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Inside this issue of
VOLUME 62, NUMBER 1 GERD Spring 2011 EDITOR IN CHIEF Joan L. Huffman, MD MANAGING EDITOR Leora Legacy ASSOCIATE EDITORS Raed Assar, MD Steven Cuffe, MD Ruple Galani, MD Kathy Harris (Alliance) Sunil Joshi, MD James Joyce, MD Neel Karnani, MD Mobeen Rathore, MD James St. George, MD
Executive Vice President Jay W. Millson DCMS FOUNDATION BOARD OF DIRECTORS Benjamin Moore, MD, President Todd L. Sack, MD, Vice President Kay M. Mitchell, MD, Secretary J. Eugene Glenn, MD, Treasurer Guy I. Benrubi, MD, Immediate Past President Mohamed H. Antar, MD Raed Assar, MD Ashley Booth Norse, MD J. Bracken Burns, DO Malcolm T. Foster, Jr., MD Jeffrey L. Goldhagen, MD Jeffrey M. Harris, MD Mark L. Hudak, MD Joan L. Huffman, MD Sunil N. Joshi, MD Daniel Kantor, MD Neel G. Karnani, MD John W. Kilkenny III, MD Sherry A. King, MD Harry M. Koslowski, MD Eli N. Lerner, MD R. Stephen Lucie, MD Jesse P. McRae, MD Senthil R. Meenrajan, MD Nathan P. Newman, MD Mobeen H. Rathore, MD Ronald J. Stephens, MD Jeffrey H. Wachholz, MD Anne H. Waldron, MD David L. Wood, MD 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: email@example.com. COVER: Photograph by Dr. Gordon Ira. Waterfall at Yellowstone National Park along the river bank.
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Northeast Florida Medicine
Patients Deserve Quick Diagnosis and Treatment for GERD Ziad T. Awad, MD, FRCSI, FACS, Guest Editor
12 Management of GERD in the Pediatric Population Daniel Robie, MD 16
The Surgical Management of GERD and Hiatal Hernia
Endoscopic Management of GERD
Laryngopharyngeal Reflux: Overview and Clinical Implications
Ziad T. Awad, MD, FRCSI, FACS
Samir Lewiz Habashi, MD 31 Impact of GERD on Common Pulmonary Diseases Abubakr A. Bajwa, MD, FCCP; Faisal Usman, MD, et al
Iman Naseri, MD
Mentors and Education Open the Door to Opportunities
Rui Fernandes, MD (Young Physician Leadership Guest Editorial)
25 Prevention of Medical Errors: Empowered to Make a Difference Constance K. Haan, MD, MS (CME) 40
DCMS Annual Meeting Details
4 From the Editor’s Desk 5 From the President’s Desk 9 Residents’ Corner Insert AMA Leadership Visit, Additional DCMS Annual Meeting coverage, Good ‘Ole Time’ Reunion, Public Health Trends
Northeast Florida Medicine Vol. 62, No. 1 2011 3
From the Editor’s Desk
Greening Your Practice The human race will be the cancer of the planet. - Attributed to Julian Huxley After a protracted, chilly winter, we welcome the spring, the re-leafing of barren trees and the green lushness of new life. It’s time to carry this theme over to your practice and become a healthy example for your community. But before you can begin to recycle, renew, and reuse intelligently, you need to determine your current use of resources. Begin with an energy audit to establish your office baseline. Review electric, gas and water bills initially and every three months. Consider a formal audit by the local electric company. Get buy-in from the staff by including them in the planning, implementation and reevaluation phases of your goals. Turn off waste, turn on energy efficiency. At night, shut off lights, equipment and perhaps even your hot water heater. Place computers in the lower energy consuming sleep mode. As your bulbs burn out, replace them with compact fluorescent bulbs (CFB), tubular T-8 fluorescent fixtures, and/or light Emitting Diode (LED) bulbs. Encourage use of task lighting as opposed to glaring overhead lights. Regulate light entry - open blinds on cool bright mornings, close them on scorching afternoons. Another low cost option is window tinting. As you retire outdated equipment, upgrade to Energy Star products, a secondary gain may be tax credits. Consider switching to a solar or tankless hot water heater, a programmable thermostat, and new double-paned insulated windows. Dial down the hot water setting to no hotter than 120° F (48° C), and insulate tanks and pipes. Adjust your heating and air conditioning: to summer Joan L. Huffman, MD, FACS settings of 74° F (23° C) and 68° F (20° C) in winter; extend your HVAC life span and efficiency with regular maintenance. Editor-in-Chief Northeast Florida Medicine
Take a look at opportunities for water conservancy as fixtures require updating, consider selfclosing faucets, low-flow faucets or low flow aerators, low flush toilets and urinals or dual flush toilets, and low flow shower-heads. In the interim, place bricks in your toilet tanks to decrease water usage. Outdoor water use is often overlooked: investigate xeriscaping, native plants, soaker hoses and rain shut off devices. An easy low cost transition is to do away with the water cooler, and to ban bottled water at your facility. Encourage tap water in reusable containers. Renewable energy sources avoid increasing your carbon footprint. Examples are solar water heaters, solar electricity via photovoltaic cells (PVC), and wind power. Power companies offer the chance to buy renewable energy or credits. In our consumer driven society, waste rapidly accumulates. Don’t just add to the mountainous landfills, instead recycle! Simple steps for your office include placing recycling bins in staff areas and waiting rooms, buying recycled paper and refillable ink cartridges. Just say “no” to styrofoam packaging, instead recycle shredded paper & cardboard. On the front end, reduce paper utilization by eliminating unnecessary forms, reducing copying, faxing and printing, especially double-sided printing.Use online resources as much as possible - bookmark or copy to a folder rather than print. Moving to an Electronic Medical Record (EMR) significantly reduces paper use. Don’t add to downstream pollution - never flush medications. Design safe disposal plans for drugs and chemicals. Use green cleaning and pest control products. Eat and drink healthy foods. Don’t provide soda or junk food machines, look at organic alternatives from local merchants. Stock the staff kitchen with recyclable/reusable containers, cups & cutlery. How do you get to work? Transportation & commuting add carbon components to our atmosphere. Encourage energy efficient vehicles, carpooling, and public transportation. Where possible organize work assignments to offices nearby staff locations. If appropriate, use telecommuting for non-patient care employees, and purchase from local vendors. Spread the green message! Post signs in waiting and exam rooms. Encourage staff and patients to expand these habits to their home and family life. The Florida Medical Association’s Environment and Health Section heartily endorses green living on their website My Green Doctor. (This effort was spearheaded by DCMS Past President and environmental champion Dr. Todd Sack.) The recommendations in this editorial encapsulate just a small snapshot of the comprehensive information available. A successful green program should be embraced not only by yourself and your office manager, but an action plan that involves the entire staff - everyone from advanced practice personnel to the janitor. Challenge your personnel not only to comply with resource saving methods, but to innovate and continually work leaner and greener. While some of these recommendations involve an up front cash outlay, the environmental savings will be coupled by long term financial advantages. Save the Earth, enhance your health and cut costs! Source:Florida Medical Association’s Environment and Health Section. www.mygreendoctor.org.
When we heal the earth, we heal ourselves. - David Orr 4 Vol. 62, No. 1 2011 Northeast Florida Medicine
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From the President’s Desk
Best or Worst of Times? It was the best of times, it was the worst of times. A Tale of Two Cities by Charles Dickens Editor’s Note: Please see the Philip H. Gilbert Young Physician Leadership Award Guest Editorial “Mentors and Education Open the Door to Opportunities” by Dr. Rui Fernandes (p.8) which shows the “enthusiasm” of the younger generation of physicians Dr. Foster refers to in his editorial.
These are trying times for medicine with Government intervention, unfunded mandates, too many uninsured patients, inadequate reimbursement and now the real possibility of the just passed Affordable Care Act. Most likely there will be decreased reimbursement for Medicaid patients as the State of Florida pushes toward a Medicaid HMO model. There have been similar “worst of times” in the past that were resisted by the house of medicine. Beginning in the 1930s health insurance such as Blue Cross and Blue Shield was established. Medicare was signed into law in 1965 and expanded in the 1970s to include the disabled and patients with renal failure in need of dialysis. In each of these situations, hospitals flourished, insurance companies prospered and medical practitioners also did well. Will history repeat itself under the Affordable Care Act?
Malcolm T. Foster, Jr., MD 2011 DCMS President
While we are letting all the changes and conflicts work their way out and we help shape our future, we need to continue to be an advocate for our patients, preserve the patient physician relationship and practice quality medicine. Never have we been able to do more for patients since we have new diagnostic tools, new therapies, better prevention, electronic medical records, etc.
Physicians need to stay engaged in the ongoing debates about medicine. We should ask ourselves: Do I join an ACO? Does my practice join with other practices? Do we affiliate with a health care organization? Do I go to work as a salaried physician? What are other physicians in similar situations doing? The DCMS is trying to address these issues in various forums, lobbying on our members’ behalf through local means and statewide and nationally through the FMA and AMA. The DCMS is not new to this advocacy role, having taken a major leadership position for 158 years. Just in my 35 years in Jacksonville I have seen superb DCMS officers work diligently for the membership and our community. Administratively we are fortunate to have a great Executive Director in Jay Millson and a dedicated staff. The officers, Board of Directors and committees work hard to keep our Society strong. They deal with the varied issues discussed above and many others such as EMR, the environment, public health, world health, social injustice, to name a few. Every day I work with young physicians and medical students. They see medicine as a great privilege and opportunity to make a change for the better in this world. Maybe those of us who have been in the medical profession a long time need to catch their enthusiasm. If we did, the worst of times could become the best of times (or at least better) as our perspective takes a more optimistic focus.
Two Physicians Remember the Past, Live in the Present and Look to the Future Dr. Gordon Ira, a retired cardiologist and now a professional photographer (see cover of this issue), recalls “the closeness of the medical community” in Jacksonville in the 1960s and 1970s. He remembers “The desire to learn and to give good patient care were the main ingredient...without the need for mandated study hall and defensive medicine.” Now that he is retired he says, “I am doing something else that I love, photography... it’s keeping me active and happy. My old brain is staying on its toes.” His photo used for this issue’s cover was taken during winter months in Yellowstone Park along the river bank where the stream enters the river. It shows runoff from one of the hot geysers and the colors in the water come from mineral deposits. Dr. Paul Mori is a retired radiologist. He is the founding partner of Mori, Bean & Brooks, PA. In retirement, he and his wife enjoy traveling. He says of his years as a physician, “Being a physician is a great privilege. The only difference between work and play is your interest in what you are doing.” Dr. Mori also has advice for all physicians - veterans or those just starting to practice. He suggests: 1) Stay in touch with the funny side of life, 2) Maintain good rapport with fellow physicians, 3) Reserve adequate time to recharge, 4) Upgrade your professional skills, 5) Practice equality, 6) Work closely with administrators, 7) Accentuate the positive, and 8) Maintain scientific curiosity. (Some comments from NEFM, Winter 2005, Vol.56, No5)
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Northeast Florida Medicine Vol. 62, No. 1 2011 5
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6 Vol. 62, No. 1 2011 Northeast Florida Medicine
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Guest Editorial: Leadership Award Recipient
Mentors and Education Open the Door to Opportunities Rui Fernandes, MD, DMD
2010 Philip H. Gilbert Young Physician Leadership Award Recipient Luke 12:48 “…to whom much is given, much is expected.” As an immigrant from Cape Verde Islands with limited opportunities, I feel that my experience in the United States is indeed the embodiment of this belief. I have been extremely fortunate since I arrived in this country to have been given amazing opportunities to study, learn and grow through assistance from merit scholarships. In my experiences, I have been exposed to great mentors that have steered me on the right path, not only through their advice but their example. This I believe is the essence of leadership. Through my mentors, I have learned that an individual can impact someone else’s life with the smallest of gestures. Living in America we have tremendous opportunities available to us and we, at times, may take them for granted. It is incumbent upon us who have achieved a certain level of academic or professional success to reach back and ensure that others will have similar opportunities. I encourage these efforts through both our professional affiliations in this country and organizations that are global in scope. In my short career, I have had the good fortune to be involved in medical education not only at the University of Florida but also through several international, multi-discipline organizations such as AONA (Arbeitsgemeinschaft fuer Osteosynthesefragen North America) and SORG (Strasbourg Osteosynthesis Research Group. These groups strive to bring surgical training to residents and practicing surgeons throughout the world. In my teaching opportunities outside the country, I am reminded of how fortunate we are to practice medicine in the United States and of our duty to share our time and resources with others. There is great opportunity for involvement in medical education both at home and abroad. I encourage you to take the lead and get involved. As we face the inevitable changes to come from new healthcare laws, I am reminded of the anonymous quote “…if you are not at the table, you may be on the menu…” I urge us all to take the lead to ensure that our views and those of our patients are represented. Now more than ever we should be involved in the dialogue that will shape the future of medical practice in our country. Also, I encourage seasoned leaders in our medical society to mentor younger physicians, i.e. residents and fellows, and welcome their participation in our organization. It is never too early for those new to practice to get involved, and it is an excellent way for experienced physicians to “pay it forward”. I have been greatly enriched professionally as well as personally through my relationship with my mentors. Through their wise counsel, I have avoided pitfalls in building my practice and have accomplished more than I thought possible in a short period of time. Much of the success that I have experienced thus far is due to their leadership by example, gift of time invested in me and their spirit of generosity. It is truly an honor to be the 2010 recipient of the Phillip H. Gilbert Young Physicians Leadership Award. I am grateful to my peers for the recognition and to the many people who have supported me throughout my professional career. I would like to thank my mentors Dr. Nelson Goldman, Dr. Francis Ong and Dr. Robert Ord for being excellent role models. Thank you to Dean Robert Nuss, Dr. Michael Nussbaum and Dr. Tirbod Fattahi for your continued administrative support. I sincerely appreciate the area’s physicians for giving me the opportunity to build my head and neck oncologic and surgical practice. Finally, I am truly grateful to my fellows and residents for allowing me to share my passion for surgery with you on a daily basis. Rui Fernandes, MD, DMD, received the 2010 Philip H. Gilbert Young Physician Leadership Award at the DCMS Annual Meeting, December 1, 2010. This award, created to honor the memory and service of Philip H. Gilbert who served as Executive Vice President of the DCMS from 1984 until his death in 2004, recognizes Young Physicians with leadership traits that Mr. Gilbert would have admired. Candidates must meet the following eligibility criteria: A “Young Physician” from Northeast Florida, under 40 years of age or within the first eight years of professional practice after residency and fellowship training, as defined by the AMA; active in the DCMS or other organized medicine service; active in civic service; medical staff (or similar) leadership experience; and be a strong advocate for medicine. Pencil sketch by Alexander Braddock
Photos: (Top, Left) Dr. Fernandes receiving his award from Dr. John Kilkenny III, now DCMS Immediate Past President. ; (Top, Right) Dr. Fernandes; (Bottom) A pencil sketch of Philip Gilbert.
8 Vol. 62, No. 1 2011 Northeast Florida Medicine
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Residents’ Corner: Naval Hospital Jacksonville Editor’s Note: In an effort to connect more Duval County Medical Society members with residents, the journal is beginning a “Residents’ Corner” In each 2011 issue, there will be information about a residency program in the area, giving details about research being done and achievements/accomplishments of the program’s residents. This first “Residents’ Corner” features Naval Air Station Jacksonville’s residency program at the Naval Hospital Jacksonville.
Overview of Residency Program
Through Naval Hospital Jacksonville’s (NH Jax) professional education and research program, NH Jax is building an infrastructure to support evidence based practices across NH Jax as well as civilian and military medicine nationwide. NH Jax values graduate medical, nursing and specialized hospital corpsman education – the lifeblood of Navy Medicine. NH Jax is home to the Navy’s oldest and largest family medicine residency program, graduating about 12 residents annually with a first-time board certification rate of 100 percent. The hospital also supports Certified Registered Nurse Anesthetist, Perioperative Nurse and Physician Assistant training programs, as well as training for hospital corpsmen such as Tactical Combat Casualty Care, Field Medical Service School and other mission-specific courses. These programs have been vital to supporting the role of Navy Medicine and NH Jax in caring for sailors, marines, soldiers, airmen and coast guardsmen on the battlefield, at sea and in support of humanitarian and disaster relief efforts. At any given time, about 15 percent of the hospital’s 1,400 military staff are deployed overseas. This year’s family medicine graduates will span the globe, with duty assignments to overseas naval hospitals and fleet surgical teams, where some will be stationed at or near the front lines. The focus at NH Jax is not simply to graduate clinicians who are able to perform duties well, but also to use their unique position to conduct research to help American troops and their families live happier, healthier lives. The residency program is uniquely positioned, with a wide scope of medical care, to incorporate multiple specialties and find practical ways of improving the practice of family medicine.
1. Being awarded a Navy Medicine $50,000 grant to research the effectiveness of a caring communications program to improve clinical outcomes, increase physician and patient satisfaction, and reduce adverse medical outcomes 2. Winning the education category for original resident research from the Uniformed Services University of the Health Sciences at its 2010 national conference 3. Receiving an annual research competition award from Naval Medical Center Portsmouth.
One of our current research projects looks at gestational diabetes mellitus (GDM). While we’ve gotten better recently at identifying women with pre-gestational diabetes and those at risk of developing GDM, this study includes screening patients earlier in pregnancy, quantifying how effective the screening is, measuring our compliance with GDM guidelines and measuring the effect of early versus standard diagnosis on maternal weight gain. Ultimately, the goal is to enable better identification and control of GDM. Another research idea, shortening the healing time of plantar fasciitis, may have major implications for service members and the population as a whole. A simple online search for plantar fasciitis spawns millions of results, including “cures.” In reality, we know that most patients heal in about nine months. Lt. J.P. Walton and Lt. T.J. Demetriou, both residents at NH Jax, will study the efficacy of autologous blood injections. Here we hope to offer patients a faster way of healing. An epidemiological project starting this spring is studying tic-borne illnesses (endemic in Northeast Florida), specifically the prevalence of Rickettsia parkeri. NH Jax’s public health director Capt. Joseph McQuade will work with Navy Medicine Research Institute and the Centers for Disease Control and Prevention to review blood samples. A recently completed study reviews primary care providers’ adherence to American Academy of Pediatrics 2008 guidelines on vitamin D supplementation. This study was inspired by a case of rickets in a local 1-year-old. Included in the study was a survey sent to pediatricians, family physicians and physician extenders. The results will be presented in a few months.
Residents Corner written by: Lt. Orlando Cabrera, Medical Corps, U.S. Navy, a 3rd year family medicine resident at Naval Hospital Jacksonville. Dr. Cabrera is a graduate of New Jersey Medical School of the University of Medicine and Dentistry of New Jersey.
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Northeast Florida Medicine Vol. 62, No. 1 2011 9
Presented by: north Florida CardiovasCular eduCation Foundation 8th Annual
M A r r I ot t S AWg r A S S H ot e l Ponte VeDrA beACH, FlorIDA
Co-sPonsored by: ameriCan College oF Cardiology Foundation Florida ChaPter, ameriCan College oF Cardiology
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ISCHeMIC HeArt DISeASe 8:30 am 8:40 am 9:10 am 9:40 am 10:00 am
introduction of speakers and Case Presentation Clinical impact of the Courage trial after 3+ years. lessons learned. has Practice Changed? – William boden, md stable ischemic heart disease: What’s optimal for evaluation and treatment? – david maron, md discussion break
MAnAgeMent oF CArotID DISeASe 10:30 am 10:40 am 11:10 am 11:40 am 12:00 pm
introduction of speakers and Case Presentation management of extracranial Carotid stenosis – sriram iyer, md Cea the “gold standard” after the randomized trials – bruce Perler, md discussion lunch evaluation of supplements and non-Cardiac drug interaction in Cardiovascular disease – mark munger, Pharmd
AntI-ClottIng StrAtegIeS 1:30 pm 1:40 pm 2:10 pm 2:40 pm 3:00 pm
introduction of speakers and Case Presentation antiPlatelet therapy: update on a rapidly evolving Field – Paul gurbel, md emerging anticoagulants in Cardiovascular disease – richard becker, md discussion break
AtrIAl FIbrIllAtIon MAnAgeMent 3:30 pm 3:40 pm 4:10 pm 4:40 pm 5:00 pm 6:00 – 7:30 pm
introduction of speakers and Case Presentation approach to Patients with atrial Fibrillation: is ablation that good? is drug therapy that bad? – douglas Packer, md Pharmacological management of atrial Fibrillation – hasan garan, md discussion Cocktail hour dinner lecture – ralph brindis, md Cardiovascular Disease in the Geriatric Patient: Who Will Advocate for the Elderly?
10 Vol. 62, No. 1 2011 Northeast Florida Medicine
AmericAn college of cArdiology FoundAtion
A Cardiovascular Education Opportunity Guest Faculty includes:
Richard C. Becker, MD, FACC William E. Boden, MD, FACC Hasan Garan, MD, FACC Paul A. Gurbel, MD, FACC Sriram K. Iyer, MD, FACC David J. Maron, MD, FACC Mark A. Munger, Pharm.D, FACC Douglas L. Packer, MD, FACC Bruce A. Perler, MD, MBA Co-Directors: Carlos Sotolongo, MD, FACC Ramon Castello, MD, FACC Featuring the latest information from faculty experts on the topics of: • Ischemic Heart Disease • Management of Carotid Disease • Anti-Clotting Strategies • Atrial Fibrillation Management and special dinner featuring:
ralph b. brindis, MD, MPH, FACC, President, American College of Cardiology speaking on
Cardiovascular Disease in the geriatric Patient – Who Will Advocate for the elderly?
Our program provides a maximum of 14 AMA PRA Category 1 CME Credits! www . DCMS online . org
For more information and to register visit www.pvcardiacsymposium.com.
This Issue’s Focus: GERD
Patients Deserve Quick Diagnosis and Treatment for GERD Gastroesophageal reflux disease (GERD) is a common condition, accounting for nearly 75% of all esophageal pathologic findings. Nearly 44% of Americans experience monthly heartburn and 18% of these individuals use over-the-counter medication for reflux symptoms. With a prevalence of nearly 19 million cases per year and an associated total cost of care of $9.8 billion in the United States, GERD is clearly a significant public health concern.1 Although medical therapy is effective in the management for GERD, it does not address the underlying mechanical problem, and the symptoms will recur in 80% of cases within 1-year of drug cessation.2 To control GERD, medical therapy may be needed for a lifetime, and that is an expense and psychological burden to the person who suffers with this condition. GERD also has unknown long term complications which interrupt one’s lifestyle and may force undesirable changes in a person’s diet or schedule. For all of these reasons, surgical treatment of GERD is an attractive option. In this issue of Northeast Florida Medicine, Daniel Robie, MD, writes about the “Management of Gastroesophageal Reflux Disease in the Pediatric Population” and concludes that “successful management of GERD in the pediatric population requires an appreciation for the broad array of possible presentations.” I write about “The Surgical Management of Gastroesophageal Reflux Disease and Hiatal Hernia” and discuss the various surgeries available for GERD and which patients are the best candidates for these procedures. Samir Lewiz Habashi, MD, addresses “Endoscopic Management of Gastroesophageal Reflux Disease,” and states “Endoscopic treatment for GERD patients Ziad T. Awad, MD, is considered an option for patients who do not want to be on longterm antisecretory medicaFRCSI, FACS Assistant Professor of Surgery, tions and they do not consider surgical intervention as an option.” Abubakr A. Bajwa, MD, University of Florida College of et al, discuss the “Impact of GERD on Common Pulmonary Diseases” and conclude, “Despite Medicine Jacksonville the link of GERD to pulmonary disease symptoms and quality of life, there is no clinical trial data to indicate treatment of GERD improves clinical outcomes in lung disease.” Finally, Iman Naseri, MD, writes about “Laryngopharyngeal Reflux: Overview and Clinical Implications” and makes it clear, “If untreated, it can manifest into other chronic conditions affecting the larynx and esophagus.” It is my hope and certainly the desire of the authors for this issue that GERD will be diagnosed more accurately and treated in a more effective way once our physician colleagues have read these articles. Since such a large percentage of patients suffer from GERD, it is imperative to recognize the symptoms quickly, seek the best method of controlling them, and, thus, keep patients from unnecessary and potentially dangerous complications. Sources: 1. Richter JE. The many manifestations of gastroesophageal reflux disease: presentation, evaluation, and treatment. Gastroenterol Clin North Am 2007;36:577–99; 2. Pace F, Tonini M, Pallotta S, et al. Systematic review: maintenance treatment of gastrooesophageal reflux disease with proton pump inhibitors taken ‘on-demand’. Aliment Pharmacol Ther 2007;26:195–204.
Register now for the 3rd Annual
Quality/Safety Forum - The Engines of Quality: Professionalism and Leadership April 26, 2011
UNF University Center/7:30 a.m.-1:30 p.m. Keynote address - Jo Shapiro, MD, FACS (Associate Professor of Surgery, Harvard Medical School)
Special Feature: Physician faculty from the Mayo Clinic, Naval Hospital, Nemours Children’s Clinic and UF & Shands Jacksonville will present their experience implementing the Patient Centered Caring Communication Course. $75.00 Registration Fee/Register now at www.unf.edu/brooks/center/Call 904-620-1211 with questions.
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Northeast Florida Medicine Vol. 62, No. 1 2011 11
Management of Gastroesophageal Reflux Disease in the Pediatric Population Daniel Robie, MD Abstract: ‘Physiologic reflux’ is common in infants but should resolve by 12-18 months of age. Pathologic reflux, GERD, can present with both esophageal and extraesophageal manifestations and it is important to recognize the various symptoms and signs of disease. A standard approach for diagnosis of GERD in the pediatric patient is not established but may include UGI, pH monitoring and/or EGD with biopsy. An empiric course of PPIs may be a useful diagnostic tool in the older child and adolescent. Treatment is provided in a step-wise manner with lifestyle changes, medical and surgical therapeutic options available. Unfortunately there remains a lack of randomized control trials comparing medical and surgical therapy as well as open versus laparoscopic surgery. Most recent reports document successful results with laparoscopic antireflux surgery though a substantial number of patients remain on antireflux medications postoperatively. The neurologically impaired child presents particular challenges in management of GERD with worse surgical outcomes frequently reported. There also remains a tendency among treating physicians to perform a ‘prophylactic wrap’ in these children when a gastrostomy tube is placed for nutritional needs. Other unique groups include patients with GERD and reactive airway disease or repaired esophageal atresia.
The contemporary management of gastroesophageal reflux disease (GERD) in infants, children and adolescents remains controversial. The key clinical dilemmas remain as such due to lack of prospective randomized studies to support A) Direct comparison of medical vs. surgical treatment; and B) whether open or laparoscopic anti-reflux surgery is superior. The clinician is therefore forced to base key treatment decisions on retrospective reports by often well meaning but biased investigators. At issue, however, is the significant impact of the chosen clinical pathway on the pediatric patient with a long life expectancy.
Regurgitation, vomiting or spitting up are frequently encountered in infants and small children. A survey of pediatricians reported by Nelson in 1997 noted an incidence of these symptoms in 67% of infants age 4-5 months, 21% age 6-7 months and 5% at 12 months.1 ‘Chalasia’ is a term used to denote the physiologically normal relaxation of the lower esophageal sphincter (LES). This so-called physiologic gastroesophageal reflux (GER) is expected to resolve between 6-12 months of age.2 In contrast and in need of clear distinction, GERD is the damage caused by reflux and can manifest in both esophageal and extraesophageal complications. (Table 1)2-4 Presenting symptoms can thus be widely variable and are broadly grouped into one of three categories; failure to thrive (FTT), esophagitis or respiratory complications. Address Correspondence to: Daniel Robie, MD, Chief, Division of Pediatric Surgery, Nemours Children’s Clinic, Jacksonville, FL 32207. Email: firstname.lastname@example.org. 12 Vol. 62, No. 1 2011 Northeast Florida Medicine
Table 1 Symptoms & Signs Potentially Associated with GER
Esophageal Recurrent regurgitation with/without vomiting Ruminative behavior Heartburn or chest pain Abdominal pain Hematemesis Dysphagia, odynophagia Upper airway/Respiratory Hoarseness Stridor Cough Wheezing Nonspecific Weight loss or poor weight gain Irritability in infants Esophageal Esophagitis Esophageal stricture Barrett’s esophagus Dystonic neck posturing (Sandifer’s yndrome) Upper airway/Respiratory Laryngeal/pharyngeal inflammation Recurrent pneumonia Dental erosion Apena spells Apparent life-threatening events Nonspecific Anemia Feeding refusal
Modified from Reference 4: Vandenplas Y, Rudolph CD, Di Lorenzo CD, etal: Pediatric gastroesophageal reflux clinical practice guidelines: Joint recommendations of the NASPGHAN and the ESPGHAN. J Pediatr Gastroenterol Nutr 2009;49: 498-547.
The significance of GERD in the larger national healthcare context is best understood in reviewing epidemiologic data. Lasser reported that over an 8 year period, 48,665 antireflux procedures were performed in children in the US.5 (approx 9 per 100,000 population) Interestingly, 45% of these were performed in infants consistent with an earlier report by Fonkalsrud.5,6
The diagnostic evaluation of the pediatric patient for possible GERD varies by age, presentation and neurologic status. In infants, it is especially important to recognize www . DCMS online . org
‘warning signs’ that suggest other potentially serious diagnoses. (Table 2)4 In adults, heartburn is the primary patient complaint whereas this cannot typically be assessed for in infants, children and nonverbal adolescents.4 Symptoms that suggest possible GERD in the pediatric patient may include abdominal pain, vomiting, rumination, weight loss or failure to thrive, irritability, dysphagia, asthma, cough, stridor or hoarseness. Signs may include Sandifer’s syndrome (neck posturing/extension), anemia, feeding refusal, RAD (reactive airway disease), ATLE (acute life threatening events), apnea or recurrent pneumonias.
Table 2 Warning Signs for Possible Alternative Diagnoses in Infants Presenting with GER Neurologic
Bulging fontanelle Macro/microcephaly Seizures
Gastrointestinal bleeding Hematemesis Hematochezia Bilious vomiting Consistently forceful vomiting Onset of vomiting after 6 months of age Diarrhea Constipation Abdominal tenderness or distention
Failure to thrive Fever Lethargy Hepatosplenomegaly Documented or suspected genetic/metabolic syndrome
Modified from Reference 4: Vandenplas Y, Rudolph CD, Di Lorenzo CD, etal: Pediatric gastroesophageal reflux clinical practice guidelines: Joint recommendations of the NASPGHAN and the ESPGHAN. J Pediatr Gastroenterol Nutr 2009;49: 498-547.
The neurologically impaired (NI) patient presents particular difficulty in diagnosis primarily due to ineffective communication. However, it is critical to consider GERD in these patients where the reported incidence is very high.7-9 In 28 children with cerebral palsy (CP) studied by pH probe, Bozhurt found evidence of significant GER (RI>4.5%) in 46%.7 Del Guidance studied 58 consecutive patients with CP referred to a pediatric neurology outpatient clinic and noted symptoms suggestive of GERD in 45 (71%).8 These 45 were further studied with a battery of tests and GERD was documented in 91%. Numerous causes for GERD in the NI child have been suggested and include; abnormal swallowing, heightened gag reflex, esophageal dysmotility, poor esophageal clearance, antro/gastro-duodenal dysmotility, LES dysfunction, higher incidence of hiatal hernias, increased intraabominal pressure (due to constipation, seizures, muscle spasticity, kyphoscolisos), supine feeding and medication side effects.4,10
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There are numerous investigative studies available to aid in diagnosing GERD. Upper gastrointestinal contrast study (UGI) is the easiest to obtain but is only a snapshot in time and the reported sensitivity ranges from 29-86%, specificity 21-83%, and PPV of 80-82% when compared with esophageal pH monitoring.4 It is thus not considered a useful study to screen for GER but is useful in defining anatomy (location of ligament of treitz), presence of esophageal strictures or a hiatal hernia, and to look for other diagnoses. Esophageal pH monitoring is able to accurately detect GER but is difficult to correlate with symptoms and severity of disease. It seems most effective when normal (RI<3%) in supporting other diagnoses of esophagitis (such as eosinophilic esophagitis).4 Endoscopy with biopsy proves very useful in assessing for esophagitis. However, one must be careful when attributing findings to GER and consider other causes of esophagitis such as eosinophilic esophagitis, infections, Crohn’s disease and iatrogenic.4 An empiric trial of Proton pump inhibitors (PPIs) for older children and adolescents presenting with symptoms suggestive of GERD can be supported in the literature as an aid to diagnosis.4 There is insufficient data to promote this approach in infants and younger children.
Lifestyle Changes – The approach in treating the pediatric patient with GERD should be done using an escalating step approach. Lifestyle changes are the first initiated through changes in diet. Avoid caffeine, chocolate, spicy foods, fatty foods, alcohol and tobacco smoke, eliminate bedtime eating, and promote weight loss.2,3 For infants, positioning prone reduces GER but is associated with an increased risk of Sudden Infant Death Syndrome (SIDS) and is not recommended. A reduction in vomiting can be seen with hypoallergenic formulas or thickening of infant feeds. Medical Therapy – Pharmacologic treatments are introduced next. Medications available for treating GERD include cholinergic agents (bethanacol), prokinetic agents (metoclopramide, cisapride), H2 blockers (ranitidine) and PPIs (omeprazole, lansoprazole). Cisapride is no longer available for use due to cardiac side effects though it has been shown effective in reducing GER.7 The H2 blockers are less effective in comparison to PPIs primarily due to tachyphylaxis. PPIs have proven ideal due to their sustained reduction of gastric acid production (elevation of gastric pH above 4) and decrease in intragastric fluid volumes (resultant improved gastric emptying) and are considered the 1st line medical therapy for GERD.2 Recommended dosing is once a day before the morning meal and underdosing needs to be avoided (normal dosing range 0.7-3.5 mg/kg/day). Sufficient long-term use data is lacking for children, but in adults up to 11 years continuous use has been reported safe. The issues related to longterm use of PPIs is reviewed in depth by Hassall and include inducing benign gastric mucosal hyperplasia and development of fundic gland polyps.11 Northeast Florida Medicine Vol. 62, No. 1 2011 13
Surgical Therapy – Whether to proceed with antireflux surgery as the penultimate step in treating the child with GERD in part depends on their response to PPIs. A good response suggests an equally good surgical outcome.2 Unfortunately, there are no randomized controlled trials directly comparing medical therapy with PPIs with antireflux surgery. However, it is generally accepted by both pediatric gastroenterologists and surgeons that successful surgery offers the only definitive cure for GERD. The Nissen 360 degree fundoplication is the most common operation performed in children. Other frequently used alternatives include the Thal 270 degree anterior wrap and the Toupet 180 degree posterior wrap. Reported outcomes are generally similar in experienced hands. Of current interest is the comparison between open versus laparoscopic Nissen fundoplication. Though there are no randomized controlled trials comparing the two, outcomes appear similar but with a higher rate of postoperative pulmonary complications with open surgery. Rothenberg reports the largest personal series of pediatric patients (n=1048) undergoing laparoscopic Nissen and noted a postoperative complication rate of 4% and a wrap failure rate of 4%.12 However, sufficient follow-up data is not provided. Esposito reported equally good results in 238 neurologically normal patients undergoing either a laparoscopic Nissen, Thal or Toupet.13 In comparison, Pearl reported a series of 234 patients undergoing an either an open Nissen or Dor-Nissen (anterior partial wrap) and found that in the cohort of 81 neurologically normal patients there was a postoperative complication rate of 12% and a wrap failure rate of 5%.14 A retrospective comparison between 150 open and 306 laparoscopic Nissen fundoplications in patients 5 years or less in age was reported by Diaz and associates.15 They showed a reoperation rate of 14% in the laparoscopic group and 8% in the open group that reached statistical significance. However the incidence of acute respiratory complications was higher in the open group (8% vs 1.3%) as were overall complications. In a group of 55 infants either undergoing a laparoscopic (39) or open (14) reported by Somme, with short term follow-up recurrent reflux was similarly infrequent though time to initiate of feeds was shorter in the laparoscopic group.16 This study however seems to lack vigorous detailed follow-up. In contrast, several authors have found a high rate of recurrent reflux, as indicated by antireflux medication use, and/or pulmonary complications following antireflux surgery.17-20 Lee reported that 197 of 342 patients (57.6%) following Nissen fundoplication were taking antireflux medications (17). This included 47 who had previously not been medicated. In an earlier report on this same group of 342 patients, these authors noted the relative risks of readmission postoperatively for aspiration pneumonia was 0.12, other pneumonia 0.55, respiratory distress/apnea 0.50 and FTT 0.57.20 Goldin noted that among 1142 pediatric patients who underwent antireflux surgery in the State of Washington over a 14-ear period, the incidence of hospital admissions for reflux related events (RREs) declined for infants and children under 4 years of age but were either the same or greater for patients over 4.19 However for all age groups, admissions for RREs were higher than expected when compared with the outcomes reported in many single institution patient series. 14 Vol. 62, No. 1 2011 Northeast Florida Medicine
In summary, the current literature remains insufficient to provide a definitive argument either for or against antireflux surgery in children. The major reasons for this include a lack of standardization in preoperative evaluation, a lack of consensus in the clinical indications for surgery, inadequate postoperative follow-up and the absence of prospective randomized trials.
Neurologically Impaired Patient – Surgical outcomes in the NI patient were documented to be worse in comparison to neurologically normal patients in several reports from the 1990s following open surgery.6,14,21,22 However, more recent studies from the laparoscopic era have not shown a higher rate of recurrent reflux or redo-fundoplication.23-25 Despite this, the belief persists that the NI patient has a worse outcome. Possible contributing factors that place the NI patient at risk for failure are the very reasons reviewed earlier that lead to an increased incidence of GERD in this population. Another controversy is whether a ‘prophylactic’ antireflux operation should be done in the NI child who requires gastrostomy tube placement. Those in favor argue that it avoids a return to surgery in this high risk patient group. However, numerous reports have not shown an increased incidence or worsening of GER after gastrostomy tube placement alone.26-28 Burd and associates studied the issue utilizing decision analysis methodology and found that gastrostomy tube placement alone was favored over adding an antireflux procedure if the morbidity of the former was < 11% and the later > 10%, odds that would clearly support gastrostomy alone.29 Esophageal Atresia – Following repair of esophageal atresia and tracheoesophageal fistula, a high incidence of gastroesohageal reflux is noted and up to one third of patients will undergo antireflux surgery.30-32 The cause is foreshortening of the esophagus with compromise of the LES antireflux mechanism and in some patients a hiatal hernia. Esophageal dysmotility is also felt to be a contributing factor. Many pediatric surgeons believe these same issues lead to a higher rate of failure following antireflux surgery. However, definitive control of reflux is critical in successfully treating stricturing of the esophageal anastomosis. Encouraging results have been reported by Esposito who noted excellent control of reflux in 21 patients though one third experienced short-term dysphagia following laparoscopic antireflux surgery.33 Reactive Airway Disease – An association between GER and RAD is suspected especially in severe asthmatics in whom the normal antireflux barrier may be compromised.3,6 Child asthmatics studied with pH monitoring are noted to have positive findings in 25-75%. A trial of PPIs may be considered in these patients in particular when nocturnal-onset asthma is documented. Antireflux surgery should be considered when GER is documented in the severe asthmatic who requires chronic antireflux medical therapy. Tashjian reported a series of 24 patients with RAD and documented GERD and noted a reduction in antireflux and pulmonary medication use from an average of 5.5 different medicines preoperatively to 0.6 postoperatively.34 Overall, 75% of patients were able to stop all medications. www . DCMS online . org
Successful management of GERD in the pediatric population requires an appreciation for the broad array of possible presentations. The impact of the patientâ€™s age, underlying disease and neurologic status are important considerations. Numerous tools for diagnosis are available, but there does not currently exist a standard diagnostic approach. PPIs are equally effective in the child as compared to the adult, but the role of surgery is not clearly defined. Laparoscopic antireflux surgery is effective, but vigorous scientific comparison with medical therapy alone or with open antireflux surgery is not available. 1.
2. 3. 4.
Nelson SP, Chen EH, Syniar GM, etal: Prevalence of symptoms of gastroesophageal reflux during infancy: a pediatric-based survey: A Pediatric Practice Research Group Survey. Arch Pediatri Adolesc Med 1997;151:569-572. Hassall E: Decisions in diagnosing and managing chronic gastroesophageal reflux disease in children. J Pediatr 2005;146:S3-S12. Rudolph CD, Mazur LJ, Liptak GS, etal: Pediatric GE reflux+ clinical practice guidelines. J Pediatr Gastroenterol Nutr 2001;32:S1-31. Vandenplas Y, Rudolph CD, Di Lorenzo CD, etal: Pediatric gastroesophageal reflux clinical practice guidelines: Joint recommendations of the NASPGHAN and the ESPGHAN. J Pediatr Gastroenterol Nutr 2009;49: 498-547.
Lassar MS, Liao JG and Burd RS: National trends in the use of antireflux procedures in children. Pediatrics 2006;118:1828-1835.
Fonkalsrud EW, Ashcraft KW, Coran AG, etal: Surgical treatment of gastroesophageal reflux in children: a combined hospital study in 7467 patients. Pediatrics 1998;101:419-22.
Bozkurt M,Tutuncuoglu S, Serdaroglu G, etal: Gastroesophageal reflux in children with cerebral palsy: efficacy of Cisapride. J Child Neurol 2004;19:973-976. 8. Del Giudice E, Staiano A, Capono G, etal: Gastrointestinal manifestations in children with cerebral palsy. Brain and Development 1999;21:307-311.
Reyes AL, Cash AJ, Green SH, etal: Gastroesophageal reflux in children with cerebral palsy. Child Care Health Dev, 1993;March-April,19(2):109-118.
10. Pensabene L, Miele E, Del Guidice E, etal: Mechanisms of gastroesohageal reflux in children with sequelae of birth asphyxia. Brain and Development. 2008;30:563-571. 11. Hassall E: Wrap session: is the Nissen slipping? Can medical treatment replace surgery for severe gastroesophageal reflux disease in children? Am J Gastroenterol 1995:90;1212-20. 12. Rothenberg S: The first decadeâ€™s experience with laparoscopic nissen fundoplication in infants and children. J Ped Surg 2005;40:142-7. 13. Esposito C, Montupet P, van Der Zee D, etal: Longterm outcome of laparoscopic nissen, toupet and thal antireflux procedures for neurologically normal children with gastroesophageal reflux disease. Surg Endosc 2006;20:855-8. 14. Pearl RH, Robie DK, Ein SH, etal: Complications of gastroesophageal antireflux surgery in neurologically impaired versus neurologically normal children. J Pediatr Surg 1990:25;1169-73. 15. Diaz DM, Gibbons TE, Heiss K, etal: Antireflux surgery outcomes in pediatric gastroesophageal reflux disease. Am J Gastoenterol 2005;100:1844-52.
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16. Somme S, Rodriguez JA, Kirsch D, etal: Laparoscopic vs open fundoplication in infants. Surg Endosc 2002;16:54-6. 17. Lee SL, Sydorak RM, Chiu VY, etal: Long-term antireflux medication use following pediatric nissen fundoplication. Arch Surg 2008;143:873-876. 18. Gilger MA, Yeh C, Chiang J, etal: Outcomes of surgical fundoplication in children. Clin Gastroentero Hepatol 2004;2:978-984. 19. Goldin AB, Sawin R, Seidel KD, etal: Do antireflux operations decrease the rate of reflux-related hospitalizations in children? Pediatrics 2006;118:2326-2333. 20. Lee SL, Shabatian H, Hsu JW, etal: Hospital admissions for respiratory symptoms and failure to thrive before and after nissen fundoplication. J Pediatr Surg 2008;43:59-65. 21. Martinez DA, Ginn-Pease ME and Caniano DA: Sequelae of antireflux surgery in profoundly disabled children. J Pediatr Surg 1992:27;267-73. 22. Smith CD, Othersen HB Jr, Gogan NJ, etal: Nissen fundoplication in children with profound neurologic disability: high risks and unmet goals. Ann Surg 1992:215;654-9. 23. Esposito C, van Der Zee D, Settimi A, etal: Risks and benefits of surgical management of gastroesophageal reflux in neurologically impaired children. Surg Endosc 2003;17:708-710. 24. Lima M, Bertozzi M, Ruggeri G, etal: Laparoscopic antireflux surgery in neurologically impaired children. Pediatr Surg Int 2004;20:114-117. 25. Steyaert H, Mohaidly A, Lembo A, etal: Long-term outcome of laparoscopic Nissen and Toupet fundoplication in normal and neurologically impaired children. Surg Endosc 2003;17:543-546. 26. Wilson GJP, van Der Zee D and Bax NMA: Endoscopic gastrostomy placement in the child with gastroesophageal reflux: is concomitant antireflux surgery indicated? J Pediatr Surg 2006;41:1441-1445. 27. Viswanath N, Wong D, Channappa D, etal: Is prophylactic fundoplication necessary in neurologically impaired children? Eur J Pediatr Surg 2010;20:226-229. 28. Wheatley MJ, Wesley JR, Tkach DM, etal: Long-term followup of brain-damaged children requiring feeding gastrostomy: should an antireflux procedure always be performed? J Pediatr Surg 1991;26:301-305. 29. Burd RS, Price MR and Whalen TV: The role of protective antireflux procedures in neurologically impaired children: A decision analysis. J Pediatr Surg 2002;37:500-6. 30. Deurloo JA, Ekkelkamp S, Schoorl M, etal: Esophageal atresia: historical evolution of management and results in 371 patients. Ann Thorac Surg 2002;73:267-72. 31. Little Dc, Rescorla FJ, Grosfeld JL, etal: Long-term analysis of children with esophageal atresia and TEF. J Pediatr Surg 2003;38:852-6. 32. Foker JE, Linden BC, Boyle EM, etal: Development of a true primary repair for the full spectrum of esophageal atresia. Annals Surg 1997;226:533-543. 33. Esposito C, Langer JC, Schaarschmidt K, etal: Laparoscopic antireflux procedures in the management of gastroesophageal reflux following esophageal atresia repair. J Pediatr Gastroenterol and Nutr. 2005;40:349-51. 34. Tashjian DB, Tirabassi M, Moriarty KP, etal: Laparoscopic nissen fundoplication for reactive airway disease. J Pediatr Surg 2002;37:1021-23. Northeast Florida Medicine Vol. 62, No. 1 2011 15
The Surgical Management of Gastroesophageal Reflux Disease and Hiatal Hernia Ziad T. Awad, MD, FRCS, FACS Abstract: Gastroesophagealreflux disease (GERD) is a common disease
throughout the western world. This review describes the indications for surgical intervention patients with GERD. Laparoscopic antireflux surgery is safe and has a similar efficacy to open antireflux surgery and best medical therapy with proton pump inhibitors. Total fundoplication tends to produce superior reflux control, but at the cost of increased risk of dysphagia. There is a trend for antireflux surgery to be superior to best medical therapy in cancer prevention in Barrett’s esophagus, but this has not reached statistical significance.
GERD is an extremely common condition accounting for 75% of all esophageal pathologic findings. In the western world, 10% of the general population experience daily, 20% weekly, and 50% monthly reflux symptoms.1-3 The disease spectrum ranges from non-erosive reflux disease, reflux esophagitis to benign strictures, columnar metaplasia, dysplasia and esophageal adenocarcinoma. In a northern European population-based endoscopy survey, the prevalence of reflux esophagitis was 15.5%, columnar metaplasia of the esophagus was 1.6%.3
The pathophysiology underlying the disease is failure of the lower esophageal sphincter and distal esophagus to control and clear refluxing gastric contents from the lower esophagus. The m a i n components of maintenance of lower esophageal sphincter competence are: the intra-abdominal length of the esophagus, the Angle of His at the esophagogastric junction, and effective lower esophageal peristalsis and sphincteric function.4,5 In patients in whom these mechanisms are defective, g a s t r i c contents may pass retrograde into the esophagus causing various reflux symptoms.Treatment of GERD includes dietary modification and lifestyle adjustments, medical therapy, endoscopic therapy, and antireflux surgery. The aim of this article is to describe the surgical treatment for GERD and hiatal hernia.
Surgical Treatment for GERD
Allison initially described approximation of the crura and reduction of the hiatal hernia in 1948.6 However, this technique had a very high recurrence rate (49%) for GERD/hiatal hernia.7 The first fundoplication for GERD was described by Rudolph Nissen as wrapping 2 folds of the stomach around the esophagus, which were fixed anteriorly to the
esophagus.8 The first laparoscopic antireflux procedures were done by Geagea and Dallemagne in 1991.9,10
Selection of Patients for Antireflux Surgery
Patients undergoing antireflux surgery should have objective evidence of gastro-esophageal reflux. The most widely available investigation is upper endoscopy as it may demonstrate the presence of esophagitis, ulceration, stricture or Barrett’s mucosa. It will also allow assessment of the size of the hiatal hernia. Esophageal acid exposure may be evaluated by 24-hour pH analysis; this test is particularly useful in patients with non-erosive reflux disease. Candidates for surgery include: 1) Patients who have failed medical management (inadequate symptom control, severe regurgitation not controlled with acid suppression, or medication side effects); 2) Those that opt for surgery despite successful medical management (due to quality of life considerations, lifelong need for medication intake, expense of medications, etc.); 3) Patients with complications of GERD (e.g., Barrett’s esophagus, peptic stricture)11,12; and 4) Patients with extraesophageal manifestations (asthma, hoarseness, cough, chest pain, aspiration).13-16
Principles of Antireflux Surgery
The exact mechanism of action of antireflux surgery is not clear, but components of its overall action include: creation of a valve a t t h e lower esophagus, exaggeration of the angle of His, increase in lower esophageal sphincter pressure, and a positive influence on lower esophageal peristalsis and sphincter relaxation. Laparoscopic Nissen fundoplication (Figure 1) has emerged as the most widely used and accepted anrireflux procedure. Technical details of the procedure include: 1) Dissection of the esophageal hiatus and diaphragmatic crura; 2) Mobilization of the gastric fundus by dividing the short gastric vessels; 3) Closure of the hiatal
Figure 1 Nissen Fundoplication
(Floppy 360° wrap pointing at 700 o’clock)
Address Correspondence to: Ziad T. Awad, M.D, FRCS, FACS, Assistant Professor of Surgery, Director, Minimally Invasive Surgery, Department of Surgery, University of Florida College of Medicine, Jacksonville, 633 W 8th Street, Jacksonville, FL 32209, USA. Phone: +001- 904-244 3971. Fax: +001- 904 244 3870. Email: email@example.com. 16 Vol. 62, No. 1 2011 Northeast Florida Medicine
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Table 1 Antireflux Procedures
Technical Comments Aspects
Anterior fundoplication Belsey Mark IV 70
Left thoractotomy 270˚
Posterior fundoplication Donahue73
Preserve the short gastric vessels
Hill gastropexy Transabdominal Suturing the phrenoesophageal ligament to the periaortic fascia and median arcuate ligament 77
Prosthesis Angelchik78 Transabdominal Placement Not used anymore due to high of gel risk of migration and dysphagia filled band around the GEJ
defect; 4) Creation of a 360 degree gastric wrap at the distal esophagus over around a 56- to 60-french esophageal dilator. The wrap is anchored to the esophagus using non absorbable sutures; and 5) Limitation of the length of the wrap to 2.0 cm. Other antireflux procedures are shown in Table 1. ( Reference numbers included with table )
Surgeon’s Learning Curve
The learning curve for laparoscopic antireflux surgery is well documented in the literature with reports of increased failure rates, complications, reoperations, operative time, hospital days, and conversions to open surgery by less experienced surgeons.17-19 To minimize adverse outcomes as a result of the learning curve, studies have suggested that surgeons seek experienced supervision during their first 15-20 laparoscopic antireflux procedures.18
Laparoscopic vs. Open Antireflux Surgery
A number of trials have compared open to laparoscopic fundoplication with a follow-up to 11 years.20-29 All have shown advantages of the laparoscopic approach with shorter post-operative stay, lower incidence of complications, faster recovery, but longer operative time. Dysphagia is similar for both approaches, but bloating was more common following open surgery. The laparoscopic approach was also less expensive than open surgery.24
Complications of Antireflux Surgery
Paraesophageal hemiation has been reported following laparoscopic antireflux surgery, particularly in the immediate postoperative period. Its incidence ranges up to 7% in published reports series.30, 31 Factors that may predispose to paraesophageal herniation following laparoscopic surgery include an increased risk of breaching the left pleural www . DCMS online . org
membrane, the concomitant presence of a hiatal hernia, and effects associated with reduced postoperative pain.32-34 Loss of the left pleural barrier during esophageal dissection can allow the stomach to slide more easily into the left hemithorax. Reduced postoperative pain is one of the main advantages of laparoscopic surgery. However, when there is less pain, more abdominal force is transmitted to the hiatal area during coughing, vomiting, or other forms of exertion in the initial postoperative period. As a result, the stomach may be pushed into the thorax, since the normal anatomical barriers have been disrupted by surgical dissection.31 There are several strategies that can reduce the likelihood of herniation. Routine hiatal repair has been shown to reduce its incidence by nearly 80%.31,35 In addition, it would seem prudent to avoid diaphragmatic stressors in the early postoperative period. The use of modern antiemetics to obviate vomiting in the first few days following surgery should further reduce the risk of acute hemiation. At the same time, patients should be advised to avoid excessive lifting or straining for 3-months after surgery. Early resumption of heavy physical work has been associated with acute herniation.31 Dysphagia in the early postoperative period is experienced by almost all patients. Initially, the patients are placed on a liquid diet for the first few days after surgery and gradually advanced to pureed diet. Solids are usually started 4-6 weeks after surgery giving time for the edema to settle and the wrap to soften. Severe postoperative dysphagia may be treated by endoscopic dilation.Those, whose dysphagia recurs soon after or those who fail to respond to endoscopic dilation, need to be evaluated by esophageal manometry, barium esophagram and endoscopy. Common causes of severe postoperative dysphagia include: wrong diagnosis, tight wrap, tight crural closure and hiatal stenosis due to scarring (Figure 2, p.18), two compartment stomach and paraesophageal hernia. Northeast Florida Medicine Vol. 62, No. 1 2011 17
Figure 2 Paraesophageal Hernia
(Following laparoscopic Nissen fundoplication)
A further multicentre study reported that 80% of patients post laparoscopic Nissen fundoplication continued to take antireflux medication.43 However, the LOTUS trial reported a much lower rate (90% remaining in remission) of patients treated by laparoscopic antireflux surgery requiring continued (>4 weeks) medication to control reflux.44 The Spanish trial randomized 101 patients with Barrett’s esophagus to best medical treatment (ranitidine initially, followed by omeprazole) or antireflux surgery. Improvement in symptoms was equal between the groups with a higher rate of healing of inflammation in the surgical group. Barrett’s did not completely regress in any cases and there were similar rates of development of dysplasia in both groups. All surgical patients who developed dysplasia had failure of control of reflux.45
Thromboembolic disease may be more common following laparoscopic antireflux surgery than open surgery due to a combination of the head-up position, intra-abdominal insufflation of CO2 t h a t would increase lower limb venous stasis and increase the risk of deep venous thrombosis. Pneumothorax may occur in l e s s t h a n 2 % of patients due to injury to the left pleural membrane, particularly f o l l ow i n g e x tensive mediastinal dissection to mobilize the esophagus or reduce hiatal hernia sac. Chest drains are usually not required as the insufflated CO2 is rapidly reabsorbed.36 Injuries to the inferior vena cava, left hepatic vein and aorta have been reported.37, 38 Bleeding may also occur from the left lobe of liver due to liver retraction or other instrumentation, or the short gastric vessels at the time of dissection. Cardiac tamponade has also been reported.39 Perforation of the esophagus or stomach may occur due to excessive traction during passage of a bougie or dissention of the retroesophageal window. These injuries are repaired primarily and tested with an air or dye test at the time of surgery and water-soluble contrast study post-operatively.
Medical vs. Surgical Therapy for GERD
Five randomized trials compared medical therapy to surgical intervention for GERD. Three of these studies were done before the era of laparoscopic antireflux surgery or proton pump inhibitors. Behar et al. reported a small trial of 31 patients was randomized into Belsey Mark IV (An anterior 270˚ fundoplication fixed to the undersurface of the diaphragm done through a left thoractomy) or medical therapy. Good results were obtained in 73% patients treated surgically versus 19% in the medical group.40 Spechler et al. randomized 247 patients to H2 receptor antagonist or open Nissen fundoplication. Patient satisfaction and endoscopic improvement in esophagitis were higher in the surgery group at 2 years f ollow-up and at mean 9 years of follow-up but there was a higher rate of late overall mortality in the surgery group due to excess cardiovascular deaths.41,42
18 Vol. 62, No. 1 2011 Northeast Florida Medicine
Lundell et al. compared proton pump inhibitor therapy to open antireflux surgery in 310 patients.46 At a 5- year follow-up, symptomatic recurrence was significantly higher in the medical arm (49/133 compared to 20/122) and 16 patients initially treated with proton pump inhibitor crossedover and had antireflux surgery. A multicentre study of 554 patients randomized to laparoscopic antireflux surgery or esomeprazole with a 3-years follow-up found no significant difference in treatment failure rate: 95% d i d n o t fail in the medical arm and 90% did not fail in the surgical arm (including the need to commence medication for recurrent symptoms in the surgical group). There was no mortality in the surgical group and a similar rate of cardiovascular events in b o t h groups.44 There is a trend for antireflux surgery to be superior to best medical treatment in dysplasia and cancer prevention 47,48 which reached statistical significance for uncontrolled studies48 (0.28% per year among patients treated surgically compared to 0.63% per year for patients treated medically, P=0.014). There were similar results in two meta-analyses (which demonstrated a trend for superiority, but no statistically significant difference).49,50 This may be the result of prevention of reflux of carcinogenic biliopancreatic secretions by repair of the defective sphincter mechanism, rather than simply reducing the volume and acidity of the refluxate.47
Hiatal Hernia – Definitions & Etiology
Hital hernia and GERD were once considered synonyms with hiatal hernia seen as a sine qua non condition for GERD to occur. Currently, it is well known that both conditions can exist independently. However, it is recognized that hiatal hernia disrupts most of the natural antireflux mechanisms and is considered an independent factor of GERD. Diaphragmatic herniation is a common disorder of the digestive tract.51,52 It is characterized by a protrusion of the stomach into the thoracic cavity through a widening of the diaphragmatic crura. Attempts began in the 1950s to classify hiatal hernia into subtypes.53 The current classification has evolved to include a category of hiatal hernias into Types I – IV.
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Type I hernias are sliding hiatal hernias when the gastroesophageal junction migrates above the diaphragm.54 The stomach remains in its usual longitudinal alignment.55 Type II hernias are pure paraesophageal hernias with the gastroesophageal junction remaining normally located and a portion of the stomach “rolls” through the diaphragmatic hiatus. Type III hernias are a combination of Types I and II with both the gastroesophageal junction and the stomach herniating through the hiatus (Figure 3). Type IV hiatal hernias are characterized by the presence of a structure other than stomach, such as the omentum, colon or small bowel, within the hernia sac (Figure 4). Types II – IV as a group are referred to as paraesophageal hernias, and are possibly differentiated from Type I hernia by relative preservation of posterolateral phrenoesophageal attachments around the gastroesophageal junction.56 Greater than 95% of hiatal hernias are of Type I. Of the paraesophageal hernias, more than 90% are of Type II, and the least common type is Type IV.55
Figure 3 Achalasia-like Barium Study
(On exploration, the hiatus was scarred and fibrosed)
Figure 4 Giant Paraesophageal Hernia (Causing gastric outlet obstruction)
analysis modeling of contemporary data suggests that routine elective repair of completely asymptomatic paraesophageal hernias may not be indicated.58 This model, based on analysis of 5 studies, suggests that repair should be reserved for patients with symptoms of gastric outlet obstruction (dysphagia and postprandial fullness), those with severe gastroesophageal reflux or anemia, and those requiring emergent surgery for possible gastric strangulation. Furthermore, this model suggested than elective laparoscopic hiatal hernia repair in asymptomatic patients might actually decrease the quality-adjusted life expectancy for patients aged 65 years and older. Other indication for surgery includes pulmonary complication due to mechanical effect of the intrathoracic stomach resulting in shortness of breath and reduction in the forced vital capacity.69
Indications for Surgery
Very little published information exists regarding the natural course of untreated paraesophageal hernias. Of the data available, there is a suggestion that the risk of progression from asymptomatic to symptomatic paraesophageal hernia is approximately 14% per year.57,58 This information, together with early reports of near universal mortality resulting from these complications, particularly gastric necrosis, has led to the dictum that all paraesophageal hernias should be repaired electively in suitable surgical candidates, particularly for patients with symptomatic hernia where the risk of complication is said to be higher.59-61 However, more recent reports have shown that mortality rates for emergency paraesophageal hernias operations are currently much lower than those reported in the last century.62,63 Mortality rates for emergency have been reported to be as low as 5.4% in large series and as low as zero in smaller series.58,64 Average mortality rates for emergency hiatal hernia surgery are around 17%.58 Moreover, the risk of developing acute symptoms requiring emergency surgery is probably less than 2% per year.58, 65-68 Decision www . DCMS online . org
Gastroesophageal reflux disease is a common problem in the western world. Medical therapy, which is quite effective, is needed to sustain life. The surgical therapy for GERD is safe and provides long term success. The surgical therapy for hiatal hernia should be individualized for the best results.
Oelschlager BK, Quiroga E, Parra JD, Cahill M, Polissar N, Pellegrini, CA. Long-term outcomes after laparotireflux surgery. Am J Gastroenterol 2008;103:280-7.
Locke GR, Talley NJ, Fett SL, Zinsmeister AR, Melton LJ. Prevalence and Clinical Spectrum of Gastroesophageal Reflux: A Population-Based Study in Olmsted County Minnesota. Gastroenterology 1997;112:1448-56.
Ronkainen J, Aro P, Storskrubb T, Johansson SE, Lind T, Bolling-Sternevald E et al. Prevalence of Barrett’s esophagus in the general population: an endoscopic study. Gastroenterology 2005;129:1825-31.
Kahrilas PJ, Shi G, Manka M, Joehl, RJ. Increased fre-quency of transient lower esophageal sphincter relaxation induced by gastric distension in reflux patients with hiatal hernia. Gastroenterology 2000;118:688-95.
de Vries DR, van Herwaarden MA, Smout AJ, Samsom M. Gastroesophageal pressure gradients in gastroe- sophageal reflux disease: relations with hiatal hernia, body mass index, Northeast Florida Medicine Vol. 62, No. 1 2011 19
and esophageal acid exposure. Am J Gastroenterol 2008; 103:1349-54.
prospective randomized study with a 3-month followup. J Am Coll Surg 1999;188:368-76.
Allison PR. Peptic ulcer of oesophagus. Thorax 1948; 3:20-42.
Allison PR. Hiatus hernia (a 20-year retrospective study). Ann Surg 1973;178:273-6.
25. Perttila J, Salo M, Ovaska J, Gonroos J, Lavonius M, Katila A et al. Immune response after laparoscopic and conventional Nissen fundoplication. Eur J Surg 1999;165:21-8.
Nissen R. Eine einfache Operation zur Beeinflussung der Refluxoesophagitis. Schweiz Med Wschr 1956;86: 590-2.
Geagea T. Laparoscopic Nissen’s fundoplication: preliminary report on ten cases. Surg Endosc 1991;5:170-3.
10. Dallemagne B, Weerts JM, Jehaes C, Markiewicz S, Lombard R. Laparoscopic Nissen fundoplication: preliminary report. Surg Laparosc Endosc 1991;1:138-43. 11. Spechler S J, Goyal R K. The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. Gastroenterology 1996; 110:614-621. 12. Lagergren J, Bergstrom R, Lindgren A, Nyren O. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999; 340:825-831. 13. Rakita S, Villadolid D, Thomas A, Bloomston M, Albrink M, Goldin S, Rosemurgy A. Laparoscopic Nissen fundoplication offers high patient satisfaction with relief of extraesophageal symptoms of gastroesophageal reflux disease. Am Surg 2006; 72:207-212. 14. Meyer T K, Olsen E, Merati A. Contemporary diagnostic and management techniques for extraesophageal reflux disease. Curr Opin Otolaryngol Head Neck Surg 2004; 12:519-524. 15. Lindstrom D R, Wallace J, Loehrl T A, Merati A L, Toohill R J. Nissen fundoplication surgery for extraesophageal manifestations of gastroesophageal reflux (EER). Laryngoscope 2002; 112:1762-1765. 16. Oelschlager B K, Eubanks T R, Oleynikov D, Pope C, Pellegrini C A. Symptomatic and physiologic outcomes after operative treatment for extraesophageal reflux. Surg Endosc 2002; 16:1032-1036. 17. Soper N J, Dunnegan D. Anatomic fundoplication failure after laparoscopic antireflux surgery. Ann Surg 1999; 229:669-676; discussion 676-667. 18. Watson D I, Baigrie R J, Jamieson G G. A learning curve for laparoscopic fundoplication. Definable, avoidable, or a waste of time? Ann Surg 1996; 224:198-203. 19. Deschamps C, Allen M S, Trastek V F, Johnson J O, Pairolero P C. Early experience and learning curve associated with laparoscopic Nissen fundoplication. J Thorac Cardiovasc Surg 1998; 115:281-284; discussion 284-285. 20. Laine S, Rantala A, Gullichsen R, Ovaska J. Laparoscopic vs conventional Nissen fundoplication. A prospective randomized study. Surg Endosc 1997;11:441-4. 21. Salminen PT, Hiekkanen HI, Rantala AP, Ovaska JT. Comparison of long-term outcome of laparoscopic and conventional nissen fundoplication: a prospective randomized study with an 11-year follow-up. Ann Surg 2007;246:201-6. 22. Hakanson BS, Thor KB, Thorell A, Ljungqvist O. Open vs laparoscopic partial posterior fundoplication. A prospective randomized trial. Surg Endosc 2007;21:289-98. 23. Heikkinen TJ, Haukipuro K, Bringman S, Ramel S, Sorasto A, Hulkko A. Comparison of laparoscopic and open Nissen fundoplication 2 years after operation. A prospective randomized trial. Surg Endosc 2000;14:1019-23. 24. 24. Heikkinen TJ, Haukipuro K, Koivukangas P, Sorasto A, Autio R, Sodervik H et al. Comparison of costs between laparoscopic and open Nissen fundoplication: a
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26. Chrysos E, Tsiaoussis J, Athanasakis E, Zoras O, Vassilakis JS, Xynos E. Laparoscopic vs open approach for Nissen fundoplication. A comparative study. Surg Endosc 2002;16:1679-84. 27. Luostarinen M, Virtanen J, Koskinen M, Matikainen M, Isolauri J. Dysphagia and oesophageal clearance after laparoscopic versus open Nissen fundoplication. A randomized, prospective trial. Scand J Gastroenterol 2001;36:565-71. 28. Nilsson G, Larsson S, Johnsson F. Randomized clinical trial of laparoscopic versus open fundoplication: blind evaluation of recovery and discharge period. Br J Surg 2000;87:873-8. 29. Ackroyd R, Watson DI, Majeed AW, Troy G, Treacy PJ, Stoddard CJ. Randomized clinical trial of laparoscopic versus open fundoplication for gastrooesophageal reflux disease. Br J Surg 2004;91:975-82. 30. Collard JM, CA de Gheldere, De Cock M, Otte JB, Kestens PJ. Laparoscopic antireflux surgery: what is real progress? Ann Surg 1994; 220:146-54. 31. Watson DI, Jamieson GG, Devitt PG, Mitchell PC, Game PA. Paraoesophageal hiatus hernia: an important complication of laparoscopic Nissen fundoplication. Br J Surg 1995; 82:521-523. 32. Biswas TK, Smith JA. Laparoscopic total fundoplication: anaesthesia and complications. Anaesth Intens Care 1993; 21:127-128. 33. Joris JL, Chiche J-D, Lamy ML. Pneumothorax during laparoscopic fundoplication: diagnosis and treatment with positive endexpiratory pressure. Anesth Analg 1995; 81:993-1000. 34. Carlson MA, Richards CG, Frantzides CT. Laparoscopic prosthetic reinforcement of hiatal herniorrhaphy. Dig Surg 1999; 16: 407-410. 35. Gotley DC, Smithers BM, Rhodes M, Menzies B, Branicki FJ, Nathanson L. Laparoscopic Nissen fundoplication -- 200 consecutive cases. Gut 1996; 38:487-491. 36. Watson DI, Mitchell P, Game PA, Jamieson GG. Pneumothorax during laparoscopic mobilization of the oesophagus. Aust N Z J Surg 1996; 66:711-2. 37. Baigrie RJ, Watson DI, Game PA, Jamieson GG. Vascular perils during laparoscopic dissection of the oesophageal hiatus. Br J Surg 1997;84:556-7. 38. McKenzie T, Esmore D, Tulloh B. Haemorrhage from aortic wall granuloma following laparoscopic Nissen fundoplication. Aust N Z J Surg 1997;67:815-6. 39. Firoozmand E, Ritter M, Cohen R, Peters J. Ventricular laceration and cardiac tamponade during laparoscopic Nissen fundoplication. Surg Laparosc Endosc 1996;6:394-7. 40. Behar J, Sheahan DG, Biancani P, Spiro HM, Storer EH. Medical and surgical management of reflux esophagitis. A 38-month report of a prospective clinical trial. N Engl J Med 1975;293:263-8. 41. Spechler SJ. Comparison of medical and surgical therapy for complicated gastroesophageal reflux disease in ve t e r a n s . T h e De p a r t m e n t o f Ve t e r a n s A f f a i r s Gastroesophageal Reflux Disease Study Group. N Engl J Med 1992;326:786-92. 42. Spechler SJ, Lee E, Ahnen D, Goyal RK, Hirano I, Ramirez F et al. Long-term Outcome of Medical and
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Surgical Therapies for Gastroesophageal Reflux Disease. JAMA 2001;285:2331-8.
59. Hill LD. Incarcerated paraesophageal hernia. A surgical emergency. Am J Surg 1973; 126:286-291.
43. Madan A, Minocha A. Despite high satisfaction, majority of gastroesophageal reflux disease patients continue to use proton pump inhibitors after antireflux surgery. Aliment Pharmacol Ther 2006;23:601-5.
60. Skinner DB, Belsey RH (1967) Surgical management of esophageal reflux and hiatus hernia. Long-term results with 1,030 patients. J Thorac Cardiovasc Surg 1967; 53:33-54.
44. Lundell L, Attwood SE, Ell C, Fiocca R, Galmiche JP, Hatlebakk JG et al. and Lotus trial collaborators. Comparing laparoscopic antireflux surgery with esomeprazole in the management of patients with chronic gastroesophageal reflux disease: a 3-year interim analysis of the LOTUS trial. Gut 2008;57:1207-13. 45. Parrilla P, Martinez de Haro LF, Ortiz A, Munitiz V, Molina J, Bermejo J et al. Long-Term Results of a Randomized Prospective Study Comparing Medical and Surgical Treatment of Barrett’s Esophagus. Ann Surg 2003;237:291-8. 46. Lundell L, Miettinen P, Myrvold HE, Pedersen SA, Liedman B, Hatlebakk JG et al. Continued (5-year) followup of a randomized clinical study comparing antire-flux surgery and omeprazole in gastroesophageal reflux disease. J Am Coll Surg 2001;192:172-9. 47. Gatenby PAC, Ramus JR, Caygill CPJ, Charlett A, Winslet C, Watson A. Treatment modality and risk of development of dysplasia and adenocarcinoma in columnar- lined esophagus. Dis Esophagus 2008; Nov 12.
61. Harriss DR, Graham TR, Galea M, Salama FD. Paraoesophageal hiatal hernias: when to operate. J R Coll Surg Edinb 1992; 37:97-98. 62. Sihvo EI, Salo JA, Rasanen JV, Rantanen TK (2009) Fatal complications of adult paraesophageal hernia: a populationbased study. J Thorac Cardiovasc Surg 137:419-424. 63. Polomsky M, Jones CE, Sepesi B, O’Connor M, Matousek A, Hu R, Raymond DP, Litle VR, Watson TJ, Peters JH (2010) Should elective repair of intrathoracic stomach be encouraged? J Gastrointest Surg 14:203-210. 64. Bawahab M, Mitchell P, Church N, Debru E. Management of acute paraesophageal hernia. Surg Endosc 2009; 23:255-259. 65. Allen MS, Trastek VF, Deschamps C, Pairolero PC. Intrathoracic stomach. Presentation and results of operation. J Thorac Cardiovasc Surg 1993; 105:253-258; discussion 258-259. 66. Hallissey MT, Ratliff DA, Temple JG. Paraoesophageal hiatus hernia: surgery for all ages. Ann R Coll Surg Engl 1992; 74:23-25. 67. Pitcher DE, Curet MJ, Martin DT, Vogt DM, Mason J, Zucker KA. Successful laparoscopic repair of paraesophageal hernia. Arch Surg 1995; 130:590-596.
48. Chang EY, Morris CD, Seltman AK, O’Rourke RW, Chan BK, Hunter JG et al. The effect of antireflux surgery on esophageal carcinogenesis in patients with Barrett esophagus. Ann Surg 2007;246:11-21.
68. Gantert WA, Patti MG, Arcerito M, Feo C, Stewart L, DePinto M, Bhoyrul S, Rangel S, Tyrrell D, Fujino Y, Mulvihill SJ, Way LW. Laparoscopic repair of paraesophageal hiatal hernias. J Am Coll Surg 1998; 186:428-432; discussion 432-423.
49. Bammer T, Hinder RA, Klaus A, Trastek VF, Achem SR. Rationale for Surgical Therapy of Barrett’s Esophagus. Mayo Clin Proc 2001; 76:335-42.
69. Awais O, Luketich JD. Management of giant paraesophageal hernia. Minerva Chir 2009; 64:159-168.
50. Corey KE, Schmitz SM, Shaheen NJ. Does a Surgical Antireflux Procedure Decrease the Incidence of Esophageal Adenocarcinoma in Barrett’s Esophagus? A Meta-Analysis. Am J Gastroenterol 2003;98: 2390-4. 51. Altorki NK, Yankelevitz D, Skinner DB. Massive hiatal hernias: the anatomic basis of repair. J Thorac Cardiovasc Surg 1998; 115: 828–835 52. Andujar JJ, Papasavas PK, Birdas T, Robke J, Raftopoulos Y, Gagne DJ, Caushaj PF, Landreneau RJ, Keenan RJ. Laparoscopic repair of large paraesophageal hernia is associated with a low incidence of recurrence and reoperation. Surg Endosc 2004; 18: 444–447. 53. Barrett NR. Hiatus hernia: a review of some controversial points. Br J Surg 1954; 42:231-243. 54. Kavic SM, Segan RD, George IM, Turner PL, Roth JS, Park A. Classification of hiatal hernias using dynamic threedimensional reconstruction. Surg Innov 2006; 13:49-52 55. Hutter MM, Rattner DW. Paraesophageal and other complex diaphragmatic hernias. In: Yeo CJ (ed) Shackelford’s Surgery of the Alimentary Tract Saunders Elsevier, Philadelphia, 2007. pp 549-562. 56. Landreneau RJ, Del Pino M, Santos R. Management of paraesophageal hernias. Surg Clin North Am 2005; 85:411-432. 57. Treacy PJ, Jamieson GG. An approach to the management of para-oesophageal hiatus hernias. Aust N Z J Surg 1987; 57:813-817. 58. Stylopoulos N, Gazelle GS, Rattner DW (2002) Paraesophageal hernias: operation or observation? Ann Surg 236:492-500; discussion 500-491.
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70. Belsey R. Functional disease of the esophagus. J Thorac Cardiovasc Surg. 1966;52:164-88. 71. Ancona E, Peracchia A, Zaninotto G, Rossi M, Bonavina L, Segalin A. Heller laparoscopic cardiomyotomy with antireflux anterior fundoplication (Dor) in the treatment of esophageal achalasia. Surg Endosc. 1993;7:459-61. 72. Watson DI, Jamieson GG, Pike GK, Davies N, Richardson M, Devitt PG. Prospective randomized double-blind trial between laparoscopic Nissen fundoplication and anterior partial fundoplication. Br J Surg. 1999; 86:123-30. 73. Donahue PE, Samelson S, Nyhus LM, Bombeck CT. The floppy Nissen fundoplication. Effective long-term control of pathologic reflux. Arch Surg. 1985;120:663-8. 74. Nicholson DA, Nohl-Oser HC. Hiatus hernia: a comparison between two methods of fundoplication by evaluation of the long-term results. J Thorac Cardiovasc Surg. 1976;72:938-43. 75. Pozo F, Giganto F, Rodrigo L. Clinical efficacy of the Toupet technique performed by laparoscopic surgery. Medium-term follow-up in 122 cases. Surg Endosc. 2001;15:1171-4. 76. Walker SJ, Holt S, Sanderson CJ, Stoddard CJ. Comparison of Nissen total and Lind partial transabdominal fundoplication in the treatment of gastro-oesophageal reflux. Br J Surg. 1992;79:410-4. 77. Moores D, Hill LD. Open repair of hiatus hernia: abdominal approach. Chest Surg Clin N Am. 1998;8:411-29. 78. Maxwell-Armstrong CA, Steele RJ, Amar SS, Evans D, Morris DL, Foster GE, Hardcastle JD. Long-term results of the Angelchik prosthesis for gastro-oesophageal reflux. Br J Surg. 1997;84:862-4. Northeast Florida Medicine Vol. 62, No. 1 2011 21
Endoscopic Management of Gastroesophageal Reflux Disease Samir Lewiz Habashi, MD Editorâ€™s Note: To ensure reproduction quality, the author has agreed to post the graphics in this article online at dcmsonline.org.
Abstract: Gastroesophageal reflux disease (GERD) is a common
disorder that can cause life threatening complications if not properly treated. Medical treatment by Proton Pump Inhibitors (PPIs) is effective in most of the patients.Unfortunately, the treatment is lifelong and is not without complications. Other treatment options include surgery and endoscopic treatment. The aim of this article is to review the endoscopic treatment modalities available at the present time. It also provides the data available regarding the efficacy, safety and durability of such techniques.
Gastroesophageal reflux disease (GERD) is a prevalent disease in society that often requires long-term medical treatment or surgery. The prevalence of heartburn and/or acid regurgitation experienced at least weekly by sufferers was 19.8 per 1001 The current therapy for GERD begins with lifestyle modification and medical treatment, mainly PPIs. Such regimen is effective in the majority of patients. However, treatment must be maintained for a long time because of a high relapse rate after cessation of the medications. Also, long term treatment is associated with increased cost, decreased compliance and also more reports of the side effects of PPI s (i.e. pneumonia, osteoporosis and C-diff associated colitis).2
Surgical Treatment of GERD
Patients who want to avoid long-term therapy may consider surgical treatment. The most common surgical procedure is Nissen Fundoplication that can be performed either by open surgery or laparoscopically. Such surgery requires anesthesia. It has a mortality of 0.2% and can be associated with dysphagia, gas-bloat syndrome and increased flatus.3 Recently, minimally invasive endoscopic procedures are used as an alternative to surgical intervention and also for patients who have failed surgical treatments.
Endoscopic Treatment for GERD
Endoscopic Treatment for GERD is considered an option for those patients who do not want to be on longterm antisecretory medications and they do not consider surgical intervention as an option. Such procedures include: 1. Delivery of radiofrequency (RF) energy to the lower esophageal sphincter (LES) and the cardia (Stretta; Curon Medical, Inc., Sunnyvale, CA, USA) 2. Creation of gastroplications (Bard EndoCinch suturing Address Correspondence to: Samir Lewiz Habashi, MD, Assistant Professor of Medicine, Division of Gastroenterology, University of Florida, Jacksonville. Email: firstname.lastname@example.org.
22 Vol. 62, No. 1 2011 Northeast Florida Medicine
system; C.R. Bard, Inc., Murray Hill, NJ, USA) 3. Injection of filler materials into cardia (enteryx). (This procedure was voluntarily recalled in 2005 because of increased risk of bleeding, fistula formation and even death.) 4,5 Stretta Procedure The Stretta Procedure is most commonly performed on an outpatient basis with either moderate sedation or general anesthesia. The mechanism of action for this procedure is delivery of RF energy into tissue which causes a circumferential coagulative necrosis that will heal with fibrosis. This may increase the Lower Esophageal Sphincter (LES) pressure and strengthen its antireflux barrier. The Stretta catheter is formed of a bougie-tip, a balloonbasket assembly, and four electrode delivery sheaths positioned radially around the balloon. (Figure 1, dcmsonline.org) The catheter is placed transorally over a guidewire and positioned 1 cm above the Gastroesophageal (GE) junction. The balloon is then inflated to a low pressure and 4-nickel titanium needles are deployed. Temperature-controlled levels of RF energy are delivered to each electrode placed in the submucosa while the overlying mucosa is cooled with irrigation. The target tissue temperature is 85 degree Celsius (Figure 2, dcmsonline.org). On average, 56 lesions are created in the region from 1 cm above to 2 cm below the GE junction (Figure 3, dcmsonline.org). When the lesion heals, the barrier function of the LES is restored (Figure 4, dcmsonline. org). Contraindications are: 1. 2. 3. 4. 5. 6.
Pregnant women Subjects under the age of 18 Patients without the diagnosis of GERD Hiatal hernia > 2 cm Achalasia Poor surgical candidates6
Complications are rare, but the following transient complications may occur: bleeding, chest pain, difficulty belching, dysphagia, epigastric discomfort and fever. Other rare complications include: injury to esophageal mucosa, perforation, pharyngitis, vomiting or bloating. Noar et al reported the sustained improvement in symptoms of GERD and antisecretory drug use after 4-year follow-up of the Stretta procedure. The study was a prospective case series on intent-to-treat basis. Patients included were GERD patients with persistent symptoms despite twice-daily proton pump inhibitor (PPI) medications. The patients were diagnosed by the presence of endoscopically evidenced esophagitis or abnormal esophageal pH testing. Symptom assessment was performed with a validated health-related quality-of-life
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questionnaire (with and without medication) at baseline and 6, 12, 24, 36, and 48 months after treatment. Complications of the procedure and medication usage were analyzed. Main outcome measurements included significant changes in symptom scores, GERD quality-of-life parameters, and medication usage on the basis of clinical outcomes.6 Results have been recorded in 109 consecutive patients who were treated with the Stretta Procedure that had reached a 4-year follow-up. Complete long-term follow-up assessment was available in matched data for 109 patients at 12 months, 108 patients at 24 months, 102 patients at 36 months, and 96 patients at 48 months. A second procedure was performed in 13 patients. Heartburn scores decreased from 3.6 to 1.18 (P < .001), total heartburn score (GERD health-related quality-of-life questionnaire) decreased from 27.8 to 7.1 (P < .001), and patient satisfaction improved from 1.4 to 3.8 (P < .001). Medication usage decreased significantly from 100% of patients on twice-daily PPI therapy at baseline to 75% of patients showing elimination of medications or only as-needed use of antacids/over-the-counter PPIs at 48 months (P < 0.005). There were no serious complications of the procedure.6 This study in drug-refractory patients with GERD found the Stretta procedure to be a safe, effective, and durable treatment that produced significant improvements in heartburn and quality of life and decreased medication usage during a 4-year period of follow-up. Only one treatment session is sufficient to improve the LES pressure and barrier function. However, a recent study done by Aziz et al showed that a double dose Stretta procedure significantly reduced the use of PPI medications, improved the GERD health related quality of life (GERD HRQL) and the grade of esophagitis compared to a single Stretta procedure. It also has a more significant normalization of the HRQL scores compared to the single Stretta.7 Regarding the role of Stretta after acid reflux surgery, McClusky found that the Stretta procedure significantly reduces subjective symptoms of GERD. It may serve as an additional management strategy for recurrent GERD symptoms after acid reflux surgery.8
First developed in the 1980s, endoscopic gastropliction allows endoscopic placement of sutures in the gastric cardia, thereby augmenting the barrier function of the GE junction. The most common Brand is Bard EndoCinch. (Figure 5, dcmsonline.org) The mechanism of placement is the EndoClinch system (Figure 6, dcmsonline.org) This system has a sewing capsule that is attached to the distal end of the gastroscope. The capsule has a hollow chamber through which the esophageal tissue is suctioned. A handle mounted to the biopsy port of the gastroscope then drives a hollow core needle containing the suture material through the tissue to create a suture through the submucosa. A second gastroscope should be applied to fasten the ends of the suture together.9
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The Filipi et al study was published in Gastrointest Endosc in 2001. The study was prospective and multi-center. Sixty-four patients with symptomatic GERD were enrolled. Patients were randomized to two stitch configurations. Post procedure visits were at 1, 3 & 6 months. The study showed that the device is safe and effective. At least 73% of patients had improvement in HRQL score, 75% had reduction in multiple meds or daily PPIs, 90% have no or mild regurgitation, 87% experienced an improvement or maintenance of esophagitis. There was no significant effect on pH and manometry and there was a significant decrease in number of reflux episodes.9 Schiefke et al studied the long term failure of endoscopic gastroplication (EndoCinch). A total of 70 patients treated with EndoCinch at a single referral center were studied prospectively. All patients were interviewed using a standardized questionnaire regarding their symptoms and medication prior to and 18 months after EndoCinch. In addition, follow up included endoscopy, 24-hour pH monitoring, and esophageal manometry.The procedure was well tolerated without major short or long term complications. Eighteen months after EndoCinch, 56/70 patients (80%) were considered treatment failures as their heartburn symptoms did not improve or proton pump inhibitor medication exceeded 50% of the initial dose. Endoscopy showed all sutures in situ in 12/70 (17%) patients while no remaining sutures could be detected in 18/70 (26%). In 54 and 50 patients examined, respectively, no significant changes in 24 hour pH monitoring (median pH <4/24 hours, 9.1% v 8.5%; p=0.82) or lower esophageal sphincter (LOS) pressure (7.7 v 10.3 mm Hg; p=0.051) were observed while median LOS length slightly increased (3.0 to 3.2 cm; p<0.05).10 The conclusion was that endoscopic gastroplication (EndoCinch) is a safe and minimally invasive endoscopic treatment for GERD with reasonable short term results. In contrast, long term outcome is disappointing, probably due to suture loss in the majority of patients. Therefore, technical improvements to ensure suture durability are mandatory before endoscopic suturing can evolve as a therapeutic option for GERD treatment.10
Endoscopic treatment for GERD patients is considered an option for those who do not want to be on longterm antisecretory medications and the patients do not consider surgical intervention as an option. Currently, the Stretta Procedure is a safe and effective minimally invasive procedure that provides a sustained longterm efficacy. Studies are currently being conducted to improve the long term efficacy of the gastroplication technique.
Locke GR 3rd, Talley NJ, Fett SL, et al. Prevalence and clinical spectrum of gastroesophageal reflux: a population-based study in Olmsted County, Minnesota. Gastroenterology. May 1997; 112(5):1448-56.
Kim Jw, Lee KL, Jeong JB, Kim BG, Shin S, Kim JS, Jung HC, Song IS. Proton pump inhibitors as a risk factor for
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recurrence of Clostridium-difficile – associated diarrhea. World J Gastroenterol. 2010 Jul 28;16(28):3753-7. 3.
Rantanen TK, Oksala NK, Oksala AK, Salo JA , Sihvo EL. Complications in antireflux surgery : national-based analysis of laparoscopic and open fundoplications. Arch Surg. 2008 Apr;143(4):359-65.
Schumacher B, Neuhaus H, Ortner M, Laugier R, Benson M, Boyer J, Ponchon T, Hagenmylluer F, Grimand JC, Rampal P, Rey JF, Fuchs KH, Allgaier HP, Hochberger J, Stein HJ, Armengol AR, Siersema PD, Deviere J: Reduced medication dependency and improved symptoms and quality of life 12 months after Enteryx implantation for gastroesophageal reflux. J Clin Gastroenerol 2005;39:212–219.
Wong RF, Davis TV, Petersen KA: Complications involving the mediastinum after injection of Enteryx for GERD. Gastrointest Endosc 2005;61:753–756.
Noar MD and Lofti-Emran S. Sustained improvement in symptoms of GERD and antisecretory drug use: 4-year follow-up of the Stretta procedure. Gastrointest Endosc 2007; 65: 367–372.
Aziz AM, El-Khayat HR, Sadek A et al. A prospective randomized trial of sham, single-dose Stretta, and double-dose Stretta for the treatment of gastroesophageal reflux disease. Surg Endosc 2010; 24(4):818-25.
McClusky DA 3rd, Khaitan L, Swafford VA, Smith CD. Radiofrequency energy delivery to the lower esophageal sphincter (Stretta procedure) in patients with recurrent reflux after antireflux surgery: can surgery be avoided? Surg Endosc. 2007 Jul;21(7):1207-11.
Filipi CJ, Lehman GA, Rothstein RI et al. Transoral, flexible endoscopic suturing for treatment of GERD: a multicenter trial.Gastrointest Endosc 2001; 53(4):416-22.
10. Schiefke I, Soeder H, Zabel-Langhennig A, et al. Endoluminal gastroplication: what are the predictors of outcome? Scand J Gastroenterol 2004; 39:1296–303.
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Malcolm Foster, Jr., MD, DCMS President
Peter W. Carmel, MD,
our national champion on many levels, is currently President-Elect of the American Medical Association. Dr. Carmel will become AMA President in June, 2011. A Pediatric Neurosurgeon from Newark, NJ, Dr. Carmel practices at the University Hospital of the New Jersey Medical School, and is chair of the school’s Neurological Surgery Department, and comedical director of the Neurological Institute of New Jersey. A long-time advocate of organized medicine, Dr. Carmel served on the AMA Board of Trustees for eight years, and in the AMA House of Delegates for 24 years. He chaired the AMA Council on Long Range Planning and Development, actively advocating for international medical graduates and proportional representation for specialty medical society members. Dr. Carmel is committed to neurological research, and served as chair of the National Coalition for Research in Neurological Disease and Stroke, and later as chair of the National Foundation for Brain Research. He has also served on the board of directors for the National Patient Safety Foundation. Dr. Carmel and his wife, Jacqueline Bello, MD, a neuroradiologist, live in Manhattan, NY. We are pleased to welcome Dr. Carmel to Jacksonville!
Join us for an evening with our national, state and local champions of medicine
with our guest speaker,
Peter W. Carmel, MD
President-Elect American Medical Association Monday, May 9, 2011
Reception – 6:15 PM Speaker & Dinner – 7:00 PM
Epping Forest Yacht Club 1830 Epping Forest Drive Jacksonville, Florida 32217
$60 per person Please RSVP by May 2
Cancellations received after this date cannot be refunded.
Watch for your invitation and details on www.dcmsonline.org
Northeast Florida Medicine
Vol. 62, No. 1 2011
158th DCMS Annual Meeting a Success The 158th DCMS Annual Meeting, December 1, 2010, was a success, with many members attending and a full Exhibit Hall area featuring vendors displaying their products and services. (see list, below) In addition, there were Scientific Poster Presentations. Below are some Annual Meeting photos. Refer to the full Annual Meeting story and more photos on p.40. Nova SE University PA Program Platinum Sponsor Pfizer, Inc. Professional Medical Insurance Svcs. FPIC ZymoGenetics
2010 DCMS Foundation Donations Dr. Janet Betchkal Dr. Ulises Caraballo Dr. Loren Clayman Dr. James Clower Dr. Robert Duncan Dr. Joe Ebbinghouse Dr. Enio Fontanelli Dr. Walter Gilbert Dr. J. Eugene Glenn Dr. Anthony Godboldt Dr. Marla Golden Dr. Eugene Griffin Dr. P. Vernon Jones Dr. Daniel Lestage Dr. Alan Marks Dr. Marianne McEuen Dr. Russell Metz Dr. Kay Mitchell Dr. H. Lynn Norman Dr. Francis Ong Dr. Charles Perniciaro Dr. Chalermchai Punya Dr. Mary Robinson Dr. Frank Schiavone Dr. Guy Selander Dr. Leonard Shvartzman Dr. N.H. Tucker
Associated Medical Office Experts, LLC Akerman Senterfitt Baptist Health Baptist Home Health Care/Baptist Blue Cross Blue Shield of Florida Infusion Therapy Community Hospice of NE Florida Live Well Networks, LLC Beson 4 Media Group Signet Diagnostic Imaging Services Cardinal Health SunTrust Bank Clinet University of Florida College of DrFirst, Inc. Medicine/Jacksonville Heartland Rehabilitation Heritage Publishing, Inc. Silver Sponsors Jacksonville Sports Medicine Program Morgan Stanley Smith Barney Alliance Solutions Group/Sage North Florida Builders Health Ray Howard & Associates Amedisys Home Health RS & H Apex Home Healthcare US Navy Medical Recruiting Baline MD We Care Jacksonville Brooks Rehabilitation Millennium Laboratories
Thank You for Your Support!
(Right) DCMS President-Elect Dr. Ashley Booth Norse and her husband, Ronald (Below, L to R) Photo 1: (L to R) FMA President Dr. Madelyn Butler (a former student of Dr. Fosterâ€™s) and DCMS President Dr. Malcolm Foster, Jr. Photo 2: (L to R) Clyde M. Collins, MD, Humanitarian Award recipient Dr. John Lovejoy, Jr. with Dr. John W. Kilkenny III, now DCMS Immediate Past President. Photo 3: (L to R) Dr. Kilkenny and the DCMS Community Service Award recipient Dr. Jeffrey Goldhagen, MD, MPH.
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26th Annual Good ‘Ole Time’ Reunion DCMS Members who practiced during the “Golden Age” of Medicine in Jacksonville (prior to 1970)
Sixty-five physicians and spouses gathered Sunday, February 13, 2011 at the Timuquana Country Club for the 26th Annual DCMS Good ‘Ole Time’ Reunion. Around every table were smiling faces of friends from past days reconnecting and reminiscing. Four DCMS Past Presidents attended. (Left above, L to R) Dr. George S. Trotter (1994); Dr. C. Ted Montgomery (1989); Dr. J. Eugene Glenn (1993); and Dr. Faris S. Monsour (1981). Also in attendance were five DCMS Auxiliary/Alliance Past Presidents. (Right, above, L to R) Mrs. Kathy Harris (2006); Mrs. Jerry Ferguson (1971); Mrs. Ruth Glenn (1981); Mrs. Paula Beale (1953); and Mrs. Margaret Ludwig (1959).
Read in the DCMS History Book how these physicians and others shaped medicine in Duval County for 158 years - Coming early 2012 Contact Mr. John Compton, Publisher, if you want to be a part of this publication by recounting your years in medicine or your practice’s history. Call 904-355-6561 x110 or email firstname.lastname@example.org. Insert
Northeast Florida Medicine
Vol. 62, No. 1 2011
Trends in Public Health
GERD and Obesity in Duval County Niketa Walawalkar, Thomas Bryant III, MSW and Robert G. Harmon, MD, MPH GERD or reflux disease is one of the most common gastric diseases. The prevalence of GERD is estimated to range from 8% to 26% in the general adult population based on surveys. In Jacksonville, GERD caused 783 emergency room and 708 hospital ambulatory care visits during 2009. Many studies have supported the association between weight gain and GERD. A large population-based case-control study published in 2003 JAMA found that excessive weight gain [greater than 3.5 body mass index (BMI) units] was associated with a 3-fold increased risk of developing reflux symptoms, and an incremental increase in symptoms related to an increase in BMI. People with higher BMIs were also found to have higher hospitalization rates for reflux related codes compared to people with normal weight. It has been estimated that half of all American adults will be obese by 2025. Florida is currently ranked 20th in the USA for prevalence of obesity, with about 26% of adults being obese. According to the CDC, during 1998-2000 the national cost of obesity-driven medical expenditures was more than $75 billion, with Florida alone spending ~$3.5 billion. In 2007, ~62% of adults in Jacksonville were either overweight or obese, a considerable rise from 57% in 2002. According to the 2009 Youth Risk Behavior Survey (YRBS), ~30% of high school students in Jacksonville were either overweight or obese. Men in Jacksonville were 13% more likely to be overweight than women, whereas women were 6% more obese than men. Obese women were found to be at higher risk of developing GERD symptoms compared to obese men, suggesting that estrogen might play a role in modulating the relationship between obesity and GERD. Though various researchers have reached conclusions for and against this theory, all demonstrated a significant positive association between obesity and GERD, irrespective of gender. According to a study published in the New England Journal of Medicine, this association is a dose-response relationship and GERD symptoms are found to occur even in individuals who gain weight but continue to have a BMI in the normal range. Thus, not only the obese and overweight, but also near overweight individuals are at risk of GERD. In Jacksonville, 38% of blacks increased body weight by five pounds in 2007, as compared to 20% of whites. Studies showed that abdominal obesity or an increase in waist circumference was more closely linked to reflux symptoms independent of BMI.
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Unhealthy diet and lack of exercise contribute to overweight and obesity. The USDA recommends consuming five fruits and vegetables a day. According to the 2007 BRFSS, 23.9% of Jacksonville adults consumed the recommended amount compared to 26.2% in Florida and 24.4% in the U.S. Jacksonville females were more likely to follow the recommendation than males. In 2009, about 82% of high-school students did not eat the recommended amount of fruits and vegetables. The CDC recommends 150 minutes of moderate activity weekly for the average adult. In Jacksonville, only 32% of residents met moderate physical activity recommendations while 23.5% of adults were sedentary compared to 25.4% of adults in Florida and 22.6%
Find CME on the Website Looking for the Post Test for the CME article in this issue or for other CME courses to complete? Go to the DCMS website at www. dcmsonline.org. Click “NEFM”,“Current Issue”, and then “Table of Contents”. The current CME article is listed there (with a Post Test link)... ...OR click “CME Articles” under “NEFM” and see a list of all the CME articles still available for credit.
See the digital version of the journal! (follow directions above)
Prevention of Medical Errors: Empowered to Make a Difference
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: Empowered to Make a Difference” authored by Constance K. Haan, MD, MS (see pp. 27-30), which has been approved for 2.0 AMA PRA Category 1 credit(s).™ For a full description of CME requirements for Florida physicians (MD/DO), please visit the DCMS website (http://www.dcmsonline. org/cme_requirements.aspx).
Faculty/Credentials: Constance K. Haan, MD, MS, is a Professor, Department of Surgery, University of Florida College of Medicine (UFCM) in Jacksonville, FL, Senior Associate Dean for Educational Affairs at UFCM in Jacksonville and Designated Institutional Official for UFCM in Jacksonville. Dr. Haan received her MD degree from the University of South Dakota School of Medicine and did residencies in surgery and thoracic surgery and fellowships in cardiothoracic surgery research and adult cardiac surgery. Her MS degree is in Evaluative Clinical Sciences from Dartmouth College of Arts and Sciences, Center for the Evaluative Clinical Sciences. Objectives for CME Journal Article 1. Identify and describe the significance and types of medical errors in healthcare delivery 2. Describe the National Patient Safety Goals and the implementation aspects of each 3. Identify and discuss individual and team tools and approaches to prevention of medial errors
Date of Release: March 4, 2011 Date Credit Expires: March 4, 2013 Estimated time to complete: 1 hr.
Methods of Physician Participation in the Learning Process
1. Read the “Prevention of Medical Errors: Empowered to Make a Difference” article on pages 27-30 2. Complete the Post Test and Evaluation on page 26 3. Fax the Post Test and Evaluation to DCMS (FAX) 904-353-5848 OR members can also go to www.dcmsonline.org & submit test online
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 one year to submit the post test and earn CME credit. A certificate of credit/completion will be emailed, faxed or USPS mailed within 4-6 weeks of submission. If you have any questions, please contact the DCMS at 355-6561, ext. 103, or email@example.com.
Faculty Disclosure Information
Dr. Haan 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.
www . DCMS online . org
Northeast Florida Medicine Vol. 62, No. 1 2011 25
Prevention of Medical Errors: Empowered to Make a Difference CME Questions & Answers (Circle Correct Answer) /Free-DCMS Members/$50.00 charge non-members*
(Return by March 4, 2013 by FAX: 904-353-5848, by mail: 555 Bishopgate Lane, Jacksonville, FL 32204 OR online: www.dcmsonline.org) 1. What is the #1 root cause of death or disability due to clinical error? a. Orientation, training b. Competency, credentialing c. Care planning d. Communications e. Staffing 2. What are common reasons or contributing factors for clinical error? a. Incomplete information b. Environmental factors c. Miscommunication d. Complexity e. All of the above 3. What procedure(s) require(s) employing the Universal Protocol i.e. a time-out, when not performed emergently? a. Thoracentesis b. Foley catheter placement c. Nasogastric tube insertion d. Peripheral IV e. All of the above 4. Which of the clinical areas below is not one of the top five for misdiagnosis in the past biennium in Florida? a. Cardiac condition b. Pregnancy/stage of pregnancy prior to treatment or surgery c. Stroke or neurologic condition d. Cancer e. Acute abdomen 5. What of the following is/are key to improving clinical communication? a. Avoiding banned abbreviations b. Correct use of leading & trailing zeros with decimal point c. Read-back of verbal order & critical results d. Legible order writing e. All of the above
6. When is medication reconciliation important to patient safety? a. At admission to inpatient setting b. At discharge from inpatient setting c. At outpatient visit d. At transfer to another facility e. All of the above 7. What is the most important activity you can do to decrease your patient’s risk of hospital-acquired infections? a. Stay home when you are sick b. Wash your hands c. Use sterile technique d. Order the correct prophylactic antibiotic (PA) e. Discontinue PA within 24 hours of surgery 8. Which of the following cannot be used as a patient identifier? a. Name b. Age c. Medical record number d. Room number e. b and d 9. How can the authority gradient contribute to error or allow error to reach the patient? a. Reluctance to admit a mistake b. Bullying and intimidation c. Reluctance to speak up to challenge a team member on an error d. Awe of the pedestal e. All of the above 10. What is your response when questioned about safe practice or challenged about decision-making? a. “When you have MD behind your name, you can tell me what to do.” b. “Thanks for bringing that to my attention. I appreciate you helping me ensure patient safety. Let’s look to see if we’ve got it right.” c. “I’m much too busy to explain why I’m right and you’re wrong.” d. “You obviously need to read more about this matter.” e. Ignore the comment and the individual, and they’ll probably let it go.”
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:______________________________________________________________________________________ ____________________________________________________________________________________________ Name (Print)___________________________________________Email_____________________________________ Address/City/State/Zip_____________________________________________________________________________ Phone__________________________Fax_____________________DCMS Member (circle) YES NO *Non-Member Charge ($50.00) - See payment options below Credit card: Visa MasterCard American Express Discover Account #___________________________________Expiration date:_______________________________________ Signature_______________________________________________________________________________________ 26 Vol. 62, No. 1 2011 Northeast Florida Medicine
www . DCMS online . org
Prevention of Medical Errors: Empowered to Make a Difference Constance K. Haan, MD, MS Abstract: Understanding the nature of medical errors, the root causes and contributing factors in healthcare delivery systems lays the foundation for prevention of errors. However, knowing is not enough. Providers must actively strive to narrow the gap between what we know and what we do. This article opens with review of the frequency and impact of medical error, followed by a review of the types of error and their root causes. The National Patient Safety Goals (NPSGs) provide fundamental principles for reduction of error. With focus on systems of care, rather than individual provider knowledge, skill or judgment, this article presents strategies and approaches for providers to actively lead in system safety and prevention of error. Key points for providers to implement, beyond adherence to the NPSGs, are to 1) anticipate opportunities for error, and intervene; 2) encourage a team approach with attention to a culture of safety, with team members encouraged to speak up or challenge if they see something unsafe; and 3) work on system errors together to address system issues, and disseminate the learning. The final take-away is for providers to be physician leaders in changing the culture of healthcare delivery to one of recognizing how frequently and easily errors and harm can occur. They need to encourage the care team to be vigilant for error and to speak up and advocate for safety.
You have just called 9-1-1, and you or someone close to you, are about to enter the healthcare system for urgently needed care. How do you feel? Confident? Relieved? Or are you apprehensive, anxious and even fearful? An acute change in one’s health is cause enough for anxiety, but for many, the event of entering the healthcare system as a customer or patient is not accompanied by a sense of, “Oh, thank goodness, they’re here for me; now everything will be alright.” Medical errors are not the rare fluke or aberrancy that many in healthcare would like to believe. Rather, error, and injury or death from error, is a clear and present danger. Safety in healthcare is not a matter a luck, but of careful and thoughtful planning and execution of systems. To that end, and because our patients would like to assume we’re attending to safety (which is why they evaluate us on our courtesy and respect), this article will lay out a systematic manner of considering errors and safety and suggest tools and methods that empower the clinician/physician to be a leader of and advocate for system improvement for high-quality, safe care.
When the Institute of Medicine (IOM) published its landmark report, To Err is Human, up to 98,000 deaths and more than 1 million injuries each year occurred in the United States due to medical errors.1 This seminal work triggered a wide range of responses and initiatives to address patient safety in healthcare on the national, regional, and local levels. In November 2010, after ten years of patient safety improvement endeavors, Landrigan, Sharek and colleagues, reported Address Correspondence to: Constance K. Haan, MD, MS, University of Florida College of Medicine – Jacksonville, Jacksonville, FL. Email: firstname.lastname@example.org. www . DCMS online . org
in the New England Journal of Medicine a study designed to look at the impact made on reducing medical errors with change in rates of harm. In a study of ten randomly selected hospitals in North Carolina from 2002 through 2007, they found evidence of 588 harms among 2341 admissions; 25.1 harms per 100 admissions, with 95% confidence interval of 23.1-27.2. The authors found no significant changes in the overall rate of harms per 1000 patient-days or the rate of preventable harm.2 As scientists, we like to work, research and analyze to a high degree of accuracy and precision, and we often frame our discussions of occurrences in the context of reference to a denominator or to statistical significance. Yet if 99.9% were “good enough,” then in terms of delivery of care and errors, there would be 500 wrong operations performed per week, and 12 babies given to the wrong parents per day.3,4 Moreover, from a patient’s point of view, or that of a family member or caregiver, absence of statistical significance is not reassuring to their experience of needs met against expectations.
Nature of Unsafe Healthcare
Errors in delivery of healthcare may be in the form of commission or omission, and of the commission types, either error in planning or error in execution or action. Errors may be due to individual error—lack of knowledge, skill, and/or judgment. Alternatively, errors may be systems errors or issues—related to characteristics of the system in which the individual is working to deliver care. This article will focus on system errors and issues. To better understand the nature of medical errors, we must look at the types of error that occur and the underlying root cause of errors, especially those that have resulted in harm to the patient. One source of data in healthcare on medical errors comes at the national aggregate level from the reporting of a sentinel event: an unexpected occurrence involving death or serious physical or psychological injury, or the risk thereof, where serious injury specifically includes loss of limb or function.5 The Joint Commission has studied and reported on sentinel events and their root causes for years, and the types of error and their frequency for 2008 and 2009 are displayed in Table 1 (page 28) as derived and modified from Joint Commission online sources.6,7 Of particular concern is that the data trends for several types of error show increase from 2008 to 2009, namely in wrong site surgery, operative or postoperative complication, delay in treatment, patient fall, and unintended retention of foreign body. The number one root cause of sentinel events has consistently been, and continues to be, communication.8 Other system errors at the root of errors and harm include: patient assessment, leadership, orientation/training, procedural compliance, environmental Northeast Florida Medicine Vol. 62, No. 1 2011 27
Table 1 Joint Commission Data Trends for Sentinel Events Types of errors Wrong site surgery Suicide Operative/postoperative complication Delay in treatment Medication error Patient fall Unintended retention of foreign body Perinatal death / loss of function Patient death or injury in restraints
Table 2 System Errors - A List of Root Causes of Sentinel Events
2008 116 102 63 82 46 60 71 32 13
2009 149 87 90 115 43 82 118 31 11
Patient identification process
and specifically the Board of Medicine, have been monitoring the areas of highest frequency of misdiagnosis for a number of years, and over the past biennium, the top five clinical areas for misdiagnosis are: cancer, cardiac condition, acute abdomen, postoperative complication, and pregnancy or stage of pregnancy prior to treatment or surgery.10
Patient observation procedures
Reasons for Unsafe Healthcare
Care planning process
Continuum of care
Orientation and training of staff
Competency assessment / credentialing
Supervision of staff
Communication with patient / family
Communication among staff members
Availability of information
Adequacy of technological support
Equipment maintenance / maintenance
Security systems and processes
Patient assessment process
Adapted from The Joint Commission Root Cause Analysis Matrix, at http://www.jointcommission.org/assets/1/18/se_root_cause_analysis_matrix.pdf.
safety, and availability of information, with a more complete listing found in Table 2.9 Another source of data on errors comes from the Florida Board of Medicine, which periodically looks at the data (closed claims and Agency for Health Care Administration reports) for trends in medical errors. The area of misdiagnosis is a particular concern in that there may be significant delay in determining that an error has even occurred, especially in the handing off of care from provider to provider, or organization to organization. Misdiagnosis may take several forms, including wrong diagnosis, missed diagnosis, delayed diagnosis, or missed complication(s). The Florida Department of Health, 28 Vol. 62, No. 1 2011 Northeast Florida Medicine
There are numerous contributing factors to medical error, especially in communication. Unclear written or verbal communication, incomplete information, and use of the same words but meaning different things all play a part. Moreover, there are the additional contributions to error from environmental factors, high complexity of care and of technology used in care delivery, as well as the ever-present authority gradient. Policies, protocols and checklists are important aids to safeguarding the patient from error and harm. Dr. James Reason has used Swiss cheese as the analogy for our serial layers and processes that are intended to ensure safety, but that may actually fail to prevent error and learn—due to the “holes in the cheese.” 11 Assumptions that may interfere with the layers to ensure safety include: 1) assumptions that error is rare; 2) the desire to trust, combined with the fear or intimidation or awe of the pedestal that prevents challenges; 3) assumption that one has all the information needed to make good decisions; and 4) the assumption that if one simply tries hard enough to do the right thing, all will be well.
Keys to Action
There are a number of things we can do as individual providers, and as physician leaders. They are simple, common sense principles, but need to be integrated and moved from what we know to what we do, thus narrowing the knowledge practice gap, as described by Don Berwick and the Institute for Healthcare Improvement. 12
Implement the National Patient Safety Goals – The first key to action in decreasing medical errors and improving patient safety is integration of the safety principles found in the NPSGs into the way we think and work. The fundamental principles are captured in the categories of NPSGs: identify patients correctly, improve staff communication, check patient www . DCMS online . org
medications and use medications safely, prevent infection, and identify patient safety risks.13,14 The Universal Protocol (note, this does not refer to the Universal Precautions for prevention of infection spread), commonly referred to as a “time-out,” is a particularly critical tool for prevention of wrong site, wrong patient, and wrong procedure. There are three principal components of the Universal Protocol - pre-procedure verification, site marking and a time-out. The Universal Protocol applies to procedures including those that are performed in the outpatient or ambulatory setting, such as a biopsy, lumbar puncture or thoracentesis.15 Proper identification of a patient and all information and specimens pertaining to that patient is performed with at least two patient identifiers. These must be identifiers that are consistently patient-specific identifiers, i.e., not age or room number, and ideally by two individuals. “The gall bladder in room 3” is not an acceptable identifier since neither the diagnosis nor room are consistently unique to an individual patient. In the clinic or in the hospital, proper use of at least two patient identifiers helps assure that the right patient gets the assessment (e.g., exam, laboratory tests), diagnosis (e.g., laboratory or radiology reports, pathologic specimen report), and treatment (e.g., medication or prescription, procedure, transfusion). Medication errors provide a major area for improvement with opiates, insulin, concentrated electrolytes and anticoagulants all posing high risk for patients. Moreover, the soundalike, look-alike drugs pose significant opportunity for error and the associated risk or harm. With the growing sites and complexity of healthcare delivery, it is imperative that medication reconciliation is performed and clearly communicated in the transfers or hand-offs across the continuum of care. Communication among providers and staff in the inpatient and outpatient settings must be conducted with efforts to minimize interruption and distraction, and to provide information in a consistent and standardized manner. Read-back of orders and critical results is imperative, but beneficial as applied more broadly, to reduce or correct miscommunication. Identification and prevention of safety risks includes attention to risk of suicide and of falls. Risk of healthcare-associated infection is another major area of risk and attention to hand hygiene and infection prevention is critical. Additionally, it is important for providers in all types of care settings to have a strategy for timely recognition of and response to deterioration in a patient’s condition. Anticipate opportunities for error and harm – Rather than assume that well-educated, highly skilled, hard-working, well-intentioned caregivers rarely make mistakes if they just try hard enough, we must acknowledge that opportunities for error and slips, and harm from error and slips, abound. Our default position must move from: “If you’re not sure it’s wrong, assume it’s right” to “If you’re not sure it’s right, assume it’s wrong.” Shift the focus to how error could occur www . DCMS online . org
in spite of good intentions and hard work, and in so doing, anticipate and identify the opportunity for error and harm, and intervene. Create a culture of safety – At the institutional and departmental levels, lead and encourage a culture of safety versus a culture of low expectations, or acceptance of “stuff happens.” A culture of safety is an atmosphere of mutual trust in which all staff members can talk freely about safety problems and how to solve them without fear of blame or punishment.16 Flatten the authority gradient – Within the clinical department and teams, identify and address the authority gradient. Whether it takes the form of bullying, reluctance to admit a mistake, or awe of the pedestal, the authority gradient can be a barrier to someone on the team being willing to speak up when an error or potential harm is identified. Flattening the authority gradient and setting the expectation for “if you see something, say something,” helps everyone on the team to take their role of accountability more seriously. Encourage empowerment among the clinical team at all levels of training and expertise. Don’t just accept, but encourage challenge. Setting this expectation among the team members sets the tone that all are focused on anticipating and looking out for opportunities for error. In so doing, all become advocates on the patient’s behalf for safety and increase the possibility for intervention to prevent error. Communicate clearly and challenge error – Clear communication among team members is critical, with increasing complexity, distractions and hand-offs. Checklists and standardized hand-off processes help assure and facilitate patient safety communication. Communicate as a multidisciplinary team, especially one that includes the patient and family, so that all know the plan of care. This serves to reinforce the patient-centered focus that Don Berwick has described as, “Nothing about me, without me.” Among the team, all are accountable, to watch out for and check on each other for focus, clarity and vigilance for error prevention. Work on system errors together – At the clinical service or department level, morbidity and mortality conferences can start the identification of system errors, but the process of addressing system errors or issues should not stop at the end of the conference. Discussion should only start there, with action plans for identifying how to proceed to engage the other key components of the system to work on issues and workarounds that have been identified as contributing to error and patient harm. Disseminate learning – Another key action is to work together as providers to analyze and reflect so as to learn from errors, and then disseminate and deploy lessons learned to share the safety improvements throughout the department, organization…and beyond, wherever possible. Learning from near misses should also be a priority, rather than waiting to pay attention to a system error or issue only after a patient has been harmed. Practice, practice, practice – The habits we cultivate determine those behaviors that become “automatic”, thus minimizing Northeast Florida Medicine Vol. 62, No. 1 2011 29
dependence on memory.17 Particularly under stress, we as humans default to the most entrenched practices and procedures; the things we “do without thinking” or “old habits.” It is therefore imperative to instill habits and practices that apply the principles of patient safety. Since we work as we train, it is imperative for individuals and teams to move beyond the education on safety and talking about safety to practicing safety-focused interactions and processes. Whether in a dedicated simulation environment, or in the day-to-day work and care environment, we must actively drill and practice the patterns and behaviors that set us up for minimizing errors and ensuring patient safety. Especially when developing a new team or a new procedure, it is critical to define roles and expectations for the team members, and then practice those roles and interactions so they become embedded. Be accountable – Each of us is personally accountable to speak up and challenge respectfully, yet persistently, to be sure we “get it right.” Each has the responsibility to listen to each other and to listen to the patient. Encourage questions and challenges. And perhaps one of the simplest, yet most overlooked actions is each individual has the responsibility for hand hygiene. It is low-tech and low-cost yet it is one of the most important things we can do to protect our patients from healthcare-associated infections.
Healthcare providers are knowledgeable, well-educated, skilled, hard-working, well-intentioned individuals. Yet, patients are at too high a risk for error and injury from error. In summary, there are fundamentals that we can do and we must do to keep our patients safe: • Acknowledge that opportunities for error and harm abound, look for them and anticipate them, to better identify and intervene. • Listen to each other and to the patient and patient’s family. Each may be acting to be a line of defense against error and potential harm. • Communicate….communicate…communicate! • Wash your hands! • Be accountable, as an individual and as a member of the healthcare delivery team. Take and maximize the opportunity to learn by learning from near-misses as well as errors. Closing the knowledge-practice gap, we can help move conversation, discussion, and analysis to action and behavior or practice pattern changes. We have before us a great opportunity to move the profession’s view of medical errors from one of focus on recognizing when an error has occurred and reporting it, to a focus on anticipating opportunity for error and speaking up and/or intervening to prevent it. Together we move forward.
Kohn LT, Corrigan JM, Donaldson MS, eds, for Institute of Medicine. To err is human: building a safer health system. Washington, DC: National Academies Press; 1999.
Landrigan CP, Parry GJ, Bones CB, Hackbarth AD, Goldmann DA, Sharek PJ. Temporal trends in rates of patient harm resulting from medical care. N Engl J Med 2010;363:2124-2134.
Lowstuter B. Is 99.9% good enough in healthcare? http:// www.leanhealthcareexchange.com/?p=123. Published May 14, 2008. Accessed December 3, 2010.
Quinley KM. 99.9% may not be good enough: beware of “statistical insignificance” defense. http://www.claims-portal. com/nlps/story.cfm?nlpage=557. Accessed December 3, 2010.
The Joint Commission. Sentinel events. http://www. jointcommission.org/assets/1/1/SE_chapter_july07.pdf. Accessed December 3, 2010.
The Joint Commission. Sentinel event trends reported by year. http://www.jointcommission.org/assets/1/18/se_stats_ trends_year.pdf. Accessed December 3, 2010.
The Joint Commission. Patient safety: updated sentinel event statistics. http://www.jointcommission.org/assets/1/18/ jconline_April_7_10.pdf. Accessed December 3, 2010.
The Joint Commission Center for Transforming Healthcare. Facts about hand-off communication. http://www. centerfortransforminghealthcare.org/projects/about_handoff_ communication.aspx. Accessed December 5, 2010.
The Joint Commission. Root cause analysis matrix. http:// www.jointcommission.org/assets/1/18/se_root_cause_ analysis_matrix.pdf. Accessed December 5, 2010.
10. Florida Department of Health. Continuing medical education. http://www.doh.state.fl.us/mqa/medical/me_ceu.html. Accessed November 29, 2010. 11. Reason J. Human Error. Cambridge, UK: Cambridge University Press; 1990. 12. Berwick DM. Case for improvement—the problem. http:// www.ihi.org/IHI/Topics/Improvement/caseforimprovement. htm. Accessed December 5, 2010. 13. The Joint Commission. Accreditation program: hospital – national patient safety goals. http://www.jointcommission. org/assets/1/18/July_2010_NPSGs_Scoring_HAP2.pdf. Accessed December 5, 2010. 14. The Joint Commission. 2010 Hospital National Patient Safety Goals. http://www.jointcommission.org/assets/1/18/ HAP_2010_NPSG.pdf. Accessed December 5, 2010. 15. The Joint Commission. Facts about the Universal Protocol 16. Institute for Healthcare Improvement. Patient safety-getting started. http://www.ihi.org/IHI/Topics/PatientSafety/ SafetyGeneral/. Accessed December 5, 2010. 17. Gosbee JW, Gosbee LL, eds. Using human factors engineering to improve patient safety: problem solving on the front line. 2nd ed. Oakbrook Terrace, IL: The Joint Commission; 2010.
Check out the DCMS website and the digital journal at www.dcmsonline.org 30 Vol. 62, No. 1 2011 Northeast Florida Medicine
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Impact of GERD on Common Pulmonary Diseases Abubakr A. Bajwa, MD, FCCP; Faisal Usman, MD; Vinny Samuel, MD; James D. Cury, MD and Adil Shujaat, MD, FCCP Abstract: The role of Gastro-Esophageal Reflux Disease (GERD), a
common disorder that is worsened due to a number of reasons, has been the subject of significant research in the pathogenesis, disease course, symptom control and outcomes of a variety of pulmonary diseases. On the other hand, GERD may be an important factor in the exacerbation and morbidity of certain pulmonary ailments, i.e., asthma, Chronic Obstructive Pulmonary Disease (COPD), pulmonary fibrosis, chronic cough and bronchiectasis. Proper diagnosis, lifestyle modification and treatment of GERD, may lead to better symptom control and improved quality of life for those struggling with pulmonary conditions. There is lack of definite evidence that this treatment will improve long term outcomes; yet strong evidence still supports treatment.
GERD is a common esophageal disorder in which the esophagus becomes irritated or inflamed because of acid and other gastric contents refluxing from the stomach. Almost 40% of the adult population of the United States have monthly symptoms and almost 10% of adults experience GERD weekly or daily. The stomach lining secretes large amounts of protective mucus which resists damage by acid. The lining of the esophagus gets damaged by the acid because of lack of this protective mechanism. Normally the lower esophageal sphincter prevents reflux of acid, however with GERD the lower esophageal sphincter is abnormally relaxed causing the mucosa of the esophagus to become damaged as the result of regurgitation of stomach contents and corrosive acid.1 The etiology of lower esophageal sphincter incompetence is difficult to delineate in humans. There are many different contributing factors that cause relaxation of the lower esophageal sphincter making reflux worse, some of which include: 1) Lifestyle (obesity, use of alcohol or cigarettes, poor posture); 2) Eating habits (eating large meals, eating before bedtime); 3) Diet (drinks with caffeine, acid foods, fatty and fried foods, chocolate, and spicy foods); 4) Medications (calcium channel blockers, antihistamines. theophyllines, and nitrates) and 5) Other medical conditions (hiatal hernia, pregnancy, diabetes, rapid weight gain).1
Pulmonary Complications of GERD
The potential of GERD to cause pulmonary complications is very under appreciated. Up to 10% of patients with GERD have pulmonary symptoms. The relationship between GERD and lung complications was suggested in 1962 by Dr. John Hines Kennedy when he described 25 patients with chronic bronchitis, bronchiectasis or pneumonia as the result of Address correspondence to: Abubakr A Bajwa MD FCCP, Pulmonary Critical Care and Sleep Medicine, University of Florida College of Medicine/Jacksonville, 655 W 8th street, Jacksonville, FL 32209. Email: email@example.com. www . DCMS online . org
silent GERD.1 Pulmonary complications of GERD can be severe and may be the only manifestation of GERD. If the relationship between the pulmonary problem and GERD is not recognized, then the pulmonary processes are likely to worsen. The different pulmonary diseases that may occur or have significant implications due to GERD are summarized in Table 1.GERD has an impact on some of the common pulmonary diseases encountered in day-to-day practice.
Table 1 Pulmonary Conditions Due to or Complicated by GERD 1. Chronic Cough 2. Asthma 3. Pulmonary Fibrosis (Idiopathic or Secondary) 4. Sleep Apnea 5. Chronic Obstructive Pulmonary Disease (COPD) 6. Aspiration Pneumonia 7. Lung Abscess 8. Bronchiectasis 9. Laryngitis Asthma and GERD – William Osler first described the relationship between asthma and GERD in 1892.2 According to a review of literature, 32% to 84% of patients with asthma have abnormal esophageal pH testing.3-7 About half of this patient population has no symptoms of acid reflux.8-10 A systematic review of 28 epidemiological studies found a 59.2% weighted average prevalence of GERD symptoms in asthmatic patients, compared to 38.1% in controls.11 The corresponding prevalence of asthma in GERD patients was 4.6%, compared to 3.9% in controls. The occurrence of asthma depends on the duration of GERD symptoms and was more prominent in male and older subjects.1 Younger patients with nocturnal reflux symptoms tend to not only have a higher prevalence of asthma compared with patients without reflux symptoms, but they also have more frequent and severe daytime as well as night time reflux symptoms.5,12 The mechanism is not well explained. However, distal esophageal stimulation has been shown to cause bronchoconstriction and increased bronchial reactivity via vagal mechanisms. In animal models, reflux has been shown to cause microaspiration of gastric acid contents that leads to bronchoconstriction.14,15 Studies of the addition of proton pump inhibitor (PPI) therapy or H2 antagonist therapy on the control of asthma Northeast Florida Medicine Vol. 62, No. 1 2011 31
symptoms have had conflicting results. A meta-analysis published in 2001 showed no significant and consistent benefit of medical treatment with PPIs or H2 antagonists on lung function, airway hyper-responsiveness or asthma symptoms. The majority of the studies reviewed for the meta-analysis did have at least one significantly improved asthma treatment outcome, however no consistency was seen across board.16 More recent studies reinforced these same results. A study evaluating the use of esomeprazole in poorly controlled asthmatics with minimal or no reflux symptoms showed no benefit in control of asthma and failed to identify a sub-group of patients that did benefit from such treatment.17 Similarly, Heaney et al failed to show any difference in the prevalence of GERD, identified by esophageal probe monitoring, between difficult to control asthmatics and treatment responsive asthmatics.18 In summary there is a high prevalence of GERD in asthmatics, and similarly there is high prevalence of asthma in GERD patients. Although the symptoms of GERD should be treated, there is no clear evidence that such treatment improves difficult to control asthma or related symptoms. COPD and GERD – The prevalence of GERD symptoms in COPD is approximately 19% which is significantly less than in asthmatics. One reason could be the difference in questionnaires used to survey these two populations. The survey used in the COPD population had been validated for GERD while the survey used in previous studies used unvalidated general questions about symptoms of GERD.19 The prevalence was noticed to be higher in patients with severe COPD (FEV1 ≤ 50% predicted).19 In another study the prevalence was estimated to be 36% in the COPD population despite frequent use of anti-reflux medications.20 The proposed mechanisms leading to development of symptoms in this population is similar to that as described in asthma. In addition severe hyperinflation and vigorous cough leads to increased intra-abdominal pressure which may in turn worsen the reflux. Acute exacerbation of COPD results in significant morbidity and mortality. Patients with COPD on average have 2-3 acute exacerbations annually.21-23 In a study by Vega et al in patients with COPD, there was an average of 1.56 more exacerbations seen in patients with weekly GERD symptoms compared to COPD patients who had either controlled symptoms or none.20 This relationship was again shown by Pourmoghaddas et al.24 To date there have not been any prospective trials evaluating the efficacy of treating GERD in preventing COPD symptoms or exacerbations. Pulmonary Fibrosis and GERD – The Interstitial Lung Diseases (ILD) are a heterogenous group of diffuse parenchymal lung diseases which can be idiopathic or secondary to a number of systemic diseases, most commonly connective tissues diseases (CTD). It has been shown in both animal and human models that pulmonary fibrosis can occur after aspiration of gastric contents.25-27 A small study by Raghu et 32 Vol. 62, No. 1 2011 Northeast Florida Medicine
al in 1998 showed that patients with Idiopathic Pulmonary Fibrosis (IPF) had a higher prevalence of GERD and typically had little or no symptoms. The reflux events tended to occur at night with proximal esophageal reflux and the authors proposed that GERD might play a role in the pathogenesis of IPF.28 ILD is reported in 57-86% of patients with Systemic Sclerosis (SSc).29,30 Patients with SSc and ILD tend to have more severe reflux (more reflux episodes and more reflux reaching the proximal esophagus) compared to SSc patients who do not have ILD.31 Whether or not prevention of GERD results in prevention of development of ILD remains to be answered. Currently the guidelines recommend aggressively treating GERD in symptomatic patients who have ILD, whether it is idiopathic or secondary to CTD. Cough and GERD – Cough lasting longer than three weeks is classified as a subacute cough while cough lasting eight weeks or longer is classified as a chronic cough.32 GERD is the second or third most common cause of subacute or chronic cough.32,33 GERD can cause cough by stimulating cough receptors in the larynx, by stimulating lower respiratory tract cough receptors through aspiration of gastric contents, and by stimulating an esophageal-trachobronchial cough reflex by reflux of acid into the distal esophagus. It is important to note that at least 40% of people with GERD induced cough do not have symptoms of GERD.33 Upper endoscopy and barium swallow exams may suggest GERD as the cause of subacute or chronic cough. However, the most sensitive and specific test to diagnose whether GERD is the cause of cough is esophageal pH monitoring coupled with an event monitor. Many people have GERD, but few have cough so that esophageal pH drops must be temporally related to the cough to prove cause and effect.32, 33 However, if GERD is strongly suspected, then medical therapy should be instituted empirically without formal testing.32 GERD induced cough usually responds to lifestyle modification and acid suppression medication.33 Since it has been shown that proton pump inhibition is more effective than H2 antagonist therapy in cough control, a medical trial of these therapies lasting at least eight weeks using the recommended moderate dose of proton pump inhibitors as initial therapy should be instituted.32, 37, 38, 39 If the cough has been proven to be due to GERD and is refractory to medical therapy (with or without the addition of metaclopramide), then laparoscopic or open Nissen fundoplication has been show to be effective in up to 83% of patients to control cough.40 Bronchiectasis and GERD – Bronchiectasis is defined as abnormal dilation of bronchi. While chronic aspiration is associated with bronchiectasis and recurrent pneumonia, usually these disorders occur due to swallowing disorders rather than GERD. However, it is postulated that GERD with chronic aspiration can cause both bronchiectasis and recurrent pneumonias without swallowing disorders.40,41 In contrast with GERD causing cough where evaluation and
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treatment are fairly well defined, the evaluation and treatment of GERD in the setting of bronchiectasis and/or recurrent pneumonia is much less defined.
GERD appears to have impact on a number of pulmonary disease symptoms and related quality of life. Despite the link of GERD to pulmonary disease symptoms and quality of life, there is no clinical trial data to indicate treatment of GERD improves clinical outcomes in lung disease. Potential treatment modalities include lifestyle modification, control of co-morbid diseases, adjustment of exacerbating medications, and addition of acid suppression treatment.
Gaude GS. Pulmonary manifestations of gastroesophageal reflux disease. Ann Thorac Med. 2009; 4(3):115-23.
Osler, WB. Bronchial asthma. The principles and practice of medicine ,497-501 Appleton. New York, NY. 1892, pp.497-501.
Field SK, Underwood M, Brant R, and Cowie RL. Prevalence of gastroesophageal reflux symptoms in asthma. Chest 1996;109:316-322.
Harding SM, Guzzo MR, and Richter JE. 24-h esophageal pH testing in asthmatics: respiratory symptom correlation with esophageal acid events. Chest 1999;115:654-659.
Sontag SJ, O’Connell S, Khandelwal S, et al. Most asthmatics have gastroesophageal reflux with or without bronchodilator therapy. Gastroenterology 1990;99:613-620.
Vincent D, Cohen-Jonathan AM, Leport J, et al. Gastrooesophageal reflux prevalence and relationship with bronchial reactivity in asthma. Eur Respir J 1997;10:2255-2259.
Simpson WG. Gastroesophageal reflux disease and asthma: diagnosis and management. Arch Intern Med 1995;155:798-803.
Harding SM, Guzzo MR, and Richter JE. The prevalence of gastroesophageal reflux in asthma patients without reflux symptoms. Am J Respir Crit Care Med 2000;162:34-39.
Irwin RS, Curley FJ, and French CL. Difficult to control asthma: contributing factors and outcome of a systematic management protocol. Chest 1993;103:1662-1669.
10. Kiljander, TO and Laitinen, JO. The prevalence of gastroesophageal reflux disease in adult asthmatics. Chest 2004;126:1490-1494. 11. Vaezi MF. Atypical manifestations of gastroesophageal reflux disease. MedGenMed 2005; 7:25-6. 12. Theodoropoulos DS, Pecoraro DL, and Efstratiadis SE. The association of gastro-esophageal reflux disease with asthma and chronic cough in adults. Am J Respir Med 2002; 1:133-46. 13. Irwin RS, Richter JE. Gastroesophageal reflux and chronic cough. Am J Gastroenterol 2000; 95:S9-14. 14. Herve, P, Denjeen, A, Jian, R, et al. Intraesophageal perfusion of acid increases the bronchomotor response to methacholine and to isocapnic hyperventilation in asthmatic subjects. Am Rev Respir Dis 1986;134:986-989. 15. Tuchman, DN, Boyle, JT, Pack, Al, et al. Comparison of airway responses following tracheal or esophageal acidification in the cat. Gastroenterology 1984;10:2255-2259.
Asthma The American Lung Association Asthma Clinical Research Centers. N Engl J Med 2009; 360:1487-1499. 18. Heaney LG, et al. Prevalence of Gastroesophageal Reflux in Difficult Asthma- Relationship to Asthma Outcome. Chest 2005; 127(4):1227-1231. 19. Mokhlesi, B, Morris, AL, Huang, CF, et al. Increased prevalence of gastroesophageal reflux symptoms in patients with COPD. Chest 2001;119:1043-1048. 20. Rascon‐Aguilar IE, Pamer M, Wludyka P, et al. Role of gastroesophageal reflux symptoms in exacerbations of COPD. Chest 2006; 130:1096-1101. 21. Anthonisen, NR, Manfreda, J, Warren, CP, et al. Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease. Ann Intern Med 1987; 106:196-204. 22. Seemungal, TA, Donaldson, GC, Bhowmik, A, et al. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000;161:1608-1613. 23. Seemungal, TA, Donaldson, GC, Paul, EA, et al Effect of exacerbation on quality of life in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157:1418-1422. 24. Rogha M, Behravesh B, and Pourmoghaddas Z. Association of gastroesophageal reflux disease symptoms with exacerbations of chronic obstructive pulmonary disease. J Gastrointestin Liver Dis. 2010; 19(3):253-6. 25. Moran, T J. Experimental aspiration pneumonia: IV. Inflammatory and reparative changes produced by intratracheal injections of autologous gastric juice and hydrochloric acid. Arch. Pathol. 1965; 60: 122-129. 26. Downs, JB, Chapman, RL, Modell, JH, and Hood, CI. 1974. An evaluation of steroid therapy in aspiration pneumonitis. Anesthesiology 1974; 40:129-135. 27. Sladen, A, Zanca, P, and Hadnott, H. Aspiration pneumonitis: the sequelae. Chest 1971;59:448-450. 28. Tobin, RW, Pope II, CE, Pellefrini, CA, Emond, MJ, Sillery, J and Raghu, G. Increased prevalence of gastroesophageal reflux in patients with idiopathic pulmonary fibrosis. Am. J. Respir. Crit. Care Med.1998; Dec; 158(6): 1804-1808. 29. D’Angelo WA, Fries JF, Masi AT, and Shulman LE. Pathologic observations in systemic sclerosis (scleroderma): a study of fifty-eight autopsy cases and fifty-eight matched controls. Am J Med 1969;46:428–440. 30. McCarthy DS, Baragar FD, Dhingra S, Sigurdson M, Sutherland JB, Rigby M, and Martin L. The lungs in systemic sclerosis (scleroderma): a review and new information. Semin Arthritis Rheum 1988;17:271–283. 31. Savarino E, Bazzica M, Zentilin P, Pohl D, Parodi A, Cittadini G, Negrini S, Indiveri F, Tutuian R, Savarino V, Ghio M. Gastroesophageal Reflux and Pulmonary Fibrosis in Scleroderma - A Study Using pH-Impedance Monitoring. Am J Respir Crit Care Med. 2009;179(5):408-13. Epub 2008; Dec 18. 32. Irwin, RS, Baumann, MH, Bolser, DC, et al. Diagnosis and management of cough executive summary: ACCP evidencebased clinical practice guidelines. Chest. 2006; 129:1S.
16. Coughlan JL, Gibson PG, and Henry RL. Medical treatment for reflux oesophagitis does not consistently improve asthma control: a systematic review. Thorax 2001;56:198-204.
33. Irwin, RS, Curley, FJ, and French, CL. Chronic cough: the spectrum and frequency of causes, key components of the diagnostic evaluation and outcome of specific therapy. Am Rev Respir Dis 1990; 141:640.
17. Efficacy of Esomeprazole for Treatment of Poorly Controlled
Continued on page 34
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Northeast Florida Medicine Vol. 62, No. 1 2011 33
In a MEDICaL MaLPRaCTICE CLaIM: Be ready for anything and everything.
Continued from page 33 34. Irwin, RS, French, CL, Curley, FJ, et al. Chronic cough due to gastroesophageal reflux. Clinical, diagnostic, and pathogenetic aspects. Chest. 1993; Nov;104(5):1511-7. 35. Fontana, GA, and Pistolesi, M. Cough. chronic cough and gastroeosophageal reflux. Thorax 2003; 58:1092. 36. Irwin, RS and Richter, JE. Gastroesophageal reflux and chronic cough. Am J Gastroenterol. 2000; 95:S9.
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37. Irwin, RS. Chronic cough due to gastroesophageal reflux disease: ACCP evidence-based clinical practice guidelines. Chest. 2006; 129:80S. 38. Chang, AB, Lasserson, TJ, Gaffney, J, et al. Gastro-oesophageal reflux treatment for prolonged non-specific cough in children and adults. Cochrane Database Syst Rev 2006; Oct 18;(4):CD004823. 39. Kahrilas, PJ, Shaheen, NJ, and Vaezi, M. American Gastroenterological Association Medical Position Statement on the Management of Gastroesophageal Reflux Disease. Gastroenterology 2008; 135:1383. 40. Allen, CJ and Anvari, M. Gastro-oesophageal reflux related cough and its response to laparoscopic fundoplication. Thorax 1998; 53:963. 41. Vandenplas, Y and Rudolph, CD. Pediatric gastroesophageal reflux clinical practice guidelines: joint recommendations of the North American Society of Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN). J Pediatr Gastroenterol Nutr 2009; 49:498. 42. El-Serag, HB, Gilger, M, Kuebeler, M, and Rabeneck, L. Extraesophageal associations of gastroesophageal reflux disease in children without neurologic defects. Gastroenterology 2001; 121:1294.
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Duval BW 3.5x9.5.indd 1
www . DCMS online . org 4/26/10
Laryngopharyngeal Reflux: Overview and Clinical Implications Iman Naseri, MD Abstract: Laryngopharyngeal reflux (LPR) is the backflow of stomach contents into the larynx and pharynx. Consequently it causes supraesophageal manifestations with distinct symptoms unlike those usually seen in gastroesophageal reflux (GER). Several other terms are synonymous with LPR in the medical literature and they are listed in Table 1.1 Due to the lack of similarities in presentation when compared to GER, the diagnosis of LPR may not be as obvious and is often referred to as ‘silent reflux’. This presents a challenge to clinicians and may lead to missed diagnoses or incomplete treatment. In comparison, there is only a 20% overlap of LPR with GERD.2-4 Practicing physicians involved in the treatment of patients with reflux disease should have a basic insight about LPR to ensure optimal management of such conditions.
The mechanisms leading to LPR along with its physiologic sequelae are distinct and are unlike the characteristic symptoms seen in GER.5,6 Nonetheless, they both share fundamental similarities in their etiology and presentations. These similarities, however, are dwindling and being replaced by differences as we continue to learn about this enigmatic subset of reflux-related conditions. People suffering from LPR have reflux episodes usually in upright position (daytime), whereas GERD reflux episodes are predominantly in supine position (nocturnal).5,7-10 The primary site of dysfunction in LPR is the upper esophageal sphincter (UES) rather than the lower esophageal sphincter (LES) involved in GER. Patients with documented LPR have a prevalence of esophagitis and Barrett’s esophagus (BE) only in 19%, suggesting that the patterns, mechanisms and manifestations of LPR differs from those of GER.4 These contrasts account for the variability between the diagnostic approaches towards the two. Therefore, esophagoscopy is not the method of choice for diagnosing LPR as it has been for GERD. To fully understand and successfully treat LPR, an allied effort spanning multiple medical disciplines (pulmonary, gastroenterology, gastrointestinal surgery, otolaryngology) is essential. In contrast to GER, LPR is a new entity which has gained recognition only during the past two decades as research has emerged defining the differences LPR versus GERD. Nonetheless, LPR remains a controversial topic with inconsistent data with respect to its etiology, diagnosis and management.3 Few prospective evidence-based investigations have significantly increased our understanding of this dynamic condition which exerts its effects on the entire upper aerodigestive system. Physiologically, its understanding has Address Correspondence to: Iman Naseri, MD, Assistant Professor University of Florida College of Medicine - Jacksonville, Department of Surgery, Division of Otolaryngology - Head and Neck Surgery, 653 West 8th St, 2nd Fl Faculty Clinic, Jacksonville, FL 32209. Phone: 904-244-3498 Fax: 904-244-7730. Email:iman. firstname.lastname@example.org. www . DCMS online . org
Table 1 Other Names for Laryngopharyngeal Reflux
been a challenge because it manifests via a complex interaction involving both peripheral and central neurologic input and feedback, all performing in synchrony with intricate biochemical interactions.
The symptoms of LPR can be nebulous and misleading so it may lead clinicians in the wrong direction in terms of diagnosis and management. The typical presenting symptoms of LPR include hoarseness, chronic cough (especially nocturnal), globus sensation, dysphagia, excess phlegm production and throat clearing (Table 2). A majority of LPR patients do not have the typical symptoms associated with gastroesophageal reflux disease (GERD), including heartburn. Patients with LPR usually do not have sub-sternal or epigastric burning sensation and their symptoms are usually not worsened after eating or in supine position. Studies have found that less than 40% of patients with LPR have heartburn, but almost 75% of them have esophagitis.7,8,11 The dichotomous presentation of symptomatology between GERD and LPR may often lead such patients into
Table 2 Symptoms and Conditions Associated with Laryngopharyngeal Reflux
Hoarseness (chronic or intermittent)
Chronic upper airway obstruction
Excessive phlegm or postnasal drip
Chronic throat clearing
Northeast Florida Medicine Vol. 62, No. 1 2011 35
Table 3 Reflux Symptom Index (RSI*)
Within the last MONTH, how did the following problems affect you? 1. Hoarseness 2. Clearing 3. Excess
or a problem with your voice
throat mucous or postnasal drip
0 = no problem 5 = severe problem 0
swallowing food, liquids, or pills
after you ate or after lying down
difficulties or choking episodes
7. Troublesome 8. Sensations
or annoying cough
of something sticking in your throat or a lump in your throat
chest pain, indigestion, or stomach acid coming up
*RSI score greater than 13 is suggestive of LPR. entirely different paths in terms of medical management. The vaguely recognized symptoms of LPR often result in misled and delayed diagnosis and treatment. In patients with symptoms akin to typical GERD, therapeutic treatment is usually initiated by primary care practitioners. Patients that do not symptomatically improve after medical therapy (often daily proton pump inhibitors) may be referred to a gastroenterologist via consultation. The other subset of patients with vague symptoms like chronic cough or postnasal drip may undergo workup for reactive airway conditions like asthma by their primary care or via consultation to a pulmonologist. In such cases, patients along with their primary care providers would exhaust diagnostic and treatment options without improvement. An otolaryngologist may be the final consultant in this chain of events.
Figure 1 Laryngopharyngeal Reflux
Laryngeal in-office examination findings seen in Laryngopharyngeal reflux; a. Symmetric enlargement of the lingual tonsils with diffuse cobble-stoning & blunted visualization of the vallecula (asterisks). b. Larynx during inspiration/vocal fold abduction: Pachydermia, thick edematous tissue seen in posterior glottis (white arrow) along with erythema present along the arytenoid processes in proximity to the esophageal inlet (black arrows). c. Pseudosulcus vocalis: caused by edema of the inferior portion of the vocal fold causing the appearance to be like a groove or sulcus (double black arrows).
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Diagnosis The diagnosis of LPR remains contentious among many otolaryngologists who treat this condition. The current gold standard for diagnosing LPR is an ambulatory dual-probe (simultaneous esophageal and pharyngeal) 24-hour pH monitoring, rather than an upper gastrointestinal endoscopy as used in the diagnosis of GERD.7 However, LPR treatment is begun as a therapeutic trial as similarly done in initial treatment for GER. In the case of LPR patients, they are treated empirically based on symptoms and laryngeal findings seen on the office examination of the larynx. Examination of the larynx is routinely performed by otolaryngologists in the outpatient clinic setting, typically done on the initial visit. This is in the form of flexible transnasal or rigid trans-oral examination of the larynx and surrounding structures. No advanced preparation or notification is required by patients, as only topical anesthetic spray is sufficient to ensure comfort. For an otolaryngologist, this is the only tool available to supplement the clinical examination and to provide some objective findings to aid in the diagnosis of LPR. Typical findings seen on office examination of the larynx that are known to be suggestive of LPR include: posterior glottic hyperemia, vocal cord edema, isolated arytenoid hyperemia and pseudosulcus vocalis (Figure 1).12-14 Among other instruments used to assess the degree of findings, the Reflux Finding Score is a validated instrument used for quantifying the physical symptoms and severity of LPR based on the findings seen on laryngoscopy examination. The level of these findings are not directly related to the severity of the LPR, and they often do not correspond to the symptoms or success of treatment. Therefore, laryngeal examination only serves a small role in the diagnostic workup of LPR.15,16 The lack of robust physical exam findings for any reflux www . DCMS online . org
condition has served as the driving force to increase the reliability of subjective data collection to aid in diagnosis. For LPR, one of the most reliable methods based on symptoms has been the reflux symptom index (RSI), a self-administered nine-item questionnaire which is routinely used by otolaryngologists to assist in the diagnosis of LPR (Table 3, p.36).14 Belafsky and colleagues found that patients with high RSI scores (>13) had significant improvement in both their followup scores in addition to their examination findings after LPR treatment.14 Although symptomatic improvement is expected after 2-3 months, the laryngeal findings of LPR do not resolve until 6 months of continued treatment.
Patients suspected to have LPR are usually treated initially with a therapeutic trial of a proton pump inhibitor (PPI). This is similar to the initial treatment of GER. Resolution of symptoms is expected after 2-3 months of therapy with twice daily proton pump inhibitors (PPIs) as well as diet and lifestyle modifications (Table 4).17 A more aggressive regimen is often required for LPR patients. This may be due to multiple mechanisms, including the slow reestablishment of mucosal homeostasis in the upper aerodigestive system and its higher vulnerability due to lack of protection to stomach reflux contents. Therefore, twice daily PPI treatment in addition to strict diet and lifestyle modifications are essential in the treatment of LPR.
Table 4 Diet and Lifestyle Modifications/ Recommendations for Reflux •
Avoidance of heavy meals, smoking, alcohol, late meals
Weight loss if BMI>35
Food avoidance: chocolate, spicy foods, citrus fruits and juices, carbonated beverages, fatty foods, mint, caffeinated drinks
Sleep with head of bed elevated
Avoid clothing that is constricting around the waist
Avoid lying on right side while in bed
Treatment failure is believed to indicate inadequacy of diagnosis, treatment regimen or resistance.18 Such patients may undergo further diagnostic testing including a pH study. Furthermore, patients that fail medical therapy or suffer from intolerable side effects or struggle with the cost of medications are offered surgical treatment. There are several types of surgical options available today, with the Nissen fundoplication as the most common type of surgery performed for this condition. This procedure essentially reinforces the LES and appears to improve both GERD and LPR symptoms.19,20 There is a significant difference in both the time and degree of response during similar treatments of LPR versus GER. A more aggressive and longer duration of treatment is often needed to gain symptomatic improvement in LPR as opposed to GER. The reason for this phenomenon is poorly understood. We know the larynx is more susceptible to injury www . DCMS online . org
from reflux in comparison to the esophagus due to its lack of both intrinsic and extrinsic epithelial defenses.21,22 Although our knowledge about the mechanisms involved in the tissue injury seen in LPR is incomplete, we understand the damage from reflux to be manifested from both direct contact and secondary cause. The direct injury is from acid, bile salts and pepsin in contact with the surface mucosa of the larynx and pharynx.8,23 Wong and colleagues have suggested the possibility of a nerve reflex system named the ‘esophageal-nasal reflex’ via the vagus nerve which may be responsible for an increase in nasal mucus production after esophageal stimulation.21 This may explain the increased postnasal drip, excess phlegm and throat clearing typically seen in LPR. Also, direct stimulation of vagal sensory nerves in the upper airway may be linked to chronic cough, throat clearing. Additionally, direct stimulation of these vagal sensory nerves could be a possible trigger to asthmatic exacerbation.25,26 Because of this known vulnerability in the larynx and surrounding structures to the effects of reflux, there is a diversity of clinical manifestations related to LPR. Convincing data has revealed that a majority of patients with voice disorders have LPR.27 Data emerging from studies also supports the theory that protracted exposure to refluxate increases the likelihood for development of precancerous or cancerous lesions, namely laryngeal carcinoma.28-31 Other studies have shown links between LPR and symptomatic asthma, chronic cough, laryngospasm, paradoxical vocal cord movement, tracheal stenosis and lingual tonsil hypertrophy.16,32-37 Patients with confirmed LPR along with symptoms of GERD may additionally undergo esophagoscopy to screen for BE. The office use of transnasal esophagoscopy (TNE) has recently gained equivocal diagnostic ability. The office-based TNE is an unsedated small-caliber endoscopy that is equivalent to conventional sedated esophagogastroduodenoscopy (EGD) in screening and surveillance for BE.11,38 It gives the clinician the ability to perform a variety of diagnostic and therapeutic procedures in the outpatient setting without sedation.
Laryngopharyngeal reflux is a complex and difficult to diagnose manifestation of reflux which is present in up to 50% of patients with voice disorders.27 If untreated, it can manifest into other chronic conditions affecting the larynx and esophagus. Although related to GER, LPR is distinct in its cause, symptoms and management. These characteristic variations are specifically involved in causing unique clinical manifestations manifesting in differing vague presentations. It often presents with a variety of ubiquitous and nonspecific symptoms that challenge many clinicians involved in the diagnosis and management of such patients. Conversely, the lack of practical objective diagnostic tools presents a further challenge in the diagnosis and management of LPR. This often leads to frustration among patients as they are often misdiagnosed and undergo unnecessary diagnostic testing and empirical treatments for other causes while their symptoms continue to progress due to undiagnosed and untreated LPR. Therefore, clinicians involved in treating patients with complaints of the upper aerodigestive system should be aware of the diagnosis of LPR and be able to recognize its symptoms to ensure optimal management of such conditions. Northeast Florida Medicine Vol. 62, No. 1 2011 37
Koufman JA, Aviv JE, Casiano RR, Shaw GY. Laryngopharyngeal reflux: position statement of the committee on speech, voice, and swallowing disorders of the American Academy of Otolaryngology-Head and Neck Surgery. Otolaryngol Head Neck Surg. Jul 2002;127(1):32-35.
Groome M, Cotton JP, Borland M, McLeod S, Johnston DA, Dillon JF. Prevalence of laryngopharyngeal reflux in a population with gastroesophageal reflux. Laryngoscope. Aug 2007;117(8):1424-1428.
Gupta R, Sataloff RT. Laryngopharyngeal reflux: current concepts and questions. Curr Opin Otolaryngol Head Neck Surg. Jun 2009;17(3):143-148.
Koufman JA, Belafsky PC, Bach KK, Daniel E, Postma GN. Prevalence of esophagitis in patients with pH-documented laryngopharyngeal reflux. Laryngoscope. Sep 2002;112(9):1606-1609.
Koufman J, Sataloff RT, Toohill R. Laryngopharyngeal reflux: consensus conference report. J Voice. Sep 1996;10(3):215-216.
Postma GN, Tomek MS, Belafsky PC, Koufman JA. Esophageal motor function in laryngopharyngeal reflux is superior to that in classic gastroesophageal reflux disease. Ann Otol Rhinol Laryngol. Dec 2001;110(12):1114-1116.
Wiener GJ, Koufman JA, Wu WC, Cooper JB, Richter JE, Castell DO. Chronic hoarseness secondary to gastroesophageal reflux disease: documentation with 24-h ambulatory pH monitoring. Am J Gastroenterol. Dec 1989;84(12):1503-1508. Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. Laryngoscope. Apr 1991;101(4 Pt 2 Suppl 53):1-78. Richter JE. Ambulatory esophageal pH monitoring. Am J Med. Nov 24 1997;103(5A):130S-134S.
10. Postma GN. Ambulatory pH monitoring methodology. Ann Otol Rhinol Laryngol Suppl. Oct 2000;184:10-14. 11. Belafsky PC, Postma GN, Daniel E, Koufman JA. Transnasal esophagoscopy. Otolaryngol Head Neck Surg. Dec 2001;125(6):588-589. 12. Belafsky PC, Postma GN, Koufman JA. Laryngopharyngeal reflux symptoms improve before changes in physical findings. Laryngoscope. Jun 2001;111(6):979-981. 13. Belafsky PC, Postma GN, Koufman JA. The association between laryngeal pseudosulcus and laryngopharyngeal reflux. Otolaryngol Head Neck Surg. Jun 2002;126(6):649-652. 14. Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS). Laryngoscope. Aug 2001;111(8):1313-1317. 15. Postma GN, Johnson LF, Koufman JA. Treatment of laryngopharyngeal reflux. Ear Nose Throat J. Sep 2002;81(9 Suppl 2):24-26. 16. Remacle M, Lawson G. Diagnosis and management of laryngopharyngeal reflux disease. Curr Opin Otolaryngol Head Neck Surg. Jun 2006;14(3):143-149. 17. Kaltenbach T, Crockett S, Gerson LB. Are lifestyle measures effective in patients with gastroesophageal reflux disease? An evidence-based approach. Arch Intern Med. May 8 2006;166(9):965-971. 18. Bough ID, Jr., Sataloff RT, Castell DO, Hills JR, Gideon RM, Spiegel JR. Gastroesophageal reflux laryngitis resistant to omeprazole therapy. J Voice. Jun 1995;9(2):205-211. 19. Catania RA, Kavic SM, Roth JS, et al. Laparoscopic Nissen 38 Vol. 62, No. 1 2011 Northeast Florida Medicine
fundoplication effectively relieves symptoms in patients with laryngopharyngeal reflux. J Gastrointest Surg. Dec 2007;11(12):1579-1587; discussion 1587-1578. 20. Sala E, Salminen P, Simberg S, Koskenvuo J, Ovaska J. Laryngopharyngeal reflux disease treated with laparoscopic fundoplication. Dig Dis Sci. Sep 2008;53(9):2397-2404. 21. Axford SE, Sharp N, Ross PE, et al. Cell biology of laryngeal epithelial defenses in health and disease: preliminary studies. Ann Otol Rhinol Laryngol. Dec 2001;110(12):1099-1108. 22. Little FB, Koufman JA, Kohut RI, Marshall RB. Effect of gastric acid on the pathogenesis of subglottic stenosis. Ann Otol Rhinol Laryngol. Sep-Oct 1985;94(5 Pt 1):516-519. 23. Adhami T, Goldblum JR, Richter JE, Vaezi MF. The role of gastric and duodenal agents in laryngeal injury: an experimental canine model. Am J Gastroenterol. Nov 2004;99(11):2098-2106. 24. Wong IW, Rees G, Greiff L, Myers JC, Jamieson GG, Wormald PJ. Gastroesophageal reflux disease and chronic sinusitis: in search of an esophageal-nasal reflex. Am J Rhinol Allergy. JulAug 2010;24(4):255-259. 25. Kollarik M, Ru F, Undem BJ. Acid-sensitive vagal sensory pathways and cough. Pulm Pharmacol Ther. 2007;20(4):402-411. 26. Tomonaga T, Awad ZT, Filipi CJ, et al. Symptom predictability of reflux-induced respiratory disease. Dig Dis Sci. Jan 2002;47(1):9-14. 27. Koufman JA, Amin MR, Panetti M. Prevalence of reflux in 113 consecutive patients with laryngeal and voice disorders. Otolaryngol Head Neck Surg. Oct 2000;123(4):385-388. 28. Koufman JA, Burke AJ. The etiology and pathogenesis of laryngeal carcinoma. Otolaryngol Clin North Am. Feb 1997;30(1):1-19. 29. Maronian NC, Azadeh H, Waugh P, Hillel A. Association of laryngopharyngeal reflux disease and subglottic stenosis. Ann Otol Rhinol Laryngol. Jul 2001;110(7 Pt 1):606-612. 30. Ozlugedik S, Yorulmaz I, Gokcan K. Is laryngopharyngeal reflux an important risk factor in the development of laryngeal carcinoma? Eur Arch Otorhinolaryngol. Apr 2006;263(4):339-343. 31. Galli J, Cammarota G, Volante M, De Corso E, Almadori G, Paludetti G. Laryngeal carcinoma and laryngo-pharyngeal reflux disease. Acta Otorhinolaryngol Ital. Oct 2006;26(5):260-263. 32. DelGaudio JM, Naseri I, Wise JC. Proximal pharyngeal reflux correlates with increasing severity of lingual tonsil hypertrophy. Otolaryngol Head Neck Surg. Apr 2008;138(4):473-478. 33. Eryuksel E, Dogan M, Golabi P, Sehitoglu MA, Celikel T. Treatment of laryngopharyngeal reflux improves asthma symptoms in asthmatics. J Asthma. Sep 2006;43(7):539-542. 34. Murry T, Tabaee A, Owczarzak V, Aviv JE. Respiratory retraining therapy and management of laryngopharyngeal reflux in the treatment of patients with cough and paradoxical vocal fold movement disorder. Ann Otol Rhinol Laryngol. Oct 2006;115(10):754-758. 35. Kothe C, Schade G, Fleischer S, Hess M. [Vocal cord dysfunction. An important differential diagnosis to bronchial asthma]. HNO. Mar 2004;52(3):261-264. 36. Weldon DR. Differential diagnosis of chronic cough. Allergy Asthma Proc. Sep-Oct 2005;26(5):345-351. 37. Roland MM, Baran AS, Richert AC. Sleep-related laryngospasm caused by gastroesophageal reflux. Sleep Med. May 2008;9(4):451-453. 38. Postma GN, Bach KK, Belafsky PC, Koufman JA. The role of transnasal esophagoscopy in head and neck oncology. Laryngoscope. Dec 2002;112(12):2242-2243. www . DCMS online . org
LEADER Malcolm Foster Jr., MD Adjunct Professor, Department of Medicine University of Florida College of Medicineâ€“Jacksonville
Malcolm Foster Jr., MD President, Duval County Medical Society
www . DCMS online . org
Northeast Florida Medicine Vol. 62, No. 1 2011 39
DCMS Annual Meeting - Dr. Foster Inaugurated 124th President Malcolm T. Foster, Jr., MD, was inaugurated as the 124th president of the Duval County Medical Society (DCMS) at its 158th Annual Meeting, Wednesday, December 1, 2010 at the Hyatt Regency Jacksonville Riverfront. His close friend, Dr. Robert Nuss, Dean of the Regional Campus and Associate Vice President for Health Affairs, University of Florida College of Medicine/Jacksonville, administered the Oath of Office. (photo below)
forward thinking so you can stay in control of your practice” and DCMS Foundation President Dr. Benjamin Moore who reminded the audience this is the 51st year of the Academy of Medicine/Foundation. Mrs. Shar Donovan, FMA Alliance President recognized Mrs. Jean Henderson, 2010 DCMS Alliance President who installed Mrs. Dena Pulley as the 2011 DCMS Alliance President. The Alliance presented flowers to Dr. Pat Foster, wife of Dr. Malcolm Foster. (photo below)
Dr. Foster, an internal medicine physician specializing in infectious diseases and rheumatology, is the Karl B. Hanson Professor of Medicine at the University of Florida/ Jacksonville Department of Medicine and Professor, Division of General Internal Medicine at the University of Florida Health Science Center – Jacksonville. (UFHSC) In addition to his responsibilities at UFHSC, Dr. Foster is President of the Attending Staff Foundation which is a group of Jacksonville physicians interested in the education of resident physicians. He is also Vice Chairman of The Blood Alliance and Immediate Past Governor of the Florida Chapter of the American College of Physicians.
DCMS Annual Awards were given and special recognitions were also made. Jeffrey L. Goldhagen, MD, MPH, received the 2010 DCMS Community Service Award for over 15 years of advocacy for the underserved and disadvantaged population in the Northeast Florida health community. This award was established by the Duval County Medical Society in 1998 to recognize outstanding volunteer efforts of DCMS Physicians performed in the community. John F. Lovejoy, Jr., MD, received the 2010 Clyde M. Collins Humanitarian Award a second time for his hurricane relief work in Haiti and his mentoring of local physicians who join his humanitarian teams that go to help this impoverished nation. This award was created in 1997 in memory of Dr. Clyde Collins to recognize volunteer efforts by physicians. Rui P. Fernandes, MD, received the 2010 Philip H. Gilbert Young Physician Leadership Award (see p. 8). DCMS Life Members (those who have been members 35 years) recognized were David Dalton, MD; Andrew Coley, MD; Lorenzo Garcia, MD; Richard Glock, MD; Robert Miller, MD; and Robert Moore, MD. Guest Editors for 2010 issues of Northeast Florida Medicine were presented with commemorative plaques by Editor-in-Chief Dr. Joan Huffman. The editors were Dr. Ziad Awad, Dr. Bracken Burns, Dr. Mobeen Rathore and Dr. Neel Karnani. Dr. Kilkenny was presented with the Past President’s Plaque.
Dr. Foster was inaugurated before DCMS members and guests attending the Annual Meeting. During his inaugural remarks, he emphasized the need for the Society to “reach out to younger physicians and get them involved” in organized medicine. A teacher and mentor himself, he recognized several of his past “trainees” in attendance.They included: Dr. Kay Mitchell, a past DCMS President; Dr. Ronald Renuart, a Florida legislator; and Dr. Madelyn Butler, current FMA President. 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. A tribute was also given to the 2010 deceased members. DCMS and FMA Past Presidents were recognized as well as special guests. Annual elections took place during the meeting, and the slate of officers, directors, FMA delegates and alternate delegates was approved. Ashley Booth Norse, MD, is the DCMS president-elect. Other 2011 officers are: Vice Presidents Neel G. Karnani, MD and Eli N. Lerner, MD; Jeffrey H. Wachholz, MD, secretary; Nathan P. Newman, MD, treasurer; and John W. Kilkenny III, MD, immediate past president. The 2010 DCMS Board of Directors was recognized. Other speakers on the program were FMA President Dr. Madelyn Butler who encouraged physicians to “be aware and 40 Vol. 62, No. 1 2011 Northeast Florida Medicine
There was a full Exhibit Hall area featuring vendors displaying their products and services and also scientific poster presentations. (complete list in the insert/center of journal) The Platinum Sponsor of the Annual Meeting was First Professionals Insurance Company (FPIC) and Gold Sponsors were Associated Medical Office Experts, Baptist Health, Blue Cross Blue Shield of Florida, Community Hospice of Northeast Florida, Live Well Networks LLC, Signet Diagnostic Imaging Services, SunTrust Bank, and the University of Florida College of Medicine, Jacksonville, and there were Silver and Exhibitor Sponsors as well. (see more Annual Meeting photographs in the insert/center of journal) www . DCMS online . org
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 Membership Committee Chair (904-244-4106 or Barbara Braddock, Membership Director (904-3556561 x107).
Javed I. Akhtar, MD Pediatrics Wolfson Children’s Hospital Pediatric Critical Care Medical Degree: Quaid-I-Azam Medical College Residency: Woodhull Medical Center Fellowship: Children’s Hospital & Health Center Nominated by: UFJP Kerry M. Bachista, MD Emergency Medicine UF Emergency Medicine 655 W. 8th St. 1st FL Clinical Center Medical Degree: Florida State University Medical School Residency: University of Florida College of Medicine-Jacksonville Nominated by: UFJP Solange Benjamin-Thorpe, MD Pediatrics 800 Prudential Dr. 4th FL Medical Degree: University of West Indies Medical School Residency: The Brooklyn Hospital Center Fellowship: Schneider Children’s Hospital Nominated by: UFJP Alexander S. Berk, MD Emergency Medicine UF Emergency Medicine 655 W. 8th St. 1st FL Clinical Center Medical Degree: Tufts University Medical School Internship: National Naval Medical Center Residency: Harbor-UCLA Medical Center Nominated by: UFJP Erin S. Berk, MD Emergency Medicine UF Emergency Medicine 655 W. 8th St. 1st FL Clinical Center Medical Degree: Brown Medical School Residency: Harbor-UCLA Medical Center Nominated by: UFJP Vikram S. Brar, MD Ophthalmology UF Ophthalmology 580 W. 8th St. 3rd FL Tower II Medical Degree: Medical College of Virginia Internship: Christiana Hospital/Christiana
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Care Health System Residency: Medical College of Virginia Nominated by: UFJP Julius Dean, MD Cardiology/Nuclear Cardiology St. Luke’s Cardiology 6867 Southpoint Dr. N. #111 Medical Degree: Yale University School of Medicine Residency: Harlem Hospital Center Fellowship: St. Luke’s Episcopal Hospital Nominated by: Peter Kuhlman, MD; Rogers Cain, MD; Mel Carbonell, MD Steven G. Dimmitt, DO Family Medicine Shands Community Health Center 655 W. 8th St. 4th FL ACC Medical Degree: University of Osteopathic Medicine Internship: Garden City Hospital Residency: Providence Hospital Nominated by: UFJP Dalia Elramady, MD Family Medicine Merrill Road Family Medicine Center 7645 Merrill Road #301 Medical Degree: University of Alexandria Medical School Residency: St. Vincent’s Family Medicine Program Nominated by: UFJP
Nilmarie Guzman, MD Infectious Disease Duval County Health Dept. 1833 Boulevard #500 Medical Degree: Ponce School of Medicine Residency: Damas Hospital Fellowship: University of Florida Health Science Center Nominated by: UFJP Hank C. Hill, MD Surgical Oncology/General Surgery 21st Century Oncology/Surgical Oncology Specialties 7751 Baymeadows Rd. E. Medical Degree: Morehouse School of Medicine Residency: Harlem Hospital Center Fellowship: Roswell Park Cancer Institute Nominated by: Alan Marks, MD; Joseph Mignone, MD; Joanne Dragun, MD Hsiao-Yen Kuo, MD Internal Medicine UF Internal Medicine 653 W. 8th St. 3rd FL Faculty Clinic Medical Degree: Institute of Medicine Residency: Wyckoff Heights Medical Center & Unity Health System Fellowship: University of Florida College of Medicine Nominated by: UFJP
Jeffrey Mark Fliesser, MD Psychiatry/Forensic Psychiatry 24 Cathedral Place #605, St. Augustine Medical Degree: Medical College of Wisconsin Residency: SUNY Stony Brook Medical School Fellowship: Mass Mental Health/Harvard Medical School Nominated by: Carl Burak, MD; Stephen Trigg, MD; Anthony Capasso, MD
Thomas A. Lupoli, DO Allergy, Asthma & Immunology Allergy & Asthma Specialists of North Florida PA 1895 Kingsley Avenue Medical Degree: Kirksville College of Osteopathic Medicine Residency/Fellowship: University of Missouri Kansas City School of Medicine Nominated by: Edward Mizrahi, MD; Patrick DeMarco, MD; Christopher Scuderi, MD
Marlene S. Goodfriend, MD Pediatrics Hope Haven Medical Degree: Northwestern University Medical School Internship: Michael Reese Hospital Residency: Children’s Memorial Hospital & Michael Reese Hospital Nominated by: Hope Haven
Barry M. McCook, MD Radiology UF Radiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: University of Florida College of Medicine Residency/Fellowship: Vanderbilt University Medical Center Nominated by: UFJP
Nelson V. Guevara, MD Anesthesiology UF Anesthesiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: Luis Razetti Medical School Internship/Residency/Fellowship: Jackson Memorial Hospital Nominated by: UFJP
Pramod K. Reddy, MD Internal Medicine UF Internal Medicine 655 W. 8th St. 2nd FL LRC Medical Degree: Sri Dev Raj Urs Medical College Internship/Residency: Stony Brook University Hospital Nominated by: UFJP Continued on page 44
Northeast Florida Medicine Vol. 62, No. 1 2011 41
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42 Vol. 62, No. 1 2011 Northeast Florida Medicine
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AHIT is your trusted IT advisor. Our team of IT professionals has over a decade of experience implementing systems within the Florida medical community. Designated as northern and southwestern FLâ€™s Regional Extension Center (REC), AHIT is federally funded to provide free and subsidized IT services to providers. We can assist you with: x Unbiased, accurate information x EHR system selection, implementation & project management assistance x Group purchasing program x Privacy & security best practices x Workflow redesign x EHR optimization and meaningful use achievement x Incentive funding attainment
To apply for REC services in Duval County, contact Radley Remo at firstname.lastname@example.org or at (904) 253-2052. Space is limited, so enroll today.
AHIT, a program of Community Health Centers Alliance, Inc., wishes to acknowledge support from the Office of the National Coordinator, Department of Health and Human Services, Award #90RC0051/01.
www . DCMS online . org
Northeast Florida Medicine Vol. 62, No. 1 2011 43
Continued from page 41 Miguel A. Rosada, MD Family Medicine UF Community Health/Family Medicine 655 W. 8th St. 3rd FL LRC Medical Degree: Pedro Henriquez Urena National University Residency: University of Florida Health Science Center/ Jacksonville Nominated by: UFJP Nigel W. Sparks, MD Orthopaedic Surgery UF Bone & Joint Center at Emerson 4555 Emerson Exwy. #100 Medical Degree: Hahnemann University Medical School Residency: Union Memorial Hospital Fellowship: UHZ Sports Medicine Institute Nominated by: UFJP Thiruppathi Sureshkumar, MD Anesthesiology UF Anesthesiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: Thanjavur Medical College Internship: Our Lady of Mercy Medical Center Residency: Albert Einstein College of Medicine & Medical College of Wisconsin Fellowship: University of Maryland Medical System Nominated by: UFJP Zhiqiang B. Wang, MD Pathology UF Pathology 655 W. 8th St. 1st FL Clinical Center Medical Degree: Shandong Medical University Residency: The Methodist Hospital Fellowship: University of Pittsburgh College of Medicine Nominated by: UFJP
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44 Vol. 62, No. 1 2011 Northeast Florida Medicine
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A financial advisor dedicated to the medical industry can help you navigate changes in your practice’s finances. The business of medicine, much like your practice itself, is forever evolving. And with new financial opportunities and ongoing concerns — like protecting against fraud, managing risk and anticipating the impact of insurance and reimbursements on cash flow — you need the guidance of an advisor who uniquely understands your industry. At SunTrust, advisors with our Private Wealth Management Medical Specialty Group work solely with physicians and their practices to deliver solutions designed for the medical community. To schedule an appointment with an advisor, call 904.632.2854 or visit suntrust.com/medicine to learn more.
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Securities and Insurance Products and Services: Are not FDIC or any other Government Agency Insured • Are not Bank Guaranteed • May Lose Value SunTrust Private Wealth Management Medical Specialty Group is a marketing name used by SunTrust Banks, Inc., and the following affiliates: Banking and trust products and services are provided by SunTrust Bank. Securities, insurance (including annuities and certain life insurance products) and other investment products and services are offered by SunTrust Investment Services, Inc., an SEC-registered investment adviser and broker/dealer and a member of FINRA and SIPC. Other insurance products and services are offered by SunTrust Insurance Services, Inc., a licensed insurance agency. ©2011 SunTrust Banks, Inc. SunTrust and Live Solid. Bank Solid. are federally registered service marks of SunTrust Banks, Inc.
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Northeast Florida Medicine Vol. 62, No. 1 2011 45
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Enroll in Florida SHOTS today at www.flshots.com or call (877) 888-SHOT and enjoy the freedom of electronically certified 680s.
46 Vol. 62, No. 1 2011 Northeast Florida Medicine
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Stephen J. Clark, MD Jacksonville family medicine physician and practice owner for nearly 30 years Joined Community Hospice as Chief Medical Officer, June 2009
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Our Spring 2011 issue on Gerd was guest edited by DCMS member Dr. Ziad T. Awad. It offers CME credit on the Prevention of Medical Errors. CM...