleeding (“clean base”).

IGV are often a consequence of pre-hepatic portal hypertension. IGV are also divided into two groups: IGV1 and IGV2. IGV1 are located in the fundus, and IGV2 reside in the antrum, body, and around the pylorus. It is important to note that IGV1 are caused by splenic vein occlusion, in which case splenectomy may be curative. Due to the lower frequency of bleeding, therapy of gastric varices is not as well studied. Though not established, pharmacologic and prophylactic therapies for acute gastric variceal bleed are the same as for esophageal varices.10 Endoscopic treatment options for gastric varices are limited. EVL does not work well for gastric varices. TIPS is the therapy of choice.

Introduction: Non-Variceal Hemmorage Nonvariceal upper gastrointestinal bleeding (NVUGIB) is a common medical emergency with hospitalizations showing an annual incidence of approximately 100 per 100,000 adults in the early 1990’s. The incidence and mortality of UGIB has decreased significantly, likely due to the advances made such as introduction of proton pump inhibitors and treatment of Helicobacter pylori. Given the recent increasing proportion of elderly patients presenting with UGIB who are more likely to be receiving non-steroidal anti-inflammatory drugs (NSAIDs), NVUGIB can have considerable morbidity and mortality. The etiology of NVUGIB is varied but the most common etiology is Peptic Ulcer Disease (PUD) and for this reason, this review will focus mainly on bleeding from PUD and the current evidence for management of this disease. The most common causes of PUD at this time are NSAID use and Helicobacter pylori infection. Initial Evaluation — The management of NVUGIH involves assessment of hemodynamic status with initiation of volume-resuscitation as needed and timely endoscopy to diagnose and treat the lesion. Multiple scoring systems have been created in order to risk-stratify patients in terms of re-bleeding, need for intervention and mortality. These include APACHE II, Forrest Classification, Glasgow-Blatchford, pre-endoscopic Rockall, Baylor College, Cedars-Sinai Medical Center and Rockall indexes. There have been numerous

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studies done to determine the best scoring system. Current evidence shows that the Glasgow-Blatchford score can be used to predict need for hospital-based intervention, although Attar et al found GBS not helpful in this regard.13,14,15 The utility of the scoring systems in predicting 30-day mortality is also unclear. Other methods of stratifying patients that have been explored also include use of nasogastric aspirate. NG aspirate is thought to be helpful if bloody, as can predict high risk lesion. However, absence of blood is less helpful as high risk lesion can still be present. Pharmacologic Therapy — Proton pump inhibitor has become a standard of therapy in patients suspected of having NVUGIB and high dose Proton pump inhibitor (PPI) given prior to endoscopy has been found to reduce risk of lesions with high risk stigmata as well as reduce the need for endoscopic therapy.17,18 However, it has not been shown to impact clinical outcomes such as mortality, risk of re-bleeding or of need for surgery. Adjuvant PPI therapy after endoscopic treatment of PUD has been found to be of benefit in prevention of re-bleeding and is also superior to H-2 antagonists. 19,20 PPI bolus followed by continuous-infusion significantly improved outcome21 and high-dose PPI has been found to be superior to standard-dose PPI.22 Recent studies have found conflicting evidence regarding the need for high-dose PPI vs. non high-dose PPI after endoscopic treatment.23 More recent studies have shown no significant difference found between the route of administration of PPI.24 Guidelines recommend continuous infusion of high-dose PPI for 72 hours after endoscopic therapy for high risk lesions. Endoscopic Intervention and Care — Endoscopy is recommended within a 24-hour window as a general consensus, however, the optimal time within the 24-hour period is not yet known.25,26 The need for therapy at the time of endoscopy is decided based on endoscopic findings with regard to high-risk stigmata (HRS) (Figure 1).27 Lesions with HRS have different risks of rebleeding as seen in Table 1.26 Therapy is indicated for ulcers with nonbleeding visible vessels or those with active bleeding. The management of adherent clots is controversial but Kahi et al showed that endoscopic therapy is superior to medical therapy for preventing recurrent bleeding. 28 There are different modalities of endoscopic therapy including thermal www . DCMS online . org

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Table 1 1.Stigmata Endoscopictreatment Treatment Table StigmataofofHemorrhage Hemorrhageand andRisk risk of of Bleeding bleeding Without without endoscopic (modified from reference #26)

Endoscopic Characteristic Arterial bleeding Visible vessel without bleeding Adherent Clot without bleeding Ulcer oozing blood (without other stigmata) Flat pigmented spot Ulcer with clean base devices, injectable agents, hemostatic clips and injection of epinephrine. It has been shown that epinephrine as a single modality is not recommended and a second modality must be used.21 Re-bleeding and Management Post-Endoscopy — Despite endoscopic therapy, further bleeding can occur in up to 14% of patients after hemostasis.29 It is generally recommended to pursue repeat endoscopic therapy initially. Surgery is an alternative when endoscopy is unsuccessful at achieving hemostasis. Transcatheter arterial embolization (TAE) has also been explored as an alternate means of hemostasis. Ripoll et al performed a retrospective study comparing TAE and surgery for refractory bleeding that showed no significant difference in recurrent bleeding, need for further intervention or death.30 TAE has even been explored as a first-line treatment after endoscopic hemostasis with good results, however, TAE remains poorly studied and a well-designed prospective study is needed for further recommendations.31 Routine second-look endoscopy after endoscopic hemostasis is currently not recommended. There have been conflicting results from various studies. Earlier studies have proposed that second-look endoscopies would reduce recurrent bleeding and improve outcomes.32 A recent meta-analysis showed that rebleeding and surgery were significantly decreased by second-look endoscopy in the setting of lesions with HRS, but mortality was not affected.33 Of note as well, was the fact that when high dose PPI was used, there was no benefit seen. Thus, at this time, in this era of high-dose PPI, there is no present consensus advocating routine second-look endoscopies. It is recommended to administer high dose PPI (80mg bolus followed by 8mg/h continuous infusion for 72h) to reduce rebleeding in patients with HRS. Patients should also be treated with a PPI for 4 weeks and the underlying etiology of the ulcer addressed such as H. Pylori infection or NSAID use.

Conclusion Variceal and Nonvariceal Bleeding can have significant morbidity and mortality. Endoscopy is the mainstay of treatment as discussed, but there are certain steps that should be taken www . DCMS online . org

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Risk of Rebleeding without Endoscopic Therapy ~ 90% ~ 50% ~ 25% ~ 10% ~7-8% ~3% pre- and post-endoscopy. Pharmacologic therapy continues to remain significant in the management of both classes of hemorrhage. Endoscopic treatment is not always successful and salvage treatments are available. Further studies are needed for specific recommendations regarding salvage therapy in the setting of non-variceal bleeding.

References

1. Groszman RJ, Garcia-Tsao G, Bosch J, et al. Betablockers to prevent gastroesophageal varices in patients with cirrhosis. N Engl J Med. 2005; 353(21): 2254-2261. 2. Pagliaro L, D’Amico G, Pasta L, Politi F, Vizzini G, Traina M, et al. Portal hypertension in cirrhosis: Natural history. In: Bosch J, Groszmann RJ editor. Portal Hypertension: Pathophysiology and Treatment. Oxford: Blackwell Scientific Publications; 1994: 72-92. 3. Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N Engl J Med. 2010; 362(9): 823-832. 4. Garcia-Tsao G, Sanyal AJ, Grace ND, Carey W. Practice Guidelines Committee of the American Association for the Study of Liver Diseases, Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007; 46(3): 922-938. 5. Corley DA, Cello JP, Adkisson W, Ko WF, Kerlikowske K. Octreotide for acute variceal bleeding: a meta-analysis. Gastroenterology. 2001; 120(4): 946-954. 6. Banares R, Albillos A, Rincon D, et al. Endoscopic treatment versus endoscopic plus pharmacologic treatment for acute variceal bleeding: a meta-analysis. Hepatology. 2002; 35(3): 609-615. 7. Bendsten F, Krag A, Moller S. Treatment of acute variceal bleeding. Dig Liver Dis. 2008; 40(5): 328-336. 8. Bosch J, D’Amico G, Garcia-Paga JC. Portal hypertension and nonsurgical management. In: Schiff ER, Sorrell MF, Maddrey WC, eds. Diseases of the Liver. 10th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2007: 419. Northeast Florida Medicine Vol. 64, No. 1 2013 17

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9. Garcia-Pagan JC, Caca K, Bureau C, et al. Early use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med. 2010; 362(25): 2370-2379. 10. Ryan BM, Stockbrugger RW, Ryan JM. A pathophysiologic gastroenterologic, and radiologic approach to the management of gastric varices. Gastroenterology. 2004; 126(4): 1175-1189. 11. Longstreth GF. Epidemiology of hospitalization for acute upper gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol.1995; 90(2): 206-210 12. Lau JY, Sung J, Hill C, Henerson C. Systematic Review of the Epidemiology of Complicated Peptic Ulcer Disease: Incidence, Recurrence, Risk Factors and Mortality. Digestion. 2011; 84: 102-113 13. Laursen SM, Hansen JM, Schaffalitzky de Muckadell OB. The Glasgow Blatchford score is the most accurate assessment of patients with upper gastrointestinal hemorrhage. Clin Gastrotenterol Hepatol. 2012; 10 (10): 1130-1135 14. Dicu D, Pop F, Ionescu D, Dicu T. Comparison of risk scoring systems in predicting clinical outcome at upper gastrointestinal bleeding patients in an emergency unit. Am J Emeg Med. 2012 Sep 20. pii: S07356757(12)00334-8. doi: 10.1016/j.ajem.2012.06.009. [Epub ahead of print] 15. Attar A, Sebbagh V, Vicaut E, et al. Urgent endoscopy in severe non-variceal upper gastrointestinal hemorrhage: does the Glasgow-Blatchford score help endoscopists? Scand J Gastroenterol. 2012;47:1086-1093 16. Aljebreen A, Fallone C, Barkun A. Nasogastric aspirate predicts high-risk endoscopic lesions in patients with acute upper-GI bleeding. Gastrointest Endosc. 2004; 59(2): 172-178 17. Sreedharan A, Martin J, Leontiadis GI, et al. Proton pump inhibitor treatment initiated prior to endoscopic diagnosis in upper gastrointestinal bleeding. Cochrane Database Syst Rev 2010 (7): CD005415 18. Lau JY, Leung WK, Wu JC, et al. Omeprazole before endoscopy in patients with gastrointestinal bleeding. N Engl J Med. 2007; 356(16): 1631-1640 19. Hsu PI, Lo GH, Lo CC, et al. Intravenous pantoprazole versus ranitidine for prevention of rebleeding after endoscopic hemostasis of bleeding peptic ulcers. World J Gastroenterol.2004; 10 (24): 3666-3669 20. Lin HJ, Lo WC, Cheng YC, Perng CL. Role of intravenous omeprazole in patients with high-risk peptic ulcer bleeding after successful endoscopic epinephrine injection: a prospective randomized comparative trial. Am J Gastroenterol. 2006;101(3):500-505 21. Laine L, McQuaid KR: Endoscopic therapy for bleeding ulcers: an evidence-based approach based on meta-analyses of randomized controlled trials. Clin Gastroenterol Hepatol. 2009; 7:33-47

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22. Chan WH, Khin LW, Chung YF, et al. Randomized controlled trial of standard versus high-dose intravenous omeprazole after endoscopic therapy in high-risk patients with acute peptic ulcer bleeding. Br J Surg. 2011; 98(5):640-644 23. Wang CH,Ma MH, Chou HC. High-dose vs non-highdose proton pump inhibitors after endoscopic treatment in patients with bleeding peptic ulcer: a systematic review and meta-analysis of randomized controlled trials. Arch Intern Med. 2010; 170 (9): 751-758 24. Javid G, Zargar SA,U-Saif R, et al. Comparison of p.o or i.v. proton pump inhibitors on 72-h intragstric pH in bleeding peptic ulcer. J Gastroenterol Hepatol. 2009; 24(7): 1236-1243 25. Sarin N, Monga N, Adams P. Time to endoscopy and outcomes in upper gastrointestinal bleeding. Can J Gastroenterol. 2009; 23(7): 489-493 26. ASGE Guideline. The role of endoscopy in the management of acute non-variceal upper GI bleeding. Gastrointestinal Endoscopy. 2012; 75(6): 1132-1138 27. Seung Young Kim, et al. Forest classification of peptic ulcers in UGIB. Clin Endosc. 2012 September; 45(3):220-223. 28. Kahi CJ, Jensen D, Sung JJY, et al. Endoscopic Therapy Versus Medical Therapy for Bleeding Peptic Ulcer with Adherent Clot: A Meta-analysis. Gastroenterology. 2005: 129:855-862 29. Barkun A,Sabbah S, Enns R, Armstrong D, et al. The Canadian Registry on Nonvariceal Upper Gastrointestinal Bleeding and Endoscopy (RUGBE): Endoscopic hemostasis and proton pump inhibition are associated with improved outcomes in a real-life setting. Am J Gastroenterol. 2004; 7:1238-1246 30. Ripoll C, Banares R,Beceiro I, et al. Comparison of transcatheter arterial embolization and surgery for treatment of bleeding peptic ulcer after endoscopic treatment failure. J Vasc Interv Radiol. 2004; 15(5):447-450 31. Katano T, Mizoshita T, Senoo K, Sobue S et al.The efficacy of transcatheter arterial embolization as the first-choice treatment after failure of endoscopic hemostasis and endoscopic treatment resistance factors. Dig Endosc. 2012; 5:364-369 32. Saeed ZA. Second thoughts about second-look endoscopy for ulcer bleeding? Endoscopy 1998;30(7): 650-2 33. El Ouali S,Barkun AN, Wyse J, Romagnuolo J, et al. Is routine second-look endoscopy effective after endoscopic hemostasis in acute peptic ulcer bleeding? A meta-analysis. Gastrointest Endosc. 2012; 76(2): 283-292

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Managing Complications of Peptic Ulcer Disease Andrea McNab, MD; Reginald Griffin, MD; and Ziad T. Awad, MD, FACS

Abstract: Peptic ulcer disease (PUD) and its complications are a

significant cause of morbidity and mortality worldwide. Complications are on the rise in older patients due to increased use of non-steroidal anti-inflammatory drugs (NSAIDS) and the chronic nature of their disease, and declining in younger patients.1 Previously, diagnosis of PUD generally meant operative intervention was necessary. However, the condition today is mostly treated medically and operations are not indicated for uncomplicated disease. Most operations are being performed for emergent complications of PUD, which are discussed in this article. These procedures are aimed at treating the emergent situation, preventing recurrence, and assessing for malignancy.2

Introduction Early studies in the pathophysiology of gastric acid secretion were made in the early 19th through mid-20th centuries. In the early 20th century, two major theories were developed in St. Petersburg by Pavlov and his protĂŠgĂŠ Popielski. Pavlov postulated that gastric acid secretion was stimulated by vagus nerve or acetylcholine responses, whereas Popielski advocated a histamine mediated response.3,4 Around the same time, British physiologist Edkins proposed the role of gastrin as a stimulant of gastric acid secondary to stimulation by peptides in the stomach.5 Major gastric operative procedures were described by Theodor Billroth while he was professor of surgery at the University of Vienna in the late 1800s, where he performed the first successful gastrectomy for cancer in 1881.6

surgical intervention.11 In patients with refractory PUD despite maximal medical management, it is important to rule out hypergastrinemia. Hypergastrinemia can be caused by achlorhydria and atrophic gastritis, both of which are associated with chronic use of proton pump inhibitors (PPI). Rarely, sporadic and familial gastrinoma (multiple endocrine neoplasia I), or Zollinger-Ellison syndrome, must be ruled out with intractable or recurrent PUD.2

Diagnosis PUD can remain asymptomatic or with vague symptoms. It may be associated with nausea, vomiting, bloating, weight loss, gastroesophageal reflux symptoms relieved with antacids, or intermittent abdominal pain sometimes related to eating. Presentations of patients with complications are described later in this article. Symptoms alone do not definitively distinguish gastric from duodenal ulcers. Location can be specified on upper endoscopy, where ulcers appear with sharp edges and visible submucosa, most often with a clean base (Table 1).2

Table 1 Classification of Peptic Ulcers Modified Johnson Classification of peptic ulcers2

Type

Location

Acid Secretion

Gastric body, lesser curvature

Low

Gastric body, also with duodenal ulcer

High

Causes

Helicobacter pylori was first identified as a potential cause of PUD in the early 1980s by Marshall and Warren of Australia. This was in contrast to prior theories involving spicy food or stress as inciting factors.7 This association was further evaluated during the National Institutes of Health conference in 1994 and in 1997 by the Centers for Disease Control.8 It is now generally believed that H. pylori is responsible for up to 85% of the changes to the gastric mucosa seen in peptic ulcers. Many people harbor H. pylori but have no ulceration, suggesting the inciting events are multifactorial.9

Prepyloric region

High

High on lesser curvature near GE junction

Low

Several other factors have been found to have strong causal relationships to PUD. Aspirin and NSAIDs both alone or in combination with H. pylori cause increase in peptic ulcers10 in both the duodenum and stomach.9 Smoking also increases recurrence, impairs ulcer healing, and increases chances of Address correspondence to: Ziad T. Awad, MD, University of Florida, Shands Jacksonville. Email: ziad.awad@jax.ufl.edu.

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5 Anywhere in the stomach

Associated with NSAIDS use

Bleeding Bleeding is the most common complication of PUD and its frequency is increasing.1 It is also the most common cause of death from the condition.9 The elderly and patients with rebleeding are at highest risk of mortality. It usually presents with hematemesis or melena and has the potential to induce hypovolemic shock from significant blood loss. Such patients should get immediate intravenous access with resuscitation.

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Endoscopic therapy is the diagnostic tool and treatment of choice for bleeding peptic and duodenal ulcers.1 Urgent upper GI endoscopy is an important part of localizing the bleeding as well as providing therapeutic interventions. Active bleeding is characterized as active oozing, pulsatile bleeding, or oozing under an adherent clot. Recent bleeding is associated with adherent clot without oozing, a visible vessel at the ulcer base, or adherent slough. Sources of bleeding may be injected with epinephrine, coagulated, sclerosed, or clipped to control hemorrhage. Endoscopic therapy should also be undertaken if the patient is hemodynamically unstable, continues to require blood transfusions, has red blood per rectum, hematemesis, is rebleeding during hospitalization, or is greater than 60 years of age.9 Unfortunately bleeding may recur despite initial control, indicating evaluation for operative intervention.10 Visualization of the endoscopy by the surgeon to assist in locating the exact anatomic location of the ulcer is very helpful in operative planning. Indications for emergent operative intervention include massive hemorrhage with hypovolemic shock, transfusion requirement of greater than 6 units of packed red blood cells in 24 hours, and recurrent hemorrhage after endoscopic therapy.9 Emergency operations occur in approximately 10-20% of bleeding peptic and duodenal ulcers.1 Duodenal ulcers identified on endoscopy that are greater than 2 cm are considered giant duodenal ulcers (GDU) and are at high risk of bleeding and perforation. GDU require definitive surgical management with antrectomy and vagotomy.12

transcatheter arterial embolization are the two best options remaining, as endoscopic therapy is often unsuccessful after operation has already occurred.9

Perforation Diagnosis of a perforated duodenal ulcer often involves sudden and severe epigastric pain resulting from gastric secretions into peritoneum, and sometimes right subscapular pain due to diaphragmatic irritation from gastric contents. Patients may also have associated fever and hypoactive bowel sounds. This may occur in 10% of patients that do not undergo treatment. Upright X-Rays may diagnose intraperitoneal free air which can be sufficient for diagnosis, but they can also be falsely negative (Figure 1). CT scan of the abdomen can reveal the diagnosis in this situation if strongly suspected.9

Figure 1

Upright Chest X-ray

Bleeding peptic ulcers are best treated by excision and biopsy of the ulcer due to the possibility of malignancy. Peptic ulcers, along the greater curvature of the stomach, antrum, or body are often excised in a wedge fashion with immediate closure. However, peptic ulcers on the lesser curvature are more involved because of their anatomic location and vascularity from the left gastric artery. Excision may cause deformity and subsequent obstruction of the stomach if wedged and primarily closed. Peptic ulcers distally located along the lesser curve are often best resected as part of a Bilroth procedure, which includes an antrectomy with gastroduodenostomy (Bilroth I) or gastrojejunostomy (Bilroth II).10 Operative intervention for a bleeding duodenal ulcer typically includes an anterior longitudinal duodenotomy across the pylorus and into the distal stomach. Ligation of affected the vessel also often takes place, followed by sutures to control vascular branches. Historically, acid reducing procedures such as a truncal vagotomy with pyloroplasty or a highly selective vagotomy is then performed to decrease further ulcer formation. These operations have been decreasing in frequency due to the current beliefs that cessation of NSAIDS use and treatment of H. pylori can decrease ulcer recurrence, and also because acid secretion can be easily decreased by the use of PPI medications.9,10 However, an acid reducing procedure can still be performed in patients that were on PPI therapy prior to occurrence of complication. Despite the above measures, rebleeding can still occur. At this point, reoperation or

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Showing free air secondary to perforated duodenal ulcer

Nonoperative management is considered in patients that are very high risk for operative complications or that have a contained perforation. These patients are treated with nasogastric decompression, broad spectrum antibiotics to include Gram negative coverage and H. pylori coverage and PPI, and fluid resuscitation. Otherwise, ulcer perforation is a strong indication for operative intervention. For perforated ulcers located in the duodenum and pylorus, placement of a laparoscopic or open omental patch and abdominal lavage is sufficient treatment. This does not necessarily involve closure of the ulcer, but sutures a flap www . DCMS online . org

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of vascularized omentum over the defect (Figure 2).12 Like procedures performed for bleeding ulcers, this was traditionally followed by a highly selective vagotomy to decrease acid secretion which is now reserved for patient that failed proton pump inhibitor therapy. Similarly, this procedure is also followed by postoperative therapy for H. pylori. The operation is often done laparoscopically, which is associated with decreased amount of pain postoperatively and decreased complication rates compared to an open procedure.13

of the accumulation of scar tissue after longstanding peptic ulcer disease or a malignancy near the pylorus. Less common causes of GOO include Crohnâ&#x20AC;&#x2122;s disease, chronic pancreatitis, and benign gastric polyps. Plain films and CT scan typically shows a large dilated stomach and pylorus with decompressed bowel distally (Figure 3).

Figure 3

CT Abdomen and Pelvis

Increased age, increased American Society of Anesthesiologists (ASA) class, presence of shock or metabolic acidosis on presentation, operative time greater than 150 minutes, elevated serum creatinine are all risk factors for morbidity and mortality during an emergent operation for perforated peptic ulcer.14,15

Figure 2

Omental Patch

GOO secondary to obstructing PUD

Upper endoscopy is also indicated in obstruction to assess the cause of obstruction, specifically to evaluate for neoplasm. As with bleeding, therapeutic intervention may be done endoscopically. Balloon dilatation can be effective in up to 85% of obstructing pyloric ulcers, but only 40% have sustained success greater than 3 months.9 Therefore, more invasive operations are performed for definitive repair.

For perforated duodenal ulcer12

(Used with permission)

Obstruction Gastric outlet obstruction (GOO) is another of the most frequent complications of PUD. Acute obstruction most commonly occurs in the pylorus and first part of duodenum. Patients present with vomiting, dehydration, and hypochloremic metabolic alkalosis. Most acute obstructions can be relieved within 72 hours nonoperatively with intravenous fluids, nasogastric decompression, and antisecretory medications. Chronic obstruction is most commonly a result

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The most common operation performed to relieve GOO is antrectomy and truncal vagotomy. The antrum of the stomach is the major source of gastrin secretion, and is therefore removed in this procedure. A Billroth I may be performed, anastomosing the remaining stomach to the duodenum, creating a gastroduodenostomy. However, due to the nature of the condition, scar tissue may limit the mobility of the duodenum. In these cases a Billroth II, gastrojejunostomy, may be performed. Billroth procedures are often followed by truncal vagotomy.16

Conclusion Diagnosis and management of PUD has been evolving since early theories were developed in the 1800s. Its relationships with NSAIDS use, H. pylori infection, and smoking have transitioned the emphasis of management from primarily surgical to medical and preventative. Increasing use of PPI,

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antibiotics, and reduction in causal factors have decreased need for elective surgery. However, complications of PUD are still very frequent and definitively managed by emergency operative intervention. With the continuing development of endoscopic and laparoscopic therapies, even emergent operations are becoming less invasive.

16. Clancy TE, Ashley SW. Procedures for benign and malignant gastric and duodenal disease. In: Souba W, Fink M, Jerkovich GJ, et al, eds. ACS Surgery: Principles and practice. Hamilton, ON: BC Decker; 2007:713-728.

References

Northeast Florida Medicine

1. Milosavljevic T, Kostic-Milosavljevic M, Jovanovic I. Complications of peptic ulcer disease. Dig Dis. 2011;29(5):491-3. 2. Conter RL, Kauffman, GL Jr. Benign gastric ulcer and stress gastritis. In: Cameron JL, ed. Current Surgical Therapy. St. Louis, MO: Mosby; 1998:75-77. 3. Konturek SJ. Gastric secretion – from Pavlov’s nervism to Popielski’s histamine as direct secretagogue of oxyntic glands. J Physiol Pharmacol. 2003;54 Suppl 3:43-68. 4. Banic M, Malfertheiner P, Babic Z et al. Historical impact to drive research in peptic ulcer disease. Diag Dis. 2011;29(5):444-453. 5. Edkins JD. The chemical mechanism of gastric secretion. J Physio. 1906;34:133-144. 6. Weil PH, Buchberger R. From Billroth to PCV: A century of gastric surgery. World J Surg. 1999;23:736-742. 7. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1984;1(8390):1311-1315. 8. NIH consensus conference. Helicobacter pylori in peptic ulcer disease. NIH consensus development panel on Helicobacter pylori in peptic ulcer disease. JAMA. 1994;272(1):65-9. 9. Muholland MW. Gastroduodenal Ulceration. In: Greenfield’s surgery: Scientific principles and practice. Philadelphia, PA: Lippincott, Williams, and Wilkins;2011:699-712. 10. Lee CW, Sarosi GA. Emergency ulcer surgery. Surg Clin N Am. 2011;91:1001-1013. 11. Kato I, Nomura AM, Stemmermann GN. A prospective study of gastric duodenal ulcer and its relation to smoking, alcohol, and diet. Am J of Epidem. 1992;135(5):521-530. 12. Nussbaum M, Chavda K, Mercer D, Goede, M. Master Techniques in Surgery: Gastric Surgery. Philadelphia, PA: Lippincott, Williams, and Wilkins; 2013:112,147-148. 13. Matsuda M, Nishiyama M, Hanai T, S Saeki, T Watanabe. Laparoscopic omental patch repair for perforated peptic ulcer. Ann Surg. 1995;221(3):236-240. 14. Moller MH, Shah K, Bendix J, et al. Risk factors in patients surgically treated for peptic ulcer performation. Scand J Gastroenterol. 2009;44(2):145-52. 15. Kim JM, Jeong SH, Lee YG, et al. Analysis of risk factors for postoperative morbidity in perforated peptic ulcer. J Gastric Cancer. 2012;12(1):26-35. 22 Vol. 64, No. 1 2013 Northeast Florida Medicine

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Current Management and Future Strategies of Gastric Cancer Ziad T. Awad, MD, FACS

Abstract: The overall prognosis of gastric cancer has gradually improved over the past decades with growing awareness of potential carcinogens, surveillance programs and early diagnosis, as well as advances in surgical techniques and multimodality treatments. Nevertheless, the outcome of advanced stage disease still remains poor with currently available treatments. To improve prognosis and quality of life in gastric cancer patients, both standardization and individualization of managements are imperative. Diagnostic tests and surgical procedures need to be further sophisticated and standardized based on more recent evidences from ongoing and future randomized controlled trials, while comprehensive management should be individualized to each patient.

Introduction Gastric cancer remains a major health issue and a leading cause of cancer death worldwide, although the prevalence and mortality of the disease have gradually decreased.1,2 In Eastern Asia, including Korea and Japan, the incidence of gastric cancer is still high despite advances in treatment and subsequent improvement in prognosis. On the contrary, in the West, where the incidence has continuously decreased, the overall and stage-specific survival is worse than that in Eastern Asia.3 Although the geographical differences in terms of incidence and prognosis have not yet been clearly elucidated, they are probably attributable to various factors in gastric carcinogenesis, as well as in diagnostic and therapeutic strategies. This article will review the current management of gastric cancer, discussing gastric carcinogenesis in relation to the prevention of the disease, early detection with effective screening, and surgical treatment as the current standard of management. It will also highlight a multidisciplinary approach for advanced disease. Furthermore, the current status of molecular biomarkers and targeted therapy will be discussed as the future strategy for the tailored management of gastric cancer patients.

Primary Prevention and Gastric Carcinogenesis Tobacco smoking and the high consumption of salted and smoked foods are well known lifestyle and environÂŹmental causes of gastric cancer.4 Being overweight and resulting obe-

Address Correspondance to: Ziad T. Awad, M.D, FACS, Assistant Professor of Surgery, Director of Minimally Invasive Surgery University of Florida College of Medicine â&#x20AC;&#x201C;Jacksonville. Jacksonville, FL. Email: Ziad.Awad@jax.ufl.edu. www . DCMS online . org

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sity are also associated with increased risk of gastric cancer.5 Although previous studies showed an inconsistent correlation between gastric cancer and alcohol, a recent meta-analysis found a significant positive association between heavy alcohol intake and gastric cancer.6 On the other hand, there has been consistent evidence that vegetables and fruit are protective against gastric cancer.7 Helicobacter pylori (H. pylori) has been classified as a class I carcinogen in humans by the World Health Organization (WHO) since 1994 based mainly on epidemiological evidence of its role in the pathogenesis of gastric carcinoma.8 A recent meta-analysis of seven randomized trials mostly conducted in Asia, where the infection rate of H. pylori is substantially high, demonstrated that eradication of H. pylori has the potential to prevent gastric cancer.9 Accordingly, updated Japanese guidelines for the management of H. pylori and related diseases have finally indicated that eradication of H. pylori is useful for the prevention of gastric cancer.10

Secondary Prevention: Early Detection To improve survival in gastric cancer patients, early detection and subsequent surveillance programs are essential; currently available screening tools include radiologic imaging and endoscopy with biopsy.11 Nationwide mass screening programs in Korea and Japan, where gastric cancer is the most common malignancy, has made it possible to detect the disease in earlier stages and to improve the overall survival rates of gastric cancer patients.12 However, most countries, except for Korea and Japan, have no national guidelines or recommendations for gastric cancer screening as there are no screening tools applicable to low risk populations with respect to acceptable accuracy, minimal invasiveness, and low cost.13,14

Present Status of Gastric Cancer Management Radical Gastrectomy with D2 lymphadenectomy â&#x20AC;&#x201D; Radical (total or subtotal) gastrectomy is the gold standard of management of gastric cancer worldwide, as complete surgical removal of macroscopic and microscopic tumors (R0 resection) confers the only chance for curing the disease. However, the extent of lymphadenectomy has been debated between the East and West. Radical gastrectomy with extended D2 lymphadenectomy is the accepted standard in Eastern Asia, whereas limited D1 resection with chemoradiotherapy is more frequently used in Western countries.15,16 The well-known European Phase III randomized controlled trials in the 1990s, carried out by the Medical Research Council and Dutch Gastric Cancer Group, failed to show a Northeast Florida Medicine Vol. 64, No. 1 2013 23

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survival benefit of D2 over D1 resections with extremely high morbidity and hospital mortality in D2 group.17,18 However, it is not feasible to draw any definite conclusion of long-term survival benefit of D2 lymphadenectomy based on these trials because they had some critical problems which inevitably lead to the substantially higher morbidity and mortality rates in D2 resections compared to those reported by specialized high-volume centers in Korea, Japan, and Western countries as well. There was no standardized quality control of the participating surgeons and hospitals prior to these trials and routine resection of the distal pancreas and spleen in total gastrectomy was defined as a part of D2 dissections in the trial protocol. Splenectomy and distal pancreatectomy are no longer advocated as a routine adjunctive procedure during D2 resections.19 Furthermore, it should be noted that the fifteen-year follow-up of the Dutch trial recently reported that D2 lymphadenectomy was associated with lower locoregional recurrence and gastric cancer related death rates than D1 surgery.20 Interim report of a randomized controlled trial by the Italian Gastric Cancer Study Group showed no significant difference in postoperative mortality and overall morbidity between D1 and pancreas-preserving D2 gastrectomy, suggesting that D2 resection is a safe option of radical gastrectomy in specialized centers, although the final report of long-term survival is still awaited.21 Minimally Invasive Management of Early Gastric Cancer (EGC) — Endoscopic mucosal resection (EMR) is a treatment option of EGC with an extremely low possibility of lymph node metastasis, and endoscopic submucosal dissection (ESD) has also recently become another treatment option with advances in endoscopic instrumentation and technique.22 Considering the benefits of ESD with minimal invasiveness of the procedure, it has the potential to extend its indication. Currently, however, a long-term oncological outcome has not been established despite its extensive use. Thus, while awaiting large scale oncologic safety data, surgical resection with appropriate lymph node dissection is the standard treatment of EGC beyond conventional EMR criteria which is only limited to differentiated adenocarcinoma of less than 2 cm in diameter without ulceration and lymphovascular invasion.23 Currently, phase III multicenter trials are ongoing both in Korea (KLASS trial) and Japan (JCOG 0912) to compare the outcomes of laparoscopic distal gastrecotmy (LADG) and open distal gastrectomy (ODG) in the stage I gastric cancer. The interim report of the KLASS trial demonstrated that LADG for early cancer is equivalent to ODG in terms of short-term outcomes, assessed by operative morbidity and mortality, but the long-term outcomes of final survival results are still awaited.24,25 The application of laparoscopic techniques in advanced gastric cancer (AGC) still remains controversial and needs more compelling evidence by well-designed prospective clinical trials prior to expanding its indications. Adjuvant Chemotherapy — Although curative D2 resection is the standard treatment of operable gastric cancer, 40-60% of patients with locally advanced cancer experience recurrence after surgery.26,27 Adjuvant chemotherapy, suspected to reduce 24 Vol. 64, No. 1 2013 Northeast Florida Medicine

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this recurrence, had shown limited and inconsistent efficacy in previous trials. However, a recent large meta-analysis (GASTRIC group), in which 3,838 individual patients from 17 trials were evaluated, reported a small but significant benefit of adjuvant chemotherapy after curative resection of gastric cancer.28 The authors suggested that postoperative adjuvant chemotherapy based on fluorouracil regimens was associated with a reduced risk of death in gastric cancer, com¬pared with surgery alone. In Japan, adjuvant S-1 therapy has become the standard treatment of choice for patients with Advanced Gastric Cancer (AGC) after D2 resections based on the positive results of the Adjuvant Chemotherapy Trial of S-1 for Gastric Cancer (ACTS-GC).29 One year after enrollment and randomization of 1,059 patients, the first interim analysis showed that both overall survival and relapse-free survival were significantly higher in the S-1 group, and the trial was discontinued following the recommendation of the monitoring committee. Recently, interim analysis of international (Korea, China, and Taiwan), multicenter, randomized, phase III trials (CLASSIC) was reported as an abstract comparing capecitabine plus oxaliplatin (CapOX) adjuvant chemotherapy group with an observation group following D2 resections in a total of 1,035 patients with locally advanced cancer.30 After the median follow-up of 34.4 months, 3-year disease-free survival was significantly higher in the CapOX group (74% vs. 60%; HR=0.56, 95% CI 0.44-0.72; p<0.0001), although a difference in overall survival has not yet been observed. Grade 3 or 4 adverse events occurred in 49% of patients in the CapOX group with serious toxicity reported in 7% of them, which was consistent with well-known safety pro¬files of CapOX. 30 Based on the results of two randomized trials (ACTS-GC and CLASSIC) (29,30), it is strongly suggested that 5FU-derivative based chemotherapy in an adjuvant setting following D2 resections would invariably deliver the best current clinical benefits to the patients with resectable gastric cancer. 29,30 Postoperative Radiochemotherapy — With the positive results of the intergroup 0116 trial (Southwest Oncology Group 9008)(15), adjuvant radiochemotherapy with limited (D0 or D1) lymphadenectomy has been frequently used in the United States. Macdonald, et al. reported promising results of the adjuvant radiochemotherapy after surgery with curative intent in patients with adenocarcinoma of the stomach or gastroesophageal junction, demonstrating the significant superiority of radiochemotherapy over surgery alone in terms of relapse free survival and over¬all survival.15,16 Nonetheless it is crucial to consider that more than 50% of patients in this trial underwent gastric resection without any lymph node dissection (D0), and the limited (D1) and extended (D2) lymphadenectomy were performed in only 36% and 10% of cases, respectively. Therefore, most resections performed were insufficient and inadequate to achieve loco-regional control which was thereafter improved by adjuvant radiotherapy. In Korea and Japan, however, prophylactic D2 lymphadenectomy achieves good loco-regional control with much lower morbidity and mortality than those of radiotherapy, and the benefit of adjuvant radiochemotherapy www . DCMS online . org

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following D2 resection has yet to be established by ongoing randomized controlled trials in Europe and Korea.31 Neoadjuvant Therapy – Neoadjuvant chemotherapy has been frequently used for locally advanced gastric carcinoma in the United States and Western Europe, ever since the Medical Research Council Adjuvant Gastric Infusional Chemotherapy trial (MAGIC trial) reported their first positive results. The MAGIC trial in patients with gastric and gastroesophageal junction cancer demonstrated that the perioperative chemotherapy group, compared to the surgery alone group, showed significant improvement in resectability, as well as disease-free and overall survival.32 Likewise, a recent phase III randomized trial by the Fédération Nationale des Centres de Luttecontre le Cancer and the Fédération Francophone de Cancérologie Digestive in 28 French centers also reported positive results similar to the MAGIC trial.33 Despite their promising results, however, limitations prevent the application as a standard treatment of gastric cancer because both trials included high proportions of distal esophagus and gastroesophageal junction tumors, and less than 50% of the patients completed postoperative chemotherapy as initially planned, and, most importantly, there were no standard preoperative staging systems. Moreover, without hazard ratio analysis on the extent of surgery, the benefit of neoadjuvant chemotherapy in addition to D2 resection remains unclear.33

Future Strategy for Gastric Cancer Researchers are focusing on the following promising areas for additional exploration: • Molecular Biomarkers and Targeted Therapy—The prognosis of patients with AGC is still dismal even with marked advances in chemotherapeutic agents over the past decades. Moreover, treatment responses and prognosis are highly variable even within the same stage. Therefore, a thorough understanding of cancer biology is essential for better management of gastric cancer in the future. • Epidermal Growth Factor Receptor (EGFR) overexpression has been observed in many tumors including gastric cancer and is generally thought to correlate with increased tumor invasion, more poorly differentiated histology, and a worse prognosis.34 Trastuzumab (Herceptin®) is a humanized monoclonal antibody that interferes with human EGFR type 2.35 • The Trastuzumab for Gastric Cancer (ToGA) trial, a pivotal randomized clinical trial of patients with HER-2 positive advanced, mostly metastatic, gastric cancer, proved the efficacy of Trastuzumab in combination with chemotherapy.36 The median overall survival was significantly prolonged in the trastuzumab-containing arm (13.8 vs. 11.1 months; HR 0.74; p=0.0046) without unexpected toxicity including cardiac events. Bevacizumab (Avastin®) is a humanized monoclonal antibody against VEGF, which is an endothelial cell-specific mitogen and the most potent driver of angiogenesis in tumorigenesis as it increases microvascular permeability.

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• In gastroesophageal cancer, Vascular Endothelial Growth Factor (VEGF) is overexpressed by up to 60%, a much higher rate than HER-2/neu, and its overexpression correlates with advanced stage, higher risk of recurrence, and poor survival.37 AVAGAST was a multinational, randomized, double-blind, placebo-controlled phase III clinical trial which set out to evaluate the anti-angiogenic agent bevacizumab combined with chemotherapy (capecitabine plus cisplatin) as a firstline therapy in patients with unresectable far advanced gastric carcinoma.38 Although AVAGAST did not reach its primary endpoint with no significant difference in overall survival (12.1 months in bevacizumab plus chemotherapy vs. 10.1 months in placebo plus chemotherapy; HR 0.87; p=0.1002), both progression-free survival (6.7 vs. 5.3 months; HR 0.80; p=0.0037) and overall response rate (46.0% vs. 37.4%; p= 0.0315) were improved significantly in the bevacizumab-arm.38 It must be noted that preplanned subgroup analysis demonstrated regional differences in the efficacy of the bevacizumab, as patients enrolled only in Pan-America demonstrated a significant survival benefit with the addition of bevacizumab (median survival 11.5 vs. 6.8 months; HR 0.63; 95% CI 0.43 to 0.94). It is not clear whether the discrepancy came from genetic differences in ethnicity or from differences in treatment patterns such as palliative resection and second-line chemotherapy. Regardless, it surely provides a direction to investigate further in future research and clinical trials.38

Conclusion The overall survival of gastric cancer has gradually improved over the past few decades with advances in surgical techniques, the evolution of multimodality treatments, and earlier detection of the disease. Researchers are also approaching important discoveries that would improve treatment. However, gastric cancer, the second most common cause of cancer-related death worldwide, still represents a global health care burden. Early detection and management remains essential in improving outcomes.

References

1. Jemal A, Siegel R, Xu J, et al. Cancer statistics, 2010. CA Cancer J Clin 2010;60:277-300. 2. Ferlay J, Shin HR, Bray F, et al. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer 2010;127:2893-917. 3. Strong VE, Song KY, Park CH, et al. Comparison of gastric cancer survival following R0 resection in the United States and Korea using an internationally validated nomogram. Ann Surg 2010;251:640-6. 4. Plummer M, Franceschi S, Muñoz N. Epidemiology of gastric cancer. IARC Sci Publ 2004:311-26. 5. Yang P, Zhou Y, Chen B, et al. Overweight, obesity and gastric cancer risk: results from a meta-analysis of cohort studies. Eur J Cancer 2009;45:2867-73. 6. Tramacere I, Negri E, Pelucchi C, et al. A meta-analysis on alcohol drinking and gastric cancer risk. Ann Oncol 2011.

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7. Lunet N, Lacerda-Vieira A, et al. Fruit and vegetables consumption and gastric cancer: a systematic review and meta-analysis of cohort studies. Nutr Cancer 2005;53:1-10. 8. Schistosomes, liver flukes and Helicobacter pylori. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Lyon, 7-14 June 1994. IARC Monogr Eval Carcinog Risks Hum 1994;61:1-241. 9. Fuccio L, Zagari RM, Eusebi LH, et al. Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer? Ann Intern Med 2009; 151:121-8. 10. Asaka M, Kato M, Takahashi S, et al. Guidelines for the management of Helicobacter pylori infection in Japan: 2009 revised edition. Helicobacter 2010;15:1-20. 11. Whiting JL, Sigurdsson A, Rowlands DC, et al. The long term results of endoscopic surveillance of premalignant gastric lesions. Gut 2002;50:378-81. 12. Jung KW, Park S, Kong HJ, et al. Cancer statistics in Korea: incidence, mortality, survival, and prevalence in 2008. Cancer Res Treat 2011;43:1-11. 13. Leung WK, Wu MS, Kakugawa Y, et al. Screening for gastric cancer in Asia: current evidence and practice. Lancet Oncol 2008;9:279-87. 14. Dan YY, So JB, Yeoh KG. Endoscopic screening for gastric cancer. Clin Gastroenterol Hepatol 2006;4:709-16. 15. Macdonald JS, Smalley SR, Benedetti J, et al. Chemoradiotherapy after surgery com¬pared with surgery alone for adenocarcinoma of the stomach or gastroesophageal junction. N Engl J Med 2001;345:725-30. 16. Macdonald JS, Benedetti J, Smalley S, et al. Chemoradiation of resected gastric cancer: a 10-year follow-up of the phase III trial INT0116 (SWOG 9008). J Clin Oncol 2009;27. 17. Cuschieri A, Weeden S, Fielding J, et al. Patient survival after D1 and D2 resections for gastric cancer: long-term results of the MRC randomized surgical trial. Surgical Co-operative Group. Br J Cancer 1999;79:1522-30. 18. Bonenkamp JJ, Hermans J, Sasako M, et al. Extended lymph-node dissection for gastric cancer. N Engl J Med 1999;340:908-14. 19. Sano T, Yamamoto S, Sasako M; Japan Clinical Oncology Group Study LCOG 0110-MF. Randomized controlled trial to evaluate splenectomy in total gastrectomy for proximal gastric carcinoma: Japan clinical oncology group study JCOG 0110-MF. Jpn J Clin Oncol 2002;32:363-4. 20. Songun I, Putter H, Kranenbarg EM, et al. Surgical treatment of gastric cancer: 15-year follow-up results of the randomised nationwide Dutch D1D2 trial. Lancet Oncol 2010;11:439-49. 21. Degiuli M, Sasako M, Ponti A; Italian Gastric Cancer Study Group. Morbidity and mortality in the Italian Gastric Cancer Study Group randomized clinical trial of D1 versus D2 resection for gastric cancer. Br J Surg 2010;97:643-9. 22. Gotoda T. Endoscopic resection of early gastric cancer. Gastric Cancer 2007;10:1-11.

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23. Japanese Gastric Cancer Association. Japanese gastric cancer treatment guidelines 2010 (ver. 3). Gastric Cancer 2011;14:113-23. 24. Kim HH, Hyung WJ, Cho GS, et al. Morbidity and mortality of laparoscopic gastrectomy versus open gastrectomy for gastric cancer: an interim report--a phase III multicenter, prospective, randomized Trial (KLASS Trial). Ann Surg 2010;251:417-20. 25. Katai H, Sasako M, Fukuda H, et al. Safety and feasibility of laparoscopy-assisted distal gastrectomy with suprapancreatic nodal dissection for clinical stage I gastric cancer: a multicenter phase II trial (JCOG 0703). Gastric Cancer 2010;13:238-44. 26. Gallo A, Cha C. Updates on esophageal and gastric cancers. World J Gastroenterol 2006;12:3237-42. 27. Gunderson LL. Gastric cancer—patterns of relapse after surgical resection. Semin Radiat Oncol 2002;12:150-61. 28. GASTRIC (Global Advanced/Adjuvant Stomach Tumor Research International Collaboration) Group, Paoletti X, Oba K, Burzykowski T, Michiels S, Ohashi Y, Pignon JP, et al. Benefit of adjuvant chemotherapy for resectable gastric cancer: a meta-analysis. JAMA 2010;303:1729-37. 29. Sakuramoto S, Sasako M, Yamaguchi T, et al. Adjuvant chemotherapy for gastric cancer with S-1, an oral fluoropyrimidine. N Engl J Med 2007;357:1810-20. 30. Bang Y, Kim YW, Yang H, et al. Adjuvant capecitabine and oxaliplatin for gastric cancer: results of the phase III CLASSIC trial. 2011 ASCO Annual Meeting: J Clin On¬col 2011:29. 31. Sasako M. Principles of surgical treatment for curable gastric cancer. J Clin Oncol 2003;21:274s-5s. 32. Cunningham D, Allum WH, Stenning SP, et al. Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 2006;355:11-20. 33. Ychou M, Boige V, Pignon JP, et al. Perioperative chemotherapy compared with surgery alone for resectable gastroesophageal adenocarcinoma: an FNCLCC and FFCD multicenter phase III trial. J Clin Oncol 2011;29:1715-21. 34. Ku GY, Ilson DH. Esophagogastric cancer: targeted agents. Cancer Treat Rev 2010;36:235-48. 35. Hudis CA. Trastuzumab—mechanism of action and use in clinical practice. N Engl J Med 2007;357:39-51. 36. Bang YJ, Van Cutsem E, Feyereislova A, et al. Trastuzumab in combination with chemotherapy versus chemotherapy alone for treatment of HER2-positive advanced gastric or gastro-oesophageal junction cancer (ToGA): a phase 3, open-label, randomised controlled trial. Lancet 2010;376: 687-97. 37. Maeda K, Chung YS, Ogawa Y, et al. Prognostic value of vascular endothelial growth factor expression in gastric carcinoma. Cancer 1996;77:858-63. 38. Ohtsu A, Shah MA, Van Cutsem E, et al. Bevacizumab in combination with chemotherapy as first-line therapy in advanced gastric cancer: a randomized, double-blind, placebo-controlled phase III study. J Clin Oncol 2011;29:3968-76.

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Management of Gastroparesis Jose M. Nieto, DO, FACP Abstract: Gastroparesis is a common condition characterized with delayed gastric emptying in the absence of a mechanical gastric outlet obstruction. There are multiple etiologies that cause gastroparesis, such as diabetic, post surgical and idiopathic. The prevalence is equal among men and women. The most common clinical symptom presentation includes nausea, vomiting and early satiety. The diagnosis is commonly made by gastric emptying scintigraphy, but other tests are available. Management includes dietary changes, nutritional supplementation, psychological interventions, anti-emetic medications and prokinetic medications, endoscopic procedures, gastric electrical stimulation, and surgical procedures.

Introduction Gastroparesis is a common condition that present with symptoms of abnormal gastric emptying. Diagnostic testing reveals evidence of delayed gastric emptying in the absence of a gastric outlet obstruction. There are multiple causes of gastroparesis and the most common etiologies are idiopathic, diabetic, postsurgical, autoimmune, paraneoplastic, neurologic, medication induced and metabolic. For men and women respectively, the prevalence of gastroparesis is 9.6 and 37.8 per 100,000 persons and its age-adjusted incidence is 2.4 and 9.8 per 100,000 person-years.1 Over a 10-year period, hospital admissions due to a primary diagnosis of gastroparesis have increased by 158%.2 Hospital length of stay and costs related to gastroparesis has also increased in the last 10 years. Several studies demonstrated an inpatient costs associated to be $7,000 per month. 1,3 The main causes of rehospitalization included medical non-compliance and poor glycemic control.

Etiology Gastroparesis has multiple etiologies. We will discuss the most common causes in terms of prevalence, presentation, and pathophysiology. In multiple studies of over 700 patients with gastroparesis, the most common etiology is idiopathic (36-64%), followed by diabetes mellitus (29-31%) and post-surgical in (13%). 4,5 In a series of 243 patients, the predominant symptoms of gastroparesis were nausea (34%), vomiting (19%) and pain (23%).5 Severe anxiety and depression were present in 36% and 18% of individuals, respectively. Half of the patients reported acute symptom onset and 19% reported an infectious prodrome, however, an infectious offending organism has not been isolated. Idiopathic gastroparesis may have a similar presentation to functional disorders, such as post-prandial functional Address Correspondence to: Jose M Nieto, DO, FACP, Assistant Professor of Medicine, University of Central Florida School of Medicine. Borland Groover Clinic, 4800 Belfort Road, 2nd Floor, Jacksonville, FL 32250. Phone: 904-383-1138/904-265-4813. Email: jnieto@bgclinic.com. www . DCMS online . org

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dyspepsia, chronic idiopathic nausea, and functional vomiting.6 In a study of patients with idiopathic gastroparesis, 86% met the Rome III criteria for diagnosis of functional dyspepsia.5,6 Pathophysiologic studies in patients with idiopathic gastroparesis have identified several abnormalities, such hypersensitivity to gastric balloon inflation (29%), and impaired fundus accommodation (43%).7 Idiopathic gastroparesis tend to have higher levels of erythrocyte sedimentation rates, antinuclear antibodies, and C-reactive protein, raising the possibility that inflammatory factors may participate in the pathogenesis of this condition.8 Gastroparesis is found in 27-65% of patients with longstanding type 1 diabetes and 30% of patients with type 2 diabetes.9 Patients with type 2 diabetes are older and have a higher body mass compared to type 1 diabetics.10 There is evidence that diabetic gastroparesis co-develops with diabetic peripheral vascular disease.11 Pathophysiologic studies of diabetic gastroparesis have identified several abnormalities, which include decreased accommodation to meals, reduction in antral contractions, vagal neuropathy, and intense prolonged pyloric spasms.12 Sixty-two percent of patients with type 1 diabetes and gastroparesis have autonomic neuropathy.13 Hyperglycemia and loss of glycemic control impairs gastric motor function and worsens gastroparesis.14 Studies have shown that hyperglycemia reduces sensations of hunger in healthy individuals and it increases postprandial fullness in patients with insulin dependent diabetes.15-17 Conversely, insulin-induced hypoglycemia promotes acceleration of both solid and liquid gastric emptying in patients with type 1 diabetes.18 Post surgical gastroparesis occurs in 5% of individuals who undergo gastric surgeries.19 The Roux stasis syndrome occurs after gastrojejunostomy and presents with delayed gastric emptying that occurs as a consequence of simultaneous or retrograde Roux limb contractions. Laparoscopic fundoplication procedures for chronic reflux may be complicated by vagal nerve damage that may predispose to gastroparesis.20 Bariatric surgeries such as Roux-en-Y gastric bypass and sleeve gastrectomy increase gastric retention and lead to fundic distention that may increase reports of early satiety, anorexia and weight loss.21 Esophagectomy can also lead to gastroparesis in 11% of patients.22 Post-surgical gastroparesis occurs in 44% of patients undergoing pancreatoduodenectomy. There are other causes of associated conditions with gastroparesis, such as medications and metabolic, infectious, and collagen vascular/autoimmune diseases.23-25

Clinical Symptomatology The majority of patients complain of nausea (90%), vomiting (68-84%), and early satiety 60%).26 Abdominal pain Northeast Florida Medicine Vol. 64, No. 1 2013 27

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occurs in 46-90% of patients, in which it is the predominant symptom in 19% of patients. The abdominal pain is epigastric in origin (43%), meal-induced (72%) and nocturnal in 74% of patients.27 Bloating occurs in 80% of patients and is the predominant symptom in 8% of patients.28 Symptoms usually are persistent, but may also have episodic flares that are separated by asymptomatic periods, which may mimic cyclic vomiting syndrome.28 These symptoms have shown to impair the patientsâ&#x20AC;&#x2122; quality of life. A percentage of patients with gastroparesis are obese (BMI >40), but studies have shown daily caloric intake in such patients averaged <60% of recommended levels and 64% of patients consumed calorie-deficient diets.29 Multiple vitamin and mineral deficiencies such as vitamins A, B, C and K, iron, potassium and zinc are prominent in gastroparesis patients.30 Gastroparesis is the cause of bezoar formation, in which most cases occur after bariatric surgery.31 Bezoars may lead to complications such as gastric ulcers, gastric perforation, small bowel obstruction and small intestinal bacterial overgrowth.32 Quantification of symptom severity and characterization of symptom profiles of gastroparesis have been classified by the Gastroparesis Cardinal Symptom Index (GCSI).33 The GCSI is a subset of the Patient Assessment of Upper Gastrointestinal Symptoms (PAGI-SYM) and consists of three subscales (nausea and vomiting, postprandial fullness and early satiety, and bloating) scored by recall of symptoms over the preceding two weeks. The Patient Assessment of Upper Gastrointestinal Disorders Quality of Life (PAGI-QOL) provides numerical values for quality of life in patients with disordered gut motility.34 These patient assessments are used to determine severity of gastroparesis and are mainly for investigational use.

Diagnostic Testing Gastric emptying scintigraphy using labeled isotope (Tc99m sulfur colloid) bound to solid food is the most used test to diagnose gastroparesis. The diagnosis criteria is gastric retention of >60% of the meal at 2 h and/or >10% of the meal at 4 h is outside the range of >95% of healthy individuals, and these cut-off values are therefore used to confer a diagnosis of gastroparesis.35, 36 An alternative diagnostic method is using a wireless motility capsule (WMC) that quantifies luminal pH. Gastric emptying is identified by a significant and sustained pH increase as the capsule passes from the stomach to the proximal small intestine. This method should be used in patients who have symptoms that suggest multiple gastrointestinal motility disorder. WMC testing can measure gastric emptying, small bowel and colon transit in a single study.37,38 Breath tests using nonradioactive 13C-labeled substrates are proposed as alternatives to gastric emptying scintigraphy.39 Findings of 13C-labeled breath tests correlate well with those of gastric emptying scintigraphy, but are unreliable in individuals with conditions that impair digestive or pulmonary function.40 28 Vol. 64, No. 1 2013 Northeast Florida Medicine

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Antroduodenal manometry should be reserved for more complex cases.41 This technique should be considered for patients with unexplained nausea, vomiting, abdominal pain or other symptoms suggestive of upper gut dysmotility, and in individuals who are unresponsive to medical therapy. It could also be used for those being considered for supplemental feeding or for intestinal resection or venting enterostomy to reduce symptoms.42

Management Gastroparesis treatment requires a combination of therapies, which include dietary modifications, diet supplementation, medications to stimulate gastric emptying or reduce emesis, endoscopic or surgical, and psychological interventions. Dietary Changes and Nutritional Supplementation â&#x20AC;&#x201C; Diet changes include small frequent meals, which are predominantly liquid, and avoiding indigestible solids and fatty meals can compensate for gastric impairments. Dietary fiber should be decreased since it can cause abdominal bloating and bezoars. Medications that delay gastric emptying such as opiates should be discontinued or significantly reduced. In diabetics, tight glycemic control is highly recommended. Severe gastroparesis may require intermittent or permanent enteral or parenternal nutrition. Pharmacological Management â&#x20AC;&#x201C; Prokinetic drugs are the first line treatment for patients with moderate or severe symptoms. A meta-analysis showed that erythromycin is most potent in stimulating gastric emptying; erythromycin and domperidone are individually superior to metoclopramide for symptom control.43 Erythromycin elicits intense antral contractions by activating motilin receptors, which mediates fasting antroduodenal contractility. Tolerance to erythromycin occurs frequently due to motilin receptor down-regulation. Adverse effects include abdominal pain, gastrointestinal spastic contractions, and sudden death from cardiac arrhythmias. Azithromycin has been shown to be an equivalent prokinetic with fewer side effects and less risk for sudden death in patients with long QT syndrome.44 Metoclopramide is a serotonin 5-HT4 receptor agonist, dopamine D2 antagonist, and direct gastrointestinal smooth muscle contractile agent that also reduces vomiting via brainstem D2 receptor antagonism and vagal and brainstem 5-HT3 receptor antagonism. Adverse effects such as fatigue, agitation, sleep disruption, galactorrhea, amenorrhea, dystonias, and tardive dyskinesia (occurs in 1-10% of patients who have been taking the drug for >3 months) limit the use of metoclopramide.45 Due to the disabling nature of this complication, tardive dyskinesia, patients should be informed about its consequences and medical records should include documentation of this discussion. Domperidone is a dopamine D2 receptor antagonist that does not cross the blood-brain barrier and acts only on peripheral sites; therefore, central neural adverse effects are negligible.46 Oral domperidone is approved in most countries except the USA. The drug is as efficacious as metoclopramide in reducing nausea and vomiting. In a systematic review of multiple articles showed symptom reductions (64%) and decreased hospitalizations www . DCMS online . org

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(67%).46 Given that it acts peripherally, domperidone is useful for the treatment of dysmotility in patients with Parkinson’s disease.47 Adverse reactions include hyperprolactinemia, QT interval prolongation, and sudden death.48 Domperidone is available to clinicians who follow a multistep process that includes submission of both an Investigational New Drug application to the FDA and an Institutional Review Board proposal to the host institution. Novel investigational agents show promise in gastroparesis such as 5-HT4 agonists with prokinetic effects, prucalopride and TD-5108.49 Mitemcinal, a motilin receptor agonist without antibacterial action, is shown to accelerate gastric emptying in patients with gastroparesis.50 Ghrelin agonist TZP-101 (Ulimorelin) has been shown to reduce nausea, vomiting and overall symptoms compared with placebo.51 Antiemetic Medications – Antiemetic medications are often used alone or in conjunction with prokinetics for the treatment of gastroparesis. Antiemetics include histamine H1 (promethazine), serotonin 5-HT3 antagonists (ondansetron) and cannabinoids (dronabinol), and are commonly used in patients with gastroparesis. Endoscopic Management – Therapeutic endoscopy may be beneficial in some patients with gastroparesis. Multiple series of endoscopic pyloric botulinum toxin injection report reduced symptoms and accelerated emptying in patients with idiopathic, diabetic and postsurgical gastroparesis.52,53 High dose of botulinum toxin (200 IU) was more efficacious than lower doses and benefits were greater in women and in patients with idiopathic disease.52, 53

Surgical Management Gastric Electrical Stimulation – The gastric electrical stimulator which delivers low energy impulses received approval from the FDA as a humanitarian use device and was granted a humanitarian device exemption (HDE) for the treatment of diabetic and idiopathic gastroparesis Several studies have demonstrated an 80% reduction in nausea and vomiting for >1 year in diabetic, idiopathic and postsurgical gastroparesis.55,56 A follow-up study extended the benefits of this type of therapy to >10 years. Electrical stimuli improve nutritional parameters, decrease medication use, improve glycemic control, enhance quality of life and reduce health-care utilization. Predictors of nonresponse to this type of therapy include a nondiabetic etiology of disease, less severe vomiting, symptomatic predominance of pain, and opiate use. Adverse events include infections, lead breakage or dislodgement from the stomach, and bowel obstruction, which occur in about 25% of patients.57 There have been subsequent smaller randomized controlled trials, which have shown small or no benefit between sham and gastric electrical stimulators. The future of gastric stimulators is still in development and new more specific gastric stimulators are currently in development.58 Surgical Treatment – Pyloroplasty is reported to reduce symptoms in diabetic patients with gastroparesis, but the efficacy is limited. Completion gastrectomy provides enduring symptom relief in subsets of patients with postsurgical www . DCMS online . org

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gastroparesis.59 The benefit of surgery in this population is uncertain.

Psychological Measures Patients with severe gastroparesis experience significant psychological impairment, which include anxiety and depression. Studies have shown the degree of psychological disease correlates with gastroparesis severity.3 The role of mental health specialists in managing gastroparesis is undefined, but may benefit in patients with severe disease.

Summary Gastroparesis is a condition that is associated with recurrent hospitalizations, worsening quality of life, and increase health costs. Multidisciplinary approach in the management of these difficult patients is highly recommended.

References

1. Jung, H. K. et al. The incidence, prevalence, and outcomes of patients with gastroparesis. Gastroenterology.2009; 136:12251233. 2. Wang, Y. et al. Gastroparesis-related hospitalizations in the United States: trends, characteristics, and outcomes. Am. J. Gastroenterol. 2008;103:313-322. 3. Hyett, B. et al. Delayed radionuclide gastric emptying studies predict morbidity in diabetics with symptoms of gastroparesis. Gastroenterology. 2009; 137: 445-452. 4. Soykan, I. et al. Demography, clinical characteristics, psychological and abuse profiles, treatment, and long-term follow-up of patients with gastroparesis. Dig. Dis. Sci. 1998;43: 2398-2404. 5. Parkman, H. P. et al. Clinical features of idiopathic gastroparesis vary with sex, body mass, symptom onset, delay in gastric emptying, and gastroparesis severity. Gastroenterology. 2011; 140:101-115. 6. Tack, J. et al. Functional gastroduodenal disorders. Gastroenterology. 2006; 130:1466-1479. 7. Hasler, W. L. et al. Importance of abdominal pain as a symptom in gastroparesis: relation to clinical factors, disease severity, quality of life, gastric retention, and medication use. Gastroenterology. 2010; 138: M2023. 8. Parkman, H. P. et al. Inflammatory and autoimmune markers in diabetic and idiopathic gastroparesis [abstract]. Neurogastroenterol. 2010; 22: 65. 9. Bytzer, P et al. Prevalence of gastrointestinal symptoms associated with diabetes mellitus. Arch. Intern. Med. 2001;161:19891996. 10. Koch, K. L. et al. Diabetic gastroparesis: comparison of clinical features in patients with Type 2 and Type 1 diabetes mellitus . Am. J. Gastroenterol. 2009;104: S56. 11. Eisenberg, B. et al. Gastroparesis in diabetics on chronic dialysis: clinical and laboratory associations and predictive features. Nephron. 1995; 70:296-300. 12. Mearin, F. et al. Pyloric dysfunction in diabetics with recurrent nausea and vomiting. Gastroenterology. 1986; 90:1919-1925. 13. Rathmann, W. et al. Visceral afferent neuropathy in diabetic gastroparesis. Diabetes. 1991; 14: 1086-1089. 14. Nohara, S. et al. Gastric emptying in patients with Type 2 diabetes mellitus and diabetes associated with mitochondrial DNA 3243 mutation using 13C-octanoic acid breath test. J. Diabetes. 2006;20:295-301. 15. Hasler, W. et al. Mediation of hyperglycemia-evoked gastric slow-wave dysrhythmias by endogenous prostaglandins. Gastroenterology. 1995;108:727-736.

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16. Jones, K. L. et al. Hyperglycemia attenuates the gastrokinetic effect of erythromycin and affects the perception of postprandial hunger in normal subjects. Diabetes. 1999; 22: 339-344. 17. Russell, A. W. et al. The effect of acute hyperglycaemia on appetite and food intake in Type 1 diabetes mellitus. Diabet. Med. 2001;18:718-725. 18. Jones, K. et al. Blood glucose concentration influences postprandial fullness in IDDM. Diabetes. 1997;20:1141-1146. 19. Jackson, M. et al. Disruption of intestinal motility by a calcium channel-stimulating autoantibody in type 1 diabetes. Gastroenterology. 2004;126:819-828. 20. Kraft, R. et al. Post-vagotomy gastric atony. Arch. Surg. 1964;88:865-874. 21. Trus, T. L. et al. Complications of laparoscopic paraesophageal hernia repair. J. Gastrointest. Surg. 1997;1: 221-228. 22. Salameh, J. et al. Refractory gastroparesis after Roux-en-Y gastric bypass: surgical treatment with implantable pacemaker. J. Gastrointest. Surg. 2007;11:1669-1672. 23. Welsch, T. et al. Evaluation of the International Study Group of Pancreatic Surgery definition of delayed gastric emptying after pancreatoduodenectomy. Br. J. Surg. 2010;97:1043-1050. 24. Bunch, T. et al. Vagus nerve injury after posterior atrial radiofrequency ablation. Heart Rhythm. 2008;5:1327-1330. 25. McCallum, R. et al. Gastric emptying in patients with gastroesophageal reflux. Gastroenterology. 1981;80: 285-291. 26. Cherian, D., et al .Abdominal pain is a frequent symptom of gastroparesis. Clin. Gastroenterol. Hepatol. 2010;8: 676-681. 27. Hasler, W. L. et al. Bloating in gastroparesis: severity, impact, and associated factors. Am. J. Gastroenterol.,2011; 106(8): 1492-1502. 28. Christensen, C. J., et al. Patients with cyclic vomiting pattern and diabetic gastropathy have more migraines, abnormal electrogastrograms, and gastric emptying. Scand. J. Gastroenterol. 2008;43: 1076-1081. 29. Parkman, H. P et al. Dietary intake and nutritional deficiencies in patients with diabetic or idiopathic gastroparesis. Gastroenterology. 2011; 141(2):486-498 30. Lysy, J. et al. Relationships between hypoglycaemia and gastric emptying abnormalities in insulin-treated diabetic patients. Neurogastroenterol. 2006;18:433-440. 31. Hewitt, A. et al. Gastric bezoars: reassessment of clinical and radiographic findings in 19 patients. Br. J. Radiol. 2009;82:901907. 32. Reddymasu, S. et al. Small intestinal bacterial overgrowth in gastroparesis: are there any predictors? J. Clin. Gastroenterol. 2010;44:8-13. 33. Revicki, D. A. et al. Development and validation of a patient-assessed gastroparesis symptom severity measure: the Gastroparesis Cardinal Symptom Index. Aliment. Pharmacol. 2003;18:141-150. 34. De la Loge, C. et al. Cross-cultural development and validation of a self-administered questionnaire to assess quality of life in upper gastrointestinal disorders. Qual. Life. 2004;13: 1751-1762. 35. Tougas, G. et al. Assessment of gastric emptying using a low fat meal: establishment of international control values. Am. J. Gastroenterol. 2000;95:1456-1462. 36. Guo, J. P, et al .Extending gastric emptying scintigraphy from two to four hours detects more patients with gastroparesis. Dig. Dis. Sci. 2001;46: 24-29. 37. Kuo, B. et al. Comparison of gastric emptying of a nondigestible capsule to a radio-labelled meal in healthy and gastroparetic subjects. Aliment. Pharmacol. 2008;27:186-196. 38. Kloetzer, L. et al. Motility of the antroduodenum in healthy and gastroparetics characterized by wireless motility capsule. Neurogastroenterol. 2010;22:527-533.

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39. Perri, F. et al. 13C-octanoic acid breath test (OBT) with a new test meal: toward standardization for testing gastric emptying of solids. Dig. Liver Dis. 2010;42:549-553. 40. Szarka, L. A. et al. A stable isotope breath test with a standard meal for abnormal gastric emptying of solids in the clinic and in research. Clin. Gastroenterol. 2008;6: 635-643. 41. Levin, A. et al. An 8-year review of barium studies in the diagnosis of gastroparesis. Clin. Radiol. 2008;63: 407-414. 42. Chen, J. D., et al. Abnormal gastric myoelectrical activity and delayed gastric emptying in patients with symptoms suggestive of gastroparesis. Dig. Dis. Sci. 1996;41:1538-1545. 43. Sturm, A., et al. Prokinetics in patients with gastroparesis: a systematic analysis. Digestion. 1999;60:422-427. 44. Larson, J. M., et al. Advantages of azithromycin over erythromycin in improving the gastric emptying half-time in adult patients with gastroparesis. J. Neurogastrointest. 2010;16:407-413. 45. Pasricha, P. et al. Drug insight: from disturbed motility to disordered movement—a review of the clinical benefits and medicolegal risks of metoclopramide. Nat. Clin. Pract. Gastroenterol. 2006;3:138-148. 46. Sugumar, A., et al. A systematic review of the efficacy of domperidone for the treatment of diabetic gastroparesis. Clin. Gastroenterol. 2008;6: 726-733. 47. Jost, W. H. Gastrointestinal motility problems in patients with Parkinson’s disease. Effects of antiparkinsonian treatment and guidelines for management. Drugs Aging 1997;10: 249-258. 48. Strauss, S. M. et al. Non-cardiac QTc-prolonging drugs and the risk of sudden cardiac death. Eur. Heart. 2005;26: 2007-2012. 49. De Maeyer, J. et al. 5-HT4 receptor agonists: similar but not the same. Neurogastroenterol. 2008;20:99-112 50. McCallum, R. et al. Clinical trial: effect of mitemcinal on gastric emptying in patients with gastroparesis—a randomized, multicentre, placebo-controlled study. Aliment. Pharmacol. 2007;26:1121-1230. 51. Wo, J. M. et al. Randomised clinical trial: ghrelin agonist TZP-101 relieves gastroparesis associated with severe nausea and vomiting— randomized clinical study. Aliment. Pharmacol. 2011;33:679-688. 52. Arts, J. et al. Clinical trial: a randomized-controlled crossover study of intrapyloric injection of botulinum toxin in gastroparesis. Aliment. Pharmacol. 2007;26:1251-1258. 53. Friedenberg, F. et al. Botulinum toxin A for the treatment of delayed gastric emptying. Am. J. Gastroenterol. 2008;103: 416-423. 54. Lin, Z. et al. Chronic gastric electrical stimulation for gastroparesis reduces the use of prokinetic and/or antiemetic medications and the need for hospitalizations. Dig. Dis. Sci. 2005; 50:1328-1334. 55. Lin, Z. et al. Symptom responses, long-term outcomes and adverse events beyond 3 years of high-frequency gastric electrical stimulation for gastroparesis. Neurogastroenterol. 2006;18:18-27. 56. Anand, C. et al. Gastric electrical stimulation is safe and effective: a long-term study in patients with drug-refractory gastroparesis in three regional centers. Digestion. 2007;75:83-89. 57. Cutts, T. et al. Is gastric electrical stimulation superior to standard pharmacologic therapy in improving GI symptoms, healthcare resources, and long-term health care benefits? Neurogastroenterol. 2005;17: 35-43. 58. Song, G. Q. et al. A novel method of 2-channel dual-pulse gastric electrical stimulation improves solid gastric emptying in dogs. Surgery 2008;143:72-78. 59. Watkins, P. J. et al. Long-term outcome after gastrectomy for intractable diabetic gastroparesis. Diabet. Med. 2003;20:58-63.

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Gastroparesis Bijo K. John, MD; Ann J. Lee, MD; Paul Sievert, MD; and James S. Scolapio, MD

Introduction Normal gastrointestinal motor function is a complex coordinated series of events that involves the sympathetic and parasympathetic nervous system and muscles of the stomach and the intestine. Any pathology or abnormality in any of these components can lead to delayed gastric emptying and produce symptoms of gastric retention in the absence of physical obstruction.1 It has a prevalence of 9.6 per 100,000 men and 37.8 per 100,000 women.2,3 Population based studies have shown a higher incidence in patients with diabetes mellitus.4 In this article we will provide an update on gastroparesis focusing on clinical features, diagnostic evaluation and management.

Normal Physiology of Gastric Motor Function Normal gastric emptying is characterized by a coordinated activity between two functional segments of the stomach: proximal (receptive relaxation) and distal (phasic contraction). In the postprandial period, esophageal transit triggers a series of events which causes the proximal segment to relax, facilitating movement of the food bolus into the stomach; a process of accommodation called receptive relaxation. In the relaxed state, the stomach assumes a reservoir function and allows chemical digestion and gastric mixing. In the distal segment, this receptive distention stimulates intermittent pressure activity, which enables a repetitive phase of propulsion and retropulsion that further grinds and mixes solid particle; a process referred to as phasic contraction. Together the proximal receptive response and distal phasic contraction are critical components of gastric motor function and directly correlate with the rate of gastric emptying. Therefore, a regional defect in one or both segments can alter gastric motility and lead to a delay in gastric emptying.5

Etiology Idiopathic (64%) and diabetic (31%) etiologies have been implicated in the majority of cases of gasteroparesis.6 Recently, with the increasing role of surgical treatment in the management of gastroesophageal reflux disease (GERD) and Address Correspondence to: James S. Scolapio, MD, Professor of Medicine, Chief, Division of Gastroenterology, University of Florida, 4555 Emerson Street, Suite 300, Jacksonville, FL 32207. Phone: 904-633-0089. Email: james.scolapio@jax.ufl.edu

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morbid obesity, postsurgical gastroparesis has become more widely recognized, and currently represents the third most common form of gastroparesis.7 Additionally, other causes have been identified but represent only a minority of cases. Idiopathic Gastroparesis – Idiopathic gastroparesis is the most common form of gastroparesis. Up to 64% of patients with delayed gastric emptying have no identifiable cause. In many of these patients a prior history of a viral illness is reported, but a causative organism is rarely identified. In one report, an immunohistochemistry stain revealed a degeneration of the myenteric plexus and loss of interstitial cells of Cajal suggesting a potential role in the pathogenesis.8 Most of these patients are young or middle aged, and predominately women. Often time’s clinical symptoms overlap with the diagnostic criteria for chronic idiopathic nausea, functional vomiting, and functional dyspepsia. Therefore, a gastric emptying study is needed to determine a diagnosis to plan an appropriate management strategy. Diabetic Gastroparesis – Diabetes is commonly associated with gastroparesis in clinical practice. However, based on a recent population-based cohort study, the incidence of gastroparesis was low, with a significantly greater risk of disease reported in type 1 diabetes (5.2% in type 1diabetes, 1% in type 2 diabetes, and 0.2% in non-diabetic control). 9 In long standing diabetes, the process of gastric emptying is affected at two levels: impaired proximal receptive response and blunted antropyloric motility. Sustained hyperglycemia is thought to be the cause of autonomic dysfunction and/or enteric nervous system degeneration resulting in neuromuscular dysfunction. Several studies have also linked acute hyperglycemia with delayed gastric emptying, although the pathophysiology remains poorly understood. In one study of normal subjects, gastric motility was markedly reduced at serum glucose concentration of 140 to 175 mg/dL, and nearly absent at a serum glucose concentration of 250 mg/dL.10 Changes in blood glucose within the normal postprandial range was also associated with delayed gastric emptying.11 However, despite experimental studies supporting the association of acute and chronic hyperglycemia with delayed gastric motility, the evidence correlating gastric stasis with clinical symptoms remains unclear. Postsurgical Gastroparesis – Postsurgical gastroparesis (PSG) is the third most common cause of gastroparesis. Gastric stasis is often demonstrated following an intentional or accidental vagus nerve injury or after distal gastric resection. Postsurgical gastroparesis has been reported following bariatric surgery for morbid obesity, fundoplication for management of GERD, partial gastrectomy performed to correct complicated peptic Northeast Florida Medicine Vol. 64, No. 1 2013 31

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ulcer disease, and after heart and lung transplantation. Initial postoperative management of PSG should be conservative as most symptoms resolve with time.12 Other Causes â&#x20AC;&#x201C; Other causes of gastroparesis have also been identified and treatment is typically individualized. Iatrogenic causes including the use of prescription medications may have side effects which decrease gastric motility. Some of these commonly prescribed medications include opiate analgesics, tricyclic antidepressants, antihypertensive agents- clonidine and calcium channel blockers, oral hypoglycemics- exenatide and GLP-1 agonists, dopamine agonists, and phenothiazines. A thorough history that includes a comprehensive list of chronic medical conditions and prescription drugs can illicit clues to identify the potential cause for delayed gastric emptying. Discontinuing the offending medication is expected to improve symptoms and resume normal gastric motility. Several neurological disorders have also been associated with gastroparesis. Stroke, parkinsonism, multiple sclerosis, and spinal cord injuries can affect the vagus nerve and the lower thoracic spinal sympathetic outflow which control the activity of the enteric nervous system and delay gastric transit. A variety of systemic diseases have also been implicated in gastroparesis including hormonal dysregulation as in hypothyroidism, and hyperparathyroidism; connective tissues disorders such as scleroderma, systemic lupus erythematosus, and polymyositis; and other autoimmune mediated processes such as paraneoplastic syndromes. The autoantibody mediated neuropathy and myopathy cause delayed gastric emptying, in addition to a slow intestinal and colonic transit. Additionally, anorexia nervosa has been documented to cause physiologic delay in gastric emptying. Other eating disorders (bulimia) and psychiatric diseases (psychogenic vomiting, depression, anxiety neurosis) share a similar clinical presentation, but impaired gastric motility is not a typical feature. Furthermore, rumination syndrome is a rare behavioral disorder which involves an effortless regurgitation of recently ingested food with subsequent remastication and reswallowing or expectoration of the food. It has frequently been identified in children and individuals with mental disorders, however, recently this disorder has been also recognized in adults with normal mental capacity. However, contrary to the aforementioned disorders of intrinsic gastric stasis, patients with an underlying psychiatric etiology (with the exception of anorexia nervosa) often have a normal gastric emptying study. 13

18 percent.14 The character of pain typically if cramping is upper abdominal in location and is usually post prandial. Work up for the pain is negative in most cases, but showing delayed gastric emptying on scintigraphy. Other symptoms that are described include early satiety, bloating and vomiting. Symptoms may range from subtle to those affecting quality of life and in severe cases associated with decreased caloric intake.15 Several tools have been described in literature to stratify patient subgroups. The Gastroparesis Cardinal Symptom Indexâ&#x20AC;&#x201C;Daily Diary (GCSI-DD) is one such tool and comprises of three subscales (fullness/early satiety, nausea/ vomiting and bloating) and rates symptom intensities from zero (none) to five (very severe). It demonstrates validity and responsiveness to treatment for gastroparesis.16 Other clues obtained from history help in possibly identifying the etiologies that have been described earlier. Diabetics may either have uncontrolled blood sugars or episodes of hypoglycemia. Rumination syndrome and cyclical vomiting syndrome have characteristic history. A detailed medication history and prior surgical history is also very useful. Examination may be unrevealing in most cases with some patients exhibiting epigastric tenderness, but no guarding or rigidity. In cases of neuropathy, a more extensive and targeted exam may note orthostatic hypotension and absence of the pupillary reaction to light and persistence of the accommodation response. Unfortunately, these signs are easily missed on a regular office visit.

Laboratory Testing Routine laboratory testing is not considered useful in the diagnosis of gastroparesis itself but may confirm the underlying etiology. The commonly obtained tests are hemoglobin, fasting blood sugar, comprehensive metabolic panel, hemoglobin A1C level and Thyroid stimulating hormone (TSH) level. One may further work up the patient with an abdominal X- ray on the first visit as well.

Clinical Features

It is prudent to first rule out mechanical obstruction or mucosal disease in all patients presenting with vague upper abdominal symptoms. The choice of testing depends on the age, presentation and risk factors including alarm symptoms. Clinicians may choose to order a barium follow through examination (upper GI series), computed tomography of the abdomen (CT scan) or upper endoscopy.

Gastroparesis patients present with a multitude of symptoms depending on the etiology. The majority of patients complain of nausea and pain. Idiopathic gastroparetics are young (mean age 41yrs), mostly women (88 percent) with predominant complaints of nausea, vomiting and abdominal pain.6 A NIH consortium reported 72% of patients with gastroparesis had abdominal pain, but was the dominant symptom in only

If this testing is essentially normal, a Scintigraphic gastric emptying test or commonly referred to as Gastric Emptying Study (GES) is the next appropriate test. GES involves ingesting usually a radiolabelled (usually technetium) low fat, egg-white meal and imaging at 0,1, 2 and 4 hours after the meal.17 The normal values for percentage retained in the stomach are 37 to 90 percent at one hour, 30 to 60 percent at 2 hours and 0 to 10 percent at 4 hours. Values of more than

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60 percent at 2 hours and 10 percent retention at the end of 4 hours have been used for confirming and standardizing a diagnosis of gastroparesis in the clinical setting. Although differential emptying of solids and liquids from the stomach have been described, especially in dumping syndrome, the use of dual isotopic (solid and liquid) emptying studies is limited.18 When using single time measurements, the gastric residual at 2 hours has a 90 percent sensitivity and specificity for accelerated gastric emptying. This is compared to gastric residuals at 4 hours, which was more accurate in predicting delayed gastric emptying with a 100 percent sensitivity and 70 percent specificity.19,20 Hence, one must always use the gastric residual at 4 hours when assessing a patient with suspected gastroparesis. Alternatively the byproduct of nonradioactive 13 Carbon labeled substrates ( Octanate or Spirulina) that are ingested may be measured by mass spectrometry and is comparable to scinitgraphic testing with a sensitivity and specificity of 80 and 89 percent respectively. Their role in office based testing have been well described.21 An alternative to GES is wireless motility capsule (WMC“Smart Pill”) that quantifies changes in intraluminal pressure and pH. WMC gastric emptying is determined when pH increased by at least 3 units when the capsule passes from the stomach to the duodenum.22 WMC gastric emptying of over 5 hours is considered to be delayed and correlates with gastroparesis identified with scintigraphy (GES). No further testing is necessary if gastric stasis is confirmed and mechanical obstruction or other pathology has been ruled out. Gastroduodenal manometery has been suggested in these patients without an identifiable cause and could potentially differentiate a myopathic process (amyloid or scleroderma) from a neuropathic process (diabetes or amyloid neuropathy). Electrogastrography (EGG) which measures gastric slow wave activity has been reported in literature but has limited clinical application thus far. Changes in the electrical activity in the smooth muscles may identify patients with bradygastria (slow) or tachygastria (rapid).23

Management Managing patients with gastroparesis requires a multidisciplinary approach. Treatment consists of four components: nutritional support, glycemic control in diabetes, pharmacologic therapy, and endoscopic and surgical treatment. Despite maximizing treatment options, clinical symptoms are often inadequately managed. Therefore, long term follow-up with appropriate therapeutic modifications is required to optimize clinical needs and maintain quality of life. Nutritional Support – Reccurrent vomiting and poor oral intake can lead to protein-calorie malnutrition and deficiencies in vitamins and minerals. Maintaining an adequate nutritional www . DCMS online . org

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state is an important goal of therapy. Dietary interventions rely on measures to optimize gastric emptying. Oral nutrition is the preferred route to provide daily calories, vitamins, and minerals. Reducing meal size and increasing the frequency of meals to ~ 4-6 times a day is recommended to avoid gastric distention and exacerbating symptoms. Diet should also contain a low-fat and low-residue component, as lipids and fibers delay gastric emptying and can lead to the formation of food bezoars especially in patients with severe gastric stasis. Additionally, patients are also encouraged to chew food well and take plenty of fluids throughout the meal, as gastric emptying of liquids is often preserved in most patients. In the subset of patients who are unable to tolerate solid meals, an alternative form of oral nutrition in the form of homogenized solids or high calorie liquid source may be required. Generally, poor tolerance of liquids is predictive of a poor outcome with oral nutrition, and therefore, an alternative means for nutritional support may be required.24 When oral nutrition is unsuccessful, enteral alimentation should be considered ie. feeding jejunostomy tube. Indications for enteric nutrition include unintentional loss of 10% or more of body weight during a period of 3-6 months, and/ or repeated hospitalizations for refractory symptoms.25 Jejunostomy tubes can be placed endoscopically or surgically, and in select patients a gastrostomy with jejunal extension tube is placed to vent gastric secretions and prevent secondary emesis. Prior to placing the feeding tube, a trial nasojejunal feeding is required to determine if jejunal feedings will be tolerated as small bowel dysfunction may also occur in some patients with gastroparesis. Total parenteral nutrition (TPN) is not commonly recommended, and clinical use is generally limited to cases with associated intestinal dysmotility. Glycemic Control in Diabetes – The of long term glycemic control on improving gastric motility and clinical symptoms is controversial. Nevertheless, given the association between acute hyperglycemia and delayed gastric emptying, it is assumed that improving glycemic control may also improve gastric motility and gastroparesis related symptoms. Therefore, short and long term glycemic control is indicated as part of managing diabetic gastroparesis.25The use of certain oral agents for treatment of diabetes such as amylin analogs or GLP-1 analogs has been reported to cause iatrogenic gastroparesis and should be avoided.26 Pharmacologic Therapy – Pharmacologic therapy for gastroparesis consists of two classes of drugs: prokinetics and antiemetics. Metoclopramide is a dopamine D2-receptor antagonist with both antiemetic and prokinetic properties. A short term benefit in symptom reduction and accelerated gastric emptying has been supported by several comparator controlled trials.27 However, the long term efficacy is unclear and reported benefits were limited to small, open label studies.28 Currently the FDA recommends a treatment duration of no longer than 12-weeks, but extended use is considered in Northeast Florida Medicine Vol. 64, No. 1 2013 33

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patients who continue to experience benefit. Long term use has also been limited by the potential for extrapyramidal side effects including acute dystonia, parkinsonism type movements, and tardive dyskinesia which can lead to irreversible damage. Therefore, all physicians are legally obligated to discuss these adverse effects and document the discussion in the medical record. Domperidone is also a dopamine D2-receptor antagonist similar to metoclopramide. It is as effective as metoclopramide, but the risk for extrapyramidal side effects are reported to be lower(particulary tardive dyskinesia). The main concern with domperidone is its associated risk for QTc interval prolongation and the drug-drug interactions altering CYP2D6 function (antiemetic agents and antidepressants). Therefore, an electrocardiogram is recommended at the beginning of treatment, and then monitored periodically during the treatment duration. This drug has been widely used for many decades in more than 20 countries, but it is currently not approved for use by the US FDA and only available through a FDA-sanctioned Investigational New Drug process.29 Erythromycin is a motilin receptor agonist which stimulates gastric motility. This drug is often given as an infusion to treat acute episodes of gastric stasis. Prolonged use of erythromycin has been associated with tachyphylaxis and clinical response reportedly drops after 4 weeks of oral therapy. Despite this decrease in treatment response, a lesser but significant improvement is reportedly noted, thereby, supporting longer therapy in select patients who continue to demonstrate clinical benefit.30 Similar to domperidone, erythromycin is associated with the risk of prolonged QT syndrome and sudden cardiac death particularly in patients taking medications that inhibit CYP3A4 function. Therefore, an electrocardiogram is recommended both at the beginning of treatment, and then periodically during the treatment duration. Recently azithromycin was recognized to have a similar prokinetic profile as erythromycin but with a reported longer duration of treatment effect.31 Additionally, azithromycin is a weak inhibitor of the CYP3A4, so reported drug-drug interactions and related QT prolongation has been less common. In addition to prokinetics, antiemetic agents are used in conjunction to treat acute nausea. Several different classes of antiemetic drugs are available and include phenothiazines (prochlorperazine and thiethylperazine), antihistamines (promethazine), and serotonin 5-HT3-receptor antagonists. Currently there are no studies that compare the efficacy between the different drug classes. Moreover, open label studies have also suggested that tricyclic antidepressants in low doses may decrease symptoms of nausea and vomiting, and are considered in refractory cases.25

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Endoscopic and Surgical Treatment â&#x20AC;&#x201C; Patients that fail medical therapy are considered for endoscopic and surgical intervention. These second line treatments have not been well studied, so the clinical efficacy is not well established. Therefore, indications for treatment are often limited to cases of refractory gastroparesis. Intrapyloric botulinum toxin injection therapy is aimed to treat the increased pyloric tone associated with gastroparesis. Several open-label studies reported improvement in gastric emptying and symptom response.25,32,33 On the contrary, no significant symptomatic benefit was noted in randomized, placebo-controlled trials. 34,35 Therefore, intrapyloric botulinum toxin injection is currently not recommended for treatment of gastroparesis based on the available study evidence. Gastric electrical stimulation (GES) is an FDA approved humanitarian use device for refractory diabetic and idiopathic gastorparesis. Most of the data is from open-label clinical studies which suggest enhanced symptom control and improved oral tolerance of feeding. A recent meta-analysis also showed similar results, but additionally noted a greater clinical response for diabetic gastroparesis.36 Currently there is no consensus guideline for treatment indication. Nevertheless, gastric electrical stimulation should be considered in patients with refractory diabetic and idiopathic gastroparesis. Minimally invasive pyloroplasty is a very effective therapeutic modality which has shown excellent treatment outcomes. A recent study reported a significant improvement in symptoms with a reduction in mean gastric emptying time (320 to 112 minutes, p=0.001) and the need for prokinetic therapy (from 89% to 14%).37 Other surgical options include subtotal and total gastrectomy which are generally limited to patients with previous partial gastrectomy.

Conclusion Delayed gastric emptying is a hallmark of gastroparesis and it is frequently associated with nonspecific clinical symptoms. This condition must be considered as part of the differential diagnosis after mechanical causes have been ruled out. In most cases, a thorough history that includes a comprehensive list of chronic medical conditions and prescription drugs can identify the potential cause for delayed gastric emptying. The management of gastroparesis include identifying and correcting nutritional deficits, treating the underlying medical condition, control symptoms, and improving gastric motility. Patients may be on opioid analgesics or other offending prescription medications which can contribute to delayed gastric emptying. This may create a management dilemma for health care providers and requires a coordinated approach between the treatment team and the patient.

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References 1. Camilleri M, Bharucha AE, Farrugia G. Epidemiology, mechanisms, and management of diabetic gastroparesis. Clin Gastroenterol Hepatol. 2011; 9:5-12. 2. Jung HK, Choung RS, Locke GR 3rd, et al. The incidence, prevalence, and outcomes of patients with gastroparesis in Olmsted County, Minnesota, from 1996 to 2006. Gastroenterology. 2009;136(4):1225-33. 3. Rey E, Choung RS, Schleck CD, et al. Prevalence of hidden gastroparesis in the community: the gastroparesis ‘iceberg’. J Neurogastroenterol Motil. 2012; 18:34-42. 4. Jones KL, Russo A, Stevens JE, et al. Predictors of delayed gastric emptying in diabetes. Diabetes Care. 2001; 24:1264. 5. Rayner CK, Horowitz M.New management approaches for gastroparesis.Nat Clin Pract Gastroenterol Hepatol. 2005 Oct;2(10):454-62 6. Parkman HP, Yates K, Hasler WL et al. National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium. Clinical features of idiopathic gastroparesis vary with sex, body mass, symptom onset, delay in gastric emptying, and gastroparesis severity.Gastroenterology. 2011; 140(1):101-15. 7. Hyett B, Martinez FJ, Gill BM et al. Delayed radionucleotide gastric emptying studies predict morbidity in diabetics with symptoms of gastroparesis. Gastroenterology. 2009; 137:445-52. 8. N Zárate,1 F Mearin,1 X-Y Wang,2 B Hewlett,2 J D Huizinga,2 and J-R Malagelada1. Severe idiopathic gastroparesis due to neuronal and interstitial cells of Cajal degeneration: pathological findings and management. Gut. 2003 July; 52(7): 966–970.

14. Hasler WL, Wilson L, Parkman HP et al. Importance of abdominal pain as a symptom in gastroparesis: relation to clinical factors, disease severity, quality of life, gastric retention, and medication use. Gastroenterology. 2010; 138 (Suppl 1): S-461. 15. Talley NJ, Young L, Bytzer P et al. Impact of chronic gastrointestinal symptoms in diabetes mellitus on health-related quality of life. Am J Gastroenterol. 2001;96:71–76. 16. Revicki DA, Camilleri M, Kuo B, et al. Evaluating symptom outcomes in gastroparesis clinical trials: validity and responsiveness of the Gastroparesis Cardinal Symptom Index-Daily Diary (GCSI-DD).Neurogastroenterol Motil. 2012;24(5):456-63. 17. Abell TL, Camilleri M, Donohoe K, et al. Consensus recommendations for gastric emptying scintigraphy: a joint report of the American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine. Am J Gastroenterol. 2008; 103(3):753-63. 18. Ziessman HA, Okolo PI, Mullin GE, et al. Liquid gastric emptying is often abnormal when solid emptying is normal.J Clin Gastroenterol. 2009;43(7):639-43. 19. Thomforde GM, Camilleri M, Phillips SF, et al. Evaluation of an inexpensive screening scintigraphic test of gastric emptying.J Nucl Med. 1995 Jan;36(1):93-6. 20. Tougas G, Eaker EY, Abell TL, et al. Assessment of gastric emptying using a low fat meal: establishment of international control values. Am J Gastroenterol. 2000;95(6):1456-62. 21. Perri F, Bellini M, Portincasa P, et al.(13)C-octanoic acid breath test (OBT) with a new test meal (EXPIROGer): Toward standardization for testing gastric emptying of solids. Dig Liver Dis. 2010;42(8):549-53.

9. Choung RS, Locke GR III, Schleck CD et al. Risk of gastroparesis in subjects with type 1 and 2 diabetes in the general population. Am J Gastroenterol. 2012; 107:82-8.

22. Rao SS, Mysore K, Attaluri A, et al. Diagnostic utility of wireless motility capsule in gastrointestinal dysmotility.J Clin Gastroenterol. 2011;45(8):684-90.

10. Barnett JL, Owyang C. Serum gulcose concentration as a modulator of interdigestive gastric motility. Gastroenterology. 1988; 94:739.

23. Abid S, Lindberg G. Electrogastrography: poor correlation with antro-duodenal manometry and doubtful clinical usefulness in adults. World J Gastroenterol. 2007;13(38):5101-7.

11. Schvarcz E, Palmer M, Aman J, et al. Physiological hyperglycemia slows gastric emptying in normal subjects and patients with insulin-dependent diabetes mellitus. Gastroenterology. 1997; 113-60. 12. Shafi MA, Pasricha PJ. Post-surgical and obstructive gastroparesis. Curr Gastroenterol Rep. 2007 Aug;9(4):280-5. 13. Parkman HP, Hasler WL, Fisher RS. American Gastroenterological Association technical review on the diagnosis and treatment of gastroparesis.Gastroenterology. 2004 Nov;127(5):1592-622. www . DCMS online . org

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24. Abell TL, Bernstein VK, Cutts T et al. Treatment of gastroparesis: a multidisciplinary clinical review. Neurogastroenterol Motil. 2006; 18:263-83. 25. Camilleri M, Parkman HP, Shafi MA, et al. Clinical Guideline: Management of Gastroparesis.Am J Gastroenterol. 2012 Nov 13. 26. Linnebjerg H, Park S, Kothare PA, et al. Effect of exenatide on gastric emptying and relationship to postprandial glycemia in type 2 diabetes. Regul Pept. 2008; 151:123. Northeast Florida Medicine Vol. 64, No. 1 2013 35

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27. Patterson D, Abell T, Rothstein R et al. A double-blind multicenter comparison of domperidone and metoclopramide in the treatment of diabetic patients with symptoms of gastroparesis. Am J Gastroenterol. 1999; 94:1230-4. 28. Longstreth GF, Malagelada JR, Kelly KA. Metoclopramide stimulation of gastric motility and emptying in diabetic gastroparesis. Diabetes Care .1993; 16:1511-4. 29. Patterson D, Abell T, Rothstein R, et al. A double-blind multicenter comparison of domperidone and metoclopramide in the treatment of diabetic patients with symptoms of gastroparesis.Am J Gastroenterol. 1999;94(5):1230-4. 30. Janssens J, Peeters TL, Vantrappen G, et al. Improvement of gastric emptying in diabetic gastroparesis by erythromycin. Preliminary studies. N Engl J Med .1990; 322:1028. 31. Moshiree B, McDonald R, Hou W, Toskes PP. Comparison of the effect of azithromycin over erythromycin on antroduodenal pressure profiles of patients with chronic functional gastrointestinal pain and gastroparesis. Dig Dis Sci. 2010; 55:675. 32. Coleski R, Anderson MA, Hasler WL. Factors associated with symptom response to pyloric injection of botulinum toxin in a large series of gastroparesis patients. Dig Dis Sci. 2009; 54:2634-42. 33. Bromer MQ, Friedenberg F, Miller LS, et al. Endoscopic pyloric injection of botulinum toxin A for the treatment of refractory gastroparesis. Gastrointest Endosc. 2005; 61:833-9. 34. Arts J, Holvoet L, Caenepeel P, et al. Clinical trial: a randomized-controlled crossover study of intrapyloric injection of botulinum toxin in gastroparesis. Aliment Pharmacol Ther. 2007; 26:1251-8. 35. Friedenberg FK, Palit A, Parkman HP, et al. Botulinum toxin A for the treatment of delayed gastric emptying. Am J Gastroenterol. 2008; 103:416-23. 36. Chu H, Lin Z, Zhong L, et al. A meta-analysis: the treatment of high-frequency gastric electrical stimulation for gastroparesis. J Gastroenterol Hepatol. 2012; 27:1017-26. 37. Hibbard ML, Dunst CM, Swanstrom LL. Laparoscpic and endoscopic pyloroplasty for gastroparesis results in sustained symptom improvement. J Gastrointest Surg. 2011:15:1513-9.

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We would like to thank the following donors for their 2012 donations to the Duval County Medical Society Foundation. Clarence Boudreaux, MD Loren Clayman, MD Yank Coble, Jr., MD Steven Crenshaw, MD Lorraine Dajani, MD Rahul Deshmukh, MD Gavan Duffy, MD Robert Duncan, MD Joe Ebbinghouse, MD Walter Gilbert, Jr., MD J. Glenn, MD Christopher Goll, MD Charles Greene, MD R. Heekin, MD Mihaela Lonescu, MD Eli Lerner, MD Daniel Lestage, MD Lawrence Lisska, MD Shanan Loe, MD Alan Marks, MD Marianne McEuen, MD Russell Metz, MD Kevin Murphy, MD Ronald Rhatigan, MD Mary Robinson, MD David Ross, MD Guy Selander, MD Paul Shirley, MD Gary Soud, MD Timothy Sternberg, DMD N. Tucker, III, MD

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Prevention of Medical Errors: Root Causes and Strategies to Avoid Errors Background - Benefits that Matter!

The Duval County Medical Society (DCMS) attempts to provide its members with the benefits that consistently meet your professional needs. One example of how this is being accomplished is by providing to DCMS members free Continuing Medical Education (CME) opportunities in the subject areas mandated/and or suggested by the State of Florida Board of Medicine to obtain and retain medical licensure. The DCMS would like to thank the St. Vincent’s Healthcare (SVHC) Committee on CME for reviewing and accrediting this activity in compliance with the Accreditation Council on Continuing Medical Education (ACCME). Helena Karnani, MD, Chair of the CME Committee; Betsy Miller, Director, Medical Staff, Quality Management; and Cindy Williamson, CME Coordinator, from SVHC deserve special recognition for their work on behalf of DCMS. This issue of Northeast Florida Medicine includes an article, “Prevention of Medical Errors: Root Causes and Strategies to Avoid Errors” authored by Vicki-lynne Gloger, BA, MSSM (see pp. 39-44), which has been approved for 2.0 AMA PRA Category 1 credits.TM For a full description of CME requirements for Florida physicians (MD/DO), please visit the DCMS website (www.dcmsonline.org).

Faculty/Credentials:

Vicki-lynne Gloger, BA, MSSM, is the Executive Director of Baptist Primary Care Inpatient Medicine for the Baptist Health System in Jacksonville, FL. Prior to that position, most recently Ms. Gloger was Chief Operating Officer for Pulmonary and Critical Care Associates in Jacksonville, and Risk Management Vice President for Preferred Professional Insurance Company in Omaha, NE. Her professional background also includes positions with the American Medical Partnership, St. Vincent’s Medical Center, and the Joint Commission on Accreditation of Health Care Organizations. She served in the United States Army (active duty and reserve) with the Medical Service Corps, leaving with the rank of Captain. In the Jacksonville community she is active in the Society for Hospital Medicine, Rotary Club, Episcopal Children’s Services, and numerous other organizations. Ms. Gloger completed her BA degree at Northern Illinois University and earned a MA degree in Systems Management from Vertibri College of Engineering at the University of California.

Objectives for CME Journal Article 1. Identify significant risks for medical errors 2. Identify primary factors affecting medical errors 3. Identify strategies to avoid medical errors

Date of Release: March 1, 2013 Date Credit Expires: March 1, 2015. Estimated time to complete: 1 hr.

Methods of Physician Participation in the Learning Process

1. Read the “Prevention of Medical Errors: Root Causes and Strategies to Avoid Errors” article pages 39-44 2. Complete the Post Test and Evaluation on page 38 3. Members or non-members may fax the Post Test to DCMS (FAX) 904-353-5848 OR members can also go to www.dcmsonline.org & submit the test online. Non-members must arrange for the CME fee payment before submitting the post test by fax. Call 904-355-6561 x104 or fax.

CME Credit Eligibility

In order to receive full credit for this activity, a minimum passing grade of 70% must be achieved. Only one re-take opportunity will be granted if a passing score is not made on the first attempt. DCMS members and non-members have two years to submit the post test and earn CME credit. A certificate of credit/completion will be emailed or USPS mailed within 4-6 weeks of submission. If you have any questions, please contact the DCMS at 355-6561, ext. 104, or patti@dcmsonline.org.

Faculty Disclosure Information

Vicki-lynne Gloger reports no significant relationships to disclose, financial or otherwise with any commercial supporter or product manufacturer associated with this activity.

Disclosure of Conflicts of Interest

St. Vincent’s Healthcare (SVHC) requires speakers, faculty, CME Committee, and other individuals who are in a position to control the content of this educational activity to disclose any real or apparent conflict of interest they may have as related to the content of this activity. All identified conflicts of interest are thoroughly evaluated by SVHC for fair balance, scientific objectivity of studies mentioned in the presentation and educational materials used as basis for content, and appropriateness of patient care recommendations.

Joint Sponsorship Accreditation Statement

This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of St. Vincent’s Healthcare and the Duval County Medical Society. St. Vincent’s Healthcare is accredited by the Florida Medical Association to provide continuing medical education for physicians.The St. Vincent’s Healthcare designates this educational activity for a maximum of 2.0 AMA PRA Category 1 credit(s) .TM Physicians should only claim credit commensurate with the extend of their participation in the activity.

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

Prevention of Medical Errors: Root Causes and Strategies to Avoid Errors CME Questions & Answers (circle one answer)/Free to DCMS Members/$50.00 charge non-members*

(Return by March 1, 2015 by FAX: 904-353-5848, by mail: 555 Bishopgate Lane, Jacksonville, FL 32204 OR online: www.dcmsonline.org.)

Family history is important when assessing the prenatal patient, regardless of her health status. a. True b. False

3. Pain medication should not be given to patients presenting with abdominal pain as it may mask their symptoms making a diagnosis more difficult to determine. a. True b. False 4. Problem lists are no longer important for the physician office due to improved technology with EMR. a. True b. False

5. When a medical error occurs, the physician should allow the hospital to handle communication with the patient/ family. a. True b. False 6. Patients who return to the ER repeatedly with vague symptoms should be reassessed to ascertain if the initial diagnoses are incorrect. a. True b. False 7. Communication between physicians can enhance patient safety when: a. Medications are changed by sub-specialists b. Care regimes are identified as “at odds” when multiple physicians are caring for a patient c. Diagnoses are unclear d. All of the above 8. Wrong site surgery is avoided by: a. Marking surgical sites b. Having all caregivers reaffirm patient identity c. Having a time out immediately before incision d. Improving OR turn-over times e. All of the above f. A,B, and D g. A and B

Evaluation questions & CME Credit Information (Please evaluate this article. Circle one number using this scale: 1= Strongly Agree to 5= Strongly Disagree) The article met the stated objectives: 1 2 3 4 5 The article was appropriate to my practice: 1 2 3 4 5 The topic was current and well presented: 1 2 3 4 5 Comments:

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1. Medication errors are the result of a. Patients not knowing what medications they are taking b. Physicians in different practices not knowing what other physicians are prescribing c. Constant change in the look and feel of generic medications d. Distracted care givers e. All of the above

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Prevention of Medical Errors: Root Causes and Strategies to Avoid Errors Vicki-lynne Gloger, MSSM

Abstract: This article focuses on medical errors and the root causes

for why they occur, case reviews of some types of errors and strategies to avoid them. After reading this article, the physician should be able to identify common medical errors according to the Board of Osteopathic Medicine and the Board of Medicine, at least two root causes for each and a minimum of two strategies to effectively avoid these medical errors.

Medical Error #1: Pregnancy Complications Complications related to pregnancy can produce many medical errors. Studies conducted by the Centers for Disease Control (CDC) and American College of Obstetricians and Gynecologists (ACOG) conclude that the leading causes of maternal/pregnancy death are: hemorrhage, hypertensive disorder, pulmonary embolism, amniotic fluid embolism, infection, and pre-existing chronic conditions. One study that spanned ten years indicated that the numbers of deaths related to hemorrhage declined while mortality attributable to other conditions e.g. cardiovascular, pulmonary and neurologic significantly increased.1 Researchers are examining the role of pre-existing medical conditions in contributing to maternal death. Conditions such as Cystic Fibrosis have long been recognized as high risk factors requiring diligence. Other more “benign” conditions are now the focus as potential significant risk factors too often not managed adequately by the physician. Obesity for example, a growing epidemic, can lead to hypertensive disorders, diabetes, and other medical conditions, and thus can directly and indirectly present significant health risks for pregnant women. It has become evident that heightened physician awareness coupled with screening of pregnant women with pre-existing condition/associated risk factors will help preclude adverse outcomes. Without comprehensive medical and social histories, these underlying factors may go unrecognized and result in morbidity or mortality.

Address questions and correspondence to: Vicki-lynne Gloger, Administrator Baptist Health System Hospitalist Programs, Jacksonville, FL. Email: Vicki-lynne.Gloger@bmcjax.com.

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The Hospital Corporation of America (HCA) examined individual causes of maternal deaths among 1.5 million births within 124 hospitals occurring from 2002-2007. They concluded that while the majority of maternal deaths could not be avoided some could have been prevented by the physicians. According to the study, the most preventable errors are failure to adequately control blood pressure in hypertensive women, failure to adequately diagnose and treat pulmonary edema in preeclamptic patients, failure to monitor/respond to vital signs following C-section, and failure to control hemorrhage following C-section.2 Steven L. Clark, MD, Medical Director of Women and Newborn Services for HCA, stated, “The data showed the individual causes of death to be very heterogeneous and that the only cause of maternal death amendable to nationwide systematic prevention efforts is pulmonary embolism. Pregnancy is a known major risk factor for venous thrombosis and pulmonary embolism.”3 Unlike nearly all other adult patients undergoing major surgery, women undergoing C-sections have traditionally not received prophylactic measures for the prevention of venous thromboembolism (VTE) afforded similar surgical patients who lack this risk factor. From 1991 through 2003, the U.S. rate of severe complications and conditions associated with pregnancy was 50 times more common than maternal death.3 A review of settled obstetrical malpractice claims reveals that adverse outcomes often result from under-responding to abnormal vital signs, failing to recognize or notice indications that complications occurred and practicing in a state of denial. It is imperative to establish protocols with triggers for appropriate responses. For example, adopting VTE prophylaxis measures, coupled with comprehensive programs for identifying and responding to hemorrhage can have a significant impact. The bottom line in avoiding preventable pregnancy related morbidity and mortality is that, in addition to the safe guards discussed at the end of this article, the following should be the standard of practice: A comprehensive history and physical should be taken when care is initiated, which includes family and social history and underlying medical conditions. • Reassessment at the time of every office visit and upon hospitalization is crucial. Northeast Florida Medicine Vol. 64, No. 1 2013 39

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• The “young and healthy” status of women in labor, during delivery and post-partum should not preclude the requirement that physicians recognize and respond to changes in a patient’s condition. Whether or not the hospital has a protocol, the physician should require that his/her patients be monitored throughout hospitalization from admission to discharge, recognizing and responding as soon as a patient’s condition appears to be worsening. • Physicians who care for women with underlying medical conditions should be attuned to the additional risks that could be imposed if pregnancy were added, how to discuss these risks with patients, the use of appropriate and acceptable contraception; and pre-conceptual care and counseling. The attending physician at delivery should communicate identified pregnancy risks to all members of the health care delivery team. • The physician managing pregnant patients should evaluate for, identify and respond to pre-existing medical conditions such as hypertension, diabetes, morbid obesity, and advanced maternal age. • The physician’s orders should identify specific triggers for responding to changes in the mother’s vital signs and clinical condition and should stipulate interventions for responding to the changes. • VTE prophylaxis should be ordered for Cesarean section patients at increased risk for pulmonary embolism. • Patients at high risk for thromboembolism should be evaluated for low molecular weight heparin for postpartum care 1,3, 4,5,6,7

Medical Error #2: Surgical Complications Surgical complications are sometimes caused by medical errors. When the then president of the Joint Commission, (TJC) surgeon Dennis O’Leary, M.D., unveiled mandatory rules to prevent operations on the wrong patient or body part, he did not mince words. “This is not quite ‘Dick and Jane,’ but it’s pretty close,” he declared in an interview about the “universal protocol” to prevent wrong-site surgery.8 These rules require preoperative verification of important details, marking of the surgical site and a timeout to confirm everything just before the procedure starts. Error prevention measures that O’Leary sited include ensuring that x-rays are hung correctly, checking arm bands and having all team members reaffirm patient identity and planned procedure. Wrong site, wrong procedure and wrong patient errors are considered by TJC so egregious and avoidable that they are classified as “never events”. Medicare requires “never event” reporting and does not pay for wrong-site surgery. Medicaid announced a similar policy to take effect this year. However in 2012, researchers and patient safety experts say wrong-site/wrong patient surgery has not improved and may be getting worse. Forty-eight cases were reported in Minnesota in 2010, up from 44 in 2009; Pennsylvania 40 Vol. 64, No. 1 2013 Northeast Florida Medicine

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has averaged about 64 cases for the past few years. Based on data provided by individual states, TJC officials estimate that wrong-site surgery occurs 40 times a week.9 Mark Chassin, MD, current TJC president, speaking at the Joint Commission Center for Transforming Healthcare Conference on June 29, 2011 said he thinks such errors are growing in part because of increased time pressures on surgical teams. Preventing wrong-site surgery also “turns out to be more complicated to eradicate than anybody thought,” he said, because it involves changing the culture of hospitals and getting doctors who typically prize their autonomy, resist checklists and underestimate their propensity for error to follow standardized procedures and work in teams. Studies of wrong-site errors have consistently revealed a failure by physicians to participate in a timeout. Timeout is the minimal delay just before incision to ensure correct patient, procedure and site.10 Philip F. Stahel, M.D., Director of Orthopedic Surgery at Denver Health Medical Center was lead author of a 2010 study evaluating 132 wrong-site and wrong-patient cases reported to a Colorado malpractice carrier. The cases were reported between 2002 and 2008, and one-third resulted in death or serious injury. Among them were three men who underwent prostate cancer surgery although they were cancer-free. In 72 percent of cases there was no timeout.11 The objective of the study was to determine the frequency, root cause, and outcome of wrong-site and wrong-patient procedures. The researchers analyzed a prospective physician insurance database and de-identified cases were screened. The database contained 27, 370 self-reported adverse occurrences. Dr. Stahel and his cohorts generated descriptive statistics and examined the number of adverse events reported per year, and the root causes and occurrence-related patient outcomes. They reported that: “A total of 25 wrong-patient and 107 wrong-site procedures were identified during the study period. Significant harm was inflicted in 5 wrong-patient procedures (20.0%) and 38 wrong-site procedures (35.5%). One patient died secondary to a wrong-site procedure (0.9%). The main root causes leading to wrong-patient procedures were errors in diagnosis (56.0%) and errors in communication (100%), whereas wrong-site occurrences were related to errors in judgment (85.0%) and the lack of performing a ‘time-out’” (72.0%).11 Hospitals and surgical centers sometimes permit non-compliance with “Universal Protocol.” The American Academy of Orthopedic Surgeons states that orthopedic surgeons have a 25 percent chance of making a wrong-site error during their career. The Academy launched a voluntary “Sign Your Site” campaign in 1997, (see website http://www3.aaos.org/ member/safety/ewsurgery.cfm) putting up billboards across the country in an attempt to educate patients. A billboard at O’Hare Airport in Chicago, for example had a hand holding a Sharpie marker and the caption indicated that the marker may be the most important tool your surgeon uses The following should be the “Always” standard of practice to www . DCMS online . org

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avoid wrong site, wrong procedure, and wrong patient surgery: 1. The surgeon should review the actual diagnostic studies performed by the referring physician to ensure he/she agrees that the proposed procedure is indicated and appropriate. 2. The surgeon should ensure that x-rays are hung correctly. 3. The “Universal Protocols” for correct site, patient and procedure should be consistently complied with for all cases regardless of O.R. turn-around times a. Every member of the surgical team speaking with the patient pre-operatively should reaffirm a patient’s identity b. Every member of the surgical team speaking with the patient should reaffirm the planned procedure and location of the procedure (level, side, etc.) c. The surgeon should consistently sign the surgical site 4. In the event of surgical error or mishap, the surgeon as “captain of the ship” should always take the lead in disclosing what occurred to the patient/family, in making a sincere apology and in working with the patient/family in resolving resulting issue according to major malpractice carriers including PPIC, The Doctor’s Company, FPIC and Mag Mutual.12

Medical Error #3: Diagnosis Failures Diagnosis errors are frequent and important but can be challenging to detect and dissect to ascertain how to best avoid them in the future or what are the root causes. A study conducted by a team of physicians led by Gordon D. Schiff, MD identified why diagnostic errors occur and what can be done to avoid them. The study, published in Advances in Patient Safety: From Research to Implementation describes what federally funded programs have accomplished in understanding medical errors and implementing programs to improve patient safety over the last 5 years. This compendium, sponsored jointly by the Agency for Healthcare Research and Quality and the Department of Defense (DoD)-Health Affairs, catalogues a series of ideas for change. These include: • Reengineering follow-up of abnormal test results • Standardizing protocols for reading x-rays/lab tests, particularly in training programs and after hours • Identifying “red flag” and “don’t miss” diagnoses and situations • Using manual and automated check-lists • Engaging patients on multiple levels to become “co-producers” of safer medical diagnosis practices and

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• Weaving “safety nets” to mitigate harm from uncertainties and errors in diagnosis.13 Creating and maintaining a patient problem list can help prevent avoid diagnostic errors. It can ensure that each active problem is being addressed, with reminders about diagnoses, allergies, and unexplained findings. It is also useful in ensuring follow-up of health maintenance. Likewise, an up-to-date medication list, reconciled at each patient visit (or admission) is essential for patient safety.10 A Harris poll commissioned by the National Patient Safety Foundation found that one in six people had personally experienced a medical error related to misdiagnosis. Most medical error studies find that on average, 20% percent of errors are errors in diagnosis. They further reported that a recent review of 53 autopsy studies found an average rate of 23.5 percent major missed diagnoses. Selected diseasespecific studies also show that around 30 percent of patients experienced missed or delayed diagnoses. While the studies used different criteria and methodologies, what emerged was compelling evidence for the frequency and impact of diagnosis error and delay.11 Obviously the severity varies greatly in missed and delayed diagnoses, but the Florida Boards of Medicine and Osteopathic Medicine have identified what they believe to be the most common in our state. At the same time, according to “Up to Date”14 it is likely that few physicians would disagree that diagnoses such as ectopic pregnancy, myocardial infarction, dissecting aortic aneurysm, and pericardial effusion with tamponade and fast growing cancers when missed or delayed, could unquestionably be life-threatening. Physicians are frequently confronted with rapid changes in diagnostic testing and care pathway expectations. New imaging modalities, lab tests, and testing recommendations have been introduced, often leaving physicians confused about what to order and how to interpret contradictory results from one sub-specialist to the next. If diagnosis errors are to be avoided, physicians must be aware of the limitations of diagnostic tests they order. For example, a normal mammogram in a woman with a breast lump does not rule out the diagnosis of breast cancer, as test sensitivity is only 70 to 85%. A recurring theme of case reviews was failure to appreciate pitfalls in weighing test results in the context of the patient’s pretest disease probabilities. Local factors, such as the variation in quality of test performance and readings, combined with communication failures between radiology/laboratory and ordering physicians (results reported as “positive” or “negative,” overlooking subtleties and limitations) provide further sources of error.12 Active listening is an essential component of an accurate diagnosis and often the physician has only partial information, resulting in diagnostic errors. The physician can fall victim to bias based on what he/she did hear and as a result “went down the incorrect biased diagnostic pathway”.15

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Medical Error #4: Diagnostic Pitfalls Errors occur when physicians are trying to make an accurate diagnosis of a medical problem. Some closed case reviews help us understand why errors in ascertaining the correct diagnosis occur. CASE ONE: The diagnosis of aneurysms (e.g., aortic, intracranial) arises repeatedly in discussions of misdiagnosis. Many physicians seem to recall a case of a missed aneurysm with catastrophic outcomes where, in retrospect, warnings may have been overlooked. A Wall Street Journal article recently won a Pulitzer Prize for publicizing such aneurysm cases. Case review showed that one patient’s back pain was initially dismissed because of frequent visits; she had been labeled as a “frequent flyer” and drug seeker due to her nonspecific symptom of “back pain”. A review of literature on the frequency of dissecting aortic aneurysm reveals that it is surprisingly rare, perhaps less than 1 out of 50,000 ED visits for chest pain, and likely an equally rare cause for back pain. The patient ultimately underwent a recommended imaging study after a suspicious plain chest x-ray; however it was read as “negative.” The CT had a fair amount of movement artifact but was not repeated. Several days later the patient succumbed to a dissected aneurysm at home. One important take away in this case is clinician bias have about “frequent flyers”. What needs to be recognized is that often this results from the original diagnosis being wrong, the disease accelerating, there being new diseases/ co-morbidities and/or the patient cannot follow the treatment plan for whatever reason.13 CASE TWO: A 76-year-old female was placed on Coumadin therapy by her cardiologist on January 29. She alleged that monitoring her INR (which monitors the time it take for blood to clot and compares it to an average) was not instructed. She returned to her cardiologist on February 14, complaining of excessive nosebleeds and bruising. On February 27, she noted a hematoma growing on her right arm and called her cardiologist’s office. His partner responded and advised to stop Coumadin and report to the lab the next day (March 1). The tests results were markedly abnormal and the partner advised the patient to report to the ED with an order for a vitamin K injection. Although not ordered by the partner cardiologist, another INR was run in the ED. While not “critical”, it was still well out of range. No discussion was conducted between the physicians (ED and partner cardiologist), and the lab result was not forwarded to the cardiology office. The patient received the vitamin-K injection and was discharged from the ED. She returned to the ED soon after, complaining of severe back pain. Narcotics were prescribed and again she was discharged. When the patient awoke on March 2, she was unable to move her lower extremities. She was taken to the hospital via rescue and diagnosed with large spinal epidural hematoma, which caused prolonged compression on her spinal cord resulting in permanent paraplegia. When we look at this case in retrospect, we find the following omissions; lack of Coumadin monitoring by the physician 42 Vol. 64, No. 1 2013 Northeast Florida Medicine

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(cardiologist), Orders for Vitamin-K as response to grossly abnormal INR, lack of communication between the physicians after ED- run INR came back abnormal, lack of ED followup on INR and lack of consideration of possible link between patient’s bleeding problems and back pain. The contributions to this untoward outcome include errors in clinical judgment, inadequate assessments, insufficient monitoring and responses to changes in condition and numerous communication lapses What might have helped avoid the outcome was better physicianphysician communication, a cardiology office problem list and documentation of phone calls in the medical record.

Medical Error #5: Abdominal Pain Acute abdominal pain is one of the most common symptoms bringing patients to the ED. Appendicitis can be easily missed if the clinical presentation isn’t classic, as seen in almost half the cases. While overall mortality for appendicitis is low (0.2 deaths per 100,000 cases), delay can lead to perforation and an increased risk of death. When evaluating a patient with abdominal pain, an organized and evidence-based approach should be utilized.16 Acute abdominal pain of less than 1-2 weeks duration accounts for up to 10% of admissions to the ED. Of those, 20-40% are admitted to hospital for investigation and symptom management. The reason for the acute pain remains undetermined in approximately half of these patients. The spectrum of diseases that present as abdominal pain ranges from life-threatening to benign and often the diagnosis can’t be established in a single encounter. It may be most prudent to exclude life-threatening etiologies than to make a specific diagnosis.17 A focused assessment is critical, related to the characteristics of the pain, (location, quality, severity, onset pattern, radiation and aggravating/relieving factors) presence or absence of associated symptoms that are systemic, and those that are organ-specific (e.g. nausea and vomiting or vaginal bleeding) must be assessed. A general physical examination is essential as are noting vital signs blood pressure, heart rate, respiratory rate, temperature and O2 saturation. The exam should include inspection, auscultation, percussion and palpation of the abdomen and external genitalia. A speculum and bimanual pelvic examination may be indicated. Urinalysis is cheap, simple and readily available. Either the dipstick test or routine analysis with microscopy exhibits high yield when results fit with the clinical scenario. A screening urine pregnancy test is recommended for all women of childbearing potential. The two features that have the highest positive impact on correct diagnosis are pain in the Right Lower Quadrant (RLQ) and migration of initial periumbilical pain. In ruling out appendicitis, a few features of the history proved to be useful, particularly absence of RLQ pain. Microscopic

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hematuria and pyuria are present in 20-30% of patients with appendicitis, but they also occur in many other conditions and asymptomatic individuals.

reviewed with the patient at each visit. • There should be effective follow-up systems for managing diagnostic study results

Contrast-enhanced CT of the abdomen has become the most favored of tests to diagnose most intra-abdominal surgical conditions. It is highly sensitive and specific for detecting appendicitis, diverticulitis, perforation, abdominal aortic aneurysm, abscess formation and mesenteric ischemia.17

• Routine documentation is needed of phone conversations with patients during and after office hours.

Medical Error #6: Medication Errors

• Reassessment throughout hospitalization is essential as is a thorough examination at discharge.

The Institute of Medicine (IOM) issued a press release on July 20, 2006, stating that medication errors account for the largest number of errors within the health delivery system and annually injure 1.5 million people and treatment of consequences of medication errors costs three billion dollars.18 Medication packaging, labeling, prescribing and administration systems are fraught with opportunities for error and breakdown. It has the biggest exposure for error due to multiple ways medications are procured, and the constant changing of the look and feel of various medications as they are created and reincarnated in iterations of generic medications. The mainstream popularity of over- the-counter medications and supplements make the situation even more complex. The report estimates that hospitalized patients incur an average of one medication error per day. Luckily, most cause no real harm. Again with the topic of communication, inadequate/untimely communication between physician offices can exacerbate the problem when patient medication regimens are altered or augmented and interactions are not recognized.19-20

• Patients should be monitored for changes in condition with actions taken to address the changes, as needed.

To avoid preventable medication errors the following be considered: • Improve prescription/over-the-counter medication communication with printed hand-outs • Improve communication between physicians • Utilize of the National Library of Medicine as an information repository • Use IT devices to store prescription and over-the-counter medication data • Use E-scribing universally • Review medications with the patient at each visit updating the medical record accordingly.19

Overall Strategies to Avoid Medical Error Unfortunately, medical errors will probably always occur in some measure, however there are some key strategies that can help avoid such errors.17,21-25. These include: • Problem and medication lists should be comprehensively www . DCMS online . org

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• Patient assessments in the office and at the hospital need to be thorough (include social and family history) and should be updated regularly.

• Communication between physicians and other care providers needs to occur routinely. • Physicians need to communicate with their patients and listen to what they tell them, avoiding bias to get to the root of their problems. • Every patient encounter should be documented as concurrently as possible to ensure accuracy. • “Universal Protocols” should be consistently followed to avoid surgical errors.

References 1. Cynthia Berg, MD, Isabella Danel, M.D. Hani Atrash, MD, Suzanne Zane, DVM, Linda Bartlett, MD. Strategies to reduce pregnancy-related deaths from identification and review to action, Centers for Disease Control and Prevention Division of Reproductive Health Safe Motherhood Activity, 2001. 2. Heron MP, et al. Deaths: Final data for 2006. National Center for Health Statistics, National Vital Statistics Reports, 57(14), 2009. 3. Sentinel Event Alert, The Joint Commission, Issue 44, January 26, 2010. 4. SE Geller, et al. A descriptive model of preventability in maternal morbidity and mortality. Journal of Perinatology, 2006, (26(2):79-84). 5. Centers for Disease Control and Prevention (CDC). Pregnancy-related mortality surveillance. Surveillance Summaries, Morbidity and Mortality Weekly Report, February 21, 2003, 2003:52. 6. Berg CJ, et al. Pregnancy-related mortality in the United States, 1991-1997. Obstetrics & Gynecology, 2003, 101(2):289-296. 7. Geller SE, et al. The continuum of maternal morbidity and mortality: Factors associate with severity. American Journal of Obstetrics & Gynecology, 2004, 191(3):939944. Northeast Florida Medicine Vol. 64, No. 1 2013 43

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8. Sandra G. Boodman, “The Pain of Wrong Site Surgery”, Washington Post Newspaper, January 21, 2011. 9. Diane Rydrych, MA; Julie Apold, MA; and Kathleen Harder, PhD. Preventing wrong-site surgery in Minnesota: A 5-year journey. Patient Safety and Quality Healthcare, November/December 2012. 10. Mark Chassin, MD, Mary Cooper MD, Lisa Lewis, RN, and Rudy Manthei, MD Presented at the Joint Commission Center for Transforming Healthcare Conference, June 29, 2011 11. Philip F. Stahel, M.D, et al.Wrong-Site and Wrong-Patient Procedures in the Universal Protocol Era: : Analysis of a Prospective Database of Physician Self-reported Occurrences, JAMA Archives of Surgery October, 2010. 12. Adverse health care events reporting system: what have we learned? A 5-year review. Minnesota Department of Health, January 2009. 13. Gordon D. Schiff, et al. Diagnosing Diagnosis Errors: Lessons from a Multi-institutional Collaborative Project, Advances in patient safety. Agency for Healthcare Quality, Vol 2.256, February 2005. 14. Up to Date (13.1 2005), (UpToDate® is an evidence-based, physician-authored clinical decision support resource which clinicians trust to make the right pointof-care decisions). 15. Kevin Helliker and Thomas Burton Deadly Discrepancy: New Light on Aortic Aneurysms February 2004 16. Staniland JR et al. Clinical presentation of acute abdomen: study of 600 patients. BMJ 1972; 3(5823):393-8. 17. Rusnak RA et al. Misdiagnosis of acute appendicitis: common features discovered in cases after litigation. American

Journal of Emergency Medicine 1994;12(4):397-402. 18. Brewster GS et al. Medical Myth: Analgesia should not be given to patients with an acute abdomen, Western Journal of Medicine 2000;172(3):209-10. 19. Daniel M. Feinberg, MD. Measurement as an essential step in patient safety. Patient Safety Colloquium: Communications in Patient Safety: It’s A No-Brainer, presented April 2, 2006. 20. Institute of Medicine, Preventing Medication Errors: Quality Chasm Series, July 20, 2006 updated from Corrigan JM, Donaldson MS, editors. To err is human: building a safer health system. A report of the Committee on Quality of Health Care in America, Institute of Medicine. Washington, DC: National Academy Press; 2000. 21. James D. Carpenter, RPh, MS and Paul N. Gorman, MD. Using medication list: mismatches as markers of potential error. US National Library of Medicine/ NIH, 2002. 22. Allan Goroll, MD, Albert Mulley, Jr., MD. Primary Care Medicine: Office Evaluation and Management of the Adult. Philadelphia, PA, Wolters Kluwer Health, Dec 1, 2006. 23. Baker GR, Norton P. Patient safety and healthcare error in the Canadian healthcare system. Ottawa, Canada, Health Canada, 2002. pp. 1-167. 24. Leape L, Brennan T, Laird N, et al. The nature of adverse events in hospitalized patients: Results of the Harvard medical practice study II. NEJM 1991;324-384. 25. Phillips R, Bartholomew L, Dovey S, et al. Learning from malpractice claims about negligent, adverse events in primary care in the United States. Quality Safe Health Care 2004;13:121-6.

DCMS History Book ON SALE NOW! Buy “Florida’s Pioneer Medical Society: A History of the Duval County Medical Society & Medicine in Northeast Florida” for you, family members and for your office. Limited copies for sale. See www.dcmsonline.org for an order form. 44 Vol. 64, No. 1 2013 Northeast Florida Medicine

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Dr. Eli Lerner Inaugurated 126th DCMS President and Awards Presented During the 160th DCMS Annual Meeting Eli N. Lerner, MD, was inaugurated as the 126th president of the Duval County Medical Society (DCMS) at its 160th Annual Meeting, Thursday, November 29, 2012 at the Hyatt Regency Jacksonville Riverfront. Rabbi Joshua Lief administered the Oath of Office. Dr. Lerner, an Attending Surgeon at the University of Florida, Shands Jacksonville, also is active in academic activities, presents papers, and does videos and lectures on various medical topics such as “Laparoscopic Surgery” and “Gastroesophageal Reflux Disease.” He received his Doctor of Medicine degree from the Chicago Medical School, did an internship at Hennepin County General Hospital in Minneapolis, MN, and a residency at Loyola University Medical Center in Maywood, IL. Prior to coming to Jacksonville in November, 2004, he practiced in Sun City and Bradenton, FL. Dr. Lerner has been active in organized medicine since the mid-1970s. He was the DCMS treasurer and then Vice President before being inaugurated as the Society’s president. He is a past member of the Florida Medical Association (FMA) Board of Directors and Immediate Past Chairman of the FMA Specialty Society Section. Dr. Lerner is a member of the American Medical Association House of Delegates, a Board Member of the Society of American Gastrointestinal and Endoscopic Surgeons, a Past President of the Florida Surgical Society, and a Board member of the Florida Society of General Surgeons. He is a Diplomate of the American Board of Surgery and a Fellow of the American College of Surgeons. As DCMS President, Dr. Lerner says his main goal is “to engage more physicians and help make the practice of medicine even more palatable in North Florida.” He also hopes to interest members in the political process of medicine because he strongly believes, “If we don’t participate, we are not going to be heard.” Finally, he would like to have secure finances and a strong membership when he leaves office. Since there are “various generational gaps in DCMS,” he is trying to reach all of them via electronic media, website resources and even small focus-type group meetings. Dr. Lerner hopes through these methods to help DCMS members and their colleagues understand the Patient Protection and Affordable Care Act (PPACA) or Obamacare. During the meeting, DCMS and DCMS Foundation past presidents and FMA past presidents were recognized as well

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as current and past DCMS staff, and special guests. Annual elections took place, and the slate of officers, directors, FMA delegates and alternate delegates was approved. Neel G. Karnani, MD, was elected as DCMS President-Elect. Other 2013 officers are: Vice Presidents Daniel Kantor, MD and Mobeen Rathore, MD; Raed Assar, MD, secretary; Sunil N. Joshi, MD, treasurer; and Ashley Booth Norse, MD, immediate past president. (Dr. Lerner presented to her a President’s Plaque and Past President’s Pin.) The 2012 DCMS Board of Directors was recognized and thanked for their efforts. George Trotter, MD, gave the traditional Roll Call. Dressed in 1880s attire, he called the name of “Francis P. Wellford, MD” as a way to honor this important DCMS Past President who died in 1887 after treating those afflicted with Yellow Fever. After their names were read, a moment of silence was observed as a tribute for DCMS members who died in 2012. DCMS Life Members (members for 35 years) recognized were: Carlos Alosilla, MD; Robert Baker, MD; Leonardo del Rosario, MD; Malcolm Foster, MD; Tajvar Goudarzi, MD; and Lawrence Lisska, MD. Speakers on the program were Florida Department of Health Surgeon General and Secretary Dr. John Armstrong and FMA President Dr. Vincent DeGennaro. Dr. Armstrong said, “The Department of Public Health will be listening for ways DOH can strengthen physician practices, and also communicate better with the public.” Dr. Vincent DeGennaro gave a Legislative update and advised, “Look at what political candidates support, not just if there is a ‘D’ or “R” after their name.” Mrs. Dena Pulley, DCMS Alliance President, and Joan Marmon, FMA Alliance President, presented a floral gift to Neva Lerner, wife of Dr. Eli Lerner. Abraham Lerner, Dr. Lerner’s son, also attended. A number of awards were presented. Sunil Joshi, MD, received the 2012 Philip H. Gilbert Young Physician Leadership Award created to honor the memory and service of Philip H. Gilbert, Executive Vice President of the DCMS from 1984 until his death in 2004. James Burt, MD received the 2012 Clyde M. Collins Humanitarian Award in recognition as co- founder of Volunteers in Medicine, a free medical clinic opened in 2003 to meet the health care needs of the working uninsured in Jacksonville. Dr. Burt remains active in the www . DCMS online . org

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1. 3.

4. 7.

11.

12.

10.

13.

14.

1. DCMS EVP Bryan Campbell, Mrs. Neva Lerner, DCMS President Dr. Eli Lerner, DCMS Immediate Past President Dr. Ashley Booth Norse, FMA President Dr. Vincent A. DeGennaro 2. Current and retired DCMS staff. Deana Hadden, Laura Townsend, Patti Ruscito, Bryan Campbell, Karen Pan, Leora Legacy and Marigrace Doran. (Not pictured is Barbara Braddock) 3. Florida State Surgeon General Dr. John Armstrong giving the Florida Department of Health Update. 4. Dr. Ashley Booth Norse presented Dr. James Burt with the 2012 Clyde M. Collins Humanitarian Award. 5. Dr. Eli Lerner giving his inauguration speech. 6. FMA President Dr. Vincent A DeGennaro giving the FMA Update 7. Dr. George Trotter as Dr. Frances Wellford giving the official “Roll Call” 8. Mrs. Neva Lerner, Dr. Eli Lerner and son Abraham. 9. Dr. Ashley Booth Norse with Dr. Irfan Qureshi, Dr. Cameron Adkisson, Dr. Joseph Tepas and Dr. Mobeen Rathore. 10. Dr. Ashley Booth Norse and Dr. Raed Assar presenting Dr. James St. George his Northeast Florida Medicine Guest Editor plaque. 11. Dr. Ashley Booth Norse presented Dr. Robert Harmon the DCMS Distinguished Service Award. 12. Mrs. Neva Lerner and FMA Alliance President, Mrs. Joan Harmon. 13. Dr. Ashley Booth Norse receiving the Past President Plaque from incoming DCMS President, Dr. Eli Lerner. 14. Dr. Ashley Booth Norse presented Dr. Sunil Joshi with the 2012 Philip H. Gilbert Young Physician Leadership Award. 15. Dr. Ashley Booth Norse presented Dr. Mobeen Rathore with the 2012 DCMS Community Service Award. 16. Rabbi Joshua Lief administered the Oath of Office to 2013 DCMS President, Dr. Eli Lerner.

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15.

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clinic and serves as the VIM-Jacksonville Clinic’s president and medical director. This award was created in 1997 in memory of Dr. Clyde Collins to recognize volunteer efforts by physicians. Mobeen Rathore, MD, received the 2012 DCMS Community Service Award. Dr. Rathore, a pediatrician specializing in infectious disease provides healthcare to children with communicable diseases and is a tireless public educator on the topic. For 22 years he has provided HIV services to patients in Northeast Florida. Dr. Rathore is the founding and current director of the University of Florida Center for HIV/AIS Research, Education & Service. (UFCares) The DCMS Community Service Award was established in 1998 to recognize the outstanding volunteer efforts of the DCMS Physicians that have been performed outside of DCMS sponsored activities. Guest Editors for 2012 issues of Northeast Florida Medicine were recognized by Editor-in-Chief Dr. Raed Assar. They were: Dr. Raymond Pomm, Dr. James St. George, Dr. Kamal Bohsali and Dr. Ghaith Mitri. A DCMS Distinguished Service Award was presented to Robert Harmon, MD to recognize his past leadership as director of the Duval County Health Department (DCHD) and his continued partnership with DCMS in helping promote and implement health information technology in Northeast Florida. Dr. Joseph Tepas, Chair of the DCMS Beals/Shahin Awards Committee, presented the 2012 John A. Beals and 2012 G. Shahin Awards. Recipients were: Beals Award – Dr. Mobeen Rathore for Original Investigation and Review categories; Shahin Award - Dr. Cameron D. Adkisson for Original Investigation, Dr. Irfan Qureshi for Clinical Observation and Dr. Andreas Puschmann for Review. The Beals Award was begun by Dr. John Beals in 1950 to recognize outstanding research and publications by DCMS members. Dr. Shahla Masood created the Shahin Award in 1995 in honor of her mother, G. Shahin, whom she considered an exemplary teacher. The award is presented to residents or fellows in Duval County who have published papers based on research done during their training. Special features at the Annual Meeting were Poster Presentations by DCMS members and resident physicians. Another feature was a booth featuring the newly released DCMS history book, entitled “Florida’s Pioneer Medical Society: A History of Duval County Medical Society and Medicine in Northeast Florida”. Order this book at www.dcmsonline.org! There was a full Exhibit Hall area featuring vendors displaying their products and services. The Platinum Sponsors were The Jacksonville Bank, First Coast Cardiovascular Institute, PA, TD Bank and The Doctors Company. Gold Sponsors were Baptist Health/Jacksonville Orthopedic Institute, Beson4 Media Group, Florida Blue, Jacksonville Surgery Center, Jax Boat Club, and the University of Florida College of Medicine-Jacksonville. There were also Silver and Exhibitor Sponsors. (see sidebar list)

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THANK YOU

Wells Fargo Practice Finance

We’re here to help you take the next step Whether you’re preparing for ownership or planning for growth, Wells Fargo Practice Finance can help you achieve your practice goals. • Acquire or start a new practice • Expand, relocate, or upgrade your office • Finance equipment • Consolidate debt Let’s talk about how we can support you. Call us today. Wendy Catone 866-337-5550

Clay Churchill 904-351-7421

Toni Higgs 904-351-7392

Or visit us at wellsfargo.com/physicians

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Sharon Basile, PharmD | Dr. Alan and Mrs. Mary Berger John and Dianne Giehrl; Dixon Hughes Goodman, LLP Harden and Associates | Randy Meg Kammer and Jeffry Wollitz Korn and Zehmer Professional Association James G. Lernley and Beverly L. Cheveallier | T.R. Lowe, R.Ph, C.Ph Dr. Daniel and Mrs. Helen Lestage Dr. Charles B. and Mrs. Anne G. McIntosh | Metro Diner Sherry Murray | Platinum Cuts | Resource Logix Drs. Todd L. Sack and Barbara L. Sharp | Mr. Robert T. Shircliff Dr. George and Mrs. Ann Trotter IN KIND

AB-Brewmaster, Steve Foppee and Gary Parker | Coca Cola Friends of Dr. George S. Trotter | Dr. Jeffrey and Mrs. Kathy Harris Dr. Stanton Longenecker | Dr. Francis Ong | Dr. Patricia Schroeder

More than 330 attendees came together November 15th at the Marriott Southpoint for the 2012 Caring Awards to thank Dr. George S. Trotter for starting We Care Jacksonville by honoring him with the Founder’s Award. The 13 Free Primary Care Clinic Partners in the We Care Network each received the Award of Service. Over $90,000 was raised to show Jacksonville’s low-income and uninsured We Care!

Wells Fargo Practice Finance is the preferred provider of practice financing through the AMA Member Value Program. All practice financing is subject to credit approval. © 2013 Wells Fargo Bank, N.A. All rights reserved. Wells Fargo Practice Finance is a division of Wells Fargo Bank, N.A. All trademarks are the property of their respective owners. 1770-0113-AMA-Quarter-Page

Thinking About.... Selling a Practice? Terry Flanagan 877-988-0911 t.flanagan@murphybusiness.com

Murphy Business and Financial Services www.wecarejacksonville.org

www . DCMS online . org

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Trends in Public Health

Suicide in Duval County: A Growing Crisis Katryne Lukens Bull, MPH, Ryan Butterfield, DrPH(c), Thomas Bryant III, MSW, Bonita Sorensen, MD, MPH. Suicide is the 10th leading cause of death in the U.S., with 36,891 deaths per year. In 2011, suicide was also the 10th leading cause of death in Duval County with 127 deaths. Suicide trends demonstrate an overall reduction since 1990, especially from 1993-2000, but starting in 2001 rates have increased and are now higher in Duval County (14.6/100,000) than Florida (13.8/100,000) and the U.S. (12.0/100,000). Suicide is recognized as a major public health issue by the U.S. Surgeon General and decreasing suicide morbidity and mortality is a Healthy People 2020 goal. Suicide is a gender, race, and religion neutral issue which affects civilians and military alike. The U.S. Armed Forces is now averaging over one suicide per day among active duty soldiers and reservists. Since July 2012, more servicemen and women were lost to suicide than killed in combat. Suicide attempts often result in significant morbidity. In 2011 in Duval County, 876 individuals were hospitalized due to a suicide attempt, 58% were female and 42% were male. Suicide is considered an external factor leading to hospitalization with an additional primary reason for being admitted (injury, mental health problem, etc.). Attempted suicide hospitalizations were most often due to an injury (70%) or a mental health diagnosis (27%). Over half of all individuals hospitalized were uninsured (30%) or on Medicaid (23%). Eighty-one percent (81%) reported their race as White. According to the CDC and the American Association of Suicidology, the majority of people who complete suicides have a history of up to 25 attempts. Completed suicides are most prevalent among White males 45 year and older, while attempts are most prevalent among adolescent females. Duval County currently has fewer adolescent deaths due to suicide than Florida (1.3 versus 1.9/100,000) but according to Duval’s 2011 Youth Risk Behavior Survey many still seriously consider suicide (14.9%) or have made a plan to commit suicide (14.7%). Duval’s high school students report more attempts (12.7%) than U.S. students (7.8%). In 2011, 60 Duval County high school students were hospitalized for a suicide attempt, 43% for a mental health diagnosis, most often adjustment reaction (75%), and 53% for an injury, most often poisoning (88%). From 2009-2011, seven students succeeded in committing suicide. The highest rates of suicide are among Duval residents ages 20 to 64 with rates peaking in the 40-59 year age group (26.2/100,000). In 2011, 775 individuals 20-64 years old were hospitalized for a suicide attempt; 72% for an injury, most often poisoning (86%) and 25% for a mental health 50 Vol. 64, No. 1 2013 Northeast Florida Medicine

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diagnosis, most often Episodic Mood Disorder (66%). From 2009-2011, 326 people 20-64 years of age succeeded in committing suicide. Individuals over 65 years of age are at risk for suicide, which often is under reported. In 2011, there were 25 hospitalizations for attempted suicide including 16% for a mental health diagnosis and 72% for an injury, most often poisoning (83%). From 2009-2011, 53 people 65 years of age and older succeeded in committing suicide. Suicide poses a significant public health problem, not only to those who attempt and/or commit suicide but for those who survive the suicide of a loved one. Surviving the loss of a loved one due to suicide is a risk factor for suicide. Surviving family members and close friends experience a range of complex grief reactions including, guilt, anger, abandonment, denial, helplessness, and shock. The Northeast Florida Coalition for Suicide Prevention and Awareness, the Northeast Florida Chapter of the American Foundation for Suicide Prevention, and the Florida Youth Suicide Prevention Project at Daniel are community organizations that provide educational training on identifying and responding to suicidal individuals. Clinician specific training is offered by Dr. Elise Fallucco at Nemours and through the Jacksonville System of Care Initiative (JSOCI). Downloadable screening tools, posters and handouts are available for Emergency Departments, Hospitals, and office settings at http://www.sprc.org/for-providers. Help numbers include: United Way Crisis Center (800) 346–6185, 1 800 SUICIDE (784- 2433), and the Crisis Line for suicide intervention for service members, veterans and families at 1-800-273-8255, Press “1.” Duval County is experiencing a growing suicide crisis among adolescents, adults, and service members; and Duval County clinicians have a unique opportunity to provide essential preventative care – screen and refer. Resources: 1) Agency for Health Care Administration: Hospitalization Discharge and Emergency Department Data 2011; 2) FDOH, Office of Vital Statistics, Death File 2011; 3) American Association of Suicidology. Accessed on December 20, 2012 at http://www.suicidology.org/home; and 4) Department of Defense accessed on December 20, 2012 at http://www.defense.gov/releases/. www . DCMS online . org

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American Cancer Society

COWFORD BALL Sat., April 27, 2013 Jacksonville Fairgrounds 6:00 PM Gourmet Dinner Live and Silent Auctions

What's the new normal?

Live Entertainment by The NashTones

Come to The Diamond Group dinner workshops "The New Normal - 6 Investment Strategies That Do Not Work in Today's Investment World"

Special Appearance by The Rat Pack â&#x20AC;˘ March 5, 2013 - Duval County member event â&#x20AC;˘ March 14, 2013 - Clay County (monthly membership meeting)

For more information and to register, go to www.dcmsonline.org or call 904-730-3744. For information: Cowfordball.org Or Therese Yanochik, 904-391-3613 or therese.yanochik@cancer.org

Attend these exclusive Society events designed specifically for physicians to learn strategies to protect their assets. These workshops are free to Society members and spouses. Come and learn about "The New Normal." Registered Representative of and securities offered through Berthel Fisher Company Financial Services (BFCFS, member FINRA/SIPC. The Diamond Group is independent of BFCFS).

www . DCMS online . org

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DCMS Membership Applications These physicians’ applications for membership in the Duval County Medical Society are now being processed. Any information or opinions you may have concerning the eligibility of the applicants listed here may be directed to Ashley Booth Norse, MD, DCMS President (904-244-4106) or Barbara Braddock, Membership Director (904-355-6561 x107). Christina S. Adams, MD OB-GYN North Florida OB-GYN Medical Degree: University of Miami School of Medicine Residency: University of Florida College of Medicine/Jacksonville Tricia R. Andrews, MD Dermatology Jacksonville Dermatology Associates Medical Degree: Mayo Medical School Residency: Mayo Graduate School of Medicine Sarah C. Austin, MD Obstetrics & Gynecology North Florida OBGYN Medical Degree: Medical College of Georgia Residency: University of Florida Health Sciences Center Jessica N. Bahari-Kashani, MD Radiation Oncology Florida Radiation Oncology Group Medical Degree: University of Minnesota Residency: University of California-Irvine David A. Boyd, MD Dermatology Advanced Dermatology and Cosmetic Surgery Medical Degree: Uniformed Services University of Health Sciences Residency: Naval Aerospace Medical Institute & National Capital Consortium Kristin B. Caldow, MD OB-GYN UF Obstetrics & Gynecology Medical Degree: Florida State University Residency: UFHSC/Jacksonville Kenneth O. Cintron, MD Orthopedic Surgery/Foot and Ankle Surgery Heekin Orthopedic Associates Medical Degree: University of Puerto Rico School of Medicine Residency: University of Puerto Rico School of Medicine Stacie W. Cook, MD OB-GYN North Florida OB-GYN Medical Degree: State University of New York Upstate Medical University Residency: West Pennsylvania Allegheny Health System Sharon M. Desmarais, MD – Active Member Obstetrics & Gynecology North Florida OBGYN Medical Degree: University of Florida Residency: Orlando Regional Medical Center Madeliene E. Gainers, MD Dermatology Advanced Dermatology & Cosmetic Surgery Medical Degree: University of Pittsburgh School of Medicine Residency: Washington University Erika D. Glas, DO OB-GYN North Florida OB-GYN Medical Degree: Des Moines University School of Osteopathic Medicine Residency: University of Illinois College of Medicine

Joseph H. Habib, MD Surgery UF Surgery Medical Degree: West Virginia University School of Medicine Residency: West Virginia University School of Medicine/Charleston Area Medical Center Fellowship: Ohio State University Medical Center John B. Hunt, MD Pain Medicine NexStep Integrate Pain Care, Inc Medical Degree: University of Arizona Residency: Naval Hospital San Diego Fellowship: University of Florida Robert K. Hurford, Jr., MD Orthopedic Surgery/Spine Surgery Heekin Orthopedic Specialists Medical Degree: Harvard Medical School Residency: Massachusetts General Hospital Fellowship: Barnes Hospital/Washington University Jennifer R. Maynard, MD Family Medicine/Sports Medicine Mayo Clinic, Beaches Primary Care Medical Degree: University of Maryland Residency: Christiana Care Family Medicine Fellowship: Mayo Clinic Andrew D. McBride, MD Diagnostic Radiology/Interventional Radiology Drs. Mori, Bean & Brooks, PA Medical Degree: University of Pennsylvania Residency: Stanford University Medical Center Fellowship: Baptist Cardiac and Vascular Institute Casey M. McClone, MD Family Medicine/Sports Medicine Orthopaedic Associates of St. Augustine Medical Degree: Ross University Residency: Mayo School of Graduate Medicine James P. Oberman, MD Otolaryngology Naval Hospital Jacksonville Medical Degree: Tufts University School of Medicine Residency: Naval Medical Center Portsmouth Margaret P. Oberman, MD Internal Medicine US Naval Hospital – Jacksonville Medical Degree: Tufts University Internship: US Naval Hospital - Portsmouth Derrick C. Pau, MD Ophthalmology UF Ophthalmology Medical Degree: George Washington University Residencies: Nassau County Medical Center/ Stony Brook University Medical Center Fellowships: The Methodist Hospital/ Devers Eye Institute Christopher H. Perkins, MD Orthopaedic Surgery UF Bone & Joint Institute at Shands Medical Degree: Baylor College of Medicine Residency: Baylor College of Medicine Fellowship: University of Miami-JMH

Jinous Saremian, MD Anatomic Pathology & Clinical Pathology/ Cytopathology UF Pathology Medical Degree: Tabriz University Medical Sciences Faculty of Medicine Residency: University of Oklahoma Fellowship: University of Florida Jacksonville Aristides A. Sastre, MD Family Medicine Baptist Primary Care Medical Degree: University of Illinois Residency: Mayo Clinic Christine L. Sears, MD Urology Naval Hospital Jacksonville Medical Degree: Feinberg School of Medicine, Northwestern University Residency: Naval Medical Center San Diego Fellowship: Walter Reed Army Medical Center Terrence L. Soldo, DO Family Medicine St. Vincent’s Family Medicine Residency Medical Degree: Kirksville College of Osteopathic Medicine Residency: Naval Hospital-Camp Pendleton Fellowship: UNC-Faculty Development Kristen M. Stewart, MD Dermatology Advanced Dermatology & Cosmetic Surgery Medical Degree: Temple University School of Medicine Residency: National Capital Consortium Kristen L. Vanderhoef, MD Anesthesiology UF Anesthesiology Medical Degree: University of South Florida Residency: Mayo Clinic Fellowship: Forsyth Medical Center Lynn Michael Waters, Jr., MD Family Practice UF Crossroads Family Medicine Center Medical Degree: Nova Southeastern University Residency: St. Vincent’s Family Medicine Amy Wrennick, MD – Active Member Obstetrics & Gynecology North Florida OBGYN Medical Degree: University of Miami Residency: University of Texas Houston

Residents/Fellows Mayo Clinic Family Medicine Alexander “Trevor” Hray, MD

Michelle Quinones Maldonado, MD OB-GYN North Florida OB-GYN Medical Degree: Ponce School of Medicine Residency: Winthrop University Hospital

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Sharon L. Reinertsen, MD Family Practice UF New Berlin Family Medicine Center Medical Degree: Uniformed Services University of the Health Sciences Residency: Naval Hospital

www . DCMS online . org

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We hate lawsuits. We loathe litigation. We help doctors head off claims at the pass. We track new treatments and analyze medical advances. We are the eyes in the back of your head. We make CME easy, free, and online. We do extra homework. We protect good medicine. We are your guardian angels. We are The Doctors Company. The Doctors Company is devoted to helping doctors avoid potential lawsuits. For us, this starts with patient safety. In fact, we have the largest Department of Patient Safety of any medical malpractice insurer. And, local physician advisory boards across the country. Why do we go this far? Because sometimes the best way to look out for the doctor is to start with the patient. To learn more about our medical professional liability program, call us at (800) 741-3742 or visit www.thedoctors.com. Endorsed by

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Aetnaâ&#x20AC;&#x2122;s Payment Estimator Knowing health costs before you get a bill. Learn more at www.aetna.com. Plans offered by Aetna Life Insurance Company and its affiliates. Health benefits and insurance plans contain exclusions and limitations. Providers are independent contractors and are not agents of Aetna. Provider participation may change without notice. ÂŠ2012 Aetna Inc. 2012025

www . DCMS online . org

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SAVE THE DATE!

North Florida Cardiovascular Foundation

4.13.13

A Cardiovascular Education Opportunity

Saturday, April 13, 2013

Location: Marriott Sawgrass Hotel, Ponte Vedra Beach, FL Date: Saturday, April 13, 2013 Credits: CME Event

10th Annual Ponte Vedra Beach

For more information and to register, visit

presents

www.pvcardiacsymposium.com

Cardiovascular Symposium

Florida CHAPTER

Co-Sponsored by Florida Chapter of the American College of Cardiology

PROGRAM SCHEDULE

SATURDAY APRIL 13, 2013

All sessions will be conducted in the Champions Ballroom E

Registration & Breakfast Welcome

7:00 AM – 8:15 AM 8:15 AM – 8:30 AM

DIABETES AND THE HEART Introduction of Speakers and Case Study New Molecular Research in Diabetic Heart Disease Cardiovascular Impact of Diabetes Therapies Panel Discussion

Jorge Plutzkey, MD Silvio Inzucchi, MD

BREAK

8:30 AM 8:40 AM 9:10 AM 9:40 AM 10:00 AM

BEYOND STATINS Introduction of Speakers and Case Study Statin Intolerance New Approaches to Lipid Management Panel Discussion

Paul Ziajka, MD Evan Stein, MD

LUNCH AND PRESENTATION Multimodality Testing in the World of Accountable Care

10:30 AM 10:40 AM 11:10 AM 11:40 AM 12:15 PM

NEW ERA IN COMBINING SURGICAL AND CATHETER TECHNIQUES Introduction of Speakers and Case Study Emerging Hybrid Procedures in Electrophysiology Hybrid Procedures for Valvular and Ischemic Heart Disease Panel Discussion

1:30 PM 1:40 PM 2:10 PM

Paul Mounsey, MD Isaac George, MD

2:40 PM

BREAK

3:00 PM

WEIRD CARDIOMYOPATHIES Introduction of Speakers and Case Study Cardiomyopathy and Genetics Sudden Death in Athletes Panel Discussion

RECEPTION AND DINNER Entitlement Reform and Implications On Cardiology

3:30PM 3:40 PM 4:10 PM 4:40 PM

Ray Hershberger, MD Barry Maron, MD

5:00 – 7:30 PM

Dipti Itchhaporia, MD Chair ACC Board of Governors

Thomas Ryan, MD

54 Vol. 64, No. 1 2013 Northeast Florida Medicine

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Your Compassionate Guide leads to quality time.

Your patients have a guide to walk with, listen to and help them find quality time through all stages of advanced illness—Community Hospice of Northeast Florida. Ask us how we can help your patients find that quality time. Call Community Hospice today.

904.407.6500 • 866.253.6681 toll free • CommunityHospice.com Community Focused • Community Supported www . DCMS online . org Florida Medicine Serving Baker, Clay, Duval, Nassau and St. Johns Northeast counties since 1979Vol. 64, No. 1 2013 2013_NFM_GastricDisease.indd 55

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Duval County Medical Society Foundation 555 Bishopgate Lane Jacksonville, FL 32204

NON-PROFIT ORGANIZATION

U.S. Postage Paid Jacksonville, Florida

Permit No. 2981

ADDRESS SERVICE REQUESTED

The Doctors Company is devoted to helping doctors avoid potential lawsuits. For us, this starts with patient safety. In fact, we have the largest Department of Patient Safety of any medical malpractice insurer. And, local physician advisory boards across the country. Why do we go this far? Because sometimes the best way to look out for the doctor is to start with the patient. To learn more about our medical malpractice insurance program, call our Jacksonville office at (800) 741-3742 or visit www.thedoctors.com.

Endorsed by

www.thedoctors.com 56 Vol. 64, No. 1 2013 Northeast Florida Medicine Duval_8x8_color.indd 1 2013_NFM_GastricDisease.indd 56

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