Fall 2012 NE Medical Journal

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Inside this issue of

VOLUME 63, NUMBER 3 Orthopaedics Fall 2012 EDITOR IN CHIEF Raed Assar, MD (Chair) MANAGING EDITOR Leora Legacy ASSOCIATE EDITORS Abubakr Bajwa, MD Steven Cuffe, MD Ruple Galani, MD Kathy Harris (Alliance) Sunil Joshi, MD (Vice Chair) James Joyce, MD Daniel Kantor, MD Neel Karnani, MD Mobeen Rathore, MD James St. George, MD

EXECUTIVE VICE PRESIDENT Bryan Campbell DCMS FOUNDATION BOARD OF DIRECTORS Malcolm T. Foster, Jr., MD, President Ashley B. Norse, MD, President Elect Eli Lerner, MD, Vice President Mobeen Rathore, MD, Vice President Neel Karnani, MD, VP & Treasurer Daniel Kantor, MD, Secretary Benjamin Moore, MD, Im. Past President Bouli Amoli, MD, Resident Raed Assar, MD Elizabeth Burns, MD J. Bracken Burns, DO Kelli Deese, MD, Resident Ruple Galani, MD Jeffrey M. Harris, MD LCDR James Hodges, MC, USN, Resident Mark L. Hudak, MD TraChella Johnson, MD Sunil N. Joshi, MD James Joyce, MD Harry M. Koslowski, MD Stephen Mandia, MD Jesse P. McRae, MD Jason D. Meier, MD Amit Grover, MD, Resident Nathan P. Newman, MD Sanjay Swami, 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: llegacy@dcmsonline.org. COVER: Tree of Andry sculpture by Dr. Douglas Kiburz and Bob Schwickrath. Used with permission from Cavc Folk Creations.

www . DCMS online . org

Northeast Florida Medicine

Features

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Musculoskeletal Diseases Challenge Patients, Physicians & Society

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Kamal I. Bohsali, MD, FAAOS, FACS, Guest Editor

Innovations in theTreatment of Dupuytren's Contracture

Garry S. Kitay, MD

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Lumps and Bumps: Initial Evaluation and Management of Bone and Soft Tissue Tumors (CME) Courtney E. Sherman, MD and Mary I. O'Connor, MD

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Management of Neck Pain and Cervical Radiculopathy

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Joint Replacement Options for the Shoulder

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Contemporary Treatment of Rotator Cuff Tendinopathy

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Pediatric and Adolescent Sports Injuries of the Knee

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Robotic Assisted Partial Knee Replacement: An Advance in Surgical Technique

Ali Chahlavi, MD; Eric Nottmeier, MD and John Matthew Hale, PA-C

Kamal I. Bohsali, MD, FAAOS, FACS LCDR Emeka Ofobike, Jr., MD

Eric D. Shirley, MD and Mary Anderson, BS

Kenneth Kaminski, MD; Cedric Ortiguera, MD and Mary I. O'Connor, MD

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Lateral Ankle Ligament Injuries: Treatment Decisions Involving the Ankle Sprain Malik Abraham, DPM

Departments

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From the Editor’s Desk From the President’s Desk Philip H. Gilbert Invited Editorial Residents' Corner Patient Page Cover - Sculptor's Feature Trends in Public Health

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Northeast Florida Medicine Vol. 63, No. 3 2012 3


From the Editor’s Desk

Community Health Education Key to Fulfilling DCMS Mission The mission of the Duval County Medical Society (DCMS) is to promote the delivery of and access to high quality, ethical medical care for the community, and to serve as an advocate for physician members and their patients. Executing this mission is the focus of the DCMS Journal and Communications Committee as it oversees the publishing the Northeast Florida Medicine journal and the DCMS Membership Directory, manages the development of the DCMS website dcmsonline.org, as well as directs any other communication initiatives or projects. Recently, DCMS has taken an active role in educating the community on healthcare issues through the Florida Times-Union newspaper and a column entitled “Doctors On Call.” Some topics and authors have been: “Woman’s multiple sclerosis initially treated as major depression” by Dr. Daniel Kantor; “Smoke, pollen double the misery,” by Dr. Sunil Joshi; and “Peripheral arterial disease, a silent but serious health threat,” by Dr. Yazan Khatib. DCMS also has plans to utilize television and radio as ways to better disseminate medical information. When the Supreme Court decision on the affordable care act was announced, DCMS President Dr. Ashley Booth Norse and DCMS Secretary Dr. Daniel Kantor were interviewed by TV reporters to present DCMS perspective. There are definite benefits to the community, physicians, and DCMS through the published news column and electronic media appearances. All help promote the overall mission of DCMS. Educating the public has a positive impact on health care outcomes. An Agency for Healthcare Research and Quality (AHRQ) report published in January 2004, indicated low literacy is associated with several adverse health outcomes including low health knowledge, increased inciRaed Assar, MD, MBA dence of chronic illness, poorer disease markers, and less than optimal use of preventive health Editor-in-Chief services. Interventions to alleviate the effects of low literacy have been studied and some have Northeast Florida Medicine shown promise for improving patient health and receipt of health care services. This report on literacy and health outcomes was requested by the American Medical Association and funded by AHRQ. (http://archive.ahrq. gov/downloads/pub/evidence/pdf/literacy/literacy.pdf ) The newspaper column and other media initiatives will promote the delivery of high quality ethical medical care, a major component of DCMS mission. The DCMS Board of Directors wants to extend DCMS activities to other print media and to television and radio stations to educate the community at large on health issues. The Society’s engagement in this media campaign with newspapers, television stations, and radio stations will highlight the value DCMS brings to the medical community and the public. Several DCMS physicians have already volunteered to represent Society in such educational efforts. In addition, as non-member physicians become interested in publishing articles and supporting community education, they will join DCMS. In fact, several non-members have already joined DCMS in order to participate. Adding to our membership makes DCMS a stronger organization that is more capable of achieving its mission. DCMS needs your help to continue this effort. Please let us know if you would like to represent DCMS in this important activity. Not only would you be able to share information that would help prevent disease and better inform patients so they can make more informed decisions about their health issues, but your practice would gain exposure through this media publicity. Please contact Laura Townsend, the DCMS Communications Coordinator, at ltownsend@dcmsonline.org or by phone at: 904.355.6561 ext. 101 if you are interested in participating. She can provide the overall guidelines and suggest beneficial topics. Please indicate the areas of your interest whether it is writing newspaper articles or conducting television or radio interviews. There is a need for more physicians who are willing to fill television station requests for health care experts to address national and seasonal issues or just questions from the public on various health care concerns. The DCMS Journal and Communication Committee will guide this effort to ensure consistency, validity, and responsiveness. Your contributions are welcomed and greatly encouraged. Dr. Assar is Aetna’s Medical Director for North Florida. Articles or opinions provided by Dr. Assar do not necessarily reflect the views of Aetna.

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From the President’s Desk

PPACA's Effects and DCMS' Commitment to Members On June 28, 2012, the U.S. Supreme Court (the Court) ruled on the Patient Protection and Affordable Care Act. (PPACA) By the time this editorial reaches your desk, this information may or may not have changed several times. But I thought I would take the opportunity to inform Duval County Medical Society (DCMS) members where the DCMS stands regarding the ruling. Let me preface by saying I understand that our members have different views of the PPACA and of the Court’s ruling. Some physicians approve of the PPACA and the ruling; others do not. Many just want to know how the latest developments will affect their practices and more importantly, their patients. In a 5-4 decision, the Court upheld the constitutionality of PPACA in a complex ruling, including the law’s individual responsibility and Medicaid expansion provisions. Simplifying the primary points of the ruling, the Court announced that the individual mandate requiring people to purchase healthcare insurance is sustained as a tax. The second impact affects states’ expansion of Medicaid eligibility. The Court ruled that the Federal government cannot force states to expand eligibility by threatening to pull existing Medicaid allocations. The most crucial issue before the Court was the individual mandate, known technically as the “minimum coverage” provision. S striking it down would jeopardize the ability of insurers to comply with other, more popular elements of the healthcare law without drastically raising premiums. Under those other provisions, for example, insurers can no longer limit or deny benefits to children because of a preexisting condition, and young adults up to age 26 are eligible for insurance coverage under their parents’ plans.

Ashley Booth Norse, MD 2012 DCMS President

On the Medicaid question, the Court’s judges found that the law’s expansion of Medicaid can move forward, but not its provision that threatens states with the loss of their existing Medicaid funding if they decline to comply with the expansion. The finding immediately raises questions as to how effectively the Federal government will be able to implement the expansion of the joint federal-state insurance program for the poor.

As we go to press, here’s what we know about future timing of PPACA: • January 1, 2013 – Expansion of Medicaid: The expansion of Medicaid eligibility and Medicaid payments to primary care physicians takes effect, pending state participation. Florida Governor Rick Scott has stated Florida will not be taking part in this expansion, yet many question this. • January 1, 2014 – Insurance Exchanges: People without access to insurance through their employer will be able to purchase insurance through insurance exchanges. • January 2, 2014 – If financially able to purchase health insurance and one chooses not to, that person will be taxed. The tax will phase in starting at $95/person in the household for the lowest income levels in 2014 and will increase to a minimum $695/person by 2016. No filing household will be taxed for more than three individuals. So what does this mean for physicians in Florida? It’s probably too early to say. Because of the primary care shortage, some have predicted that there will be an increase in emergency room visits. Others have speculated that there will be diminished access to care. Most agree that insurance rates will increase. No one knows how the Medicaid expansion will play out in the state or what impact that will have on the healthcare delivery system. This means that in Florida, the final impact of this ruling still remains to be determined. The DCMS will work closely with our contacts in the Florida Legislature and with the Florida Medical Association on the timing and implementation of the provisions and will bring you updates as they are available. The DCMS is committed to supporting you, our members, and ensuring that the care of your patients is not interrupted. Our focus is not on the partisan debate. It is on protecting our patients. Northeast Florida has one of the best medical systems in the state and this ruling from the Supreme Court does not change that. We will continue to work to resolve outstanding issues and advocate for physician and patient rights through local, regional and national advocacy efforts.

www . DCMS online . org

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Rehabilitation Hospital • Outpatient Clinics • Home Health • Nursing • Medical Group Practice • Research • Community Programs

6 Vol. 63, No. 3 2012 Northeast Florida Medicine

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Northeast Florida Medicine Vol. 63, No. 3 2012 7


Philip H. Gilbert Invited Editorial

Funding for Indigent Care in Jacksonville Daniel R. Wilson, MD, PhD Vice President, University of Florida Health Science Center, Jacksonville and Dean, UF College of Medicine-Jacksonville Editor's Note: Philip H. Gilbert served as the Executive Vice President of the Duval County Medical Society (DCMS) from 1984 until his unexpected death in 2004. During those decades, he was an outspoken advocate for the physicians he served and for the needs of their patients. With no fear of retribution, Phil shared his honest informed opinions with his DCMS colleagues and with the community they served. In his honor, the DCMS Board of Directors established the Philip H. Gilbert Invited Editorial to celebrate his spirit for addressing issues that he championed such as advocacy, tort reform, community activism and caring for the underserved. The “Request for the 2011 Philip H. Gilbert Invited Editorial” invitation was sent in July to local, state, and national leaders (physician or layperson). All editorials received were reviewed by the DCMS Journal and Communications Committee and two were chosen for publication. One is published in this issue and the one will appear in the winter journal.

The numbers are staggering. State and federal dollars to care for the underinsured in Jacksonville have been cut $53 million over the past four years. Costs to care for Duval County’s indigent at UF&Shands Jacksonville, The University of Florida Academic Health Center, are rapidly increasing while the city of Jacksonville’s contribution for such care has remained flat for a decade at $23.8 million per year. This annual contribution represents less than half of what the true costs of care represent. And, in the past decade Shands Jacksonville and the University of Florida medical professionals have provided without reimbursement nearly $300 million worth of care to those in need. University of Florida College of Medicine-Jacksonville doctors provide exemplary care to all citizens, mainly at Shands Jacksonville, but also at clinics across the city and with key Daniel R. Wilson, MD, PhD partners. Moreover, we do VP UF Health Science Center this with extraordinary efand Dean, UF College of ficiency. Of 71 U.S. teaching Medicine - Jacksonville hospitals surveyed last year by the UHC, an alliance of academic health centers, Shands Jacksonville ranked the best for lowest supply expense per case and ninth for lowest total cost. One would be hard-pressed to find a business in America that can suffer such funding deficits and remain operationally viable. We are the lifeboat upon which the city’s sickest and poorest people depend.We cannot sink. Can we? One of our missions as an academic health center is to care for the uninsured and under insured. It is a mission we embrace. But it is also a mission in jeopardy – immediate and serious jeopardy. The current funding model is inadequate and increasingly unsustainable. But, we are not just sitting around waiting for funding to magically reappear. 8 Vol. 63, No. 3 2012 Northeast Florida Medicine

Our groundbreaking research continues to help change the lives of patients in Jacksonville and across the country. In support of this, we secured $22 million in outside funding for research last year – the seventh consecutive increase for our campus. Plans are underway for Shands Jacksonville North, a hospital across from the booming River City Marketplace. This will help improve our payer mix with a result being to subsidize operations of the 8th Street campus that serves the entire region as the basic source of uncompensated care. Recently, we implemented a medical home model to help these most medically and socially vulnerable in our community live healthier lives. Such patients will soon be seen by a dedicated team of clinicians in a unique total care clinic rather than over reliance on our Emergency Room.This medical home will allow us to better treat growing numbers of uninsured for less and do so in a manner tailored to their unique needs via care rendered with culturly competence. But this group is only a fraction of the nearly 300,000 uninsured in Jacksonville. Community-wide care for those in need cannot continue to be a Shands Jacksonville-only responsibility. It is undeniably a Jacksonville issue that the city and all its citizens need to recognize, accept and address. The medically needy, uninsured and indigent must be recognized as the responsibility of the entire county and all its health systems – not justUF&Shands. Despite our creative changes that attempt to cover gaping losses, can we continue this key societal mission alone much longer? No, we cannot. UF&Shands carries far more than its fair obligation both morally and fiscally but cannot do so much longer. Our elected officials and civic leaders must make dealing with this dire situation a priority. The problem is not going to self-correct. The remarkable humanitarian mission of UF&Shands will have to be greatly reduced if Jacksonville cannot better address this crisis urgently and achieve alternative solutions. We simply do not have the money to continue giving away more than $50 million dollars a year to a social end that is the moral responsibility of a far, far broader group than the faculty at UF and the staff at Shands Jacksonville. www . DCMS online . org


Residents’ Corner: Naval Hospital Jacksonville Editor’s Note: In an effort to connect more Duval County Medical Society members with residents, in each 2012 issue there will be a “Residents’ Corner” with information about a residency program in the area, details about research being done and/or a list of achievements/accomplishments of the program’s residents. This “Residents’ Corner” features the Naval Hospital Jacksonville.

Overview of Residency Program

Naval Hospital (NH) Jacksonville is home to the oldest and largest accredited of six Family Medicine Residency Programs in the Navy, and it earned the 2011 Clinical Site of the Year Award from the Uniformed Services University of the Health Sciences. NH Jacksonville is a busy community hospital, providing the entire continuum of care for active and retired service members and their families such as primary and specialty care, surgical and maternity services, wellness centers and ancillary services, along with programs for warfighters. It has 91 active beds, over 5,000 admissions and 1,000 deliveries annually. Family Medicine (one of three primary care clinics) has over 14,000 enrolled beneficiaries with 75,000 outpatient visits per year. The Family Medicine Residency Program is a three-year program with 12 residents per class and a first-time board certification pass rate of 98% for the past 41 years. Graduates can expect to be deployed around the world, with duty assignments afloat and ashore, on ships, with Marine Corps battalions, and at stateside and overseas naval hospitals and with fleet surgical teams. Many of these assignments are in austere environments with limited resources. To meet the needs of patients in these settings, residents cross-train at other facilities to broaden their experience. The core curriculum includes rotations in MICU, NICU and trauma at the University of Florida & Shands Jacksonville, and inpatient pediatrics and pediatric emergency medicine at Wolfson Children’s Hospital. All Family Medicine providers (including residents and faculty) work on one of four Medical Homeport teams, each of which functions much like a group practice with the patient at the center. Many faculty members have additional fellowship training, and residents obtain a superb mix of experiential and academic instruction with an abundance of opportunities for hands-on learning. Robust procedural training prepares residents to perform vasectomy, colposcopy, exercise treadmill tests, obstetric ultrasonography and an assortment of minor procedures. Electives include colonoscopy and advanced obstetrics. The program emphasizes evidence-based medicine and a scholarly approach to clinical problem-solving. Many of the faculty members have additional fellowship training. The residency and medical student programs benefit greatly from NH Jacksonville’s organizational commitment to excellence in both education and clinical practice.

Awards

Received Family Medicine 2011 Clinical Site of the Year Award from the Uniformed Services University of the Health Sciences .

At the Uniformed Services Academy of Family Physicians annual symposium in 2012 which included 17 Department of Defense Family Medicine Residency Programs, NH Jacksonville: submitted 27% (22/79) of the research works, represented 28% (7/25) of the research works accepted, and earned 67% (4/6) of the awards in the categories entered.

Community Outreach

Tar Wars: Lt. Amy Watkins (PGY-3) along with 7 other residents and Lt. Cmdr. Michelle Overton (staff physician) coordinated this American Academy of Family Physicians program to educate local students about being tobacco-free, provide tools to make positive decisions, and promote personal responsibility for their well-being.

Research •

• • • •

Lt. Anne McLendon (PGY-3) and Lt. Patricia Reichert (PGY-2) are carrying out a research project looking into gestational diabetes mellitus (GDM). This study screens patients earlier in pregnancy, quantifies the efficacy of screening, measures compliance with GDM guidelines, and examines the effect of early versus standard diagnosis on maternal weight gain. Ultimately, the goal is to better identify and control GDM. Lt. Theodore Demetriou (PGY-3) has an institutional review board study evaluating a method to shorten the healing time of plantar fasciitis with the use of autologous blood injections. Lt. Liz Rodnez (PGY-2) has contributed three chapters to an encyclopedia by Dr. Jill Grimes, MD, about sexually transmitted infections for adolescents Lt. Patricia Reichert (PGY-2) and Lt. Mona Singh (PGY-2) have a study to evaluate the efficacy of pediatric obesity management using increased clinic visits, teaching, and nutrition programs. Lt. Cmdr. Mike Arnold (PGY-3) is drafting a study to evaluate EKG training methods, comparing 20 five-minute sessions with a single 100-minute didactic session.

Lt. Cmdr. James Hodges, MD, Medical Corps, U.S. Navy, is a 3rd year Family Medicine resident at Naval Hospital Jacksonville. Dr. Hodges was a Navy submarine officer for 10 years before graduating from the Uniformed Services University of the Health Sciences in Bethesda, Maryland. www . DCMS online . org

Northeast Florida Medicine Vol. 63, No. 3 2012 9


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Patient Page* - Knee Replacement

Are You Considering Knee Replacement? Written by Leora Legacy, Northeast Florida Medicine Managing Editor In March 2009, I had my right knee replaced. Because of the novelty, I took photos of the stapled knee, the bruising, the flowers sent, the therapists who helped me, my orthopedist…I just documented it all. In March 2012, I had my left knee replaced because osteoarthritis had damaged it too. I even had an arthritic spur wearing away my femur bone. No photo documentation this time. (other than x-rays/See below) I guess I had “been there, done that,” so I didn’t need photos. I’ve learned quite a bit about the procedure and myself while going through the joint replacement process. I’m thankful there is technology today that allows for body parts to be replaced. It means I am walking today and not in a wheelchair or using a cane. If you are thinking about knee replacement, there are some important pre-surgery, post-surgery and long term considerations.

Pre-surgery Tips: • • • • •

Find a good orthopedist. (get a referral from your Primary Care physician or friends and/or family) Get a diagnosis from two orthopedists. (choose the one to do the surgery that you relate to best) Remember, not all knees must be replaced. Ask lots of questions. If you have other medical conditions, find out how surgery and therapy may affect those. Understand the surgery risks. Get information from the internet and talk to friends or family who have had knee replacements. (Be ready for cautions. This is major surgery.) Look ahead on your work and personal calendar to make sure you have at least 3-4 weeks you can take off from regular activities. (Count on 6 weeks before you can drive again) • Plan on having some assistance at home for a couple weeks to dress, bathe, cook, do laundry, etc. • Be determined to do whatever therapy is required and STAY determined as you go through therapy.

Post-surgery Cautions

• Follow your orthopedist’s orders and the nurses’ directions in the hospital (i.e. start moving because of blood clot risks, wear compression socks for the same reason, use ice packs to help swelling, and eat sensibly so bowels will work despite effects of pain pills and inactivity) • Take prescribed pain medication when needed and then stop when over-the-counter pain medicine is enough. • Start therapy and give it your all! • Expect a low energy level and possibly interrupted sleep patterns at night. That will improve. • Be careful when walking with a walker or cane. Remove small rugs in your way. If you fall, try to land on your side and not your knee(s). • Do everything you are told for the best outcomes.

Long Term Advice • • • •

Keep exercising and moving even after therapy sessions are completed. Watch your weight. If you were told by the doctor to lose some pounds – do it! To get the longest life out of your new knee(s), do not jog, limit kneeling, and avoid stairs as much as possible. Be patient with yourself and your knee(s). For about 1-year, there will be knee stiffness and swelling . And yes, you will have a scar on your knee. (6” possible) • Expect to tire more easily for awhile. Build in some nap time. • Use common sense in how much stress you put on your knees, but stay active. • Be ready to set off the metal detectors at airports and other places that have sensitive security equipment. (Haven’t noticed a problem at any retail stores)

Knee Replacement Stats • Greater than 30 million Americans are affected by osteoarthritis annually. (70 to 90% are over the age of 75) • In 2006, more than 1.1 million hip or knee replacement surgeries were performed. (National Center for Health Statistics;Centers for Disease Control and Preventions, National Hospital Discharge Survey, 2006)

• Greater than 90% of people who have knee replacement surgery will experience reduction of knee pain and improvement in the ability to perform daily activities, although not better than before they developed arthritis (American Academy of Orthopaedic Surgeons, http://orthoinfo.aaos.org/. Look under Total Knee Replacement)

Figure 1 (Left) is the weightbearing preoperative x-ray of the left knee joint. Notice (arrow) where the bone spur on the kneecap has caused a deformity to the femur/thigh bone. Figure 2 (Right) is a postoperative x-ray of the left knee soon after surgery. The arthritic parts of the knee have now been replaced by metal and plastic and the knee alignment has been restored to normal.

• Surgery should be considered when: severe knee pain or stiffness limits everyday activities (walking, climbing stairs, and standing from a seated position); one has moderate or severe knee pain while resting, either day or night; a person has long term knee inflamation and swelling that does not improve with rest or medications (anti-inflammatory medications, cortisone shots, artificial joint fluid injections, therapy); or there is knee deformity. More information at http://orthoinfo.aaos.org/ (Look under Total Knee Replacement)

*Copy and distribute to patients or go to dcsmsonline.org, click "NEFM" and download for patient use.

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Northeast Florida Medicine Vol. 63, No. 3 2012 11


From Sketch to Icon and Now Sculpture Little did Dr. Nicholas Andry realize when he drew a “Crooked Tree” as an illustration for his 1741 book Orthopaedia: The Art of Correcting and Preventing Deformities in Children that it would survive generations and become the symbol for many orthopaedic organizations around the world. Now known as the “Tree of Andry”, the crooked tree tied to a strong post is an internationally recognized icon in reference to how orthopaedic surgery corrects deformities. In Dr. Andry’s time, a crooked leg was bandaged to an iron plate to help straighten it, just as it was also commonly used to make a bent sapling tree stand tall. This analogy has stood the test of time and now symbolizes the profession. Orthopaedic literally means "straighten the child" because in Dr. Andry's time, many children had deformities as a result of polio and rickets. Over the years various artists, bonsai enthusiasts, and sculptors have based their creations on Andry’s very basic drawing. The cover of this journal is a sculpture inspired by the Tree of Andry and created by Douglas Kiburz, MD, an orthopaedist in Sedalia, Missouri and Bob Schwickrath, a retired x-ray technician. They combined their interest in sculpting and started Cave Folk Creations. Using welding cable, they make copper trees (from Aspens to Willows) by utilizing lapidary saws, blow torches, underwater diamond drills and a few surgical instruments.

Douglas Kiburz, MD

Dr. Kiburz says, “The Andry Tree is an exceptional symbol of a great profession which is dedicated to keeping the world in motion. Creating an actual piece of art which has existed as a sketch for 300 years is exciting.”

A tree climber when he was child, Dr. Kiburz adds, “As an orthopaedist, I now take care of kids who get hurt climbing trees. That is one reason I am writing a children’s book on tree appreciation and safe climbing.” A member of Sedalia, Missouri’s Tree Board, Dr. Kiburz has been in practice in Sedalia for 26 years and is Chief of Orthopaedics, Physical Therapy and Rehabilitation at Bothwell Regional Health Center. His avocation at Cave Folk Creations gives him an artistic outlet, and he is pleased many of the tree sculptures are purchased and displayed in offices and academic departments coast to coast. If interested in purchasing a Tree of Andry sculpture by Dr. Kiburz, go to http://fineartamerica.com/featured/tree-ofandry-cave-folk-creations.html. For other creations, email Dr. Kiburz at kibz@charter.net.

(Left) The original sketch of the Tree of Andry dated 1741. (Right) The Tree of Andry sculpture created by Dr. Kiburz and his Cave Folk Creations partner.

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This Issue’s Focus: Orthopaedics

Musculoskeletal Diseases Challenge Patients, Physicians & Society The treatment of pathologic conditions of the musculoskeletal system has continued to evolve with notable advances in diagnostic evaluation, pharmacologic management, and surgical intervention. Within the medical community, enthusiasm for these advances has been tempered by local, state, and federal legislative measures to curtail and control healthcare spending. According to the World Health Organization, the United States spends approximately 16% of the gross domestic product (GDP) on healthcare; more than any other industrialized nation in the world. In 2004, the total cost for the treatment and lost wages associated with musculoskeletal diseases approached $849 billion1. The current and future challenge for orthopaedic surgeons and other musculoskeletal physicians is the ability to provide contemporary treatment to an increasing volume of patients in a fiscally responsible manner, without jeopardizing the quality of care and the welfare of the patient. As the healthcare model shifts from a volume and fee based system to reimbursement based on quality measures, clinicians and surgeons alike will be tasked with preserving the patient-physician relationship. With that in mind, we have several topics specific to the subject of musculoskeletal medicine in this issue of Northeast Florida Medicine. The authors were selected to provide a balanced viewpoint from both academic and community based environments. The article subjects were chosen based upon their clinical importance and the relevance to our community populace. Kamal I. Bohsali MD, FAAOS, FACS Diplomate, American Board of Orthopaedic Surgery Bahri Orthopedics & Sports Medicine Clinic

First is “Innovations in the Treatment of Dupuytren’s Contracture” by Garry S. Kitay, MD, which discusses current treatment modalities for Dupuytren’s contracture with a focus on newer options such as collagenase therapy. Next is the CME article, “Lumps and Bumps: Initial Evaluation and Management of Bone and Soft Tissue Tumors,” by Courtney E. Sherman, MD and Mary I. O’Connor, MD. In “Management of Neck Pain and Cervical Radiculopathy,” Ali Chahlavi, MD, Eric Nottmeier, MD and John Matthew Hale, PA-C, expound on the initial diagnosis and management options of cervical radiculopathy and how problems in the cervical spine can manifest as symptoms in the upper extremities. In “Joint Replacement Options for the Shoulder”, I provide a succinct review regarding the surgical options for arthritis of the gleno-humeral joint . A related treatise on rotator cuff tear management entitled “Contemporary Treatment of Rotator Cuff Tendinopathy” by LCDR Emeka Ofobike, Jr., MD, follows. We continue with two articles that focus on the knee. The one in the pediatric population about ACL tears and cartilage injuries is “Pediatric and Adolescent Sports Injuries of the Knee,” by Eric D. Shirley, MD and Mary Anderson, BS. The other in the adult population regarding computer assisted partial knee replacement surgery is “Robotic Assisted Partial Knee Replacements: An Advance in Surgical Technique by Kenneth Kaminski, MD; Cedric Ortiguera, MD, and Mary I. O’Connor, MD. The issue ends with a timely topic for weekend warriors entitled “Lateral Ankle Ligament Injuries: Treatment Decisions Involving the Ankle Sprain,” by Malik Abraham, DPM that discusses evaluation and management of chronic ankle instability. We applaud all physicians in our community, not just orthopaedic surgeons, in their desire to provide “patient-centric”, competent, and fiscally responsible heath care. Bibliography Jacobs J et al. The Burden of Musculoskeletal Diseases in the United States: Executive Summary. American Academy of Orthopaedic Surgeons et al. Rosemont, IL; 2008: 1-9.

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Innovations in theTreatment of Dupuytren's Contracture Garry S. Kitay, MD Abstract: Dupuytren’s disease can lead to progressive and disabling flexion contractures of the hand. In the last century, the most common treatment for this condition has been surgical excision of the contracting fascial cords. However, there is a relatively high complication rate with these procedures. Over the last decade there has been greater interest in, and use of, percutaneous or needle aponeurotomy, which disrupts the cord with a minimally invasive technique. There is also a newer non-surgical technique that utilizes an injectable collagenase enzyme mixture. Both of these treatment methods are performed in the office. Their advantages and concerns are discussed.

Introduction Dupuytren’s disease is a condition of abnormal collagen production that can lead to progressive and disabling flexion contracture of the digits. It is named after the French surgeon Baron Guillome Dupuytren, who was the first to treat the condition with fasciectomy, or excision of the cord, in 1831. The condition was first described by Plater over 400 years ago in 1614.1 Henry Cline characterized it as a disease of the palmar fascia and was the first to describe division of the cord as a treatment option in 1777.2 There is a strong genetic contribution to the development of Dupuytren’s disease. Many believe the disease to have originated with Germanic tribes 2,500 years ago, and then spread by the Viking conquests.3 Hence, the condition is much more commonly seen in individuals of Scandinavian and northern European descent. The disease appears to be transmitted by autosomal dominant inheritance with variable penetration. However, no specific group of genes has been identified as the sole cause of the disease. It does appear that there is inhibition of the genes that regulate the natural breakdown of collagen.4 While palmar fascia is normally composed of Type I collagen, Dupuytren’s cords are primarily composed of Type III collagen. It is the myofibroblast that is the major contractile element in this disease, and this actively contracting tissue shortens and transforms into a static acellular matrix. Normal ligaments and fascial bands are transformed in this condition into the diseased contractile tissue, which can then lead to joint contracture as well as skin and subcutaneous tissue stiffness.5 It appears that environmental contributors to this condition exist. Both alcohol use and smoking are associated with increased risk of developing Dupuytren’s. The disease is also more common in males, diabetics, and older individuals.4,6

Presentation Dupuytren’s is most commonly seen in males over the age of forty. Men are two to seven times more likely to develop Address correspondence to: Garry S. Kitay MD, Jacksonville Orthopaedic Institute, Affiliate of Baptist Health System, 1325 San Marco Blvd., Suite 200, Jacksonville, FL 32207. Phone: 904-8586425. Email: gkitay@joionline.net. 14 Vol. 63, No. 3 2012 Northeast Florida Medicine

the condition. It often develops with nodules in the palm first, and these gradually develop into cords with myofibroblast contraction. As these cords become acellular matrices, they also become fixed to overlying skin.4 This condition generally is not painful except with forced stretching of these tissues. Most commonly, the disease begins in the palm and spreads distally, first involving the metacarpophalangeal (MCP) joints, followed by the proximal interphalangeal (PIP) joints. However, there are some individuals where the disease is isolated to the digit and only contracts the PIP joints. About 50% of individuals who have a palmar nodule will develop cords. As the disease progresses, often patients are unable to place their hand flat on a table.7 The digit most commonly affected is the ring finger, followed by the small finger. Occasionally all fingers can be affected including the thumb (Figures 1a-c, p. 16)

Treatment Many articles and book chapters have been devoted to the treatment of Dupuytren’s contracture. It is largely accepted that external management of contractures is not effective. These modalities, such as splinting, physical therapy, and even radiation therapy, have not proven helpful. Surgical procedures are generally considered indicated when the contracture is over 30 degrees at the MCP joint and over 15 degrees at the PIP joint.4 Excision of the contractile elements is an effective means of disease management. These procedures can be classified based on the degree of tissue excision. Radical fasciectomy where all subcutaneous fascia is removed has been largely abandoned due to its high morbidity and complication rate. Limited fasciectomy is the most popular surgical procedure performed for Dupuytren’s. It involves excision of diseased fascia, but not of the healthy palmar tissue. Dermato-fasciectomy includes the above with excision of the overlying contracted skin, in order to lower the recurrence rate. A local fasciectomy involves removal of diseased fascia through a smaller incision, but this leaves most of the diseased tissue in place. Finally, fasciotomy is a local division of a diseased cord without its removal at all. These latter two procedures have a higher recurrence rate with the diseased tissue being disrupted but not excised.8 With the more aggressive surgical excision procedures, complications are relatively frequent. They tend to be higher when the deformity is worse, as is the recurrence rate. Wound healing complications can occur in up to 20% of patients with nerve injury in 2% and complex regional pain syndrome in nearly 6% of patients. Infection can occur in over 2% with a major complication rate of 15%.4

New Treatment Options The relatively high complication rate for fasciectomy as well as prolonged recovery has led to research and renewed interest in less invasive techniques. Currently there are two treatment www . DCMS online . org


Figures 1 A,B,C Hands Affected by Dupuytren's Contracture

(Left to Right) (A) Dupuytren’s cord to ring finger with 70º MP and 20º PIP joint contractures. (B)The involved digit cannot be passively extended. (C) Table top test – the hand cannot be placed flat on a surface.

modalities that have gained popularity. These two modalities include collagenase injection and percutaneous fasciotomy. Collagenase Injection – Injectable collagenase is the first Food and Drug Administration approved non-surgical treatment for Dupuytren’s contracture. This is office-based, and the patient must have a palpable cord leading to a contracture such that they cannot place their hand flat on a table. The medication has two distinct enzymes from clostridium histolyticum that cleaves collagen strands at different sites. AUX1 cleaves the terminal ends of collagen and AUXII cleaves internal sections of the collagen.9 In a 2009 New England Journal of Medicine study, contractures were improved with up to three injections of collagenase into the Dupuytren’s cords to within 0-5 degrees of full extension in 77% of the MCP and 40% of the PIP joints, compared to 7% and 6% with placebo. The range of motion at the MCP joint improved by 41 degrees, and at the PIP joint by 29 degrees. Overall improvement was 94% for the MCP joints and 67% for the PIP joints.10 The results were better for less contracted joints, which is similar to surgical results. Most complications noted with this injection technique were edema, contusion, and pain, which are particularly noted for the first few days. Also, lymphadenopathy can occur as well as skin laceration. Major complications are rare, but flexor tendon rupture has occurred, which was thought to be from injecting the collagenase in proximity to the flexor tendon.11 This technique has been approved to be performed one cord at a time. Hence, individuals with multiple cords may require multiple injections at different sittings. In fact, there needs to be a one month period between injections. The injection is performed in the office, and the release, where the digit is extended and often accompanied by an audible and palpable release of the contracted tissue, is performed the following day. It is during this procedure that skin tears are sometimes seen near the site of the injection of the collagenase. Night time splinting is recommended for a four month period. Percutaneous Fasciotomy – This technique was popularized initially by French rheumatologists in the 1970s.12 Although it was first thought to be a good choice for more elderly individuals with less severe contractures,13 it has become

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popular in a wider group of Dupuytren’s patients.This procedure has similarities to the collagenase injection. In both, a confined area of the constrictive cord is disrupted. Both are also performed in areas where the skin is intact but not adherent to the underlying cord. This is also performed in the office, but the extension maneuver to the involved digits is performed immediately, also often with a palpable and audible release. Percutaneous aponeurotomy has the advantage of permitting multiple digits to be treated simultaneously. Both procedures generally employ night time splinting, but not formal hand therapy, which is extensive in the open surgical procedures. The recovery period of the needle technique, in general, is short, with a relatively low complication rate. The recurrence rate is higher than with surgical fasciectomy. Neither this technique nor collagenase injection is appropriate for contractures due to post surgical scarring, inadequate skin, or capsular contracture of the PIP joint.

Technique Hypodermic 18 to 25 gauge needles are utilized after local anesthesia is achieved with infiltration just to the level of the dermis. It is notable that the pathologic cord itself is insensate. Hence with the local anesthesia, one is careful not to anesthetize the nerves surrounding the cord. In this way the patient can warn the physician if the cutting needle approaches the digital nerve. The cord is cut with the needle by creating multiple puncture sites within it, or by using a swiping maneuver. Care needs to be exercised to keep distance from digital nerves. It can help to keep the digit passively extended while performing the fasciotomy. After completing the cord division, the finger is passively extended. If full extension is not achieved, further release may be required. Although formal hand therapy is generally not required, passive extension of the finger at night in a splint for up to four months is recommended to try to limit recurrence. Strenuous activities should be avoided the first week following the procedure, after which most patients can return to normal activities (Figures 2a-c, p.16) See technique video, as well as two week results of procedure, on htpp://youtube. com/watch?feature=player_embedded&V=QQxsxul-Uvo#!

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Figures 2 A,B,C Results of Percutaneous Aponeurotomy

(Left to Right) (A) Same patient 2 weeks following percutaneous aponeurotomy, full extension. (B) Full fist. (C) Negative table top test.

Results

5.

Al-Qattan MM: Factors in the pathogenesis of Dupuytren’s contracture. J Hand Surg Am 2006; 31(9): 1527-1534.

Needle or percutaneous aponeurotomy leads to contracture improvement of the MCP joint in 79-100% of procedures, and the PIP joint in 46-76%.11 In a recent study, there was greater correction maintained in the older age group, over 55 years old, irrespective of gender. The improvement maintained was over 50% of the initial contracture in 75% of MCP joints and in 33% of PIP joints at least three years following the procedure. Complications were infrequent. The most common were skin tears, which occurred in 3.4%, followed by transient nerve parasthesias.15 A single study directly compared percutaneous needle fasciotomy and open limited fasciectomy. Although both groups improved their extension, it was greater in the open surgical group. There was also a higher recurrence rate in the aponeurotomy group; however, the major complication rate was higher in the fasciectomy group.16 While the effectiveness of needle aponeurotomy is supported by many studies 17-20, the recurrence rate is higher when compared with open fasciectomy. However, it also has a dramatically more rapid recovery rate and lower incidence of major complications.

6.

Burke FD, Proud G, Lawson IJ, et al: An assessment of the effects of exposure to vibration, smoking, alcohol and diabetes on the prevalence of Dupuytren’s disease in 97,537 miners. J Hand Surg Eur 2007; 32(4):400-406.

7.

Reilly RM, Stern PJ, Goldfarb CA: A retrospective review of the management of Dupuytren’s nodules. J Hand Surg Am 2005; 30(5): 1014-1018.

8.

Van Rijssen AL, Werker PMN: Percutaneous Needle Fasciotomy in Dupuytren’s Disease. J Hand Surg 2006; 31B(5): 498-501.

9.

Gilpin D, Coleman S, Hall S, et al: Injectable Collagenase Clostridium Histolyticum: A New Nonsurgical Treatment for Dupuytren’s Disease. J Hand Surg 2010; 35A: 2027-2038.

Summary

13. Rowley DI, Couch M, Chesney RB, et al. Assessment of Percutaneous Fasciotomy in the Management of Dupuytren’s Contracture. J Hand Surg Br. 1984; 9B(2): 163-4.

Percutaneous aponeurotomy and collagenase injection appear to be safe and effective for Dupuytren’s, particularly in the short-term. Similar results are obtained with both procedures. Outcomes from both are better at the MCP than the PIP joints and when there are milder degrees of contracture. Almost all contractures can be improved when there is a palpable cord. However, contractures due to post surgical scarring, inadequate skin, or capsular contracture of the PIP joint will not improve with either procedure.

References

1.

Elliot D: Pre-1900 literature on Dupuytren’s disease. Hand Clin 1999; 15(1): 175-181.

2.

Cline H. Notes on pathology. London: St. Thomas Manuscript Collection. 1777:185.

3.

McFarlane RM: On the origin and spread of Dupuytren’s disease. J Hand Surg Am 2002; 27(3): 385-290.

4.

Black E, Blazar P: Dupuytren disease: an evolving understanding of an age-old disease. J Am Acad Orthop Surg 2011; 19:746-757.

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10. Hurst LC, Badalamente, Hentz VR, et al: CORD I Study Group: Injectable collagenase Clostridium histolyticum for Dupuytren’s contracture. N Engl J Med 2009; 361(10): 968-979. 11. Srinivasan R, Shah A, Jebson P. New Treatment Options for Dupuytren’s Surgery: Collagenase and Percutaneous Aponeurotomy. J Hand Surg 2010; 35A: 1362-1364. 12. Lermusiaux JL, Debeyre N. Le traitement medical de la malidie de Dupytren. Rhumatologique. Paris: Expansion Scientifique, 1979; 338-323.

14. Eaton, C. Percutaneous Fasciotomy for Dupuytren’s Contracture. J Hand Surg 2011; 36A: 910-915. 15. Pess GM, Pess RM, Pess RA. Results of Needle Aponeurotomy for Dupuytren Contracture in Over 1,000 Fingers. J Hand Surg 2012; 37A(4): 651-6. 16. van Rijssen AL, Gerbrandy FS, Ter Linden H, et al. A comparison of the direct outcomes of percutaneous needle fasciotomy and limited fasciotomy for Dupuytren’s disease: A 6-week follow-up study. J Hand Surg Am 2006; 31(5): 717-725. 17. Badois FJ, Lermusiaux C, Masse C, et al. Nonsurgical treatment of Dupuytren’s disease using needle fasciotomy. Rev Rheum Engl Ed 1993; 60:692-697. 18. Foucher G, Medina J, Navarro R. Percutaneous needle aponeurotomy: complications and results. J Hand Surg 2003; 28B: 427-431. 19. Rahr L, Sondergaard P, Bisgaard T, Baad-Hansen T. Percutaneous needle faciotomy for primary Dupuytren’s contracture. J Hand Surg (Eur) 2011; 36E(7): 548-552. 20. Cheng HS, Hung LK, Tse WL, Ho PC. Needle aponeurotomy for Dupuytren’s contracture. J Orthop Surg 2008; 16(1): 88-90.

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Lumps & Bumps: Initial Evaluation and Management of Bone & Soft Tissue Tumors 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, “Lumps and Bumps: Initial Evaluation and Management of Bone and Soft Tissue Tumors” authored by Courtney E. Sherman, MD and Mary I. O’Connor, MD (see pp. 19-23), which has been approved for 1.0 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: Courtney E. Sherman, MD, is a Fellow in the Department of Orthopedic Oncology at Mayo School of Graduate

Medical Education, Mayo Clinic in Rochester, MN. Prior to this appointment, she was a Resident in the Department of Orthopedic Surgery at Mayo Clinic and earned her MD from Northeastern Ohio University, College of Medicine in Rootstown, OH. Mary I. O’Connor, MD, is an Associate Professor of Orthopedics at the College of Medicine, Mayo Clinic Jacksonville in Jacksonville, FL. She is also Chair of the Department of Orthopedic Surgery at Mayo Clinic Jacksonville and Program Director of its Adult Reconstructive Fellowship. Dr. O’Connor serves as a consultant to the Department of Orthopedic Surgery at Mayo Jacksonville and to Nemours Childrens Clinic in Jacksonville, FL. She received her MD from the Medical College of Pennsylvania and did an internship, residency and fellowship at Mayo Graduate School of Medicine.

Objectives for CME Journal Article 1. Recognize common bone and soft tissue tumors 2. Understand worrisome clinical and radiographic findings of malignancy in bone tumors 3. Understand worrisome clinical and radiographic findings of malignancy in soft tissue tumors

Date of Release: September 1, 2012 Date Credit Expires: September 1, 2014. Estimated time to complete: 1 hr.

Methods of Physician Participation in the Learning Process

1. Read the “Lumps and Bumps: Initial Evaluation and Management of Bone and Soft Tissue Tumors” article pages 19-23. Complete the Post Test and Evaluation on page 18. 3. Members or non-members may fax the Post Test to DCMS (FAX) 904-353-5848 OR members can also go to www.dcmsonline.org & submit the test online. Non-members must arrange for the CME fee payment before submitting the post test by fax. Call 904-355-6561 x106 or fax.

CME Credit Eligibility

In order to receive full credit for this activity, a minimum passing grade of 70% must be achieved. Only one re-take opportunity will be granted if a passing score is not made on the first attempt. DCMS members and non-members have two years to submit the post test and earn CME credit. A certificate of credit/completion will be emailed or USPS mailed within 4-6 weeks of submission. If you have any questions, please contact the DCMS at 355-6561, ext. 103, or llegacy@dcmsonline.org.

Faculty Disclosure Information

Dr. Sherman and Dr. O’Connor report 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 1.0 AMA PRA Category 1 credit(s) .TM Physicians should only claim credit commensurate with the extend of their participation in the activity.

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Northeast Florida Medicine Vol. 63, No. 3 2012 17


CME Questions & Answers (Circle Correct Answer) /Free-DCMS Members/$50.00 charge non-members*

Lumps & Bumps: Initial Evaluation & Management of Bone & Soft Tissue Tumors

(Return by September 1, 2014 by FAX: 904-353-5848, by mail: 555 Bishopgate Lane, Jacksonville, FL 32204 OR online: www.dcmsonline.org)

1. The estimated incidence of primary malignant tumors of the bone in the U.S. in 2012 is 10/100,000. a. True b. False 2. The estimated incidence of primary malignant soft tissue tumors in the U.S. in 2012 is 3.3/100,000. a. True b. False 3. The most common benign bone tumor in children is: a. Aneurysmal bone cyst (ABC) b. Unicameral bone cyst (UBC) c. Non-ossifying fibroma (NOF) d. Fibrous dysplasia e. Chondroblastoma 4.

The most common benign soft tissue tumor is: a. Giant cell tumor of tendon sheath b. Glomus tumor c. Hemangioma d. Lipoma e. Myxoma

5. Periosteal new bone formation is a worrisome radiographic feature of a malignant bone tumor. a. True b. False 6. Worrisome radiographic features of a malignant soft tissue tumor include all of the following EXCEPT: a. Greater than 5 cm b. Deep location c. Hetereogenous d. Invasive lesion e. High signal intensity on T1 MRI sequences similar to subcutaneous fat 7. In patients with a metastatic lesion of unknown primary, the Rougraff strategy will identify the primary malignancy in 30% of patients. a. True b. False 8. Poorly performed biopsies can adversely affect the patient’s survival, fail to allow proper diagnosis or necessitate amputation in order to obtain clear margins. a. True b. False

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)

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Lumps and Bumps: Initial Evaluation and Management of Bone and Soft Tissue Tumors Courtney E. Sherman, MD and Mary I. O’Connor, MD Abstract: An understanding of the systematic approach to bone and soft tissue tumors can help the practitioner recognize common bone and soft tissue tumors and potential worrisome clinical and radiographic findings of malignancy. These principles will allow the practitioner to direct the patient to the appropriate specialist for further evaluation and management.

Introduction Bone and soft tissue tumors commonly present clinically as “lumps and bumps”. These tumors can be a source of diagnostic and therapeutic uncertainty. Primary malignant tumors of bone and soft tissue are rare. Missed diagnoses or inadequate management, such as poorly performed biopsies and excisions, can adversely affect the patient’s survival and fail to allow proper diagnosis or necessitate amputation in order to obtain clear margins1,2. While the likelihood of most clinicians diagnosing a primary malignant bone or soft tissue tumor is low, many providers will see several bone and soft tissue lesions present each year. It is necessary for the clinician to recognize benign versus potentially malignant bone and soft tissue lesions based on history, physical examination, and imaging findings.

Incidence Primary bone and soft tissue sarcomas are rare when compared to more prominent entities such as lung cancer. In the United States in 2012, an estimate of 2,890 people will be diagnosed with a primary malignant tumor of bone, an incidence of 0.9/100,000 people. Osteosarcoma is the most common primary malignant tumor of bone. At least 11,280 people will be diagnosed with a primary malignant soft tissue tumor, an incidence of 3.3/100,000 people. In comparison, an estimate of 226,160 people will be diagnosed with lung cancer in the United States, an incidence of 62.6/100,000 people3. There are more than 1.2 million cases of carcinoma yearly in the United States with a 30-80% incidence of metastatic bone lesions3,4. The incidence of benign bone lesions is difficult to estimate as many are asymptomatic and therefore these lesions are under diagnosed. The estimated prevalence of nonossifying fibroma is 30-40%, believed to be the most common benign skeletal lesion (tumors) in children. Osteoid osteoma accounts for 10% of benign bone tumors, enchondroma 12-24% of benign bone tumors and giant cell tumor accounts for 5% of all benign bone tumors 5,6,7. Address Correspondence to: Mary I. O’Connor, MD, Department of Orthopedic Surgery, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224. Phone: 904-953-0260.Email: oconnor.mary@mayo.edu. www . DCMS online . org

The incidence of benign soft tissue lesions is also difficult to estimate as these lesions are likely under diagnosed. Lipoma is the most common benign soft tissue lesion that presents for clinical evaluation with an incidence estimated at 1/1000 per year, or 300,000 lipomas that present for evaluation per year in the United States8. Due to urgency of early diagnosis and treatment, despite the fact that benign and metastatic tumors are far more common, primary malignant bone and soft tissue sarcomas should always be considered during the evaluation of bone and soft tissue tumors.

Clinical History Patients with a bone lesion or soft tissue tumor typically present with a clinical mass, which can be painful or painless. Patients can also present with a pathologic fracture. Often patients are referred for incidentally noted lesions on clinical examination or routine radiographs obtained for another reason. History details that should be elicited include how the patient noted the lesion, location, onset and duration of symptoms, timing of symptoms (night pain, rest pain, pain with palpation), exacerbating and alleviating factors, any changes in size over time or growth, constitutional symptoms, weight changes, personal history of cancer, medical history, and any family history of bone or soft tissue lesions that could predispose them to tumors (e.g. Neurofibromatosis, multiple hereditary exostoses, Ollier’s disease, Gardner’s syndrome, Li-Fraumeni syndrome).9 Patient age is one of the most important factors for determining a differential diagnosis for bone tumors. For example, osteosarcoma is the third most common cancer in adolescence, occurring less frequently than only lymphomas and brain tumors. Among the lesions seen almost exclusively in children and adolescents are non-ossifying fibroma, unicameral bone cyst, aneurysmal bone cyst, osteosarcoma and Ewing sarcoma. In patients >40 years of age, metastatic bone lesions and multiple myeloma are the most common malignant bone lesions.6,9,10 Differential diagnoses of benign and malignant bone tumors based on their age are noted in Table 1. (p.20)

Physical Examination For bone tumors, physical examination should focus on the problem that caused the patient to present to the physician and evaluate the area of the lesion noted on radiographs if already obtained. The clinician should evaluate the joint above and below clinically, as patient’s pain can be referred. The physical examination should also attempt to determine if the lesion is the cause of the patient’s musculoskeletal complaint or just Northeast Florida Medicine Vol. 63, No. 3 2012 19


Table 1 Most Common Bone Lesions Based on Age

Table 2 Benign & Malignant Soft Tissue Lesions

an incidental finding. For example, the patient in Figure 1 (p.21) was referred for her bone lesion found on radiographs, however clinically her pain was located over her lateral epicondyle and extensor wad consistent with tennis elbow (lateral epicondylitis). Her imaging was consistent with fibrous dysplasia and her pain improved with nonoperative measures. For soft tissue tumors, physical examination should estimate the size of the mass, location (deep or superficial), mobility, consistency (soft, cystic, firm, solid) and presence of a Tinel’s sign (suggestive of nerve sheath tumor). If the mass transilluminates it is typically cystic, often a benign ganglion cyst. If the mass is significantly painful, this may indicate an inflammatory lesion such as an abscess or inflammatory lymphadenopathy. If the mass is found to have pulsatile flow or a bruit on auscultation, this suggests a vascular lesion or pseudoaneurysm. A lymph node examination should be performed on all patients with bone or soft tissue tumors and any lymphadenopathy noted as certain soft tissue malignancies can metastasize to lymph nodes. The patient should be evaluated for signs of systemic disease such as cafÊ-au-lait spots that can be associated with familial diseases associated with bone and soft tissue tumors, such as McCune Albright syndrome and neurofibromatosis. The more common benign and malignant soft tissue lesions to be considered in the differential are noted in Table 2. In general, soft tissue masses <5 cm, superficial, soft and cystic are typically benign. Unfortunately there are some very rare soft tissue sarcomas which can be small, superficial and present for years, thus making small size and superficial location suggestive, but not diagnostic, of a benign diagnosis. In contrast, soft tissue masses >5 cm, deep, solid and firm are typically malignant and further evaluation is indicated. Often patients report no pain associated with the mass. However, if what was thought to be a benign lesion is increasing in size or more symptomatic, this should prompt further evaluation (Table 3). A helpful guideline for the clinician is that any deep soft tissue mass greater than 5 cm is malignant till proven otherwise.

Imaging Table 3 Worrisome Features/Malignant Tumors

The most essential question to be addressed by imaging is whether the lesion appears benign or malignant. The potential for a malignant lesion will direct a referral to the orthopedic oncologist. The character of the lesion will provide a differential diagnosis and direct the need for additional imaging studies, staging studies and potential biopsy.11 The plain radiograph is always the first line imaging modality that should be obtained on both bone and soft tissue lesions. (Figures 2 a-f, p.21) For bone lesions, probable benign findings include a lesion with an intact cortex although often expanded, narrow zone of transition, no soft tissue mass and no periosteal bone formation. Plain radiographs (minimum of two views) can occasionally provide a definitive diagnosis

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Figure 1 A,B Mid Humeral Lesion

Patient was referred for her mid humeral lesion. Radiographs (A, left) and MRI (B, right) demonstrated a mid humeral lesion consistent with fibrous dysplasia, however the patient’s clinical symptoms were consistent with tennis elbow. She improved with symptomatic management of lateral epicondylitis.

for benign bone lesions, for example Figure 2b, demonstrates a proximal humeral lesion consistent with a giant cell tumor. Malignant lesions may demonstrate cortical destruction, permeative changes in the bone, a soft tissue mass and periosteal bone formation. In osteosarcoma, a primary malignant bone tumor, a characteristic radiographic finding is the formation of bone like tumor tissue (mineralization of osteoid formation) as seen in Figure 2c. For chondrosarcoma, another primary malignant bone tumor, the chondroid matrix of the tumor can also mineralize but with a different pattern as shown in Figure 2d. Periosteal reaction as seen in Figure 2e can be seen in primary malignant lesions such as Ewing sarcoma and osteosarcoma, as well as metastatic disease. Metastatic and myelomatous lesions often demonstrate cortical destruction with a moth-eaten appearance as demonstrated in Figure 2f with associated pathologic fracture. For soft tissue masses, radiographs can provide important information regarding the soft tissue mass and its relationship with the underlying bone lesion, its effect on the bone, and calcification or mineralization in the mass. Soft tissue masses, including tumoral calcinosis, heterotopic ossification, myositis ossificans, phleboliths in a vascular lesion, and synovial chondromatosis all demonstrate mineralization on plain radiographs. If the lesion is concerning for malignancy or needs to be further characterized, multiplanar imaging is indicated. Ideally, the multiplanar imaging should be guided by an orthopedic oncologist and/or musculoskeletal radiologist in order to obtain optimal imaging to define the lesion11. For bone lesions, CT/MRI imaging in axial, coronal and sagittal planes allows evaluation of the extent of the lesion, evaluation of any soft tissue component and defines the regional anatomy in relationship to the neurovascular and soft tissue structures. As MRI does not afford adequate imaging of cortical bone and matrix formation, CT scans can be helpful for bone lesions with mineralization in order to characterize the type of www . DCMS online . org

Figures 2 A-F Imaging of Bone & Soft Tissue Lesions

A

B

C

D

E

F

(Top to bottom, Left to Right) A. Normal humerus radiograph; B. Proximal humeral lytic lesion in 40-year-old male which demonstrates a narrow zone of transition, cortical expansion with no evidence of cortical destruction, no soft tissue mass and no periosteal new bone formation, most consistent with a benign giant cell tumor; C. Proximal humeral lesion in 22-year-old female with mineralization consistent with osteoid formation, cortical destruction and permeative appearance, consistent with malignant osteosarcoma; D. Proximal humeral lesion with mineralization in 58-year-old male consistent with chondroid formation, permeative appearance with wide zone of transition, biopsy proved chondrosarcoma; E. Mid humeral lytic permeative lesion in 18-year-old male with periosteal new bone formation, biopsy proved Ewing sarcoma; F. Proximal humeral lytic, permeative lesion in a 75-year-old female with cortical destruction and pathologic fracture, blood and urine electrophoresis and eventual biopsy proved multiple myeloma.

Northeast Florida Medicine Vol. 63, No. 3 2012 21


mineralization (chondroid versus osteoid) and extent of the mineralization. CT/MRI can also provide three dimensional reconstructions that are often useful for pre-operative planning although this is not their primary use. For soft tissue masses, MRI is the imaging modality of choice; however, MRI can only provide a tissue specific diagnosis in approximately one third of the cases.12,13 MRI is typically able to confirm a diagnosis of a lipoma with high signal on T1 and low signal on T2 sequences (Figure 3), with the same consistency of the subcutaneous fat. In contrast, indeterminate lesions for both bone and soft tissue lesions will typically have low signal intensity on T1 and high signal intensity on T2 sequences, and these lesions require biopsy to obtain a tissue specific diagnosis to determine if the mass is benign or malignant (Figures 4, 5, 6/Figures 5 & 6, p.23).

Further Management The initial evaluation including clinical history, physical examination and imaging should allow the clinician to delineate benign versus indeterminate or malignant conditions. Asymptomatic benign bone and soft tissue lesions typically can be observed. Patients with symptomatic, large, active aggressive or indeterminate bone tumors should be referred to an orthopedic oncologist for further imaging and/or biopsy to determine the appropriate treatment. Patients with clearly

Figure 3 A,B Shoulder MRI

Shoulder MRI of a large intramuscular lipoma, demonstrating high signal intensity on T1 (A, top), low signal intensity on T2 fat suppression sequences (B, bottom). 22 Vol. 63, No. 3 2012 Northeast Florida Medicine

Figure 4 A,B Lesions in 73-Year-Old

A 73-year-old male with large > 5 cm, deep seated, firm, heterogenous mass with low signal intensity on T1 sequences (A, left) and high signal intensity on T2 sequences (B, right), a very worrisome lesion for malignancy, but is indeterminate for an exact tissue diagnosis on imaging and would require further staging and biopsy. High grade sarcomatoid carcinoma was the diagnosis on biopsy.

malignant bone lesions will fall in two groups, either a primary malignant bone sarcoma or a lesion with known or unknown primary malignancy (metastatic disease, multiple myeloma, lymphoma) and should be referred to an orthopedic oncologist or medical oncologist. If it is suspected that the patient has a metastatic lesion with unknown primary lesion, further workup as recommended by Rougraff includes in addition to history, physical examination and plain radiographs, a chest x-ray, bone scan, blood and urine studies (CBC, chemistries, serum protein electrophoresis (SPEP), Urine protein electrophoresis (UPEP), PSA, LDH, alkaline phosphatase) and CT chest, abdomen and pelvis. Per Rougraff et al, these studies will identify the primary malignancy in 85% of the cases without the need for biopsy.14 Patients with symptomatic, large, deep seated, firm or clinically changing soft tissue lesions and patients with indeterminate soft tissue tumors on three dimensional imaging should be referred to an orthopedic oncologist for further evaluation and biopsy. Needle biopsies of both bone and soft tissue tumors should be performed by an orthopaedic oncologist or interventional musculoskeletal radiologist after consultation with the orthopedic oncologist. Ideally, a needle biopsy is performed in such a manner that there is minimal contamination of surrounding soft tissues and that the tract can be excised at the time of surgery for limb salvage. Welker et al. demonstrated a 1.1% rate of overall complications with percutaneous needle biopsies in 155 patients with musculoskeletal masses. 15 Tumor seeding following percutaneous needle biopsy of bone and soft-tissue lesions is very unlikely if performed well, but awareness of compartmental anatomy and oncological surgical practice is of utmost importance for planning of definitive limb salvage surgery. At times insufficient tissue is obtained with a needle biopsy, or a larger amount of tissue is required for complex testing and an open biopsy is required. The open biopsy should be performed by the orthopedic surgeon who would proceed with additional definitive surgical treatment and not by the referring surgeon. As mentioned earlier, poorly performed biopsies can adversely affect the patient’s survival, fail to allow proper www . DCMS online . org


Figure 5 A,B Lesions in 70-Year-Old

A 70-year-old female with large >5 cm, subcutaneous mass clinically with significant growth. T1 MRI sequence with low signal intensity (A, left) and T2 MRI sequence with high signal intensity (B, right) and significant heterogeneity. Biopsy provided high grade pleomorphic soft tissue sarcoma.

diagnosis or necessitate amputation in order to obtain clear margins1,2. The location and orientation of the biopsy incision is critical, as misplaced biopsies may preclude a limb salvage procedure. The incision or percutaneous approach should be placed so that it can be excised en bloc at the time of definitive tumor resection. On the extremities, the incision should be longitudinal and not transverse (authors should explain why) unless there is some overriding consideration.15 While the biopsy is a small procedure, it is a clinically significant procedure and requires preoperative planning.

Summary The evaluation of a patient with a bone or soft tissue tumor starts with a thorough patient history and physical examination. It is important to determine if a lesion is symptomatic or asymptomatic as this often plays a pivotal role in whether this requires observation or treatment. The next step is to obtain plain radiographs with a minimum of 2 views of the lesion. Often radiographs provide the diagnosis for bone lesions and suggest whether a lesion is benign or malignant. Soft tissue lesions frequently do not show any significant findings on x-ray; however, some can have calcifications and/or affect the

Figure 6 A,B Lesions in 78-Year-Old

underlying skeletal structure. Further imaging, such as MRI or CT scan can be obtained to assist in the diagnosis. For any suspicious lesion, referral to an orthopedic oncologist to coordinate or perform a biopsy is an appropriate next step. Lumps and bumps are common in clinical practice. While most are benign, clinicians should always be alert to the possibility of malignancy.

References

1.

Mankin HJ, Lange TA, Spanier SS. The hazards of biopsy in patients with malignant primary bone and soft tissue tumors. J Bone Joint Surg. 1982;64A:1121–7.

2.

Mankin HJ, Mankin CJ, Simon MA. The hazards of biopsy, revisited. J Bone Joint Surg. 1996;78A:656–63.

3.

SEERCancer stat fact sheets. [SEERWeb Site]. 2011. Available at: http://www.seer.cancer.gov/statfacts/index.html. Accessed April 4, 2012.

4.

Abeloff MD. Abeloff’s clinical oncology. Philadelphia: Churchill Livingstone/Elsevier:2008. Ch. 57, Bone Metastases, 845-871.

5.

Betsy M, Kupersmith LM, Springfield DS. Metaphyseal fibrous defect. J Am Acad Orthop Surg. 2004;12(2):89-95.

6.

Dorfman HC, Czerniak B. Bone tumors. 1st edition. St Louis (Missouri): CV Mosby;1998. 451-456

7.

Klenke FM, Wenger DE, Inwards CY, et al. Giant cell tumor of bone: risk factors for recurrence. Clin Orthop Relat Res. 2011;469(2):591-9.

8.

Rydholm A, Berg NO. Size, site and clinical incidence of lipoma and sarcoma. Acta Orthop Scand. 1983:54(6):929-34.

9.

Damron TA. Oncology and basic science. Philadelphia:Lippincott Williams & Wilkins;2008.

10. Simon MA, Springfield DS. Surgery for bone and soft tissue tumors. Philadelphia: Lippincott-Raven;1998, 621-624. 11. O’Connor MI. Musculoskeletal imaging: What information is important to the orthopedic oncologist? Seminars in musculoskeletal radiology. 2007;11(3): 273-278. 12. Kransdorf MJ, Jelinek JS, Moser RP Jr, et al. Soft-tissue masses: diagnosis using MR imaging. AJR Am J Roentgenol. 1989;153(3):541-7. 13. Crim JR, Seeger LL, Yao L, et al. Diagnosis of soft-tissue masses with MR imaging: can benign masses be differentiated from malignant ones? Radiology. 1992;185(2)581-6. 14. Rougraff BT, Kneisel JS, Simon MA. Skeletal metastases of unknown origin. A prospective study of a diagnostic strategy. J Bone Joint Surg Am. 1993;75(9):1276-81. 15. Shives TC. Biopsy of soft-tissue tumors. Clin Orthop Relat Res. 1993;289:32-35.

DCMS History Book HERE! A 78-year-old female presented with posterior thigh lump, MRI demonstrates a myxoid appearance with low signal intensity on T1 (A, left) and very bright signal intensity on T2 sequences (B, right). Due to the indeterminate imaging findings between a benign or malignant myxoid lesion, biopsy was performed and demonstrated a benign myxoma.

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Buy "Florida's Pioneer Medical Society: A History of the Duval County Medical Society & Medicine in Northeast Florida" for you, family members and for your office. Learn about the 159-year history of DCMS.

See dcmsonline.org for an order form. Northeast Florida Medicine Vol. 63, No. 3 2012 23


Management of Neck Pain and Cervical Radiculopathy Ali Chahlavi, MD; Eric Nottmeier, MD, and John Matthew Hale, PA-C Abstract: Neck pain and cervical radiculopathy cause a significant

health burden in the U.S. general population. Appropriate health care treatment for these associated disorders requires accurate diagnosis and approved treatments. We present both non-operative management and surgical options for cervical radiculopathy. When non-operative measures fail, anterior cervical discectomy and fusion, disc replacement surgery, and selective posterior cervical foraminotomy serve as viable surgical options.

Non-operative Management of Cervical Disc Disease Degenerative cervical spine disorders will affect up to two-thirds of the U.S. population in their lifetime.1 Cervical disc disease can occur for several different reasons including traumatic injury, osteoarthritis, rheumatoid arthritis, and spontaneous disc herniation. Non-operative management is considered the first line of treatment for cervical disc disease when the patient is not experiencing associated extremity weakness or bladder/bowel incontinence. There are several modalities that can be employed either alone, or in combination, to provide relief of symptoms for the patient. Oral medications are common first-line treatments for patients. These include narcotic analgesics, anti-inflammatory medications, muscle relaxants, anti-depressants, and neuroleptic medications.1 Initial management most commonly will consist of oral NSAIDs such as Ibuprofen for a short course at high dose. If the patient is experiencing significant muscle spasms associated with axial or radicular symptoms, then a muscle relaxant medication can also be utilized. Muscle relaxers offer a two-fold benefit in this instance. First, they reduce cervical tension that causes increased axial loading and possible disc bulging or disc herniation. Second, the muscle relaxant medication will ease constant muscular tension that leads to irritability and pain. If the cycle of persistent muscle spasm can be controlled, then the need for stronger medications for pain control can be reduced. If the above mentioned medication combination is not effective, then a short steroid burst of 5-7 days can be tried as a substitute for the NSAID regimen. Patients will benefit from the anti-inflammatory effect of the steroid pack shortly after initiating therapy. The primary goal of steroid utilization for nerve root compression is to decrease the inflammation of the nerve root, thereby providing pain relief and giving the disc time to heal. Some patients experience significant pain associated with disc disease. This subset of patients will require the addition Address correspondence to: A. Chahlavi MD, St. Vincent’s Spine and Brain Institute, 4205 Belfort Road, Suite 1100, Joe Adams Building, Jacksonville, FL 32216. Phone: 904-296-3103. Email: chahlavia@yahoo.com. 24 Vol. 63, No. 3 2012 Northeast Florida Medicine

of narcotic medications. Muscle relaxants and narcotics can be of benefit, but should be prescribed for a fixed period of time to prevent tolerance.3 It is important to consider patient age, body habitus, previous exposure to narcotics, and other medical conditions when determining which pain reliever to utilize. Physical Therapy is a key component of conservative management. Initial evaluation by a therapist focuses on determining a baseline of patient ability and pain tolerance in order to formulate a plan of care. Stretching of the paraspinal structures can be utilized to prevent muscle contraction. It can also be utilized to minimize the formation of scar tissue associated with focal injury. Active range of motion exercises are the most effective for these patients, maintaining the motion of the facet joints and encouraging proper postures.1 Strengthening of the cervical musculature will also be a key component of therapy. Strengthening is designed to increase the cervical muscle mass and provide improved support for the cervical bone structures. Therapy also focuses on providing patient training for improved posture. Some patients will benefit from utilization of ultrasound and massage therapy to induce scar tissue breakdown. In instances where patients are experiencing foraminal stenosis secondary to cervical disc protrusion and herniation, cervical traction may be helpful. The benefit may arise from re-establishing appropriate disc height with temporary reduction of the herniated disc by the process of ligamentotaxis; a technique where ligaments are placed in longitudinal traction so as to cause redirection of the disc fragments away from the nerve roots and back into the interbody space. This technique may provide pain relief. When conservative treatment has failed, certain minimally invasive radiologic procedures can be applied to relieve pain.2 There are three common types of interventional procedures that may be attempted to provide pain relief. These procedures offer improvement for cervical problems. If the patient is experiencing significant posterior cervical muscle pain, then trigger point injections can be utilized to stop cervical muscle contraction. If there is mechanical pain, then the patient may benefit from facet joint injections. Patients suffering from significant arthritis of the facet joint will often gain significant improvement with a combination of anesthetic and steroid injection into the problematic facet joints. This may require a series of injections throughout the year to gain lasting improvement. The third option is epidural steroid injections (ESI). These injections are designed to provide a small, focused amount of steroid close to the degenerative cervical disc and symptomatic nerve root. ESI are usually performed in a series of three injections a year. Patients do not always have improvement with the first injection. Whenever the steroid injections fail to relieve pain from a contained cervical disc herniation, more invasive decompressive techniques should www . DCMS online . org


be proposed.2 In patients who are operative candidates, pain-relieving injections can assist in identifying the level of surgery in multilevel disease while temporizing pain as the patient awaits surgical scheduling.4 Lifestyle is often overlooked when considering management of cervical disc disease, but it can play a pivotal role in non-surgical and surgical outcomes.Tobacco cessation is one of the key behaviors that will allow for an improved outcome. Tobacco utilization will increase the rate of disc degeneration, decrease bone density over time and decrease vascular flow. In the face of cervical insult, all three of these detrimental characteristics will lead to poor outcomes. Patients should be honest about their decision to discontinue smoking, otherwise they may face persistent symptoms.

Nevertheless, it has been found in biomechanical studies that fusion causes increased stress at the adjacent levels, which may contribute to adjacent segment degeneration8. For this reason, disc arthroplasty became an alternative to ACDF, especially after biomechanical cadaveric studies demonstrated that artificial disc replacement maintains motion and mechanics within physiologic ranges at all levels of the cervical spine while decreasing stresses on adjacent segments (Figure 2).9 Artificial disc can reduce neck and radicular pain while still allowing motion throughout the spine.

Figures 1, and 2A, 2B Spine CTs

Obesity is also a significant determinant of outcome. Patients with diabetes will have increased recovery times from injury as a result of the underlying vascular disease. Diminishing patients’ body mass index will also result in less physical loading of the cervical spine, thus reducing mechanical stress on the injured area. The timeframe for non-operative management varies based on progress and symptoms. A patient that is experiencing weakness and/or bladder or bowel incontinence is usually a candidate for surgical consideration. The patient with numbness and tingling in the upper extremities without weakness can undergo initial conservative management. If symptom improvement does not occur, then the patient should undergo surgery. Patients who are experiencing exclusively neck pain should proceed through a 6-month course of conservative treatment before considering any surgical intervention. Informing patients of alternatives, while allowing them to take an active part in decision making is vital to long-term success of the chosen treatment.3

Artificial Cervical Disc Replacement Artificial disc replacement is a type of arthroplasty, a surgery in which the dysfunctional joint surface is replaced with something new, while maintaining stability.5 For many years, one of the common procedures available to treat degenerative cervical disc disease with or without radiculopathy was anterior cervical discectomy and fusion (ACDF), which has been a very successful and widely accepted option.6 Spinal fusion surgery creates a solid union between two or more vertebrae. More than 200,000 cervical fusions are performed each year in the US to relieve pressure on the spinal cord or nerve. In the last decade, adjacent segment disease (or degeneration) has been studied extensively, and the possibility that fusion may accelerate has become a concern (Figure 1). Hilebrand et al.7, in a retrospective study, reported that 25.6% of patients within 10 years developed new disease at an adjacent level requiring surgical intervention. Although, there is no prospective clinical trial that has been able to demonstrate this, few argue that adjacent segment disease is a result of the natural progression of degenerative disc disease. www . DCMS online . org

(Figure 1/above left) Anterior cervical discectomy and fusion prevents motion at the segments fused. It may also induce adjacent level disease as it can be seen in this CT of cervical spine with large osteophyte (bone spur) formation at the level above. (Figure 2A - above right at top and Figure 2B - above right at bottom) Artificial disc allows normal range of motion of the cervical spine in flexion and extension.

The first implanted artificial cervical device was in 1966 by Dr. Ulf Fernstrom.10 A stainless steel ball was inserted into the nuclear recess of the cervical intervertebral disc to help stabilize the motion segment, in a posterior approach. However, there were too many failures of adjacent-segment hypermobility, migration, and device subsidence. Therefore, cervical arthroplasty procedure lost its appeal. It was not until the early 1990s when cervical artificial disc replacement regained popularity in Europe with the Cummins-Bristol Disc.®11 Due to many instrumentation failures with the Cummins-Bristol Disc®, a new disc, The Frenchay, later named The Prestige® was made. In an initial pilot study in 2002, the disc demonstrated lower complication rates.12 The artificial disc surgery is still relatively new in the United States, only receiving FDA approval in October 2004 for lumbar disc pathology. There were four years of clinical trials before the first device, The Charite® Artificial disc, manufactured by DePuy, could be approved, but it was limited to the lumbar spine. The device was invented at Charite University Hospital in Berlin in mid-1980s by two East German scientists, and orthopedic surgeon Karin Buttner-Janz and her colleague Kurt Schellnack.13 Northeast Florida Medicine Vol. 63, No. 3 2012 25


Finally, in July 2007, the FDA approved the Prestige 速disc for cervical radiculopathy and/or myelopathy at C3-7 levels. Soon after, the Pro Disc C速, the second artificial disc, was approved in the U.S. in December 2007. The Pro Disc C速 was developed by Dr. Rudolf Bertagnoli and manufactured by Synthes. Both of these discs had comparable neurological success comparable to anterior cervical fusion, while demonstrating superior effect in having the patient return to work in a shorter time frame. In addition, the studies showed a decrease in the number of secondary surgeries within the first 24 post-operative months with the arthroplasty procedures.14-15 To this point, the FDA has approved single level cervical disc arthroplasty. There are no current plans for multi-level approval. Unfortunately, a second artificial disc at another level is also not approved even if additional surgery is required at a later date. Total disc replacement is indicated in skeletally mature patients for reconstruction at one level from the C3-7 disc levels. The discectomy with arthroplasty is performed for intractable symptomatic cervical disc disease. The symptoms can include neck or arm pain with or without associated neurological deficit (numbness and/or weakness). Patients also need imaging studies (CT and/or MRI) to confirm the herniated disc, canal or foraminal stenosis, osteophyte formation, or loss of disc height. Not all patients qualify for cervical arthroplasty. The following conditions preclude cervical disc arthroplasty: patients with active systemic infection or with infection localized close to the site of implantation, patients with more than one level disc disease, patients with severe osteoporosis defined as DEXA bone density measured T-score < or =-2.5, patients with marked cervical instability with translation > 3 mm seen during flexion/extension x-rays, patients with active malignancy, patients with rheumatoid arthritis and autoimmune disease, and patients with spondylosis characterized by bridging osteophytes and/or a loss of disc height >50%.15 The latter is a common finding in patients with disc disease and cervical radiculopathy, and for this reason, it is imperative to review the cervical films carefully prior to any decision making for cervical arthroplasty. A significantly collapsed cervical disc space requires more endplate resection to achieve enough distraction and disc height. However, this will lead to arthrodesis and highly osteogenic environment that can fuse overtime. If the cervical height is not achieved, a tight implant would limit motion, and thus encourage bone formation and possible fusion. The disc replacement is implanted via an open anterior approach; similar to the manner in which an anterior cervical discectomy is performed. Meticulous discectomy with decompression of the cord and the nerve is performed first. The cartilaginous endplate should also be excised. While it is important to remove the bone spurs pressing on the cord and the nerves, it is important to avoid performing an arthrodesis by drilling or scraping off the endplate which will promote bone fusion. The goal of the artificial cervical 26 Vol. 63, No. 3 2012 Northeast Florida Medicine

disc surgery is to remove the diseased disc, restore some disc height, decrease discogenic neck pain and associated arm pain/ weakness, preserve motion in the affected vertebral segment, and improve patient function. The patient receiving the disc replacement should have failed conservative management with non-operative measures prior to implantation of the total disc replacement. One of the most attractive aspects of cervical disc arthroplasty is that the degenerative disc disease and herniated disc can be treated with a procedure that will preserve and even possibly restore normal cervical spine motion. Most patients who are faced with the possibility of undergoing a cervical disc replacement favor arthroplasty over fusion for the reason stated above. Total cervical disc replacement has the advantage of reducing adjacent segment disease and possible future surgeries, although longer term studies are necessary to substantiate this assumption. The disadvantage to this procedure is that a large percentage of patients are not candidates for this option. Patients with more than one disc affected, segmental instability, bone disease, and patients that have undergone prior cervical fusion are not candidates for this surgical option. Revision surgeries are more problematic and have greater risks in arthroplasty surgery. Long-term patient follow-up is essential to assess the effectiveness and safety of artificial disc surgery in comparison to ACDF.

Non-arthroplasty Options for Cervical Radiculopathy and Disc Disease When a patient suffering from cervical radiculopathy is not deemed a cervical arthroplasty candidate, then other surgical options include anterior cervical discectomy and fusion (ACDF), as well as posterior cervical foraminotomy (PCF). The ACDF procedure is typically chosen for patients who have cervical disc bulging or herniation anterior to the spinal cord as this region is difficult to approach posteriorly without risking injury to the spinal cord (Figure 3). When the cervical disc is compressing the nerve root within the foramen only, then a PCF can be used. Accordingly, there are advantages and disadvantages to both procedures exist.

Figure 3 MRI of Disc Herniation Axial T2-weighted MRI image showing a disc herniation (see arrow) located anterior to the spinal cord and protruding into the neuro-foramen.

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Figure 4 Radiographs of Cervical Plate

(Left) Anterior-posterior and (Right) lateral radiographs showing an anterior cervical plate.

The ACDF procedure most commonly used today was originally introduced by Smith and Robinson in 195816. Advantages of the ACDF procedure include dissection through normal anatomical planes in the neck to approach the anterior cervical spine, which can result in minimal postoperative pain for the patient. Additionally, the anterior approach allows for complete removal of the cervical disc, which gives direct visualization and decompression of the anterior spinal canal and bilateral neuro-foramen. However, because the disc is completely removed this void needs to be filled with a structural graft. Grafting options in ACDF procedures include structural allograft or autograft, as well as cervical cages packed with morselized bone (autograft or allograft). After the bone graft is inserted, a titanium plate is applied to the front of the spine to further stabilize the segment (Figure 4). The goal is to have the bone graft that is inserted into the disc space fuse to the surrounding bone. The fusion rates reported in the literature for instrumented single-level ACDF have been reported to be greater than 90%17-18. A disadvantage of the ACDF procedure is the possibility that the bone graft does not fuse to the surrounding bone and this is termed pseudo-arthrosis. If a patient has a pseudo-arthrosis, then it may be asymptomatic with no further treatment required. If it is a painful pseudo-arthrosis causing neck pain, then a revision surgery may be necessary. Another disadvantage of the ACDF procedure is that it fuses a motion segment in the spine, and therefore poses a risk of degeneration at adjacent motion segments, otherwise termed “adjacent-segment disease�. The cumulative risk of adjacent-segment disease reported in the literature after anterior cervical fusion is approximately 3% per year in the first 10 years after surgery.19

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Anatomic structures in the neck that can be at risk for injury in ACDF procedures include the carotid and vertebral arteries, esophagus, trachea, and the recurrent laryngeal nerve (RLN). RLN injury can result in hoarseness of the voice and/ or aspiration, which can be permanent. The incidence of RLN injury in ACDF procedures is reported to be approximately 2%.20 Most cases of RLN palsy occur with simple retraction of the anterior cervical structures and not necessarily transection of the nerve. Because of this, most cases of RLN palsy resolve within 6 months and an observational approach is taken in these cases. The PCF procedure can be accomplished in minimally invasive fashion through the posterior cervical musculature. A small window of bone is removed in the cervical lamina and the herniated disc can be accessed and excised (Figure 5). An advantage of the posterior cervical foraminotomy procedure is that it does not involve fusing a motion segment and; therefore, has been shown to be associated with a low rate of adjacent-segment disease.21 Additionally, because the spine is being approached posteriorly there is no risk of injury to structures in the anterior neck including the RLN, carotid artery, trachea, and esophagus. A disadvantage of the posterior cervical foraminotomy procedure is that disc herniations anterior to the spinal cord cannot be accessed. Another disadvantage of the posterior cervical foraminotomy procedure is that a chance of disc re-herniation exists because the disc is not completely removed and a fusion is not accomplished. A small risk of instability also exists with any bone removal in the spine, possibly necessitating a subsequent fusion procedure. Though the approach for PCF does require dissection through the posterior cervical musculature, a minimally invasive approach using a tubular retractor is a method that results in less muscle dissection and can decrease the patient’s postoperative pain. PCF should not be considered in patients who display subluxation or kyphosis at the cervical level to be treated as this risks further instability at that level.

Figure 5 Laminotomy Illustration

Illustration showing placement of a tubular retractor and excision of a foraminal herniated disc through a laminotomy.

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Both ACDF and PCF are effective methods for surgically treating cervical radiculopathy, each with their own advantages and disadvantages. The location of the cervical disc herniation dictates the approach in a majority of cases. Patients with disc herniations that are anterior to the spinal cord are typically treated with ACDF. In patients with more lateral disc herniations primarily affecting the neuroforamen, then a PCF can be used. The choice of ACDF versus PCF also depends in part on the surgeon’s comfort level with each technique. The ACDF procedure is the most commonly used method as most cervical disc herniations are at least in part located anterior to the spinal cord.

Conclusion The majority of the U.S. population at one point in their lifetime will experience neck pain. Those individuals with associated neurologic symptoms may benefit from surgical intervention after non-operative modalities have been exhausted. The surgical options vary from disc replacement surgery to fusion, each with its own set of risks and long term considerations. It is imperative that those individuals with myelopathic features be referred in an expedited fashion to a spine specialist for appropriate treatment.

References

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Todd, A. Cervical spine: degenerative conditions. Curr Rev Musculoskeletal Med. 2011 December; 4(4): 168-174.

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Gangi, A., Tsoumakidou G., Buy, X., Cabral, JF., Garnon, J. Percutaneous techniques for cervical pain of discal origin. Semin Musculoskeletal Radiology. 2011 April; 15 (2): 172-180.

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Carlson, H., Carlson, N. An Overview of the Management of Persistent Musculoskeletal Pain. Posted 04/01/2011; Therapeutic Adv. Musc. Dis. 2011 3(2):91-99.

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Safriel, Y. Lumbar and Cervical Pain Management Procedures: When and How to Do Them. Posted 1/19/2011; App. Radiol. 2010;39(12):14-23.

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Albert TJ, Eichenbaum MD: Goals of cervical disc replacement. Spine J 4:292S–293S, 2004.

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Bose B: Anterior cervical fusion using Caspar plating: analysis of results and review of the literature. Surg Neurol 49:25–31, 1998.

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Hilibrand AS, Carlson GD, Palumbo MA, Jones PK, Bohlman HH: Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg Am 81:519–528, 1999.

8.

Matsunaga S, Kabayam S, Yamamoto T, Yone K, Sakou T, Nakanishi K. Strain on intervertebral discs after anterior cervical decompression and fusion. Spine 1999;24:670-5.

9.

Puttlitz CM, Rousseau MA, Xu Z, Hu S, Tay BK, Lotz JC. Intervertebral disc replacement maintains cervical spine kinetics. Spine 2004;29:2809-14.

10. Fernstrom U. Arthroplasty with intercorporal endoprothesis in herniated disc and in painful disc. Acta Chir Scand Suppl 357:154–159, 1966. 11. Le H, Thongtrangan I, Kim DH: Historical review of cervical arthroplasty. Neurosurg Focus 17:3E1, 2004.

JT. The new Frenchay artificial cervical joint: results from a two-year pilot study. Spine 27:2446–2452, 2002. 13. Buttner-Janz K, Schellenack K, Zippel H. An Alternative treatment strategy in lumbar intervertebral disk damage using an SB Charite modular type intervertebral disk endoprosthesis. Z Orthop Ihre Grenzgeb 125(1):1-6 1987. 14. Heller JG, Sasso RC, Papadopoulos SM, Anderson PA, Fessler RG, Hacker RJ, et al.: Comparison of BRYAN cervical disc arthroplasty with anterior cervical decompression and fusion: clinical and radiographic results of a randomized, controlled, clinical trial. Spine 34:101–107, 2009. 15. Murrey D, Janssen M, Delamarter R, Goldstein J, Zigler J, Tay B, et al.: Results of the prospective, randomized, controlled multicenter Food and Drug Administration investigational device exemption study of the ProDisc-C total disc replacement versus anterior discectomy and fusion for the treatment of 1-level symptomatic cervical disc disease. Spine J 9:275–286, 2009. 16. Smith GW, Robinson RA. The treatment of certain cervicalspine disorders by anterior removal of the intervertebral disc and interbody fusion. J Bone Joint Surg Am. Jun 1958;40A(3):607-624. 17. Kaiser MG, Haid RW, Jr., Subach BR, Barnes B, et al. Anterior cervical plating enhances arthrodesis after discectomy and fusion with cortical allograft. Neurosurgery. Feb 2002;50(2):229-236; discussion 236-228. 18. Wang JC, McDonough PW, Endow K, Kanim LE, et al. The effect of cervical plating on single-level anterior cervical discectomy and fusion. Journal of Spinal Disorders. Dec 1999;12(6):467-471. 19. Hilibrand AS, Carlson GD, Palumbo MA, Jones PK, et al.. Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. Journal of Bone & Joint Surgery - American Volume. Apr 1999;81(4):519-528. 20. Beutler WJ, Sweeney CA, Connolly PJ. Recurrent laryngeal nerve injury with anterior cervical spine surgery risk with laterality of surgical approach. Spine. Jun 15, 2001;26(12):1337-1342. 21. Clarke MJ, Ecker RD, Krauss WE, McClelland RL, et al. Same-segment and adjacent-segment disease following posterior cervical foraminotomy. Journal of Neurosurgery Spine. Jan 2007;6(1):5-9.

DCMS History Book HERE! Buy "Florida's Pioneer Medical Society: A History of the Duval County Medical Society & Medicine in Northeast Florida" for you, family members and for your office. Learn about the 159-year history of DCMS.

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12. Wigfield CC, Gill SS, Nelson RJ, Metcalf NH, Robertson 28 Vol. 63, No. 3 2012 Northeast Florida Medicine

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Joint Replacement Options for the Shoulder Kamal I. Bohsali, MD, FACS, FAAOS Abstract: Degeneration of the shoulder joint occurs in osteoarthritis, inflammatory arthritis, osteonecrosis (bone death), and cuff tear arthropathy (arthritis with a massive rotator cuff tear). When nonoperative measures fail, joint replacement surgery may reliably provide pain relief, restoration of shoulder motion, and improved ability to perform activities of daily living. There are multiple factors that must be considered when contemplating shoulder replacement surgery such as patient physiologic age, activity level, rotator cuff integrity, and bony deficiency. Surgical treatment options vary from partial shoulder replacement with or without biologic resurfacing to total shoulder replacement. The reverse ball and socket design serves as a new tool in the treatment of cuff tear arthropathy, failed shoulder arthroplasty, and proximal humerus fractures.

Introduction Shoulder replacement surgery was originally performed in 1893 by Jules-Emile Pean for tuberculous arthritis.1 Charles Neer modernized the surgical technique and implant design in the 1950s to address three and four-part proximal humerus fractures.2 He later developed the first “modern day” shoulder prosthesis in 1974 consisting of a metallic humeral stem and an all polyethylene glenoid component.3 At the same time, more constrained “reverse ball and socket” designs were in vogue in the treatment of patients with rotator cuff deficiency and arthritis of the shoulder. This alternate (non-Neer) prosthetic design was quickly abandoned as early catastrophic failures occurred.4 Since Neer’s initial foray, more than 70 shoulder systems have been developed, some in part to correct errors in design (i.e. reverse ball and socket) and advances in metallurgy.5 Although not as common as hip and knee replacement surgery, shoulders are the third most commonly replaced joint. According to the Department of Health and Human Services, shoulder replacement surgeries have increased approximately 145% from 1997 to 2005, with an average annual volume of 16,700.6 Despite the increased volume, approximately threefourths of shoulder replacements are performed by surgeons who do two or fewer procedures a year.7,8 Clinical outcomes after shoulder replacement surgery have been reported as more favorable when the procedures are performed by high volume surgeons in high volume hospitals.9-11

Indications for Shoulder Replacement Surgery Patients with shoulder arthritis will usually have pain, motion limitation, and loss of function. Pain can occur Address correspondence to: Kamal I. Bohsali, MD, Bahri Orthopedics and Sports Medicine, P.A., 6100 Kennerly Road Suite 101, Jacksonville, FL 32216. Phone: 904-739-0050. Email:Orthomd@ gmail.com. www . DCMS online . org

with activity and at rest. Many individuals will indicate an inability to sleep on the affected side. History regarding onset of the pain, previous injuries and/or surgeries, and systemic illnesses (i.e. rheumatoid arthritis) is helpful when deciding the treatment plan. Clinically, the person may exhibit muscle atrophy around the shoulder with or without previous surgical incisions. Crepitus, a grinding sensation of the joint, will be noted during active and passive attempts at range of motion. As with hip and knee arthritis, shoulder arthritis may be associated with medical co-morbidities that may affect the individual’s ability to recuperate from surgical intervention; thus, not all patients are candidates for operative intervention. It is incumbent upon the treating surgeon and the patient’s primary care physician (and respective consultants) to maintain an open dialogue regarding the risk-benefit ratio of surgery. Shoulder replacement surgery is generally recommended after the individual has failed a course of non-operative management consisting of oral anti-inflammatory medication, narcotic pain medication, activity modification, moist heat application, physical therapy, and cortisone injection therapy. Radiographs will usually demonstrate loss of joint space and osteophyte (bone spur) formation (Figure 1). With advanced osteoarthritis, the socket (glenoid) may demonstrate asymmetric wear. In some cases, the humeral head is situated in an elevated position with corresponding changes to the acromion, indicative of cuff tear arthropathy. MRI may portray a rotator cuff tear, an important preoperative finding that has direct implications regarding shoulder function after joint replacement surgery.

Figure 1 AP Radiograph of Shoulder Joint

AP radiograph of the shoulder joint demonstrating joint space loss and bone spur formation. (see arrow)

Indications for shoulder replacement surgery include osteoarthritis, inflammatory arthritis, post-traumatic arthritis, cuff tear arthropathy, proximal humerus fractures, tumors of the shoulder, osteonecrosis, and failed shoulder replacement. Contraindications include active or suspected infection of the joint, severe humeral and glenoid bony deficiency, axillary nerve injury with dysfunction, and host infirmity (i.e. the medically moribound patient). Due to the availability of different prosthetic options, orthopaedic surgeons have sought to establish treatment guidelines to maximize patient outcomes and minimize complication rates. Northeast Florida Medicine Vol. 63, No. 3 2012 29


Figure 2 Resurfacing Implant

Resurfacing implant for arthritis in a young patient.

Prosthetic Options for the Shoulder The three main surgical options include partial shoulder replacement (humeral head replacement, HHR), total shoulder replacement (TSR), and reverse total shoulder replacement (rTSR). Partial shoulder replacement involves placement of a metallic humeral head with or without an attached stem and is currently used in the following scenarios: degeneration of cartilage limited to the humeral head, inflammatory arthritis (i.e. rheumatoid arthritis), cuff tear arthropathy, three and four-part proximal humerus fractures, osteonecrosis, and arthritis with deficiency of the socket (glenoid).5 In young, active, and athletic patients with humeral head degeneration, partial shoulder replacement (resurfacing) may be performed with a metallic cap while preserving a majority of the humeral head. Additionally, structural parameters such as head-shaft angle, offset, version, and inclination are not altered allowing for conversion at a later date to a stemmed implant when joint degeneration has advanced.12 (Figure 2). When degenerative changes have resulted in alteration of the humeral head anatomy, the more conventional stemmed HHR is used. HHR results in reliable pain relief and functional improvement, though some surgeons have argued the superiority of TSR in terms of range of motion and patient assessment functional scores.13,14

Figure 3 Total Shoulder Replacement 1

A standard total shoulder replacement with a stemmed humeral component and polyethylene glenoid component.

A TSR involves placement of a metallic stem and head, and plastic glenoid component. Most glenoid components are all polyethylene in composition due to historical problems with metal backed components.15 (Figure 3). The primary indication for TSR is a symptomatic shoulder caused by arthritis with an intact rotator cuff. With advanced shoulder arthritis, severe asymmetric wear of the glenoid has previously 30 Vol. 63, No. 3 2012 Northeast Florida Medicine

precluded resurfacing of the glenoid. A recently released all polyethylene component (Steptech APG®) with posterior “build-up” may allow for glenoid replacement even in the setting of bony deficiency (Figure 4). Because of a current lack of biomechanical and clinical data, indications, complications, and patient outcomes regarding this specific implant have not been determined.

Figure 4 Steptech APG®

Steptech APG®, an augmented glenoid component. (Image courtesy of Depuy, Inc.)

A TSR is not appropriate for young (less than 50 years of age) and active patients due to concerns regarding accelerated wear of the glenoid component. As a temporary solution, some surgeons have advocated the use of a HHR (with or without a stem) and biologic soft tissue interposition with the understanding that conversion to a polyethylene glenoid component in the future may be necessary. The stereotypical patient is a young manual laborer with symptomatic arthritis who is involved in repetitive heavy lifting activities. Several authors have employed with varying results the use of interpositional tissues such as joint capsule, tensor fascia lata, and mensical allograft to serve as a buffer between the humeral head implant and the glenoid.16-20 A recent report by Wirth substantiates the viability of this technique for the short term (2 to 5 years), but alludes to the probability of future surgery.21 The kinematics of the shoulder are usually altered in the setting of arthritis and rotator cuff deficiency (Figure 5, p.31). The increased instability of the shoulder with cuff tear arthropathy (CTA) would lead to rapid failure of a standard (unconstrained) TSR. Subsequent to FDA approval in 2004, a renewed interest in the reverse ball and socket design has allowed orthopaedic surgeons to use joint replacement surgery as a means to address CTA (Figure 6, p.31). Indications for use of this type of prosthesis are continuing to evolve, with some surgeons advocating its use in the treatment of proximal humerus fractures, failed TSRs, and severe rotator cuff deficiency without underlying arthritis.4 As indications expand, so have the reports regarding specific complications associated with the use of this implant design. Some of the complications reported include neurologic injury, peri-prosthetic fracture, hematoma, infection, notching of the scapula, instability, implant failure, and acromial fracture.22 The procedure has shown promising short term and mid-term results for the treatment of shoulder arthritis and rotator cuff deficiency and as a salvage procedure for failed unconstrained TSR.23 Due to the complexity of the procedure, we recommend that the surgeon demonstrate additional training and familiarity with www . DCMS online . org


Figure 5 AP X-ray of Shoulder

This AP (frontal projection ) x-ray of a right shoulder indicates previous attempt at rotator cuff repair with retained metallic anchors which has failed. The humeral head has migrated superiorly, and there are corresponding degenerative changes to the shoulder joint.

the implant design, shoulder anatomy, surgical approaches, and complication rate (and type) to achieve optimal patient outcome.

Conclusion Evolution of surgical technique and implant design has provided the modern day orthopaedist powerful tools with which to address pathologic processes of the shoulder joint. Ongoing prospective studies evaluating patient derived outcome measures from shoulder replacement surgery will enable orthopaedic surgeons to tailor treatment based upon evidence based medicine and not anecdotal experience.

Figure 6 Total Shoulder Replacement 2

4.

Bohsali KI, Wirth MA, Rockwood CA Jr. Current concepts review: complications of total shoulder arthroplasty. J Bone Joint Surg Am 2006; 88: 2279 -2292.

5.

Wiater JM and Fabing MH. Shoulder arthroplasty: prosthetic options and indications. J Am Acad Orthop Surg 2009; 17: 415-425.

6.

Joshi D. Total shoulder replacement- the 3rd most replaced joint in America. Pearl Driver Inc. 08 March 2008. Web. 18 Dec 2011.

7.

Hasan SS, Leith JM, Smith KL, Matsen FA 3rd. The distribution of shoulder replacement among surgeons and hospitals is significantly different than that of hip or knee replacement. J Shoulder Elbow Surg. 2003; 12: 164-9.

8.

Hammon JW, Queale WS, Kim TK, McFarland EG. Surgeon experience and clinical and economic outcomes for shoulder arthroplasty. J Bone Joint Surg Am. 2003; 85: 2318-24.

9.

Jain N, Pietrobon R, Hocker S et al. The relationship between surgeon and hospital volume and outcomes for shoulder arthroplasty. J Bone Joint Surg Am. 2004; 86: 496- 505.

10. Jain NB, Hocker S, Pietrobon R, et al. Total arthroplasty versus hemiarthroplasty for gleno-humeral arthritis: role of provider volume. J Shoulder Elbow Surg. 2005; 14: 361-7. 11. Lyman S, Jones EC, Back PB, et al. The association between hospital volume and total shoulder arthroplasty outcomes. Clin Orthop Relat Res. 2005; 432; 132-7. 12. Bailie DS, Llinas PJ, Ellenbecker TS. Cementless humeral resurfacing arthroplasty in active patients less than fifty-five years of age. J Bone Joint Surg Am. 2008; 90: 110-117. 13. Edwards TB, Kadakia NR, Boulahia A, et al. A comparison of hemiarthroplasty and total shoulder arthroplasty in the treatment of primary gleno-humeral osteoarthritis: results of a multicenter study. J Shoulder Elbow Surg. 2003; 12: 207-13. 14. Gartsman GM, Roddey TS, Hammerman SM. Shoulder arthroplasty with or without resurfacing of the glenoid in patients who have osteoarthritis. J Bone Joint Surg Am. 2000; 82: 26-34. 15. Martin SD, Zurakowski D, Thornhill TS. Uncemented glenoid component in total shoulder arthroplasty. Survivorship and outcomes. J Bone Joint Surg Am. 2005; 87: 1284-92. 16. Burkhead WA, Hutton KS. Biologic resurfacing of the glenoid with hemiarthroplasty of the shoulder. J Shoulder Elbow Surg. 1995; 4: 263-70. 17. Ball CM, Galatz LM, Yamaguchi K. Meniscal allograft interposition arthroplasty for the arthritic shoulder: description of a new technique. Tech Shoulder Elbow Surg. 2001; 2: 247-54.

Reverse ball and socket designed total shoulder replacement.

References

1.

Lugli T. Artificial shoulder joint by Pean (1893): the facts of an exceptional intervention and the prosthetic method. Clin Orthop Relat Res. 1978; 133: 215-8.

2.

Neer CS, Brown TH Jr., McLaughlin HL. Fracture of the neck of the humerus with dislocation of the head fragment. Am J surg. 1953; 85: 252-8.

3.

Neer CS II, Watson KC, Stanton FJ. Recent experience in total shoulder replacement. J Bone Joint Surg Am 1982; 64: 319- 337.

www . DCMS online . org

18. Nowinski DO, Burkhead WZ. Hemiarthroplasty with biologic glenoid resurfacing 5-13 year outcomes. Presented at the Annual Meeting of the American Academy of Orthopaedic Surgeons; 2003 Feb 5-9; New Orleans, LA. 19. With MA. The parachute technique for interpositional meniscal allograft fixation in shoulder arthroplasty. Presented at the Annual Meeting of the American Academy of Orthopaedic Surgeons; 2004 Mar 10-14; San Francisco, CA. 20. Namdai S, Alosh H, Baldwin K, et al. Biological glenoid resurfacing for gleno-humeral osteoarthritis: a systematic review. J Shoulder Elbow Surg. 2011; 20: 1184-1190. 21. Wirth MA. Humeral head arthroplasty and meniscal allograft resurfacing of the glenoid. J Bone Joint Surg Am. 2009; 91: 1109-19. 22. Cheung E, Willis M, Walker M, et al. Complications in reverse total shoulder arthroplasty. J Am Acad Orthop Surg. 2011; 19: 439-449. 23. Guery J, Favard L, Sirveaux F, et al. Reverse total shoulder arthroplasty: survivorship analysis of eighty replacements followed for five to ten years. J Bone Joint Surg Am. 2006; 88: 1742-1747.

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Contemporary Treatment of Rotator Cuff Tendinopathy Lieutenant Commander Emeka Ofobike, Jr., MD Abstract: Rotator cuff pathology is the most frequent cause of shoulder pain in the adult population. The evaluation and treatment of these injuries represent a dilemma for both the orthopedist and non-orthopedist alike. Diagnosis requires an accurate history with emphasis on patient age and activity level, symptom duration, exacerbating factors, and level of disability. Interpretation of the shoulder exam is often difficult because of lack of specificity of the many tests and the similarity of findings among various diagnoses. As technology improves, imaging of the rotator cuff has become more diagnostic with even subtle tears being evident on MRI and ultrasound. Radiographic findings, however, often do not correlate with patient symptoms. Conflicting evidence regarding operative versus non-operative management of impingement lesions, partial-thickness and full-thickness rotator cuff tears makes choosing the correct treatment regimen highly individualized for each patient and physician. There are emerging therapies for treatment of rotator cuff pathology based on specific patho-etiologic factors. The purpose of this discussion is to review the current understanding of rotator cuff pathology and the various etiologies. Additionally, the reader should be able to understand which aspects of history, physical exam and imaging studies may render a patient a more suitable surgical candidate based on prognostic factors.

Introduction Shoulder pain is a frequent presenting complaint of patients to a physician’s office. Subacromial impingement syndrome comprises various etiologies which include subacromial bursitis, impingement related to bursal or articular-sided rotator cuff compression, and partial-or full-thickness rotator cuff tears. Rotator cuff tears (RCTs) are the most common tendon injury in the adult population, with as much as 2/3 of the elderly population demonstrating radiographic evidence of full-thickness defects.1 Manifestation of these injuries includes persistent shoulder pain, weakness, motion limitation and disability.1-2 However, there remains a high prevalence of asymptomatic full-thickness RCTs. Recent studies investigating the natural history of these tears indicate that as tear size increases with age, so does the likelihood of pain development. Tear size increase includes enlargement of full-thickness tears as well as conversion of partial-thickness to full-thickness tears.3 In the younger population (40-60 years old), increase in tear size was found in 49% of study participants after 2-3 years of conservative treatment with a correlation found between clinically significant increase in tear size and the presence of considerable pain.4 The presence of a tear in the dominant arm is a positive predictor of pain related to RCT, as is having a positive impingement sign and weakness of external rotation.1, 3

Patho-etiology of Rotator Cuff Tendinopathy Despite the common use of the term “tendonitis” to describe rotator cuff disease, implying an inflammatory mechanism, the histopathology of rotator cuff disease is a failed healing response which includes collagen disorganization, fat degeneration, fibrocartilaginous metaplasia, disorderly tendon cell proliferation and increased noncollagenous extracellular matrix.5-6 Many authors are now recommending the use of the general term “tendinopathy” in reference to the clinical entity of overuse rotator cuff disease with “tendonitis” and “tendinosis” only being used after histopathologic examination. Part of the difficulty in identifying optimal treatment of rotator cuff tendinopathy is in delineating the causative factors of pain. Numerous theories explaining rotator cuff disease continue to be debated. These include the extrinsic compression theory which holds that the rotator cuff is compressed between the humeral head and the anterior acromion and coracoacromial (CA) ligament, leading to bursitis and tendinopathy (Figure 1). This process may progress to partial-or full-thickness tearing.7 In this theory, the acromiohumeral space may be further narrowed by aberrant acromial morphology or degenerative spurring of the undersurface of the acromion or acromio-clavicular joint increasing the risk of cuff impingement. The intrinsic degeneration theory of rotator cuff tendinopathy presumes that factors intrinsic to the rotator cuff, such as a hypovascular “watershed” area of the distal supraspinatus tendon, collagen degeneration due to aging, and primary cuff failure due to eccentric overload are responsible for cuff disease.8-9 Another area of debate relates to the role that overuse plays in development of pain related to rotator cuff pathology. In all likelihood, the true pathogenesis of rotator cuff disease involves a combination of these factors.

Figure 1 View of Rotator Cuff

A front view image of the rotator cuff (supraspinatus), acromion, and subacromial bursa.

Address correspondence to: LCDR Emeka Ofobike, Jr., Department of Orthopaedics, U.S. Naval Hospital Okinawa, Japan, PSC 482, Box 45 FPO, AP 96362. Email:emeka.ofobike@med.navy.mil. 32 Vol. 63, No. 3 2012 Northeast Florida Medicine

www . DCMS online . org


It is becoming apparent that among the contributing factors of rotator cuff disease, genetics is not to be overlooked. Though no single gene may be implicated in the development and progression of cuff tendinopathy, there is a familial predisposition to rotator cuff disease, symptom presentation, and tear progression.10-11 Current research is investigating the role of apoptosis and its effect on tendon repair and regenerative capacity.11 At the molecular level, the complex and delicate balance between matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) as it relates to tendinopathy and tendon rupture continues to be investigated. The role of MMPs as regulators of tissue remodeling after injury is well established; however when MMPs themselves are left under-regulated, weakening of tendon extracellular matrix may occur.6 Increased expression of MMPs with an associated decreased expression of TIMP messenger RNA has been found in tendinopathic tendon cells.12

Patient Evaluation Obtaining an accurate and detailed patient history is a crucial step in establishing the diagnosis of rotator cuff tendinopathy. The patient’s age, hand dominance and activity level are important factors to ascertain. Additionally, knowing whether symptom onset began insidiously or after a traumatic event is of paramount importance and may affect choice and timing of treatment.13 Other potentially prognostic variables to determine are overall duration of symptoms, presence of pain at night or anything that awakens the patient from sleep, and subjective weakness.1,14-15 Identification of prior treatments such as pharmacologic therapy, physical therapy, injections or surgeries is also beneficial. The physical exam of the shoulder is notoriously difficult not only because of the numerous bony, ligamentous, musculotendinous and cartilaginous structures which may cause pain, but also because of the number of special tests used in evaluating them. Compounding this difficulty is the knowledge that many of the tests, though sufficiently sensitive in eliciting positive findings, are notoriously non-specific in identifying a particular diagnosis. For this reason, it is important for any practitioner who evaluates patients with shoulder pain to develop a working knowledge and level of comfort with the provocative tests so that the decision may be made on which ones to use based on clinical suspicion. Among the most frequently used clinical exams for the rotator cuff are: the lift-off and belly press tests for subscapularis injury; the external rotation lag sign for full thickness rotator cuff tears (noted to have a sensitivity of 56% and specificity of 98% for isolated supraspinatus tears)16; Jobe’s test for supraspinatus tears; and the impingement tests (Neer’s and Hawkins-Kennedy). Tennent et al. present an excellent review of the special tests associated with the rotator cuff which include the original author descriptions of the exams with artistic depictions.17 Imaging studies guided by appropriate history and physical exam provide significant additional information. Initial www . DCMS online . org

Figure 2 MRI Image of Shoulder

This is an MRI image of a right shoulder with the asterisk (see arrow) indicating the torn position of the supraspinatus tendon (black structure) which has pulled away from its normal attachment from the humeral head (round gray structure). The "bright" signal around the tendon indicates joint fluid and underlying inflammation. Notice the space between the tendon edge and the humeral head confirming discontinuity of the rotator cuff tendon.

studies should include plain radiographs of the shoulder in three planes (true shoulder AP, supraspinatus outlet view and axillary lateral.) Plain films may identify glenohumeral and acromioclavicular arthritic disease with associated hypertrophic spurring, evidence of prior instability, calcific tendon deposits, rotator cuff insertional sclerosis or cystic change of the greater tuberosity, or decreased acromiohumeral distance indicative of a chronic, massive rotator cuff tear. Historically, arthrography was the imaging modality of choice for identification of rotator cuff pathology, but that has been supplanted by magnetic resonance imaging (MRI) with its ability to provide detailed soft tissue images in multiple planes (Figure 2). Recently, sonography has become a popular alternative to MRI for imaging of the rotator cuff for several reasons. It has been well-established that MRI and ultrasound are equivalent in their ability to diagnose full-thickness rotator cuff tears, with ultrasound being significantly cheaper. Diagnostic efficiency of ultrasound remains operator-dependent and the ability of ultrasound to detect partial-thickness rotator cuff injuries as well as labral or articular cartilage pathology remains diminished.18

Non-operative Management Optimal treatment for rotator cuff tendinopathy has not been elucidated. In most cases, a trial of conservative treatment, which typically includes systemic anti-inflammatory medications; subacromial or intra-articular injections, which may be repeated periodically; and physical therapy, is appropriate.19-20 The American Academy of Orthopaedic Surgeons Clinical Practice Guideline on treatment of rotator cuff pathology Northeast Florida Medicine Vol. 63, No. 3 2012 33


recommends that patients with rotator cuff symptoms, in the absence of a full-thickness tear, be initially treated non-operatively with exercise and/or non-steroidal anti-inflammatory drugs.21 With subacromial cortisone injection and physical therapy, 79% of study patients with subacromial impingement syndrome did not require surgery when followed up after two years.22 Review of current literature has failed to show any significant difference between operative and nonoperative treatment of impingement syndrome.23 There is also level I evidence which shows that subacromial injections of sodium hyaluronate significantly improved pain and functional scores in patients with rotator cuff disease without full-thickness tears after a mean duration of 33 months.24 With regard to rotator cuff tears, success rates of nonoperative treatment vary between 33 and 92%.14 Recent evidence indicates that injection of triamcinolone into the glenohumeral joint followed by supervised physical therapy significantly improved night pain and activity-related pain for up to three months in patients with full-thickness rotator cuff tears compared to rehabilitation alone.25 The optimal treatment for partial-thickness tears remains controversial, whereas the trend is for surgical treatment of symptomatic full-thickness tears.4, 26-27

Surgical Treatment Despite the overall lack of consensus regarding surgical treatment of rotator cuff tears, there does appear to be one instance in which there is agreement; acute traumatic rotator cuff injuries should be repaired early.13,21 Animal models have suggested that irreversible changes occur to the rotator muscle-tendon complex as early as six weeks from date of injury. There has therefore been a shift towards operative treatment of rotator cuff tears when acute. In one report, surgery within 3 weeks of traumatic cuff injury led to significantly improved range of motion and functional scores compared to late surgery after a 3-year follow-up in one report.13 One of the long-standing surgical debates of rotator cuff pathology relates to what to do with symptomatic partial-thickness tears. The options range from arthroscopic debridement with or without acromioplasty and subacromial decompression to completion of the tear and repair as one would for a full-thickness tear. In the short term, completion of partial-thickness tears to a full-thickness defect, followed by repair has shown significant improvement of functional scores with a high rate of radiographic healing.28 One of the more attractive aspects of rotator cuff repair to emerge within the last decade is the concept of the doublerow suture anchor repair. This repair configuration, which is theorized to more closely approximate the anatomic footprint of the rotator cuff insertion, has shown in biomechanical studies increased pullout strength, improved contact area and pressure, and decreased gap formation at the bone-tendon interface as compared to single row configuration.The general theme is to create two separate points of attachment (“rows”) for the tendon, one in a medial position on the 34 Vol. 63, No. 3 2012 Northeast Florida Medicine

humeral head and another one more lateral on the greater tuberosity. Within each “row”, several suture anchors may be placed. Despite these findings, clinical and functional outcomes demonstrating superiority of one technique over the other have not emerged.29-31 Regardless of the choice of repair technique (open versus mini-open versus arthroscopic) or configuration (single-row versus double-row), greater than 85% of patients undergoing primary repair of full-thickness rotator cuff tears experience improved pain and shoulder function.13,29-34 Interestingly, these functional improvements come despite a radiographic retear rate that may be as high as 57%.33 Presently, no correlation can be made between functional improvement after rotator cuff repair and healing rates as identified on follow-up MRI or ultrasound.35 There are factors, which portend a less favorable surgical outcome after rotator cuff surgery. These include increasing patient age, MRI tear characteristics such as fatty infiltration and atrophy of rotator cuff muscles, workers’ compensation status, larger initial tear size, degree of shoulder weakness, chronic tear of the long head of the biceps, and female gender.21,32,36-38

Emerging Concepts The treatment of massive irreparable rotator cuff tears remains a clinical challenge and clear recommendations have yet to be established. The use of teres major and latissimus dorsi tendon transfers for massive postero-superior rotator cuff tears has been well reported in the literature. These two tendons, which act as internal rotators and adductors, are rerouted during transfer surgery to the greater tuberosity and/ or proximal humerus, allowing for theoretically improved external rotation and abduction. Lack of high level studies and heterogeneity of outcomes makes generalizing the results of these transfers difficult.39 The search for optimal treatment of this entity has led to interest in tissue engineering as an alternative means of cuff repair.40-41 What has been established is that the use of noncrosslinked, porcine small intestine submucosal xenograft is not recommended.21 Synthetic scaffolds such as polylactic acid and Gore-Tex patches, polyurethane scaffolds, and others are appealing because of their superior mechanical characteristics, however, they come at the cost of poor biocompatibility with foreign body reactions such as synovitis, inflammation, device failure and post-operative infection.41 In contrast to synthetic augmentation, human dermal allograft has recently been shown to be effective in improving pain and function in massive rotator cuff tears in patients after an average of three years, with high rates of radiographic healing.42 Biologic augmentation with platelet rich plasma (PRP) for full thickness rotator cuff tears is another area of active research. The use of PRP in the treatment of rotator cuff tears has gained interest in the hopes that it may enhance and accelerate healing as has been suggested for other musculoskeletal injuries. Though its use appears to be safe without evidence www . DCMS online . org


of increased perioperative morbidity, current literature fails to show improved rates of healing or function with PRP as compared to controls.43-46 Conversely, the use of recombinant human bone morphogenetic protein-12 (rhBMP-12) in an in vivo animal study of rotator cuff repair showed improved biomechanical properties and histological evidence of increased collagen organization in the experimental group when compared to controls without biologic modulation.47 Finally, stem cell research has provided a possible application in the treatment of rotator cuff tears. Scleraxis (Scx), a transcription factor related to embrylogical tendon development, is being investigated to determine whether it can drive genetically-modified pluripotent stem cells to differentiate into tenocytes and augment rotator cuff repair in an animal model.48

Conclusion

nonoperatively treated symptomatic rotator cuff tears in patients 60 years old or younger. Am J Sports Med. 2011; 39(4): 710-714. 5.

Oliva F, Giai Via A, Maffulli N. Role of growth factors in rotator cuff healing. Sports Med Arthrosc Rev. 2011; 19(3): 218-226.

6.

Garofalo R, Cesari E, Vinci E, Castagna A. Role of metalloproteinases in rotator cuff tear. Sports Med Arthrosc Rev. 2011; 19(3): 207-212.

7.

Neer CS. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: A preliminary report. J Bone Joint Surg Am. 1972; 54: 41-50.

8.

Lohr JF, Uhthoff HK. The microvascular pattern of the supraspinatus tendon. Clin Orthop Relat Res. 1990; 254: 35-38.

9.

Harrison AK, Flatow EL. Subacromial impingement syndrome. J Am Acad Orthop Surg. 2011; 19: 701-708.

10. Tashjian RZ, Farnham JM, Albright FS, et al. Evidence for an inherited predisposition contributing to the risk for rotator cuff disease. J Bone Joint Surg Am. 2009; 91: 1136-1142.

The interest in optimizing treatment of rotator cuff pathology underscores the impact this disease process has on our population. The multifactorial nature of the symptoms of rotator cuff tendinopathy makes evaluation and treatment difficult in the office, the radiology suite and the operating room. Fortunately, appropriate conservative treatment tends to be effective in the vast majority of patients . For those who eventually require surgery, improvement in shoulder pain and function is a reasonable expectation, despite a high incidence of incomplete healing. It is important to remember that the prescribed course of conservative treatment does not apply to acute, traumatic rotator cuff injuries which are better treated with early surgery. Although there is a high prevalence of asymptomatic full-thickness rotator cuff tears in the elderly population, rotator cuff tears in the younger population (<60 years old) tend to progress in size and symptoms with time, which may negatively affect chances of positive outcomes if treated late.

11. Longo UG, Berton A, Papapietro N, et al. Epidemiology, genetics and biological factors of rotator cuff tears. Med Sport Sci. 2012; 57: 1-9.

Massive rotator cuff tears are difficult to treat with no consensus on treatment. Emerging technologies and investigation of tissue engineering, biological and synthetic augmentation may provide opportunities in the future for improved outcomes in challenging cases.

17. Tennent TD, Beach WR, Meyers JF. A review of the special tests associated with shoulder examination: Part 1: The rotator cuff tests. Am J Sports Med. 2003; 31: 154-160.

1.

References

Yamamoto A, Takagishi K, Kobayashi T, et al. Factors involved in the presence of symptoms associated with rotator cuff tears: a comparison of asymptomatic and symptomatic rotator cuff tears in the general population. J Shoulder Elbow Surg. 2011; 20(7): 1133-1137.

2.

Rees JD, Wilson AM, Wolman RL. Current concepts in the management of tendon disorders. Rheumatology (Oxford). 2006; 45(5): 508-521.

3.

Mall NA, Kim M, Keener JD, et al. Symptomatic progression of asymptomatic rotator cuff tears: A prospective study of clinical and sonographic variables. J Bone Joint Surg Am. 2010; 92: 2623-2633.

4.

Safran O, Schroeder J, Bloom R, et al. Natural history of

www . DCMS online . org

12. Pasternak B, Aspenberg P. Metalloproteinases and their inhibitors: diagnostic and therapeutic opportunities. Acta Orthop. 2009; 80: 693-703. 13. Hantes ME, Karidakis GK, Vlychou, et al. A comparison of early versus delayed repair of traumatic rotator cuff tears. Knee Surg Sports Traumatol Arthrosc. 2011; 19(10): 1766-1770. 14. Longo UG, Franceschi F, Berton A, et al. Conservative treatment and rotator cuff tear progression. Med Sport Sci. 2012; 57: 90-99. 15. Ruotolo C, Nottage WM. Surgical and nonsurgical management of rotator cuff tears. Arthroscopy. 2002; 18: 527-531. 16. Castoldi F, Blonna D, Hertel R. External rotation lag sign revisited: accuracy for diagnosis of full thickness supraspinatus tear. J Shoulder Elbow Surg. 2009; 18: 529-534.

18. Churchill RS, Fehringer EV, Dubinsky EJ, Matsen FA. Rotator cuff ultrasonography: diagnostic capabilities. J Am Acad Orthop Surg. 2004; 12: 6-11. 19. Bigliani LU, Levine WN. Subacromial impingement syndrome. J Bone Joint Surg Am. 1997; 79(12): 1854-1868. 20. Millet PJ, Wilcox RB, O’Holleran JD, Warner JP. Rehabilitation of the rotator cuff: an evaluation-based approach. J Am Acad Orthop Surg. 2006; 14: 599-609. 21. Pedowitz RA, Yamaguchi K, Ahmad CS, et al. AAOS Clinical Practice Guideline on optimizing the management of rotator cuff problems. J Bone Joint Surg Am. 2012; 94: 163-167. 22. Cummins CA, Sasso LM, Nicholson D. Impingement syndrome: Temporal outcomes of nonoperative treatment. J Shoulder Elbow Surg. 2009; 18(2): 172-177. 23. Dorrestijn O, Stevens M, Winters JC, et al. Current evidence fails to show differences in effectiveness between conservative and surgical treatment of subacromial impingement syndrome. J Bone Joint Surg Am. 2010; 92: 474. 24. Chou WY, Ko JY, Wang FS, et al. Effect of sodium hyaluronate Northeast Florida Medicine Vol. 63, No. 3 2012 35


treatment on rotator cuff lesions without complete tears: a randomized, double-blind, placebo-controlled study. J Shoulder Elbow Surg. 2010; 19: 557-563.

42. Gupta AK, Hug K, Berkoff DJ, et al. Dermal tissue allograft for the repair of massive irreparable rotator cuff tears. Am J Sports Med. 2012; 40(1): 141-147.

25. Gialanella B, Prometti P. Effects of corticosteroids injection in rotator cuff tears. Pain Med. 2011; 12(10): 1559-1565.

43. Jo CH, Kim JE, Yoon KS, et al. Does platelet-rich plasma accelerate recovery after rotator cuff repair? A prospective cohort study. Am J Sports Med. 2011; 39(10): 2082-2090.

26. Papalia R, Franceschi F, Del Buono A, et al. Results of surgical management of symptomatic shoulders with partial thickness tears of the rotator cuff. Br Med Bull. 2011; 99: 141-154. 27. Dezaly C, Sirveaux F, Philippe R. Arthroscopic treatment of rotator cuff tear in the over-60s: repair is preferable to isolated acromioplasty-tenotomy in the short term. Orthop Traumatol Surg Res. 2011; 97(6 Suppl): S125-S130. 28. Kamath G, Galatz LM, Keener JD, et al. Tendon integrity and functional outcome after arthroscopic repair of high-grade partial-thickness supraspinatus tears. J Bone Joint Surg Am. 2009; 91: 1055-1062. 29. Dines JS, Bedi A, ElAttrache NS, Dines DM. Single-row versus double-row rotator cuff repair: techniques and outcomes. J Am Acad Orthop Surg. 2010; 18: 83-93. 30. Grasso A, Milano G, Salvatore M, et al. Single-row versus double-row arthroscopic rotator cuff repair: a prospective randomized clinical study. Arthroscopy. 2009; 25: 4-12. 31. Burks RT, Crim J, Brown N, et al. A prospective randomized clinical trial comparing arthroscopic single- and double-row rotator cuff repair: magnetic resonance imaging and early clinical evaluation. Am J Sports Med. 2009; 37: 674-682. 32. Iannott JP. Full-thickness rotator cuff tears: factors affecting surgical outcomes. J Am Acad Orthop Surg. 1994; 2: 87-95. 33. Zumstein MA, Jost B, Hempel J, et al. The clinical and structural long-term results of open repair of massive tears of the rotator cuff. J Bone Joint Surg Am. 2008; 90: 2423-2431. 34. Gulotta LV, Dodson SJ, Adler CC, et al. Prospective evaluation of arthroscopic rotator cuff repairs at 5 years: part I – functional outcomes and radiographic healing rates. J Shoulder Elbow Surg. 2011; 20(6): 934-940. 35. Gulotta LV, Nho SJ, Dodson CC, et al. Prospective evaluation of arthroscopic rotator cuff repairs at 5 years: part II – prognostic factors for clinical and radiographic outcomes. J Shoulder Elbow Surg. 2011; 20(6): 941-946. 36. Chung SW, Oh JH, Gong HS, et al. Factors affecting rotator cuff healing after arthroscopic repair: osteoporosis as one of the independent risk factors. Am J Sports Med. 2011; 39(10): 2099-2107. 37. Kemp KA, Sheps DM, Luciak-Corea C, et al. Systematic review of rotator cuff tears in workers’ compensation patients. Occup Med-Oxford. 2011; 61(8): 556-562. 38. Razmjou H, Davis AM, Jaglal SB. Disability and satisfaction after rotator cuff decompression or repair; a sex and gender analysis. BMC Musculoskelet Disord. 2011; 12: 66. 39. Longo UG, Franceschetti E, Petrillo S, et al. Latissimus dorsi tendon transfer for massive irreparable rotator cuff tears: a systematic review. Sports Med Arthrosc Rev. 2011; 19: 428-437.

44. Mei-Dan O, Carmont MR. Autologous blood products in rotator cuff repair. Med Sport Sci. 2012; 57: 65-75. 45. Edwards SL, Lynch TS, Saltzman MD, et al. Biologic and pharmacologic augmentation of rotator cuff repairs. J Am Acad Orthop Surg. 2011; 19: 583-589. 46. Barber FA, Hrnack SA, Snyder SJ, Hapa, O. Rotator cuff repair healing influenced by platelet-rich plasma construct augmentation. Arthroscopy. 2011; 27(8): 1029-1035. 47. Seeherman HJ, Archambault JM, Rodeo SA, et al. RhBMP-12 accelerates healing of rotator cuff repairs in a sheep model. J Bone Joint Surg Am. 2008; 90: 2206-2219. 48. Gulotta LV, Rodeo SA. Emerging ideas: Evaluation of stem cells genetically modified with scleraxis to improve rotator cuff healing. Clin Orthop. 2011; 469(10): 2977-2980.

4th Annual Quality Forum AND

6th Annual Caring Community Conference September 12, 2012 Presented by

The Center for Global Health and Medical Diplomacy at the University of North Florida in Jacksonville, FL

40. Donaldson J, Khan WS, Hazlerigg A. Functional tissue engineering for rotator cuff tendons. J Stem Cells. 2010; 5(4): 195-204. 41. Longo UG, Lamberti A, Khan WS, et al. Synthetic augmentation for massive rotator cuff tears. Sports Med Arthrosc Rev. 2011; 19: 360-365.

36 Vol. 63, No. 3 2012 Northeast Florida Medicine

Go to www.unf.edu/brooks/ center for more details. www . DCMS online . org


Pediatric and Adolescent Sports Injuries of the Knee Eric D. Shirley, MD and Mary Anderson, BS Abstract: Traumatic knee injuries in children and adolescents are common in sports participation. The knee injuries may result in anterior cruciate ligament ruptures, meniscus tears, patella dislocations, and osteo-chondral fractures. Both the history and physical examination are helpful in making the diagnosis. Radiographs with judicious use of magnetic resonance imaging may be confirmatory. Treatment will depend upon the specific injury and one must consider the patient’s activity level while preserving physeal growth.

Introduction Participation in sports has long been a rite of passage for youth. An estimated 44 million Americans under the age of 18 years participate in organized athletic activities each year.1 While participation in sports has many positive effects on youth, such as promoting healthy lifestyle decisions, there is also a risk of injury. Pediatric and adolescent sports participation results in an estimated 2 million injuries, 500,000 doctor visits, and 30,000 hospitalizations per year.2,3 Sports related knee injuries are second only to ankle injuries.4 In male athletes, knee injuries occur at the following rates per 10,000 athletic exposures; 6.91 per in football, 3.81 for wrestling, 3.60 for soccer, 2.03 for basketball and 1.05 for baseball.4 In female atheletes, knee injuries occur at a rate of 5.08 for soccer, 3.80 for basketball, 1.64 for volleyball and 1.41 for softball. Knee surgeries account for 45% to 60% of all adolescent sports-related surgeries.4 Knee injuries from sports include anterior cruciate ligament (ACL) ruptures, meniscus tears, patella dislocations, and osteochondral or other fractures. This review will focus on the evaluation, diagnosis, and treatment of these injuries.

Clinical Evaluation History – When a traumatic sports injury is sustained, a detailed history is important in determining the diagnosis. A description of the injury can be helpful, although adolescent patients may have a difficult time describing or remembering what happened.5 Injuries can be classified as contact and noncontact injuries. Contact injuries include direct blows to the knee by an opponent or a fall to the ground. Noncontact injuries involve a twisting event. Alternatively, the injury may occur with relatively little trauma, such as from walking or running in a straight line. Sometimes a “pop” is heard at the time of injury and may represent a ligament injury. Symptoms that develop later should be elicited, including pain, ability to bear weight, swelling, and the presence of mechanical symptoms or instability. Pain may be localized or diffuse. Similarly, swelling may be focal or diffuse about Address Correspondence to: Eric D. Shirley, MD, 807 Children’s Way, 5th Floor, Jacksonville, FL 32207. Phone: 904-697-3684. Fax: 904-697-3477. Email:eshirley@nemours.org. www . DCMS online . org

the knee if a traumatic effusion has occurred. A knee effusion that develops within several hours of a traumatic injury is assumed to be a hemarthrosis.6 Patients may note instability or mechanical symptoms such as catching and locking. Examination – A standardized, detailed examination should be performed on every patient with a traumatic knee injury. The musculoskeletal examination of the knee has been well described.7 It begins with a gait evaluation. In general, gait may be described as smooth, antalgic, or unable to bear weight. Depending on the level of pain and swelling, patients may be asked to perform functional tests such as double leg squat, single leg squat, and lunges. Lower extremity alignment is inspected and can be classified as neutral, varus, or valgus. Leg lengths are assessed for inequality. The knee is inspected for skin lacerations, ecchymosis, focal swelling, or effusions. To evaluate for an effusion, the patient is placed in the supine position with the knee extended.6 The suprapatellar pouch is then compressed to move the fluid distally, and ballottement of fluid medially and laterally confirms the presence of an effusion.6 The knee is palpated for areas of focal tenderness, which can localize the injury. Anatomic locations to palpate include the femoral/tibial physes (fracture), femoral condyles (osteo-chondral fracture), medial plica, medial patellar retinaculum (patella dislocation), joint lines (meniscus tear), collateral ligaments, patella, tibial tubercle, and patellar tendon. Range of motion assessment includes flexion and extension. The ability to maintain a straight leg raise should be demonstrated. A flexion contracture is noted when the patient is unable to achieve full extension actively or passively, while an extensor lag is noted when the patient is able to achieve full extension passively but not actively. Special tests will further help make the diagnosis. Patella instability may be assessed by translating the patella laterally and detecting apprehension of dislocation. Varus and valgus stresses are applied with the knee held in 30° of flexion to assess the collateral ligaments. The Lachman test evaluates the ACL. This test is performed with the knee positioned in 20° flexion by placing one hand over the joint line and a second hand under the proximal tibia. The second hand is used to provide an anterior stress on the lower leg while the other hand senses the amount of translation and firmness of the endpoint. A side-to-side difference greater than 3 mm is considered abnormal. The pivot shift test may be performed to evaluate the ACL as well. The detection of posterior sag of the tibia plateau relative to the femoral condyles greater than the contralateral side suggests a posterior cruciate ligament (PCL) injury. In addition, the posterior drawer test is performed with the knee positioned in 90° of flexion to further evaluate the PCL. The McMurray test evaluates for a meniscus tear. The knee is placed in flexion and then extended with the leg in both external and internal rotation to evaluate for lateral Northeast Florida Medicine Vol. 63, No. 3 2012 37


and medial tears, respectively. Finally, postero-lateral corner injuries, which typically occur following significant trauma, are evaluated in the prone position using the Dial test.

Figure 1 A,B Radiographs of Fractures

The remainder of the limb should be assessed for coexisting injuries. It is important to remember that a slipped capital femoral epiphysis can present with knee pain. These patients may exhibit decreased hip flexion and internal rotation. Underlying ligament laxity should be assessed as conditions such as Ehlers-Danlos syndrome can influence treatment decisions.8 Finally, a neurovascular examination should be performed.

Differential Diagnosis Traumatic knee hemarthroses often represent important injuries that may require surgical treatment.6,9-11 Luhmann reported a series of 44 acute knee hemarthroses in patients 18 years or younger, and 48% required surgery.6 Specific causes of an acute traumatic knee hemarthrosis include ACL ruptures, meniscus tears, patella dislocations, and osteo-chondral or other fractures. These fractures include patella sleeve, tibial spine, and distal femoral physeal fractures. The most common cause of traumatic knee hemarthrosis has varied from ligament injuries to osteo-chondral fractures.6,9-11 Stanitiski et al. found that ACL tears were the most common cause of acute knee injuries in an evaluation of 70 children.9 Sixty-three percent had ACL tears, and 46% had meniscus tears.9 Osteo-chondral injuries were seen in 7% of patients.9 In the series of pediatric knee injuries reported by Luhmann, ACL tears, meniscal tears, and patellofemoral pathology comprised 87% of injuries.6 Of all injuries, 29% were ACL tears, 29% meniscus tears, 25% patellofemoral subluxations/dislocations,5% medial collateral ligament sprains, 4% osteo-chondral fractures, 2% PCL injuries, and 2% tibial spine fractures.6 Girls were more likely to have patellofemoral injuries, while boys were more likely to have ACL or meniscal tears.6 Bergstrom et al. found that collateral ligament strains were the most common cause of injury in a study of 30 patients under 16 years of age with a traumatic hemarthrosis.10 Conversely, Matelic et al. found that osteochondral fracture was the most common injury in a series of 21 children with traumatic hemarthroses.11

Imaging Radiographs – General indications for obtaining plain radiographs in the evaluation of knee injuries include history of a traumatic effusion, difficulty bearing weight, and focal tenderness. Standard views include anteroposterior, lateral, and a sunrise or Merchant view to visualize the patella. A posteroanterior tunnel view may be helpful as well. Radiographs will lead to the diagnosis for many patients (Figure 1). In a series of 51 pediatric patients with acute knee trauma, radiographs were positive in 16 of 51 patients.12 These findings included 5 metaphyseal fractures, 3 patellar fractures, 4 physeal fractures, 3 tibial spine avulsions, and 1 ligament

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(A, left) Anteroposterior and (B, right) lateral radiographs of distal femur physeal fractures sustained by a 15-year-old wrestler.

avulsion.12 While radiographs are useful to identify these fractures, they may not detect all osteo-chondral fractures.11 Magnetic Resonance Imaging – Magnetic resonance imaging may be obtained to evaluate for an ACL injury, meniscal injury, intra-articular fracture, or loose body. An MRI is not required if the examination is absolutely consistent with a complete ACL rupture or meniscus tear. When a patient sustains an osteo-chondral fracture or loose body, the MRI allows the donor site and optimal surgical approach to be evaluated. It should be kept in mind that MRI for intra-articular knee disorders is less accurate in younger patients, with lower sensitivity (62%) and specificity (90%) in children younger than 12 years than in children 12 to 16 years (78% and 96%).13 Furthermore, when performed by an experienced pediatric sports medicine specialist, clinical examination and selective MRI have similar overall performance.13

Specific Injuries Anterior Cruciate Ligament Injuries – The ACL originates on the posteromedial aspect of the lateral femoral condyle and runs obliquely through the knee to insert between the tibial spines. The function of the ACL is to limit both anterior translation and rotation of the tibia. ACL injuries account for approximately 7% of pediatric sports injuries.14 Although just 1% of the 250,000 complete ACL tears per year occur in skeletally immature patients, the number of ACL injuries in this age group is rising.15,16 Girls are particularly at risk, and approximately 1 in 70 high school female athletes will sustain an ACL injury per year of varsity sports participation.17 The ACL may be injured by direct contact or more commonly by noncontact mechanisms.Patients often report hearing a “pop” and note the early onset of an effusion. Some may develop frequent instability, while others will only have www . DCMS online . org


instability during running or twisting activities. Examination may demonstrate a knee effusion, tenderness over the joint lines (when associated with a meniscus tear), and positive Lachman or pivot shift tests, or both. The pivot shift test is more helpful in patients who are relaxed and has been shown to be positive in 90% of patients under anesthesia versus 35% of awake patients.18 An MRI is helpful to evaluate patients with an equivocal examination and to evaluate associated injuries of the meniscus, cartilage, PCL, collateral ligament, and postero-lateral corner. The goals of treatment are to prevent functional instability, allow return to sports, and prevent the long-term complications associated with knee instability. Nonoperative management (physical therapy, bracing, and activity modification) of complete ACL tears has demonstrated poor results, with an increased risk of meniscus tears and chondral injury over time.19-21 Kellenberger and von Laer reported on 23 pediatric adolescent ACL ruptures treated nonoperatively; all had signs of instability, and 10 showed joint arthrosis at the 72-month follow up.21 Mizuta et al. reported the results of nonoperative treatment in 18 skeletally immature patients. 2 At the 51-month follow up, all had symptoms, 6 developed meniscus tears, 61% developed radiographic changes, and only 1 returned to pre-injury sport level. Conversely, surgical treatment has demonstrated superior results, with ACL reconstruction achieving greater stability, higher rate of return to sports, and lower rates of subsequent re-injury or meniscus tears.22,23 Treatment considerations include patient goals, compliance, and skeletal maturity. In adults, surgical treatment consists of reconstruction using bone tunnels that cross the closed proximal tibia and distal tibial physes. Treatment can proceed in a similar manner for older adolescents with closed or nearly closed physes (boys greater than 16 years of age, girls greater than 14 years of age, Tanner stage V).24 With younger patients, you must consider the risk of

Figure 2 Ligament Reconstruction (Graft position)

Graft position in physeal-sparing anterior cruciate ligament reconstruction with autogenous iliotibial band graft. (Used with

permission.)

Figure 3 Ligament Reconstruction (Tunnel position)

Tunnel position in physeal-sparing anterior cruciate ligament reconstruction with all-epiphyseal tunnels. (Used with permission.)

iatrogenic physeal injury resulting in longitudinal or angular growth disturbance. These complications have been reported, although they most often involved hardware fixation across the physis, bone plugs across the physis, or large tunnels.16 Treatment of skeletally immature patients with ACL injuries may be divided into two groups: adolescents with growth remaining (boys 13-16 years, girls 12-14 years, Tanner stage 3-4) and pre-pubescent patients (Tanner stages 1 or 2).24 For adolescent patients with growth remaining, transphyseal reconstruction with fixation away from the growth plates can be performed.25 Treatment for prepubescent patients can be more complicated. For prepubescent patients, the risks of surgical treatment are more significant because of greater growth remaining. If possible, nonoperative treatment with rehabilitation, functional bracing, and return to non-high-risk activities is advised, with surgery performed when the patient is closer to skeletal maturity. However, surgery is indicated in patients with concurrent cartilage or repairable meniscus damage or with functional instability despite nonoperative treatment. Physeal-sparing methods are performed. Options include combined intra-and extra-articular reconstruction using an autogenous iliotibial band graft (Figure 2) and intra-articular all-epiphyseal fixation (Figure 3).26,27,28 Postoperative treatment requires a commitment to a physical therapy program. Initial rehabilitation consists of range of motion exercises, patellar mobilization, proprioception exercises, and closed chain strengthening. After 3 months, straight-line jogging, plyometrics, and sport-specific training is initiated. Return to play typically occurs 6 to 8 months after surgery and may occur as early as 4 to 5 months. Given the consequences of ACL injury and complexities of treatment, attention has been given to prevention. Preventive efforts are primarily focused on improving neuromuscular deficits due to training deficiencies, developmental differences,

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Northeast Florida Medicine Vol. 63, No. 3 2012 39


or hormonal influences in the female knee.28 The deficits are targeted by neuromuscular training programs that aim to decrease peak landing forces, reduce valgus and varus torques, increase hamstring function, and increase jump height.29 Meniscus Tears – The menisci are C-shaped portions of fibrocartilage located in the medial and lateral portions of the knee. The menisci function primarily to preserve articular cartilage via load-sharing and shock absorption and secondarily to assist in joint stability.30 Meniscus tears in skeletally immature patients are more common in association with ACL tears but may also occur in isolation.31 Meniscus tears occur primarily as a result of a twisting injury. Physical examination may demonstrate an effusion, pain with knee flexion greater than 90°, joint line tenderness, and a positive McMurray’s test. An MRI may be helpful to clarify the diagnosis (Figure 4) and to identify a discoid meniscus. The discoid meniscus occupies a greater than normal amount of the lateral tibial plateau and demonstrates variable stability. Treatment options for meniscus tears include observation and surgery. Nondisplaced tears located in the periphery may have healing potential and, therefore, can be treated nonoperatively with a gradual return to pivoting, cutting, and sports approximately 3 months after injury. Surgery is indicated for displaced tears or those with mechanical symptoms. During arthroscopy, the morphology of the tear is evaluated to determine the best treatment. Vertical tears in the periphery of the meniscus may be repaired, providing the advantage of meniscal tissue preservation. Debridement can result in early arthritis due to increasing local contact stresses on the cartilage.32 However, meniscectomy (typically partial) is recommended for complex or horizontal tears as

Figure 4 MRI of Meniscus Tear

Figure 5 Patella Dislocation

Sunrise view with loose body in lateral gutter following patella dislocation in a 14-year-old baseball player.

the tissue is often not amenable to repair and success rates are lower.33 Success rates of repair are highest when performed with concomitant ACL reconstruction.34 Patients may return to sports 3 to 4 months after repair following meniscectomy. Patella Dislocations – The normal articulation of the patellofemoral joint depends on both bony conformity and softtissue constraints. The medial patellofemoral ligament (MPFL) is the main restraint against lateral patellar dislocation from full extension through 30° of knee flexion before the patella engages in the trochlea.35 Then, stability is primarily provided by the bony conformity of the trochlea. Other stabilizers include the quadriceps and patellar tendons, the vastus medialis muscle, and the patellotibial and patellomeniscal ligaments. Patella dislocations may result from contact or noncontact mechanisms. Often the patella will dislocate laterally and reduce spontaneously. The dislocation may result in a tear of the medial patellofemoral ligament or an osteo-chondral fracture of the medial patella facet or lateral femoral condyle.36 Examination may demonstrate an effusion and tenderness over the MPFL or osteo-chondral donor sites. Further examination is performed to identify predisposing factors such as genu valgum, rotational malalignment, vastus medialis weakness, ligament laxity, and flat feet .37 Radiographs are obtained to evaluate the reduction of the patella, presence of loose bodies (Figure 5), and predisposing factors such as patella alta, abnormal patella morphology, and trochlear dysplasia.

Sagittal view of T2-weighted magnetic resonance imaging (MRI) demonstrating lateral meniscus tear in 17-year-old male basketball player. 40 Vol. 63, No. 3 2012 Northeast Florida Medicine

If the patella has not spontaneously reduced, reduction can be performed in the prone position with the hips and knees extended.Treatment for the first-time patella dislocation generally involves nonoperative treatment.37 This consists of brief immobilization followed by functional rehabilitation. The length of immobilization is not well established. Surgery is indicated in the setting of an osteo-chondral fracture. Surgery may also be considered for substantial disruption of the medial soft tissue stabilizers with lateral subluxation of patella.38 However, primary repair of the torn medial structures has not been shown to improve long-term subjective or functional results.39 Despite nonoperative or operative efforts at primary treatment, recurrent dislocation rates range from www . DCMS online . org


17% to 44%40,41 and may require surgical reconstruction of the medial patellofemoral ligament.42

Figure 6 A,B Tibial Spine Fracture Radiographs

Osteo-chondral Fractures – Pediatric and adolescent patients are susceptible to osteo-chondral fractures because of a weaker cartilage-bone junction, which results from incomplete formation of the calcified cartilage.43 Osteo-chondral fractures may occur following noncontact or contact injuries (including patellar dislocations), which place shear forces on the femoral condyles. Examination will demonstrate an effusion and tenderness over donor sites or loose bodies. Although radiographs may reveal the presence of a loose body, the size can be underestimated as the cartilage will not be visualized.44 An MRI can be helpful to evaluate the location, size, and integrity of the donor sites. The differential diagnosis should include osteo-chondral fractures resulting from a previous osteochondritis dissecans. An acquired condition affecting subchondral bone, this condition represents a spectrum that may progress from softening of the overlying cartilage and partial detachment of an articular lesion to osteo-chondral separation with loose bodies.45 Potential causes include inflammation, ossification abnormalities, ischemia, and repetitive micro-trauma. The goal of treatment is to prevent progressive arthritis due to disruption of the articular cartilage surface. Surgery is recommended for large loose bodies with a donor site in weight-bearing portions of the knee as reattachment affords the potential to restore anatomy of the cartilage surface. Surgery should be performed before the osteo-chondral fragment is disrupted. Fixation can be achieved with bioabsorbable46 or metallic devices.47 Following repair, postoperative weight bearing is limited initially. Return to sports may be expected between 4 and 6 months postoperatively. If the loose body is found to be not viable for repair, the loose body is removed, and the donor site is treated with either observation, marrow stimulation, or other cartilage resurfacing techniques. Fractures – Acute knee injuries may result in fractures as well. Fractures of the distal femoral physis, patella sleeve, and tibial spine may result in a traumatic hemarthrosis. Focal tenderness will be present over the involved bone, and radiographs will identify the fracture location. Distal femur physeal fractures are important to identify to provide optimum treatment. Physeal fractures occur because the growth plate is weaker than the surrounding ligaments. Radiograph results may be normal or may demonstrate physeal widening. Traditionally, stress radiographs were advised, although these views are no longer advocated because of concerns of creating further physeal injury. Therefore, suspected nondisplaced physeal injuries can be further evaluated with an MRI or treated empirically with cast immobilization. Nondisplaced distal femur physeal fractures can be treated with immobilization, while displaced fractures will require anatomic reduction and fixation. Following treatment, these injuries need to be followed closely for growth arrest, which is not uncommon and occurred in 27% of patients in one series.48 Treatment of a growth arrest may require contralateral growth plate arrest, limb lengthening, or osteotomy.49 www . DCMS online . org

(A, left) Anteroposterior and (B, right) lateral radiographs of displaced tibial spine fracture in a 12-year-old male soccer player.

Similar to growth plate fractures, fractures may also occur through the incompletely ossified tibial spine. These injuries typically occur between the ages of 8 and 14 years. Radiographs demonstrate the fracture but may not show associated injuries such as meniscus tears. Nondisplaced or reducible fractures can be treated nonoperatively with casting.49 Displaced or irreducible fractures require surgery (Figure 6). Arthroscopic or open reduction is followed by screw or suture fixation. Complications include both stiffness and laxity. Stiffness may require further procedures such as manipulation in repeat arthroscopy; therefore, early range of motion exercises are advocated.50 Persistent laxity despite anatomic reduction is likely due to stretching of the ACL at the time of the fracture and is usually not functionally limiting.51 Patella sleeve fractures occur in the cartilaginous portion of the proximal or distal patella ossification centers, typically in patients between the ages of 8 and 12 years. Examination will reveal a palpable defect at the patellar pole and inability to extend the knee (unless the retinaculum remains intact). Radiographic diagnosis may be difficult because of the small size of the bone fragments, and, therefore, a high degree of suspicion for this injury should be maintained. Surgical treatment is required.

Conclusion Pediatric sports injuries involving the knee may result in a variety of injuries. These include ACL tears, meniscus tears, patella dislocations, and osteo-chondral fractures. The initial history and physical examination often identifies the diagnosis, with radiographs and other imaging used for confirmation. Treatment goals include restoring function, returning to sports, and preventing long-term complications such as arthritis and growth plate arrest. Northeast Florida Medicine Vol. 63, No. 3 2012 41


1.

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Butler JC, Andrews JR. The role of arthroscopic surgery in the evaluation of acute traumatic hemarthrosis of the knee. Clin Orthop Relat Res. 1988;(228):150-152.

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Luhmann SJ. Acute traumatic knee effusions in children and adolescents. J Pediatr Orthop. 2003;23:199-202.

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Hoppenfeld S. Examination of the spine and extremities. East Norwalk, CT: Appleton-Century-Crofts; 1976:1-267.

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Beighton P, Solomon L, Soskolne CL. Articular mobility in an African population. Ann Rheum Dis. 1973;32:413-418.

9.

Stanitski CL, Harvell JC, Fu F. Observations on acute knee hemarthrosis in children and adolescents. J Pediatr Orthop. 1993;13:506-510.

10. Bergstrom R, Gillquist J, Lysholm J, Hamberg P. Arthroscopy of the knee in children. J Pediatr Orthop. 1984;4:542-545. 11. Matelic TM, Aronsson DD, Boyd DW Jr, Lamont RL. Acute hemarthrosis of the knee in children. Am J Sports Med. 1995;23:668-671. 12. Wessel LM, Scholz S, Rusch M, et al. Hemarthrosis after trauma to the pediatric knee joint: what is the value of magnetic resonance imaging in the diagnostic algorithm? J Pediatr Orthop. 2001;21:338-342. 13. D. Kocher MS, DiCanzio J, Zurakowski D, Micheli LJ. Diagnostic performance of clinical examination and selective magnetic resonance imaging in the evaluation of intraarticular knee disorders in children and adolescents. Am J Sports Med. 2001 May-Jun;29(3):292-6.

of acute anterior cruciate ligament examinations. Initial versus examination under anesthesia. Am J Sports Med. 1985;13:5-10. 19. Barber FA. Anterior cruciate ligament reconstruction in the skeletally immature high-performance athlete: what to do and when to do it? Arthroscopy. 2000;16:391-392. 20. Mizuta H, Kubota K, Shiraishi M, et al. The conservative treatment of complete tears of the anterior cruciate ligament in skeletally immature patients. J Bone Joint Surg Br. 1995; 77:890-894. 21. Kellenberger R, von Laer L. Nonosseous lesions of the anterior cruciate ligaments in childhood and adolescence. Prog Pediatr Surg. 1990; 25:123-131. 22. McCarroll JR, Rettig AC, Shelbourne KD. Anterior cruciate ligament injuries in the young athlete with open physes. Am J Sports Med. 1988;16:44-47. 23. Pressman AE, Letts RM, Jarvis JG. Anterior cruciate ligament tears in children: an analysis of operative versus nonoperative treatment. J Pediatr Orthop. 1997;17:505-511. 24. Finlayson CJ, Nasreddine A, Kocher MS. Current concepts of diagnosis and management of ACL injuries in skeletally immature athletes. Phys Sportsmed. 2010;38:90-101. 25. Kocher MS, Smith JT, Zoric BJ, et al. Transphyseal anterior cruciate ligament reconstruction in skeletally immature pubescent adolescents. J Bone Joint Surg Am. 2007;89:2632-2639. 26. Kocher MS, Garg S, Micheli LJ. Physeal sparing reconstruction of the anterior cruciate ligament in skeletally immature prepubescent children and adolescents. J Bone Joint Surg Am. 2005;87:2371-2379. 27. Anderson AF. Transepiphyseal replacement of the anterior cruciate ligament using quadruple hamstring grafts in skeletally immature patients. J Bone Joint Surg Am. 2004;86-A Suppl 1:201-209. 28. Lawrence JT, Bowers AL, Belding J, et al. All-epiphyseal anterior cruciate ligament reconstruction in skeletally immature patients. Clin Orthop Relat Res. 2010;468:1971-1977. 29. Hewett TE, Myer GD, Ford KR. Reducing knee and anterior cruciate ligament injuries among female athletes: a systematic review of neuromuscular training interventions. J Knee Surg. 2005;18:82-88. 30. Brown TD, Davis JT. Meniscal injury in the skeletally immature patient. In: Micheli LJ, Kocher MS, editors. The Pediatric and Adolescent Knee. Philadelphia: Elsevier; 2006. p. 236–59.

14. Shea KG, Pfeiffer R, Jo HW, et al. Anterior cruciate ligament injury in pediatric and adolescent soccer players: an analysis of insurance data. J Pediatr Orthop. 2004;24:623-628.

31. Hede A, Jensen DB, Blyme P, Sonne-Holm S. Epidemiology of meniscal lesions in the knee. 1215 open operations in Copenhagen 1982-84. Acta Orthop Scand. 1990;61:435-437.

15. DeLee JC, Curtis R. Anterior cruciate ligament insufficiency in children. Clin Orthop Relat Res. 1983;(172):112-118.

32. Burks RT, Metcalf MH, Metcalf RW. Fifteen-year follow-up of arthroscopic partial meniscectomy.Arthroscopy. 1997;13:673-679.

16. Kocher MS, Saxon HS, Hovis WD, Hawkins RJ. Management and complications of anterior cruciate ligament injuries in skeletally immature patients: survey of the Herodicus Society and The ACL Study Group. J Pediatr Orthop. 2002;22:452-457.

33. Krych AJ, McIntosh AL, Voll AE, et al. Arthroscopic repair of isolated meniscal tears in patients 18 years and younger. Am J Sports Med. 2008;36:1283-1289.

17. Hewett TE, Lindenfeld TN, Riccobene JV, Noyes FR. The effect of neuromuscular training on the incidence of knee injury in female athletes. A prospective study.Am J Sports Med. 1999 Nov-Dec;27(6):699-706. 18. Donaldson WF 3rd, Warren RF, Wickiewicz T. A comparison

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34. Ahn JH, Lee YS, Yoo JC, et al. Clinical and second-look arthroscopic evaluation of repaired medial meniscus in anterior cruciate ligament-reconstructed knees. Am J Sports Med. 2010;38:472-477. 35. Andrish J. The biomechanics of patellofemoral stability. J Knee Surg. 2004;17:35-39.

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36. Iobst C, Kocher M. Chondral injuries and osteo-chondral fractures. In: Micheli L, Kocher M, eds. The Pediatric and Adolescent Knee. Philadelphia: Saunders; 2006. p. 294-316.

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37. Stefancin JJ, Parker RD. First-time traumatic patellar dislocation: a systematic review. Clin Orthop Relat Res. 2007 Feb;455:93-101. 38. Stefancin JJ, Parker RD. First-time traumatic patellar dislocation: a systematic review. Clin Orthop Relat Res. 2007; 455:93-101. 39. Palmu S, Kallio PE, Donell ST, et al. Acute patellar dislocation in children and adolescents: a randomized clinical trial. J Bone Joint Surg Am. 2008;90:463-470.

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40. Cash JD, Hughston JC. Treatment of acute patellar dislocation. Am J Sports Med. 1988;16:244-249. 41. Cofield RH, Bryan RS. Acute dislocation of the patella: results of conservative treatment. J Trauma. 1977;17:526-531. 42. Deie M, Ochi M, Adachi N, et al. Medial patellofemoral ligament reconstruction fixed with a cylindrical bone plug and a grafted semitendinosus tendon at the original femoral site for recurrent patellar dislocation. Am J Sports Med. 2011;39:140-145.

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43. Flachsmann R, Broom ND, Hardy AE, Moltschaniwskyj G. Why is the adolescent joint particularly susceptible to osteo-chondral shear fracture? Clin Orthop Relat Res. 2000;(381):212-221. 44. Walsh SJ, Boyle MJ, Morganti V. Large osteo-chondral fractures of the lateral femoral condyle in the adolescent: outcome of bioabsorbable pin fixation. J Bone Joint Surg Am. 2008;90:1473-1478. 45. Anderson AF, Lipscomb AB, Coulam C. Antegrade curettement, bone grafting and pinning of osteochondritis dissecans in the skeletally mature knee. Am J Sports Med. 1990;18:254-261. 46. Tabaddor RR, Banffy MB, Andersen JS, et al. Fixation of juvenile osteochondritis dissecans lesions of the knee using poly 96L/4D-lactide copolymer bioabsorbable implants. J Pediatr Orthop. 2010;30:14-20. 47. Kocher MS, Czarnecki JJ, Andersen JS, Micheli LJ. Internal fixation of juvenile osteochondritis dissecans lesions of the knee. Am J Sports Med. 2007;35:712-718.

49. Baxter MP, Wiley JJ. Fractures of the tibial spine in children. An evaluation of knee stability. J Bone Joint Surg Br. 1988;

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70:228-230. 50. Patel NM, Park MJ, Sampson NR, Ganley TJ. Tibial eminence fractures in children: earlier posttreatment mobilization results in improved outcomes. J Pediatr Orthop. 2012;32:139-144. 51. Kocher MS, Foreman ES, Micheli LJ. Laxity and functional outcome after arthroscopic reduction and internal fixation of displaced tibial spine fractures in children. Arthroscopy. 2003;19:1085-1090.

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Robotic Assisted Partial Knee Replacements: An Advance in Surgical Technique Kenneth Kaminski, MD; Cedric Ortiguera, MD and Mary I. O'Connor, MD Abstract: In today’s society, technology and the internet profoundly affect the lives of essentially all Americans. With access to the internet, patients are more informed than ever before regarding medical advances and often have high expectations that their surgeon is up-to-date on the most relevant, cutting-edge technology that medicine has to offer. This is particularly true with joint replacement surgery. Robotic assisted partial knee replacement is particularly relevant with the predicted spike in the demand for joint replacements over the next thirty years in the aging “Baby Boomer” generation.1 This article focuses on robotic-assisted partial joint replacements and reviews the fundamental details on this newer procedure.

Figure 1 X-ray of UKA Arthroplasty

Partial versus Total Knee Arthroplasty Total knee arthroplasty (TKA) is one of orthopaedic surgery’s most successful operations.2 However, replacing all three compartments (medial, lateral, and patellofemoral) is not always the ideal option, particularly in younger, high demand individuals with arthritis in only one area (compartment) of the knee. In this patient demographic, a total knee replacement may be an overly aggressive treatment option, sacrificing unaffected bone and resurfacing a majority of the knee that is otherwise asymptomatic. In patients with arthritis limited to the medial or lateral compartment of the knee, surgical options include high tibial osteotomies (HTO) and unicompartmental knee arthroplasty (UKA). With the realignment of the knee joint away from the affected compartment, HTOs typically provide good but temporary improvement in pain with joint replacement often performed approximately seven years later; however, some patients are dissatisfied with the cosmetic appearance of the limb because it can look somewhat “knock-knee”.3 Alternatively UKA can be performed, which resurfaces only the involved joint compartment, while maintaining a more “normal” kinematic motion and appearance of the knee (Figure 1) UKAs were initially introduced into orthopaedic literature in the 1970s with controversial acceptance and uncertain longevity. Implant design, surgical indications, and implantation techniques have evolved over the last 40 years, and if performed within the narrow indications of the procedure, outcomes have been successful. These narrow indications include clinical pain in only either the medial or lateral compartment, an intact anterior cruciate ligament, no arthritis in the opposite Address correspondence to: Mary I. O’Connor, Assistant Professor and Chair, Department of Orthopedic Surgery, Mayo Clinic, 4500 San Pablo Road S., Jacksonville, FL 32224. Phone: 904-953-2496. Email: oconnor.mary@mayo.edu. 44 Vol. 63, No. 3 2012 Northeast Florida Medicine

X-ray of a left medial unicompartmental knee arthroplasty. (UKA)

compartment, only moderate arthritis in the patellofemoral joint, 90 degrees or more of motion, less than a 15 degree flexion contracture, the absence of inflammatory arthritis, and less than a 5 degree correctable varus/valgus deformity. For example, a survival analysis seven to 10 years postoperatively showed a survivorship of 77% for UKA and of 60% for HTO.4 It has been postulated that improvements in UKA techniques, such as the use of navigation and a robot-assisted cutting tool, have even further improved this survival rate. Furthermore, there are early benefits of UKA in the immediate perioperative period: patients with UKA have less perioperative morbidity, regain knee motion more rapidly, have a higher percentage of excellent outcomes and state that the UKA feels more like their original knee.5-7 In appropriate patients, UKA may be a better option than TKA. One important question is whether UKA potentially compromises the ease of converting the patient to a TKA if arthritis develops in the other compartments of the knee. Some data shows that if minimal bone is resected during the UKA and modern implants are used, then the clinical results of subsequent conversion to TKA are comparable to a primary TKA.8 As the longevity of the UKA will be affected by how well the technical aspects of the surgery are performed9,10, tools to assist the surgeon to more precisely place the implants, namely robotic assisted surgery, have emerged. www . DCMS online . org


Robotic-Assisted Surgery

Figure 2 MAKO Robotic Arm

Robotic assisted surgery utilizes a surgeon controlled robotic arm to precisely prepare the bone for UKA implants. The surgical plan is based on a preoperative computed tomography scan, imported to specific software, which allows the surgeon to model the placement of the implants prior to surgery and optimize alignment, particularly rotational congruity of the implants. The surgeon may modify the preoperative plan based on intraoperative findings. Once the plan is determined, the surgeon-controlled robotic arm (Figure 2) utilizes a burr to precisely remove the required bone, minimizing the amount of bone resected.11 Data suggests that with this technology more precise and accurate leg alignment can be achieved in UKA compared with traditional non-navigated non-robot-assisted techniques.12,13 Another benefit is that the robotic-assisted burr permits the creation of individual bony surfaces of any shape, which cannot be generated by an oscillating saw or the traditional UKA cutting guides. This results in a perfectly sculpted cavity that the implant can be placed in. The preservation of the remaining bone allows for an easier and possibly more successful conversion to TKA if one is required at a later date. Use of this technology also facilitates accurate implant placement with a minimally invasive surgical approach. Prior studies of UKA performed with a minimally invasive approach without navigation or robotic assistance demonstrated increased rates of revision. This was attributed to the increased difficulty of identifying bony landmarks for appropriate implant placement.14-16 Although robotic assisted surgery demonstrates positive preliminary results, there are still potential drawbacks to the newer technology. There is a substantial learning curve for the surgeon with the adaptation of any new technology. However, the learning curve has been shown to be relatively low with the robotically assisted UKA.17 This may make the procedure more inviting to someone in the earlier stages of training and can potentially reduce surgical errors associated with minimally invasive approaches. Furthermore, computer tomography (CT)-based systems fail to incorporate soft tissue tension into the planning; gap kinematics are, however, tracked intraoperatively by monitoring the flexion/extension cycle of the knee before the burring process, allowing the implant placement to be refined based on the predicted gaps. The reliability of this practice is still unknown.11 In today’s political atmosphere of escalating health care costs and declining reimbursements, the overall costs for an additional customized CT scan and initial purchase and maintenance of the robot and software are high. The relatively new system also requires trained operating room staff who are familiar with the surgical technique, to ensure efficiency. From a healthcare systems standpoint, whether the potential clinical benefit of robotic assisted partial knee replacement will outweigh the added expense remains unknown. www . DCMS online . org

Image of the MAKO robotic-assisted surgical burr. (Used with permission)

Conclusion In summary, robotic assisted CT image-navigated partial knee replacements represent the current most advanced state of joint replacement surgery. The dynamic changes occurring in healthcare coupled with future studies and outcome evaluations will finalize the role of this innovative technique in the future of orthopedic practice.

References

1.

Kurtz SM, Lau E, Ong K, Zhao K, Kelly M, Bozic KJ. Future young patient demand for primary and revision joint replacement: national projections from 2010 to 2030. Clinical orthopaedics and related research. 2009;467(10):2606-2612.

2.

Schai PA, Thornhill TS, Scott RD. Total knee arthroplasty with the PFC system. Results at a minimum of ten years and survivorship analysis. The Journal of bone and joint surgery. British volume. 1998;80(5):850-858.

3.

Haddad FS, Bentley G. Total knee arthroplasty after high tibial osteotomy: a medium-term review. The Journal of arthroplasty. 2000;15(5):597-603.

4.

Stukenborg-Colsman C, Wirth CJ, Lazovic D, Wefer A. High tibial osteotomy versus unicompartmental joint replacement in unicompartmental knee joint osteoarthritis: 7-10-year follow-up prospective randomised study. The Knee. 2001;8(3):187-194.

5.

Patil S, Colwell CW, Jr., Ezzet KA, D’Lima DD. Can normal knee kinematics be restored with unicompartmental knee replacement? The Journal of bone and joint surgery. American volume. 2005;87(2):332-338.

6.

Laurencin CT, Zelicof SB, Scott RD, Ewald FC. Unicompartmental versus total knee arthroplasty in the same patient. A comparative study. Clinical orthopaedics and related research. 1991(273):151-156.

7.

Newman JH, Ackroyd CE, Shah NA. Unicompartmental or total knee replacement? Five-year results of a prospective, randomised trial of 102 osteoarthritic knees with unicompartmental arthritis. The Journal of bone and joint surgery. British volume. 1998;80(5):862-865.

8.

Levine WN, Ozuna RM, Scott RD, Thornhill TS. Conversion

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of failed modern unicompartmental arthroplasty to total knee arthroplasty. The Journal of arthroplasty. 1996;11(7):797-801. 9.

Hernigou P, Deschamps G. Alignment influences wear in the knee after medial unicompartmental arthroplasty. Clinical orthopaedics and related research. 2004(423):161-165.

10. Collier MB, Engh CA, Jr., McAuley JP, Engh GA. Factors associated with the loss of thickness of polyethylene tibial bearings after knee arthroplasty. The Journal of bone and joint surgery. American volume. 2007;89(6):1306-1314. 11. Pearle AD, O’Loughlin PF, Kendoff DO. Robot-assisted unicompartmental knee arthroplasty. The Journal of arthroplasty. 2010;25(2):230-237. 12. Rodriguez F, Harris S, Jakopec M, et al. Robotic clinical trials of uni-condylar arthroplasty. Int J Med Robot. 2005;1(4):20-28. 13. Cobb J, Henckel J, Gomes P, et al. Hands-on robotic unicompartmental knee replacement: a prospective, randomised controlled study of the acrobot system. The Journal of bone and joint surgery. British volume. 2006;88(2):188-197. 14. Jenny JY, Ciobanu E, Boeri C. The rationale for navigated minimally invasive unicompartmental knee replacement. Clinical orthopaedics and related research. 2007;463:58-62. 15. Keene G, Simpson D, Kalairajah Y. Limb alignment in computer-assisted minimally-invasive unicompartmental knee replacement. The Journal of bone and joint surgery. British volume. 2006;88(1):44-48. 16. Fisher DA, Watts M, Davis KE. Implant position in knee surgery: a comparison of minimally invasive, open unicompartmental, and total knee arthroplasty. The Journal of arthroplasty. 2003;18(7 Suppl 1):2-8. 17. Rees JL, Price AJ, Beard DJ, Dodd CA, Murray DW. Minimally invasive Oxford unicompartmental knee arthroplasty: functional results at 1 year and the effect of surgical inexperience. The Knee. 2004;11(5):363-367.

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Lateral Ankle Ligament Injuries: Treatment Decisions Involving the Ankle Sprain Malik Abraham, DPM Abstract: Although most patients sustaining a lateral ankle ligament

injury (ankle sprain) will suffer no long-term consequences, it is well established that a significant number will have persistent complaints of instability, pain, and the potential for future ankle arthritis. We review the diagnostic measures and treatment modalities of both acute and chronic lateral ankle ligament injuries. Rehabilitation is a critical part of treatment, but surgical options may be necessary for those patients suffering from chronic lateral ankle instability (CAI).

Figure 1 Lateral Ligament Complex of Ankle

Introduction Lateral ankle ligament injuries are one of the most common injuries in athletic and recreational activities. Estimates of 23,000 sprains occur in the U.S. per day, making it one of the most frequent injuries seen by medical practitioners.1 These injuries are often times neglected by the patient, or have insufficient rehabilitation and follow-up. It has been estimated that 55% of patients sustaining an ankle sprain do not seek medical treatment.2 This lack of treatment or poor follow-up, after an initial evaluation, most likely plays a significant role in the development of chronic lateral ankle instability (CAI). The estimates for CAI were as high as 70% in the McKay study.2 Unprotected ambulation in the untreated or “undertreated” lateral ankle sprain leads to the injured ligaments healing in an elongated state, with poor tensile strength leading to mechanical laxity found in CAI. Patients who do not seek medical treatment additionally may contribute to the development of CAI by returning to activity prematurely. This may compromise ligament healing as research indicates that mechanical stability is not seen until at least 6 weeks to 3 months post-injury.2

Initial Evaluation Ankle trauma should be evaluated in a comprehensive manner with assessment that not only includes the painful and edematous lateral ankle ligament complex (anterior talofibular,[ATFL] posterior talofibular,[PTFL] and calcaneofibular ligaments [CFL]), but also the anatomy proximal and distal to the ankle (Figure 1). A careful history prior to examination should be obtained from the patient to address mechanism of injury and secondary complaints that may warrant further investigation. The proximal fibula should be palpated to detect a Maisonneuve fracture: a spiral fracture of the proximal third of the fibula associated with a tear of the distal tibiofibular syndesmosis and the interosseous membrane. Address Correspondence to: Malik Abraham, DPM, Bahri Orthopedics & Sports Medicine, 6100 Kennerly Road Suite 101, Jacksonville, FL 32216. Phone: 904-739-0050. Email:malika7950@ yahoo.com. www . DCMS online . org

Lateral ligament complex of the ankle: ATFL (anterior-talofibular ligament and tibiofibular ligament), PTFL (posterior talo-fibular ligament), and CFL (calcaneo-fibular ligament).

There may be an associated fracture of the medial malleolus or rupture of the deep deltoid ligament. Direct palpation and the “squeeze test” of the mid-calf will help rule out a syndesmosis injury. This type of injury is sometimes called a high ankle sprain because it involves the ligaments above the ankle joint. In an ankle syndesmosis injury, at least one of the ligaments connecting the bottom ends of the tibia and fibula bones (the lower leg bones) is sprained. Examination medially should include the deltoid ligament and posterior tibial tendon, while examination laterally is vital to rule out tendonitis and subluxation of the peroneal tendons from the fibular groove. Peroneal subluxation (Peroneal tendons instability) although an infrequent finding, is often missed and leads to a delay in treatment , and consequently, adversely impacts a full return to sports or work. The anterior drawer and talar tilt tests are frequently employed to assess the integrity of the ATFL and CFL ligaments respectively. (Figures 2 and 3, p.48) With the anterior drawer test, if the ankle can be subluxated three to five millimeters more than the unaffected side, the ATFL is assumed to be incompetent. A greater than 10 degree difference in inversion when comparing injured and uninjured ankles is highly suggestive of a CFL tear. Continuing distally, palpation of the sinus tarsi for sprains and the lateral process for avulsion fractures is essential, as again, injuries to these structures are often missed. The anterior process of the calcaneus, the cuboid, and the 5th Northeast Florida Medicine Vol. 63, No. 3 2012 47


Figures 2 & 3 Ankle Tests Figure 2 (Top, left) Anterior drawer test: the examiner attempts to subluxate the ankle anteriorly with respect to the tibia. A greater than 3 to 5 mm difference from the unaffected side indicates a positive result and probable tear of the ATFL. Figure 3. (Bottom, left) Talar tilt test: the ankle is inverted passively. A greater than 10 degree difference from normal side indicates CFL tear.

metatarsal are examined.The neurovascular status regarding pulse examination, capillary refill, and sensory testing complete the clinical evaluation.

Imaging Studies Most patients will require ankle x-rays involving anteroposterior (AP), lateral, and mortise views. Radiographs of the foot are added when palpation suggests injury to the lateral column (cuboid, lateral cuneiform). When symptoms persist past six weeks, MRI or CT imaging may be required to determine the possibility of osteo-chondral talar dome lesions and occult fractures of the ankle and foot. MRI performed with 1.5 Tesla scanner with thin slices appear to offer the most utility in searching for these less obvious injuries. An MRI may show evidence of lateral ankle ligament disruption that may not be clinically significant (Figure 4). Likewise, a MRI read as “normal�, or one with limited findings, does not preclude ankle instability.3,4

Treatment Options The treatment regimen for uncomplicated ankle sprains is fairly standard consisting of RICE (rest, ice, compression and elevation) and range of motion exercises that are begun early and often.5 Protected ambulation in an aircast or short leg walker boot with crutch assistance based upon pain is beneficial.6 Functional rehabilitation should be started early whether or not the patient will be referred for a formal physical therapy program.7 The benefits of functional rehabilitation are a speedier recovery with less chance of development of chronic instability. Rehabilitation is initiated with range of motion exercises and Achilles tendon stretching. Muscle strength is improved with resistance exercises utilizing rubber resistance bands or tubing, and one pound ankle weights, followed by double and single-limb toe raise exercises. Proprioception 48 Vol. 63, No. 3 2012 Northeast Florida Medicine

is improved with training exercises on a wobble-board. In addition, shallow pool walking and kick boards, plus use of a stationary bicycle, are instrumental in a functional rehab program. Finally, athletic specific training is instituted first with walking, then jogging with advancement to running activities. Progression is based upon pain free activity before moving to more intense training, eventually progressing to pattern running, cutting and full ballistic activities.8 Cast or short leg boot immobilization without movement and protected weight-bearing are rarely indicated today when the diagnosis is a Grade 1 (a sprain with mild damage to one or more ligaments without any associated ankle joint instability) or Grade 2 ankle ligament injury. (partial ligament tear[s] where there may be some ankle joint instability) If one suspects a Grade 3 (complete tears leading to ankle joint instability) ligament injury, immobilization may be considered, but the current consensus in the literature indicates early ligament repair will provide a quicker recovery with less chance of development of chronic lateral ankle ligament instability (CAI). When the acute lateral ankle ligament injury progresses to a chronic state, then more aggressive steps are required in order to return the patient to their pre-injury status. A formal physical therapy program is initiated that continues functional rehabilitation. Modalities, such as ultrasound, electrical stimulation and iontophoresis, may be administered. Iontophoresis (a.k.a. Electromotive Drug Administration [EMDA]) is a technique using a small electric charge to deliver a medicine or other chemical through the skin. If the patient fails to achieve significant improvement to allow resumption of athletic or work activities, then an injury reassessment should be made along with a referral to an orthopedic or podiatric sports medicine specialist. The patients who fail conservative treatment of lateral ankle ligament injuries have usually developed CAI with or without concomitant osteo-chondral talar defects and tendon pathology.9 Usually a MRI , if not previously performed, would be

Figure 4 Ankle MRI

This is a coronal MRI image of the ankle joint in an individual with an ankle sprain. The asterisk (see arrow) indicates a tear in the calcaneo-fibular ligament with surrounding edema and inflammation. www . DCMS online . org


ordered to diagnose any talar dome lesions, tendon rupture or syndesmosis injury.10 Stress ankle radiographs, either performed manually or with an ankle stress device, can also be used to quantify the degree of instability. In order to prevent guarding by the patient due to the uncomfortable nature of these tests, a local anesthetic block in the ankle and/or a sedative are often required. Surgical Management – Literature and clinical experience demonstrate that a certain percentage of patients (possibly 10-15%) with CAI will require surgical intervention to return them to pre-injury activities and prevent the development of future ankle arthritis. Sometimes this determination is readily apparent, especially in the elite level athlete who has been compliant with a functional rehab program but still cannot resume pain free activities even with taping and bracing. Other patients who show some degree of improvement with their symptoms and function, but still have not reached their pre-injury status, are more difficult to determine, when and if, they require surgical intervention. In these patients, the decision to operate is often delayed and occasionally determined by the level of play and necessity to return to sports or work activities.11-14 When it is determined that surgical intervention is required, then treatment options can be divided into anatomic versus non-anatomic reconstructions. The anatomic technique was popularized by Brostrom and later refined by Gould and others.15-17 The anatomic reconstruction is aimed at re-establishing the continuity of both the ATFL and CFL through direct repair that utilizes strong non-absorbable suture and bone anchors, either metal or absorbable material, placed into the fibula. Incisions that are oblique, longitudinal or transverse are based on the associated pathology. Longitudinal incisions are most helpful when peroneal tendon pathology needs to be addressed in addition to the ankle ligament repair. Dissection is carried from the subcutaneous tissue, the inferior retinaculum and then into the joint capsule. In some chronic injuries, easy identification of the ATFL is difficult, therefore, it is sometimes brought as one unit and sutured together with the retinaculum. The sutures are tied with tension as the foot is held in an everted position. Some surgeons have found it beneficial to test the ankle after the ATFL has been repaired as it is sometimes found there is an improvement of the talar tilt and, therefore , unnecessary to repair the CFL. The “non-anatomic” repair utilizes the peroneus brevis tendon, split longitudinally, or with an allograft and aims to reestablish the function in the ruptured CFL and ATFL. The tendon or graft is woven through the distal fibula and fastened into the lateral aspect of the talus with an anchor of choice. This procedure usually requires a longer incision, and if utilizing the peroneus brevis tendon, weakens the tendon’s function as the main evertor of the foot. This can have a negative effect in patients with athletic demands. A legitimate concern with this type of repair is a decrease in subtalar motion, again potentially impacting athletic performance.18,19 The post-operative recovery is similar with both types of www . DCMS online . org

repair, but earlier weight bearing and return to activities are possible with the anatomic repair. Protected non-weight bearing in a splint or boot is usually required after repair for approximately two weeks in anatomic repairs and usually twice the duration in non-anatomic repairs. Advancement to partial weight bearing in a boot, range of motion exercises, light Thera-band® resistance, and pool exercises can then be added as pain allows. In compliant patients, weight bearing in an athletic shoe with a lace-up brace can occur in as little as three to four weeks post-operatively in anatomic repairs. Light running can begin at six weeks and sport specific training at eight weeks. Complications from Surgical Intervention – The most common complications likely to be encountered are wound dehiscence, nerve injury, lack of subtalar joint motion, chronic edema, and scar tissue formation. Chronic weakness may be encountered if the patient is not compliant with their rehabilitation.

Conclusion Lateral ankle sprains are a common injury encountered by a number of different medical disciplines. The majority of these acute injuries should heal with nonoperative treatment provided there is good follow-up and rehabilitation. It has been established that CAI and other associated chronic ankle conditions can occur when patients do not comply with treatment protocols or return to activities prematurely. When CAI has been diagnosed, most patients can still return to their pre-injury status with a functional rehabilitation program. In those patients who require surgical repair of their chronically injured ankle, well established procedures are available that reconstruct the ligaments and allow a return to athletic and work activities within a reasonable period of time.

References

1.

Kannus P, Renstrom P. Treatment for acute tears of the lateral ligaments of the ankle: operation, cast, or early controlled mobilization. J Bone Joint Surg Am. 1991: 73(2) :305-312.

2.

McKay G.D., Goldie P.A., Payne W.R., Oakes B.W. Ankle injuries in basketball: injury rate and risk factors. Br J Sports Med. 2001;35(2):103-108.

3.

Perrich KD, Goodwin DW, Hecht PJ, Cheung Y. Ankle ligaments on MRI: appearance of normal and injured ligaments. Am J Roentgenology.2009 Sep;1993(3):687-95.

4.

Martin B. Ankle sprain complications: MRI evaluation. Clin Podiat Med Surg.2008 Apr; 25(2):203-47.

5.

Lynch SA, Renstrom PA. Treatment of acute lateral ankle ligament ruptures in the athlete: conservative versus surgical treatment. Sports Medicine. 99 Jan;27(1):61-71.

6.

Wolfe MW, Uhl TS, Mattacola CG, McCluskey LL. Management of ankle sprains. Am Fam Physician. 2001Jan1;63(1):93-104.

7.

Weber JM, Maleski RM. Conservative treatment of acute lateral ankle sprains. Clin Pod Med Surg. 2002 Apr;19(2):309-18.

8.

Safran MR, Zachazewski JE, Bewedelti RS, et al. Lateral ankle sprains: a comprehensive review Part 2: treatment and

Northeast Florida Medicine Vol. 63, No. 3 2012 49


9.

rehabilitation with an emphasis on the athlete. Med Sci Sports Exer.1999 Jul:31(7suppl):s438-47.

proprioception of the functionally unstable ankle. J Othop Sports Phys Ther. 1998;27(4):264-275.

Hinterman B. Biomechanics of the unstable ankle joint and clinical implications. Med Sci Sports Exer. 1999;317 (suppl):S459-69.

15. Brostrom L. Sprained ankles. V. Treatment and prognosis in recent ligament ruptures. Acta Chir Scand. 1966;132:537-550.

10. Labovitz JM, Schweitzer ME. Occult osseous injuries after ankle sprains: incidence, location, pattern, and age. Foot Ankle Int. 1998;19;661-7. 11. Karlsson J, Lundin O, Lind K, Styf J. Early mobilization versus immobilization after ankle ligament stabilization. Scand J Med Sci Sports. 1999;9:299-303. 12. Denegar CR, Miller SJ. Can chronic ankle instability be prevented? Rethinking management of lateral ankle sprains. J Athl Train. 2002;37(4):430-435. 13. Karlsson J, Lansinger O. Chronic lateral instability of the ankle in athletes. Sports Med. 1993 Nov;16(5):355-65. 14. Bernier JN, Perrin DH. Effect of coordination training on

16. Karlsson J, Bergsten T, Lansinger O, Peterson L. Reconstruction of the lateral ligaments of the ankle for chronic lateral instability. J Bone Joint Surg Am. 1988:70:581-588. 17. Gould N, Seligson D, Gassman J. Early and late repair of lateral ligament of the ankle. Foot Ankle. 1980;1:84-89. 18. Chrisman OD, Snook GA. Reconstruction of lateral ligament tears of the ankle. An experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg Am. 1969 Jul;51(5) :904-12. 19. Hollis JM, Blasier RD, Flahiff CM, Hofmann OE. Biomechanical comparison of reconstruction techniques in simulated lateral ankle ligament injury. Am J Sports Med. 1995;23(6):678-682

DCMS Represented at 2012 AMA Annual Meeting DCMS was well represented at the 161st American Medical Association’s (AMA) Annual Meeting, June 16-20 in Chicago, IL. The following DCMS members attended: • Yank, D. Coble, Jr., MD, an AMA Past President • Florida Medical Association Delegates: DCMS members: W. Alan Harmon, MD; Nathan P. Newman, MD; Ashley Booth Norse, MD; John M. Montgomery, MD; Thomas G. Peters, MD; and Daniel Kantor, MD • Eli N. Lerner, MD, was a Delegate for the Society of American Gastrointestinal Endoscopic Surgeons.

Highlights from the meeting were the inauguration of Dr. Jeremy A. Lazarus as the 167th AMA President and the election of Dr. Ardis Dee Hoven as President-Elect. DCMS will invite Dr. Hoven to visit Jacksonville in the spring for its annual AMA Leadership Visit and Dinner. Also, Dr. Alan Harmon (DCMS member) was elected to the AMA Council on Medical Service. Some news headlines from the Annual Meeting and listed on amednews.com include: • • • • • • • • •

Doctors advised to consider costs in care choices Don’t make licensure dependent on board certification, AMA says Taxes on sugary beverages could fund obesity prevention CEO spells out AMA’s strategic direction at Annual Meeting Support given to mammography access for women older than 40 Greater range of Medicaid finance options wins support Delegates oppose giving pharmacists authority to prescribe drugs Telemedicine can pose ethical problems, delegates warn Helmets sought for wider range of sports and other activities

Find more AMA Meeting details and House of Delegate actions at www.ama-assn.org.

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NE Florida Represented at FMA Annual Meeting The Florida Medical Association Annual Meeting was July 26-29, 2012 in Boca Raton, FL. DCMS EVP Bryan Campbell said, “Tremendous thanks to those those who attended the FMA Annual Meeting from Northeast Florida. Our region was well represented with outgoing FMA President Dr. Miguel Machado, new FMA President-Elect Dr. Alan Harmon, newly elected FMA Alliance President Mrs. Joan Harmon, along with several local physicians who won awards or were elected as delegates.” The following received special recognition or were elected to an FMA Position: DCMS Past President Dr. Alan Harmon was elected FMA President-Elect

DCMS Past President Dr. John W. Kilkenny III was elected to the Surgical Specialty and Sub-Specialty seat on the FMA Board of Governors

Mrs. Joan Harmon was inducted as the FMA Alliance President

DCMS member Dr. Nitesh Paryani was elected to the Resident & Fellow section seat of the FMA Board of Governors

DCMS President Dr. Ashley Booth Norse was elected as an FMA Delegate to the AMA

DCMS member Dr. Thomas T. Chiu was awarded the FMA Certificate of Appreciation

DCMS Past President Dr. Thomas Peters was elected as an FMA Alternate Delegate to the AMA

DCMS Past President Dr. John Montgomery was elected as an FMA Alternate Delegate to the AMA

Clay County member and an FMA Past President Dr. Patrick Hutton received the Certificate of Merit St. Johns County President Dr. Michael DiBella – Received the Harold S. Strasser, MD, Good Samaritan Award. Putnam County Past President and FMA Delegate Dr. Jack Matheney II, sat on the Reference Committee III

Congratulations to All! www . DCMS online . org

Northeast Florida Medicine Vol. 63, No. 3 2012 51


Trends in Public Health

Florida's Public Health Response to H1N1 Outbreak Radley Remo, MPH; Niketa Walawalkar, MD, MPH; Nancy Winterbauer, PhD; and Robert Harmon, MD, MPH In April 2009, a novel influenza A (H1N1) virus was identified in the United States with the definitive characteristics of a pandemic virus. Within weeks, the virus had spread to every region in the country and throughout the world. The Florida State Surgeon General issued a Declaration of Public Health Emergency on May 1, 2009, as a consequence of confirmed H1N1 cases in two counties and because of the potential for the disease to spread. The public health response to H1N1 varied markedly around the country and around the state. Ultimately, the severity of this pandemic was lower than initially predicted. However, the number of hospitalizations and deaths were significant. As of June 12, 2010, Florida experienced 1,324 labconfirmed hospitalizations and 230 lab-confirmed H1N1 deaths. A large proportion, 40%, of the hospitalizations occurred in the under-25 age group. This was a deviation from seasonal influenza, which most severely affects adults over 65 and children under two years of age. Twenty percent of the H1N1 deaths in Florida occurred in healthy individuals with no underlying condition. While 13% of H1N1 deaths in Florida occurred in the under-25 age group, the majority were in adults aged 24-65. During seasonal influenza in the United States, approximately 90% of deaths occur in the over-65 age group. After the first cases in May 2009, H1N1 cases in Florida increased steadily throughout the summer. The second wave of H1N1 outbreaks began in August 2009 with the beginning of the school year. Case numbers peaked at the end of September 2009, after which they began to decline. In December 2009, the CDC reported that Florida’s H1N1 activity had decreased from “widespread” to “regional” activity, and by December 30 “widespread” flu was no longer being reported in any of Florida’s counties. The Duval County Health Department (CHD) received a Robert Wood Johnson Foundation grant to examine the statewide variation in the public health response to the H1N1 virus and its impact on the community’s acceptance of the H1N1 vaccine. The Florida Department of Health CHD 2009 Influenza A (H1N1) Pandemic Response Survey, consisting of 33 questions, was sent to a convenience sample of 67 CHDs in Florida from October 2010 to March 2011. The survey was completed by a central person at the CHD intimately involved with H1N1 response. This effort was taken to facilitate public health preparation for future influenza outbreaks and pandemic responses in the state of Florida. Florida public health responses to the H1N1 pandemic varied from county to county. Public health officials recorded variations in how and where the vaccine was administered to the community and the methods used to inform the 52 Vol. 63, No. 3 2012 Northeast Florida Medicine

community of vaccination efforts. Common vaccination point of distribution sites were CHD clinics, schools and public facilities; less common sites were migrant camps, faith-based organizations and shelters. CHD clinics and schools were perceived as the most effective dispensing sites. Faith-based, public and workplace points of distributions were associated with greater perceived community acceptance of the vaccinations. The top three methods of communication used to inform the community of public health’s H1N1 vaccination effort were local news media, radio and newspaper advertisements. The least common communication methods utilized were social networking sites, magazine advertisements and hiring of a marketing company. Despite the variation in communication, no methods were found to be significantly associated with perceived community acceptance of the H1N1 vaccine. It was also learned that CHD characteristics influenced community acceptance of the H1N1 vaccine. CHDs that had a pharmacy or a formal in-house Emergency Operation/ Incident Command Center or were NACCHO “Public Health Ready” accredited were perceived as having communities accepting of the H1N1 vaccine effort. The Florida Department of Health CHD 2009 Influenza A (H1N1) Pandemic Response initiative documented the diverse approaches in which CHDs dispensed, administered and communicated the H1N1 vaccine activities. Several key points were learned from the initiative: • Standard practices or agreement of practices were inferred from the methods used by the majority of counties. • Perceived effectiveness of sites dispensing vaccines did not necessarily foster community acceptance of the vaccine efforts. • CHD characteristics are important in the community’s acceptance of the H1N1 vaccination efforts. • Diverse methods of communication are critical to getting the word out and fostering acceptance of the vaccination process. Further research is required with significantly greater community input to understand the success or failure of the public health response to disease outbreaks. Additional research is required to measure the effectiveness of the methods used in this study. There is much work to be done to sustain and improve our capabilities before the next pandemic. www . DCMS online . org


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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Northeast Florida Medicine Vol. 63, No. 3 2012 53


A DCMS Dynamic Duo

Dr. Alan Harmon and Mrs. Joan Harmon 2013 FMA President-Elect and 2013 FMA Alliance President

Dr. and Mrs. W. Alan Harmon (Joan) are truly one of DCMS’ Dynamic Duos. For years they have been active in organized medicine at the county, state and national levels. Dr. Harmon was DCMS President in 1995 and has held many other Society positions. In July he was elected as the 2013 Florida Medical Association’s (FMA) President-Elect and in June he was chosen to serve on the American Medical Association’s (AMA) Council on Medical Service. Dr. Harmon is a gastroenterologist with Borland-Groover Clinic in Jacksonville, FL. By her husband’s side always, but sometimes stepping into her own spotlight, Joan Harmon has also been active in the DCMS Alliance (as Past President among other leadership roles), as well as the FMA and AMA Alliances. In July she was inaugurated the 86th President of the FMA Alliance. Mrs. Harmon is an RN and worked in various roles in that profession before moving to Jacksonville with her husband in 1981 and then turning her focus to her family and volunteer work. The Harmons have been married 40 years and have two grown children and one grandchild. According to an FMA press release, the Harmons “have seen so many changes in the climate of how physicians practice medicine since early days in medical school, internship and fellowship.” And though both “see a whirlwind of evolution in medical practice parameters, they continue to support medicine as an honorable profession.”

Congratulations, Dr. & Mrs. Harmon. You certainly are a Dynamic Duo! 54 Vol. 63, No. 3 2012 Northeast Florida Medicine

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DCMS Membership Applications These physicians’ applications for membership in the Duval County Medical Society are now being processed. Any information or opinions you may have concerning the eligibility of the applicants listed here may be directed to Ashley Booth Norse, MD, DCMS President (904-244-4106) or Barbara Braddock, Membership Director (904-355-6561 x107).

Alexandra D. Beier, DO Neurosurgery UF Pediatric Neurosurgery Center Medical Degree: Midwestern University

Sassan Keshavarzi, MD Neurosurgery UF Pediatric Neurosurgery Center Medical Degree: University of Rochester School of Medicine

Daniela L. Neagu, MD Pediatric Cardiology UF Pediatric Cardiology Center

Fellowship: Hospital for Sick Children

UF Cardiothoracic Surgery

Cardiothoracic Surgery Medical Degree: American University of the Caribbean

Internship/Residency: University of Texas at Houston

Residencies: Louisiana State University Medical Center Shreveport/University of South Alabama Medical Center/ Boston University Medical Center/ University of Tennessee College of Medicine/Dartmouth-Hitchcock Medical Center/Children’s Hospital Boston

Residency: University of Florida College of Medicine

Fellowship: University of Florida College of Medicine

Mayo Clinic Medical Degree: University of Florida College of Medicine

Fellowship: Vanderbilt University Medical Center

Fellowship: University of California Fawad Khawaja, MD

Radiology

Residency: UFHSC/Jacksonville

Internship/Residency: University of California San Diego

Internship/Residency: Providence Hospital

Candice Whitney Bolan, MD

Internship: Spartanburg Regional Medical Center

Fellowship: Mayo Clinic

Medical Degree: Carol Davila University of Medicine & Pharmacy Residency: Newark Beth Israel Medical Center Fellowship: University of Miami School of Medicine Saumil R. Oza, MD Cardiac Electrophysiology Diagnostic Cardiology Associates Medical Degree: University of Miami School of Medicine Residency: University of Illinois Medical Center & Loyola University Medical Center

Cristian O. Landa, MD Emely Eid, MD

Internal Medicine

Nathan J. Ranalli, MD

Gastroenterology

UF Internal Medicine Primary Care Center

Neurosurgery

UF Gastroenterology Center at Emerson Medical Degree: American University of Beirut Internship: American University of Beirut Residency: Indiana University School of Medicine Fellowship: University of Texas Southwestern Medical School Lisa Jacobson, MD

Medical Degree: Ross University Residency: University of Florida/Jacksonville College of Medicine Natesan Manimekalai, MD Anesthesiology UF Anesthesiology Medical Degree: Thanjavur Medical College Residency: Mercy Catholic Hospital & Thomas Jefferson University Hospital

Emergency Medicine UF Emergency Medicine Medical Degree: University of Wisconsin School of Medicine Residency: Mount Sinai School of Medicine

UF Pediatric Neurosurgery Center Medical Degree: University of Pennsylvania Internship: Hospital of the University of Pennsylvania Residency: University of Pennsylvania School of Medicine Fellowship: Washington University in St. Louis Katherine S. Tzou, MD Radiation Oncology Mayo Clinic

Patrick Natter, MD Diagnostic Radiology

Medical Degree: Ohio State University College of Medicine

UF Radiology

Internship: Fletcher Allen Health Care-UVM

Medical Degree: University of Alabama

Residency: Mayo Clinic

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Oleksly Zyernov, MD

Dorothy M. Russ, MD

Jason Siegel, MD

Anesthesiology

Gastroenterology

Jose Raul Valery, MD

Raul Jose Badillo, MD

Neurohospitalist

Michal Bartel, MD

Maisha T. Robinson, MD

Kondal R. Kyanamkabir, MD

Neurological Surgery

Internal Medicine

Ramon L. Navarro Balbuena, MD

Jenna Beasley, MD

Jang Won Yoon, MD

Casey Cable, MD

Physical Medicine/Rehabilitation

Jeffrey David Duncan, MD

Stephan M. Esser, MD

Gautam V. Matcha, MD

Radiation Oncology

Luke M. H. McCrone, MD

Ajaykumar Patel, MD

Chad McRee, MD

Radiology

Lindsey Minshew, MD

Brittany Albers, MD

Jason Steele Prater, MD

Dana Amiraian, MD

Ronald Glen Racho, DO

Kathleen E. Carey, MD

Steven P. Sears, DO

Christopher Coleman, MD

Kristina Seeger, MD

Dermatology

Tara Otto, MD

Musculoskeltal Radiology

Ryan P. Reddy, MD

Stephanie Ortman, MD

Heman K. Dave, MD

Rheumatology

Family Medicine

Nephrology

Florentina Berianu, MD

Jonathan Balog, DO

Asad Ayub, MD

Melissa Duart, MD

Neurology

Admire Kuchena, MD

Dredla Brynn, MD

Yuan Liu, MD

Christian Burrell, MD

Katherine McMullan, MD

Andrea Harriott, MD

Candice North, MD

Iris Vanessa Marin Collazo, MD

UF Anesthesiology Medical Degree: Crimean State Medical University Internship/Residency: University of Missouri Hospitals & Clinics Fellowship: Washington University RESIDENTS/FELLOWS MAYO CLINIC Anesthesiology John Emmanuel, MD Babak Golbaba, MD Pallavi Gupta, MD Tim Howard, MD Matthew Isenhower,MD Juan Ramos, MD

RESIDENTS/FELLOWS NEMOURS CHILDREN’S CLINIC Child Neurology Daniel D. Bui, MD

2012 BEALS AND SHAHIN AWARDS If you have published peer reviewed articles (listed in MEDLINE/PubMed journal database) between January 2011 and December 2011 and are a DCMS member in good standing, you are eligible to submit for the Beals and/or Shahin Awards. Categories are: Original Investigation, Clinical Observation and Review Articles. Participants can only submit in one category. Beals Award submissions must come from DCMS members for work done in Duval County. Shahin Award submissions are strictly for Residents/Fellows in Duval County. (Winners last year for either award cannot win this year.) The submission deadline is October 1, 2012. Winners will be notified by November 12 and awards will be presented at the DCMS Annual Meeting, November 29, 2012. For more award guidelines, go to dcmsonline.org or to answer any questions, contact Laura Townsend at 355-6561 x101 or email her at ltownsend@dcmsonline.org.

www . DCMS online . org

Northeast Florida Medicine Vol. 63, No. 3 2012 57


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