Indiana Orthopaedic Journal - Department of Orthopaedic Surgery

Transcription

Indiana Orthopaedic Journal
INDIANA UNIVERSITY DEPARTMENT of ORTHOPAEDIC SURGERY
2010
Clarian Human Motion offers complete care for
bones, joints, spine and muscles — everything that
keeps humans in motion. Through our affiliation with
Indiana University School of Medicine and some
of the most prestigious private physician practices in
Central Indiana, Clarian Human Motion provides
preeminent musculoskeletal care at all Indianapolisarea Clarian Health facilities.
When it comes to your orthopedic referrals, you can
rest assured that Clarian Human Motion will provide
your patients with the specialized care they need.
We work with top physicians in the state to deliver the
highest quality of care in a wide range of orthopedic
specialties, including:
s!RTHRITISand Rheumatology
s"ONE#ANCER
s&OOTand!NKLE
s(AND
s*OINT2EPLACEMENT2ECONSTRUCTION
and Revisions
s+NEE
s0AIN-ANAGEMENT
s0EDIATRIC/RTHOPEDICS
s0HYSICAL-EDICINEand Rehabilitation
sRehabilitation Services
sShoulder and Upper Extremity
sSpine
sSports Medicine
s3PORTS0ERFORMANCE
s4RAUMA&RACTURE#ARE
To receive more information on Clarian Human Motion,
PLEASECALL)-!#3/NE#ALLAT1-800-265-3220 or visit us
at www.clarian.org/hm.
/UROrthopedic specialists
cover a full range of
human motion.
Volume 4 – 2010
Table of Contents
Annual Reports
1
3
4
5
7
8
10
12
14
15
19
22
23
24
27
28
30
Chairman’s Report – Jeff Anglen, MD
Residency Program Director’s Report – Randy Loder, MD
Orthopaedic Research Lab Report – Melissa Kacena, PhD
Faculty of the Department of Orthopaedic Surgery
Volunteer Faculty and Lecturers
Residents and Fellows
Faculty Awards, Grants, and Selected Publications
Garceau-Wray Lectureship
Lindseth Lectureship and Mark Brothers Lectureship
Endowment of the Bill and Louise Capello Chair of Orthopaedic Surgery:
An Interview with Bill Capello, MD
Faculty Volunteer Orthopaedic Service in South India – Alex Mih, MD
In Memoriam: Charles H. Turner, PhD
Arthroscopy Skills Trainer for Residency Program
Event Photos
Alumni List by Graduation Year
Alumni News
Indiana Orthopaedic Society
Manuscripts
32
Adult Trauma: Getting Through the Night. An Instructional Course Lecture, American
Academy of Orthopaedic Surgeons.
Andrew H. Schmidt, MD, Jeffrey Anglen, MD, Arvind D. Nana, MD, Thomas F. Varecka, MD
44
Current and Future Trend in Articular Cartilage Restoration.
Jack Farr, MD
48
Minimum 10-Year Results after Anterior Cruciate Ligament Reconstruction: How the Loss of
Normal Knee Motion Compounds Other Factors Related to the Development of Osteoarthritis
after Surgery.
K. Donald Shelbourne, MD, Tinker Gray, MA
i
50
55
Volume 4 – 2010
The Use of Implantable Bone Stimulators in Nonunion Treatment.
Michael S. Hughes, MD, Jeffrey O. Anglen, MD
Pediatric Diaphyseal Femur Fractures: A Comparison of Flexible Versus Rigid Intramedullary
Nailing.
Daniel J. Cuttica, DO, Allan C. Beebe, MD, John R. Kean, MD, Jan E. Klamar, MD, Kevin E. Klingele, MD
60
Slipped Capital Femoral Epiphysis Associated With Consumer Products.
64
Valgus Slipped Capital Femoral Epiphysis:Prevalence, Presentation, and Treatment Options.
70
Randall T. Loder, MD
Craig F. Shank, MD, Eric J. Thiel, MD. Kevin E. Klingele, MD
Outpatient Microdiscectomy for Lumbar Disc Herniation in Adolescent Patients: Long-Term
Follow-up Study.
Natalie M. Best MD, Rick C. Sasso MD
74
Clinical Outcomes of Scaphoid and Triquetral Excision With Capitolunate Arthrodesis Versus
Scaphoid Excision and Four-Corner Arthrodesis.
R. Glenn Gaston, MD, Jeffrey A. Greenberg, MD, Robert M. Baltera, MD, Alex Mih, MD, Hill Hastings, MD
79
Arthroscopic Coracoclavicular Ligament Reconstruction Utilizing a Semitendinosis Graft and
Titanium Flip Button Tension Band Construct.
Vivek Agrawal, MD
84
Metastatic Disease of the Extremities: Tips for Management.
91
Advances in Orthopaedic Oncology for 2010.
94
Instructions for Authors
Daniel Wurtz MD, Judd Cummings MD
Bruce T. Rougraff, M.D.
Judy R. Feinberg, PhD
Editor
Donna L. Roberts
Assistant
ii
Volume 4 – 2010
Chairman’s Report
The end of summer and coming of fall always bring a sense of
transition. Summer vacation is over, and the kids are heading back
to school; the new academic year is in full swing, and football season
is just around the corner. The time seems to fly by from our annual
picnic at the Anglen house where we welcome the newbies, to the
Garceau-Wray dinner when we say goodbye to old friends. This year
we welcome four new faculty members along with the five new interns
who have been at work for a couple of months now. Two new pediatric
orthopaedic surgeons (Drs. Kishan and Gantsoudes) join Drs. Loder
and Caltoum at Riley Hospital; a fifth fellowship trained orthopaedic
traumatologist (Dr. Shively) joins the team working at Wishard Hospital;
and Dr. Nolan, a shoulder and elbow surgeon comes on board as well.
This brings our number of new faculty hires in the past five years to 13
– a number both exciting and challenging. The expansion of capacity,
opportunity and teaching manpower is exciting. Fitting everyone into
already tight facilities and schedules is the challenging part. As usual,
our faculty has continued the tradition of IU Orthopaedic excellence,
as you will see in the pages to come.
In 2011, our Department will make another transition by becoming part of a new venture you may have heard
about, the Indiana Clinic. This union of the IU School of Medicine faculty practice plan with the Clarian Hospital
system (soon to be the Indiana University Health Care System) will allow us to provide care to patients from across
the state and beyond in a more efficient, coordinated, safe and effective manner, and will position us to prosper in the
face of health care reform. Becoming the musculoskeletal arm of this new system will provide strategic advantages,
stability, and strength to our clinical enterprise, allowing us to better secure the future of our academic mission.
Over the past year, we learned of two exciting and significant gifts to the Department, which I announced to those
of you who were able to attend the Indiana Orthopaedic Reception at the AAOS annual meeting in New Orleans.
Dr. Richard Halfast of Kokomo, an orthopaedic surgeon and graduate of IU School of Medicine made a generous
bequest to our Department for support of an orthopaedic fellowship. Dr. Bill Capello, a current and long-time
member of the faculty, made the outstanding commitment necessary to endow a Chair in Orthopaedics, our second
endowed Chair. Read more about Dr. Capello’s career in an interview in this journal. His many contributions to our
Department, including this wonderful gift, have helped us to produce many outstanding orthopaedic surgeons.
To advance our educational, research and clinical missions, and to train the next generation in our profession, we
need your help. These are challenging times for orthopaedic education. Declining reimbursement from government
and insurers affects all orthopaedic practices, but academic departments are particularly hard hit. The increasing
number of uninsured patients in this economy means that more underfunded care falls on our clinics and doctors,
as we become the last resort for patients turned away from private groups and facilities because they cannot pay.
Shrinking government support for research and education coupled with increasing regulatory burden from quasigovernmental entities like the ACGME and JCAHO, more demands on reduced clinical revenues, continually
increasing time requirements for faculty and staff, and cut-throat competition from private groups (many staffed by
former IU trainees) make it harder than ever to continue to maintain the traditions of our profession and renew our
ranks. It simply cannot be done successfully without the support and engagement of a wide spectrum of orthopaedic
surgeons – not just the few who chose a full-time academic career. We greatly appreciate the support of alumni
and colleagues who have donated their time to lectures, conferences, journal club, and mentorship for the residents,
1
Volume 4 – 2010
Chairman’s Report (continued)
intern applicant interviews, and help with recruiting. We also appreciate those who appropriately refer complex
patients to our faculty, and those who provide call coverage and indigent care for patients in their own community.
For those of you who may be inclined, we have a variety of other ways you can contribute financially. In addition
to our lectureship funds, we have started an alumni/ally fund to obtain an arthroscopy simulator for the residency.
After the great success of our campaign for the resident electronic learning center, this seemed like a natural next
step. Read more about the simulator in AAOS NOW at the website, http://Aaos.Org/news/aaosnow/oct09/cover2.
Asp. If you are willing to contribute to the project, either with dollars or time, please let us know!
Sadly, another transition occurred this past year when we lost Dr. Charles Turner to cancer. Charles was an
amazingly productive research scientist who worked with orthopaedic faculty, residents, and students for the past
two decades at IUPUI. His work in bone biomechanics brought both great credit and significant research support to
IU. He will be sorely missed by his many friends and collaborators on campus.
We hope you will plan to visit with us annually at the Lindseth Lectureship, the Indiana Reception at AAOS, or
the Garceau-Wray Professorship – or any other time you happen to be in Indianapolis. Thank you for your continued
support and good will. It has been a great pleasure for us to become closer to our alumni and to reconnect with our
IU orthopaedic family over the past six years, and we look forward to growing our relationships in the future.
Jeffrey O. Anglen, M.D.
Professor and Chairman, Indiana University School of Medicine,
Department of Orthopaedic Surgery
2
Volume 4 – 2010
Residency Program Director’s Report
Since the last issue of the Indiana Orthopaedic Journal, several noteworthy events have occurred regarding
our residency program.
Resident Applications
We again used our out-patient clinics as the site of the resident interviews. This location and format also
allow for more interviews per interviewee, thus affording the interviewee to get a more complete perspective of
the program. This has been very popular with the applicants. Some comments we have received are: “Having
time to speak with the current residents was very valuable.” “There was more time allotted to interview with
each set of attendings/residents than other programs.” “It was nice to be able to engage in conversation rather
than repeat skimming the surface due to time limitations in other interviews.” “It was great getting to meet
so many of the faculty and residents.” “The residents’ presence at the interviews was great. They were very
enthusiastic and knowledgeable.” “I liked that all the chief residents were involved in the interview process.”
Dr. Loder
This year we received 449 applications for the five positions, up from 409 last year. Of these 449 applicants, 205 were screened
out simply on the basis of USMLE Part I Board Scores; 244 files were then reviewed, and 88 applicants were offered interviews. These
interviews took place over three days, two for non-IU students and one specifically for IU students. The day for IU students is shorter as they
are acquainted with the facilities and program. The addition of this third day reserved for IU students allows us to interview more non-IU
students on the other two days, thus potentially increasing the diversity and number of potential residents. We wish to extend our appreciation
to all the faculty, both full-time and volunteer/alumni, who participated in the resident interview process this year.
Our five new PGY-1 residents who began their studies July 1, 2010 are: Dr. Matthew Beck from Wake Forest University, Dr. Eric
Dockter from the University of Toledo, Dr. Isaac Fehrenbacher from Indiana University, Dr. Austin McPhilamy from Wayne State University,
and Dr. Justin Millard from the American University of the Caribbean.
Resident Awards
Dr. Jonathon Wilhite, PGY-4, was nominated for induction into the IUSM Chapter of the Gold Humanism Society.
Dr. Kirk Reichard, PGY-5, was nominated for induction into the IUSM Chapter of the Gold Humanism Society.
Dr. Susan McDowell, PGY-3 resident, continues as one of the co-PIs on a Biomedical Research Grant from the IU School of Medicine
entitled “Structural and Functional Evaluation of Stainless Steel and PMMA Induced Membranes as a Graft Bed for Segmental Bone
Defects’.
Dr. Katie Peck, PGY-3 resident, is one of the co-PIs on and IU Simon Cancer Center Institutional Research Grant entitled “Effects of
Platelet Number and Adhesion on Osteosarcoma Growth and Metastatic Potential”.
Overseas Volunteerism
Dr. Susan McDowell, PGY-3 resident, volunteered in the Barefoot
Doctors School, a school which has been outside Chiang Mai, Thailand
for over 20 years. Their mission is to educate Burmese village health care
workers from the villages in Myanmar. These people are local leaders in
the villages, and they vary in age, education levels, and backgrounds. It was
the first 6-week session of a 3-year program. The focus was on learning the
basics of primary health care from taking blood pressure to treating tropical
diseases. Dr. McDowell taught the Orthopaedic/Neuro sessions covering
fracture types and basic splinting (with bamboo and banana leaf stalks) for
adjunct treatment of arthritis and polio. The Barefoot Doctor School is
backed by the Frontier Labourers for Christ, a mission in Chiang Mai. She
was in Thailand for five days teaching at the school. Further information
can be obtained from http://barefootschool.blogspot.com/
Randall T. Loder, M.D.
PGY-3 Resident, Dr. Susan McDowell, teaching Orthopaedics
to Burmese health care workers as part of a mission program, George J. Garceau Professor of Pediatric Orthopaedics
Residency Program Director, Department of Orthopaedic Surgery
The Barefoot Doctor School, in Thailand.
3
Volume 4 – 2010
Orthopaedic Research Laboratory Report
Orthopaedic research at IU is primarily located in laboratories within Fesler Hall, Medical Sciences, and the Engineering/Science &
Technology Building. There are five main orthopaedic research laboratories directed by Drs. Stephen Trippel, David Burr, Tien-Min Gabriel
Chu, Melissa Kacena, and Robyn Fuchs. The research group includes approximately 25 scientists and clinicians, eight of whom have grants
from the National Institutes of Health (NIH). These scientists come from four different disciplines: Orthopaedic Surgery, Anatomy and Cell
Biology, Physical Therapy, and Restorative Dentistry. Below are brief research updates from the five research directors as well as a brief update
on additional orthopaedic research endeavors/grants awarded.
Research Update
Stephen Trippel, MD, Professor of Orthopaedic Surgery: Dr. Trippel’s research focuses on cartilage-related disorders. The research
team consists of Stephen Trippel MD, Shuiliang Shi PhD and Albert Chan BS. Recent work includes the investigation of gene therapy and the
regulation of articular cartilage by growth factors. His work is funded by the NIH and VA.
David Burr, PhD, Professor and Chair of Anatomy and Cell Biology: Dr. Burr’s research is directed towards increasing the understanding
of the effects of changes in bone collagen on the mechanical properties, and of increased fracture risk, of bone in osteoporosis and in Type II
diabetes. Dr. Burr currently serves as President of the American Association of Anatomists and the Orthopaedic Research Society. He recently
was awarded the Borelli Award from the American Society of Biomechanics. Much of his work is funded by the NIH and NSBRI.
Tien-Min Gabriel Chu, DDS, PhD, Associate Professor of Restorative Dentistry: Dr. Chu’s research is focused on the development of
tissue engineering strategies to enhance the regeneration in long bones and in craniofacial areas. He is particularly interested in the fabrication and
characterization of high strength three dimensional (3D) biodegradable scaffolds capable of carrying mesenchymal stem cells and/or releasing
growth factors. He has funding from IU School of Dentistry and the Oral and Maxillofacial Surgery Foundation to investigate the use of polymerreinforced calcium phosphate as novel 3D scaffolds to enhance regeneration in rabbit cranial defects.
Melissa Kacena, PhD, Assistant Professor of Orthopaedic Surgery, Chair, Orthopaedic Research Committee: Dr. Kacena’s overall research
goal is to improve the understanding of the interaction of the bone and hematopoietic systems, thereby potentially improving the treatment
of metabolic bone disease and fracture healing. To achieve this goal, her research will focus in three areas: 1) The role of megakaryocytes,
megakaryocyte growth factors, and their receptors in bone homeostasis; 2) Translational/clinical studies examining the genetic regulation of
skeletal homeostasis; and 3) The molecular mechanisms underlying bone repair/fracture healing. She has received numerous honors, young investigator
awards, and grants for her research, including NIH funding. This past year she served as an ad hoc member on several NIH study sections.
Robyn Fuchs, PhD, Assistant Professor of Physical Therapy and Adjunct Assistant Professor in the Department of Anatomy and Cell
Biology: The goal of Dr. Fuchs research is to develop a better understanding of the genes and molecular pathways involved in regulating
periosteal bone apposition at the tissue and cellular level in response to anabolic therapies and fracture healing. Dr. Fuchs is currently funded by
NIH under the division of NIAMS for her work evaluating the role of the extracellular matrix protein periostin in bone formation.
Additional Basic Orthopaedic Research Studies/News:
Dr. Charles H. Turner, Director of Orthopaedic Research, lost is battle with cancer July 16, 2010. We mourn his loss and our thoughts are
with his family. Please see the memorial on page 22 of the journal for further details.
Drs. Brian Mullis, Janos Ertl, Jeffrey Anglen, Matthew Allen, Tien-Min Gabriel Chu, and Melissa
Kacena are working together on a rabbit study examining the structural and functional evaluation of
stainless steel and PMMA induced membranes as a graft bed for segmental bone defects. Dr. Mullis
recently received a Biomedical Research Grant from the IU School of Medicine to support this work.
Orthopaedic surgery resident, Dr. Susan McDowell, is also assisting on this project.
Drs. Brian Mullis, Peter Hoggs, Tien-Min Gabriel Chu, and Mr. Daniel Alge (PhD student in
Biomedical Engineering, Purdue University) are working together to compare the load and mode of
failures in fresh-frozen cadaver femurs fixed by sliding hip screws implants with non-locking plates and
locking plates. Dr. Mullis recently received funding from Synthes Inc. to support this work.
Drs. Judd Cummings, Melissa Kacena, Daniel Wurtz and Lindsey Mayo are working together to
examine the role of platelets and megakaryocytes in osteosarcoma. Dr. Cummings recently received
Ying-Hua Cheng, MD, PhD, is a an American Cancer Society Grant from the IU School of Medicine to support this work. Orthopaedic
Research Associate in the Department of surgery resident, Dr. Katie Peck, is assisting with this research.
Orthopaedic Surgery. Dr. Cheng is the
Dr. Theresa Guise and her research and clinical group moved from UVA to IU School of Medicine
manager of the orthopaedic cell biology
in the summer 2009. Their research primarily focuses on bone cancers. The arrival of their group on
laboratory. In addition, as a trained
orthopaedic surgeon, Dr. Cheng performs campus has significantly strengthened our already strong bone research program.
the bulk of the orthopaedic animal
surgeries. Surgical models include:
Masqulet membrane (rabbits); critical Melissa A. Kacena, Ph.D.
sized defect bone healing (rats and mice); Assistant Professor of Orthopaedic Surgery
and fracture healing (mice).
Chair, Orthopaedic Research Committee
4
Volume 4 – 2010
Department of Orthopaedic Surgery Faculty
Jeffrey O. Anglen, MD
Professor and Chairman
Clinical Interests: Orthopaedic trauma and post-traumatic complications with
special interest in pelvis and acetabulum fractures, peri-articular fractures of both
upper and lower extremity, bone healing, nonunions, malunions, deformity and
post-traumatic infections.
Contact Information: 317-274-7913 (office phone);
janglen@iupui.edu (e-mail)
Thomas A. Ambrose, MD, FACS
George J. Garceau Professor of
Pediatric Orthopaedics and Vice Chairman
Clinical Interests: Pediatric orthopaedics with special interest in scoliosis,
pediatric hip disorders (hip dislocation, Perthes’ disease, slipped capital femoral
epiphysis), clubfoot, and cerebral palsy.
rloder@iupui.edu (e-mail)
Associate Professor and
Chief of Surgery at Clarian West
Clinical Interests: Adult reconstruction (total joint replacements), Sports
Medicine and treatment of post-traumatic complications such as non-unions and
malunions. T reatment of severe musculoskeletal injuries, such as pelvic and
acetabular fractures as well as complex long bone fractures.
tambrose@iupui.edu (e-mail)
Christine B. Caltoum, MD
Randall T. Loder, MD
Assistant Professor
Clinical Interests: Pediatric orthopaedic surgery with special interest in Perthes
disease and shoulder problems secondary to obstetrical brachial plexus palsies
ccaltoum@iupui.edu (e-mail)
G. Peter Maiers, II, MD
Assistant Professor
Clinical Interests: Sports medicine with a focus on total knee care, adult and
pediatric athletic injuries, ligament reconstruction, cartilage restoration, and hip
arthroscopy
gmaiers@gmail.com (e-mail)
Alexander D. Mih, MD
Associate Professor,
and Chief of Upper Extremity Service
Clinical Interests: Reconstructive surgery of the upper extremity, brachial
plexus reconstruction and repair, pediatric upper extremity disorders,
microsurgery, shoulder reconstruction
amih@iupui.edu (e-mail)
William N. Capello, MD
Professor Emeritus
Clinical Interests: Hip replacement with special interest in revision hip
replacement
wcapello@iupui.edu (e-mail)
Brian H. Mullis, MD
Assistant Professor and
Chief of Orthopaedic Trauma Service
Clinical Interests: Orthopaedic trauma and post-traumatic complications with
special interest in pelvic and acetabular fractures, peri-articular fractures of both
upper and lower extremities, bone healing, nonunions, malunions, deformities,
and post-traumatic infections
bmullis@iupui.edu (e-mail)
Judd E. Cummings, MD
Assistant Professor
J. Andrew Parr, MD
Chief of Adult Reconstruction Service
Clinical Interests: Management of adult and pediatric patients with bone and
soft tissue tumors or tumor-like conditions utilizing a comprehensive and multidisciplinary approach. Operative treatment incorporates contemporary surgical
techniques for removal of extremity, pelvic tumors, and spinal tumors. Reconstructive techniques include limb sparing surgery using both endoprostheses and
structural allografts. Metastatic lesions of bone are managed with prophylactic
stabilization, internal fixation, or resection and reconstruction.
Clinical Interests: Minimally invasive total hip and knee surgery, alternative
bearing surfaces and complex revision hip and knee replacement.
Janos P. Ertl, MD
Stephen B. Trippel, MD
Contact Information: 317- 274-3227 (office phone);
judcummi@iupui.edu (e-mail)
Assistant Professor, and
Chief of Orthopaedics, Wishard Hospital
Clinical Interests: Bridging orthopaedic trauma and sports medicine including surgical
procedures of arthroscopic assisted periarticular fractures, long bone fractures, non-unions,
minimally invasive fracture treatment arthroscopy, autogenous and allograft chondral
transplantation, ligament reconstruction and amputation reconstruction.
japarr@iupui.edu (e-mail)
Professor
Clinical Interests: Arthritis treatment, joint preserving and joint replacement
surgery.
strippel@iupui.edu (e-mail)
jpertl@iupui.edu (e-mail)
Paul E. Kraemer, MD
Assistant Professor
Clinical Interests: General spine surgery, spinal trauma, adult spinal deformity,
and metastatic disease to the spine, adjacent segment disease, and revision /
deformity surgery.
Contact Information: 317- 713 6879 (office phone);
pkraemer@indianaspinegroup.com (e-mail)
Richard E. Lindseth, MD
Professor Emeritus
Mark D. Webster, MD
Chief of Orthopaedic Service at VA
Clinical Interests: Sports medicine, fractures, total joints, trauma.
mdwebste@iupui.edu (e-mail)
L. Daniel Wurtz, MD
Associate Professor and
Chief of Orthopaedic Oncology Service
Clinical Interests: Operative and non-operative treatment of musculoskeletal
tumors
dwurtz@iupui.edu (e-mail)
5
Volume 4 – 2010
Research Faculty
David B. Burr, PhD
Melissa A. Kacena, PhD
dburr@iupui.edu (e-mail)
mkacena@iupui.edu (e-mail)
Professor and Chair of Anatomy
Professor of Orthopaedic Surgery (Indiana University)
Professor of Biomedical Engineering (Purdue
University, IUPUI)
Assistant Professor of Orthopaedic Surgery (Indiana
University)
Assistant Professor of Biomedical Engineering (Purdue
University, IUPUI)
New Faculty
George D. Gantsoudes, MD
Pediatrics
Dr. Gantsoudes completed his undergraduate work at the University of Michigan and his MD degree from the University of IllinoisChicago College of Medicine. After completing his residency in Orthopaedic Surgery at the Mount Sinai School of Medicine in New
York City in 2009, he was spent a year as a Fellow in Pediatric Orthopaedics and Scoliosis at the San Diego Children’s Hospital before
joining the faculty at IU. He will be seeing patients at both Riley and Clarian North Hospitals.
Shyam Kishan, MD
Pediatrics
Dr. Kishan is a 1991 graduate of the Jawaharlal Institute of Postgraduate Medical Education and Research. He then completed his residency in Orthopaedic Surgery at Bombay University in Bombay, India. Since coming to the United States in 1997 initially as a Research Fellow in the Department of
Surgery at Staten Island University Hospital, he completed a residencies in General Surgery and Orthopaedic Surgery at the New Jersey Medical School
in Newark. In 2005, he was a Fellow in Pediatric Orthopaedics and Scoliosis at the San Diego Children’s Hospital. He then spent a year as an attending
orthopaedic surgeon at Shriner’s Hospital for Children in Erie, PA and then four years as a pediatric orthopaedic surgeon at Loma Linda Hospital in Loma
Linda, CA, before joining our faculty. He will be seeing patients at both Riley and Clarian North Hospitals.
Elizabeth (Betsy) M. Nolan, MD
Shoulder and Elbow
Dr. Nolan received her medical doctorate in 2003 from The University of Texas Health Science Center at San Antonio, and completed her specialty
training in Orthopaedic Surgery at Los Angeles County University of Southern California Medical Center in 2008. Dr. Nolan then went on to complete
two Shoulder and Elbow fellowships. The first was at Balgrist Hospital, University of Zurich, Switzerland, 2008-2009. The second was at William
Beaumont Hospital in Royal Oak, MI, 2009-2010. She then joined the Department as a specialist in problems of the Shoulder and Elbow at Wishard,
the VA Hospital, and the Clarian system. The combination of the European and American fellowships give her unique and extensive training in newer
techniques and implants in Shoulder and Elbow Surgery. This includes the Reverse Total Shoulder Replacement, which has been performed in Europe
for over 20 years, but received FDA approval for use in the US only in 2004. Dr. Nolan’s research interests include clinical outcomes of Total Shoulder
and Reverse Total Shoulder Replacement surgeries, as well as biomechanical wear properties and durability of these types of joint replacements, elbow
injuries, shoulder instability, and rotator cuff tears. She is also actively involved in teaching with the IU School of Medicine Orthopaedic Surgery
Residents and Students.
Karl D. Shively, MD
Trauma
Dr. Shively received his medical degree from the University of Illinois College of Medicine, and then completed his residency here at Indiana University.
Following his residency, he completed a fellowship in trauma at the University of Texas Southwester, Department of Orthopaedic Surgery. He joined
our faculty this fall and will be working with Drs. Ertl and Mullis doing trauma care at Wishard Hospital.
6
Volume 4 – 2010
The Indiana University Department of Orthopaedic Surgery would like to thank the
following individuals for their valuable contributions to our residents’ education
during the 2009-2010 academic year
Volunteer Faculty Chiefs of Service
Thomas J. Fischer, MD
Chief of Hand Service
David A. Porter, MD, PhD
Chief of Foot & Ankle Service
Lance A. Rettig, MD
Chief of Sports Medicine Service
Rick C. Sasso, MD
Chief of Spine Service
Resident Conference Lecturers 2009
Jack Farr, MD ..................................................................... Specialty Centers for Orthopaedics
Thomas Fisher, PhD ............................................. IUPUI Department of Occupational Therapy
Eric Horn, MD ...................................................................University Neurosurgery Associates
Daniel Lehman, MD ..................................................................................................Ortho Indy
John McCarroll, MD ........................................................................ Methodist Sports Medicine
Alex Meyers, MD .....................................................Reconstructive Hand Surgeons of Indiana
Gary Misamore, MD ........................................................................ Methodist Sports Medicine
Michael Pannunzio, MD ...........................................Reconstructive Hand Surgeons of Indiana
Christopher Perry, CP, LP ................................................................................ Perry Prosthetics
Arthur Rettig, MD............................................................................ Methodist Sports Medicine
Lance Rettig, MD............................................................................. Methodist Sports Medicine
Peter Sallay, MD .............................................................................. Methodist Sports Medicine
Rick Sasso, MD ......................................................................................... Indiana Spine Group
David Schwartz, MD .................................................................................................Ortho Indy
K. Donald Shelbourne, MD .................................................................... The Shelbourne Clinic
Terry Trammell, MD ..................................................................................................Ortho Indy
Scott Urch, MD ....................................................................................... The Shelbourne Clinic
7
Volume 4 – 2010
PGY-2 through PGY-5 Residents
PGY-2
David Barba, MD
University of California
Los Angeles
Edgar Fernandez, MD
University of Texas
Galveston
Scott Pepin, MD
University of Minnesota
Chad Turner, MD
University of Utah
Jason Watters, MD
Indiana University
Ryan R. Jaggers, MD
Indiana University
School of Medicine
Raymond J. Metz, Jr., MD
Indiana University
School of Medicine
Justin A. Miller, MD
University of Louisville
School of Medicine
W. Lee Richardson, MD
Ohio State University
College of Medicine
Susan M. McDowell, MD
Indiana University
School of Medicine
Kathryn M. Peck, MD
Indiana University
School of Medicine
Daniel R. Sage, MD
SUNY Downstate College
of Medicine
Tarek A. Taha
Medical University
of South Carolina
David M. Fang, MD
Washington University
School of Medicine
Stephen P. Jacobsen, MD
University of Medicine
& Dentistry of New Jersey
Christopher B. Vincent, MD
University of Colorado
School of Medicine
Jonathan H. Wilhite, MD
Indiana University
School of Medicine
PGY-3
Matthew D. Abbott, MD
Indiana University
School of Medicine
PGY-4
Scott R. Bassuener, MD
University of Wisconsin
School of Medicine
& Public Health
PGY-5
Joseph E. Bellamy, MD
University of Illinois
College of Medicine
8
Volume 4 – 2010
Left To Right:
A. Kirk Reichard, MD
Medical School: University of Louisville School of Medicine
Research Project Title: Radiographic Identification of Total Hip
Stems: How Good Are We?
(mentor: J. Andrew Parr, MD)
Fellowship: Adult Reconstruction (Anderson Orthopaedic Research
Institute, Alexandria, VA)
Good Luck to our 2010 PGY-5 Residents
Megan A. Brady, MD
Medical School: Iowa Carver College of Medicine
Research Project Title: The Incidence of Wound Complications
Following Open Reduction Internal Fixation
of Calcaneal Fractures (mentors: Gregory D.
Dikos, MD, David Brokaw, MD)
Fellowship: Trauma (MetroHealth, Cleveland, OH)
Justin W. Miller, MD
Medical School: Indiana University School of Medicine
Research Project Title: Lumbar Extraforaminal Decompression:
A Retrospective Study Looking at Surgical
Outcomes and Complications as an Outpatient Procedure (mentor: Rick C. Sasso, MD)
Fellowship: Spine (University of Wisconsin, Madison, WI)
Larry Martin, Jr., MD
Medical School: Meharry Medical College
Research Project Title: The Relationship of Posterior Inferio Tibial Slope and Anterior Cruciate Ligament Injuries (mentor: K. Donald Shelbourne, MD)
Fellowship: Sports (University of Cincinnati, Cincinnati, OH)
Not pictured:
Conor D. Dwyer, MD
Medical School: Indiana University School of Medicine
Research Project Title: Fracture Union Rates Secondary to Gunshot Wounds: A Retrospective Review (mentors: Janos Ertl MD, Brian Mullis, MD, Jeffrey Anglen, MD)
Practice: Witham Health Services (Lebanon, IN)
Good Luck to the 2009-2010 Fellows
Arup Bhadra, MBBS
Methodist Sports Medicine Center
Creso C. Bulcão, M.D.
IUSM Department of Orthopaedic Surgery
Melissa Gorman, MD
OrthoIndy Trauma
Charan Gowda, MD
Indiana Hand to Shoulder Center
John Hildenbrand, MD
William T. Page, MD
Michael Krosin, MD
OrthoIndy Trauma
William T.J. Payne, MD
William Kurtz, MD
OrthoIndy Trauma
Chad Weber, DO
OrthoIndy Trauma
Robert LeBlanc, MD
Matthew D. Welsch, MD
Welcome…
to the
PGY-3 Class
Kartheek K. Reddy
Texas Tech University
Health Sciences Center
School of Medicine
Raj Kakarlapudi, MD
OrthoIndy Spine
to the New PGY-1 Class
Matthew Beck, MD
Wake Forest University
School of Medicine
Eric R. Dockter, MD
Isaac W. Fehrenbacher, MD
The University of Toledo
Indiana University
College of Medicine
School of Medicine
9
Austin M. McPhilamy, MD
Wayne State University
School of Medicine
Justin D. Millard, MD
American University
of the Caribbean
Volume 4 – 2010
2009-2010
Faculty Awards, Grants
& Publications
Faculty Awards
Jeffrey O. Anglen, M.D. was designated as one of Indy’s Top Docs in Indianapolis Monthly. He was also an invited speaker as
part of the AAOS/OTA delegation to the 46th Congreso Argentino de Oropedia Y Traumatologia held in Salta, Argentina in
November, 2009. He is also vice president of ABOS and is on the Board of Directors of AAOS.
Melissa A. Kacena, Ph.D. was elected to the Board of Directors for the journal, Advances in Mineral Metabolism (AIMM).
J. Andrew Parr, M.D. won the 2010 Trustee Teaching Award for Orthopaedic Surgery. Award recipients must have demonstrated a sustained level of teaching excellence in the form of documented student learning and must have completed at least
three years of service at IUPUI to be eligible. A review committee selects 53 recipients based on the criterion of excellence
in teaching as the primary factor for selection, including the review of student and/or course evaluations. The award is presented annually at the IUSM Commencement, and recipients are also honored at the Spring Faculty Meeting and the annual
campus Chancellor’s Honors Convocation.
L. Daniel Wurtz, M.D. was selected as one of three Healthcare Heroes by the Indianapolis Business Journal. He was a finalist
for the award in the Advancements in Health Care category for his work in limb-saving research for children with cancer.
Grants
Project Director Project Title
Granting Agency
Cummings, Judd
Effects of Platelet Number and Adhesion on Osteosarcoma Growth and Metastatic
Potential
Am Cancer Society / IU
Simon Cancer Center
Ertl, Janos
Rhbmp2 vs. Autograft for Critical Size Tibial Defects: A Multicenter Randomized Trial
OTA
Ertl, Janos
Ankle Fracture Plating: A Multicenter Randomized Trial Comparing Lateral and
Antiglide Plating in Displaced Lateral Malleolus Fractures
Ohio State U Research
Foundation
Kacena, Melissa
The Role of OPG in GATA-1 Deficiency
NIH-NIAMS
Kacena, Melissa
Young Investigator in Basic Science Award
CTSI
Kacena, Melissa
Collaboration in Translational Research Award
CTSI
Mullis, Brian
Research Assistant Funding
Synthes
Mullis, Brian
A Multicenter, Randomized, Double-Blind Placebo-Controlled Study of Adults
with a Fresh Unilateral Tibial Diaphyseal Fracture Statue Post Definitive Fracture
Fixation with an Intramedullary Nail
Amgen
Mullis, Brian
A Multicenter, Randomized Double-Blind, Placebo-Controlled Study of AMG 785
in Skeletally Mature Adults with a Fresh Unilateral Tibal Diaphyseal Fracture Status
Post Definitive Fracture Fixation with an Intramedullary Nail
Amgen
Mullis, Brian
Hip Fracture Evaluation with Alternatives of Total Hip Arthroplasty versus
Hemi-Arthroplasty: A Multicenter, Randomized Trial Comparing Total Hip
Arthroplasty and Hemi-Arthroplasty on Revision Surgery and Quality of
Life in Patients with Displaced Femoral Neck Fractures
Boston U
Mullis, Brian
Fixation using Alternative Implants for the Treatment of Hip Fractures
U of Minnesota
Trippel, Stephen
Gene Transfer Treatment of Articular Cartilage Damage
NIH-NIAMS
Trippel, Stephen
Selection of Therapeutic Agents for Articular Cartilage Repair
VA Merit Grant
10
Volume 4 – 2010
Selected Publications
Anglen JO, Bosse MJ, Bray TJ, Pollak AN, Templeman DC, Tornetta P 3rd, Watson JT. The Institute of Medicine report on resident
duty hours. Part I: The Orthopaedic Trauma Association response to the report. J Bone Joint Surg – Am. 91(3):720-2, 2009.
Barrett MO, Anglen JO, Hoernschemeyer DG, Schnetzler KA. Case report: associated both-column acetabulum fracture with an ipsilateral centrally dislocated intertrochanteric femur fracture. J Trauma-Inj Infect Crit Care. 66(3):918-21, 2009.
Anglen JO, Archdeacon MT, Cannada LK, Herscovici D Jr, Ostrum RF. Avoiding complications in the treatment of humeral fractures.
Instr Course Lect 58:3-11, 2009.
Archdeacon MT, Cannada LK, Herscovici D Jr, Ostrum RF, Anglen JO. Prevention of complications after treatment of proximal femoral
fractures. Instr Course Lect. 58:13-9, 2009.
Ostrum RF, Anglen JO, Archdeacon MT, Cannada LK, Herscovici D Jr. Prevention of complications after treatment of femoral shaft and
distal femoral fractures. Instr Course Lect. 58:21-5, 2009.
Cannada LK, Anglen JO, Archdeacon MT, Herscovici D Jr, Ostrum RF. Avoiding complications in the care of fractures of the tibia. Instr
Course Lect. 58:27-36, 2009.
Herscovici D Jr, Anglen JO, Archdeacon MT, Cannada LK, Scaduto JM. Avoiding complications in the treatment of pronation-external
rotation ankle fractures, syndesmotic injuries, and talar neck fractures. Instr Course Lect. 58:37-45, 2009.
Templeman DC, Anglen JO, Schmidt AH. The management of complications associated with tibial fractures. Instr Course Lect. 58:47-60,
2009.
Engsberg JR, Steger-May K, Anglen JO, Borrelli J Jr. An analysis of gait changes and functional outcome in patients surgically treated
for displaced acetabular fractures. J Orthop Trauma. 23(5):346-53, 2009.
Schmidt AG, Anglen JO, Nana AD, Varecka TF. Adult trauma: Getting through the night. Instr Course Lect. 59:437-53, 2010.
Schmidt AG, Anglen JO, Nana AD, Varecka TF. Adult trauma: Getting through the night. J Bone Joint Surg – Am. 92(2):490-505, 2010.
Capello WN, D’Antonio JA, Geesink RG, Feinberg JR, Naughton M. Late remodeling around a proximally HA-coated tapered titanium
femoral component. Clin Orthop. 467(1):155-65, 2009.
Vail TP, Mont MA, McGrath MS, Zywiel MG, Beaule PE, Capello WN. Hip resurfacing: patient and treatment options. J Bone Joint
Surg – Am. 91(Suppl 5):2-4, 2009.
Capello WN, Feinberg JR. Use of an alumina ceramic-on-alumina ceramic bearing surface in THA in a 13 year old with JIA--a single case
study. Bull NYU Hosp Jt Dis. 67(4):384-6, 2009.
Cummings JE, Smith RA, Heck RK Jr. Argon beam coagulation as adjuvant treatment after curettage of aneurismal bone cysts: a preliminary study. Clin Orthop. 468(1):231-7, 2010.
Ciovacco WA, Goldberg CG, Taylor AF, Lemieux JM, Horowitz MC, Donahue HJ, Kacena MA. The role of gap junctions in megakaryocyte-mediated osteoblast proliferation and differentiation. Bone. 44(1):80-6, 2009.
Ciovacco WA, Cheng YH, Horowitz MC, Kacena MA. Immature and mature megakarocytes enhance osteoblast proliferation and inhibit
osteclast formation. J Cell Biochem. 109(4):774-81, 2010.
Lemieux JM, Horowitz MC, Kacena MA. Involvement of integrins alpha(3)beta(1) and alpha(5)beta(1) and glycoprotein IIb in megakaryocyte-induced osteoblast proliferation. J Cell Biochem. 109(5):927-32, 2010.
Chitteti BR, Cheng YH, Poteat B, Rodriguez-Rodriguez S, Goebel WS, Carlesso N, Kacena MA, Srour EF. Impact of interactions of
cellular components of the bone marrow microenvironment on hematopoietic stem and progenitor cell function. Blood. 115(15):323948, 2010.
Gaston RG, Greenberg JA, Baltera RM, Mih A, Hastings H. Clinical outcomes of scaphoid and triquetral excision with capitolunate
arthrodesis versus scaphoid excision and four-corner arthrodesis. J Hand Surg – Am. 34(8):1407-12, 2009.
Foulk DM, Mullis BH. Hip dislocation and management. J Am Acad Orthop Surg. 18(4):199-209, 2010.
Shi S, Mercer SA, Dilley R, Trippel SB. Production of recombinant AAV vectors encoding insulin-like growth factor I is enhanced by interaction among AAV rep regulatory sequences. Virology. 6:3, 2009.
Shi S, Mercer S, Eckert GJ, Trippel SB. Growth factor regulation of growth factors in articular chondrocytes. J Biol Chem. 284(11):6697704, 2009.
Shi S, Mercer S, Trippel SB. Effect of transfection strategy on growth factor overexpression by articular chondrocytes. J Orthop Res.
28(1):103-9, 2010.
11
Volume 4 – 2010
The Garceau-Wray Lectureship
In 1966, the Riley Memorial Association began the Garceau Lectureship in honor of Dr.
George Garceau, the first Chairman of the Department of Orthopaedic Surgery at the Indiana
University School of Medicine. The combined Garceau-Wray Lectureship was begun in 1976
in memory of Dr. James B. Wray, the second Chairman of the Department of Orthopaedic
Surgery, following his untimely death.
Dr. Garceau (1896-1977) was recognized around the world as a both a fine pediatric
orthopaedic surgeon and as a true gentleman. He joined the staff at Riley Hospital in 1928 and
rose through the academic ranks to become Professor and Chairman of Orthopaedic Surgery,
then a section of General Surgery, in 1948. He was instrumental in forming an independent
Department of Orthopaedic Surgery in 1960 and served as the Chairman until his retirement in
1966. During his career, he served as Vice President of the American Academy of Orthopaedic
Surgery, President of the American Board of Orthopaedic Surgery, and President of the Clinical
Orthopaedic Society. In addition to being a skilled surgeon, he was an inspiring and innovative
teacher, developing the model of the residency program still in use at Indiana University.
Dr. Wray (1926-1973) was recruited as the second Chairman of the Department in 1966.
He was dedicated to the investigation and research of metabolic and vascular responses to fracture and to the general metabolic responses
to trauma, and he established the orthopaedic basic science research laboratories in 1967. In addition to multiple scientific publications, he
was the recipient of three research awards for excellence. Like his predecessor, he was an inspiring and dedicated surgeon and teacher. His
sudden and untimely death left a void in the hearts of his colleagues, residents, and medical students by whom he was liked and respected.
The Garceau-Wray Lectureship is supported by generous donations from our alumni and industry. Each year two nationally known
speakers are invited to address the faculty, residents, alumni, and community surgeons in honor of these two fine gentlemen. This year’s
meeting was held on June 3-4, 2010 at the University Place Conference Center and Hotel on the IUPUI campus. Keynote speakers were:
Roy W. Sanders, M.D.
University of South Florida School of Medicine, Tampa, Florida
Dr. Sanders is a highly respected specialist in trauma and post-traumatic reconstruction as well as foot and ankle surgery, and has
published nearly 100 articles and abstracts on orthopaedic trauma. Dr. Sanders attended medical school at NYU and completed his residency
at the Hospital for Joint Diseases Orthopaedic Institute in NYC. After completing his fellowship in musculoskeletal trauma at Vanderbilt
University, he was granted the prestigious AO/ASIF Jack McDaniels Memorial Trauma Fellowship, trained under the tutelage of Thomas
Ruedi, MD, in Chur, Switzerland, and then completed a foot and ankle fellowship at Harborview Medical Center in Seattle, WA. He currently
serves as the Director of the Orthopaedic Trauma Service and
Chief of the Department of Orthopaedic Surgery at Tampa General
Hospital. In addition he is President of the Florida Orthopaedic
Institute and the Editor-in-Chief of the Journal of Orthopaedic
Trauma. As the George J. Garceau lecturer, he presented a paper
entitled, The Operative Management of Displaced Intra-Articular
Fractures of the Calcaneus.
Arnold-Peter Weiss, M.D.
Brown University, Providence, Rhode Island
Dr. Weiss is a highly respected specialist in wrist and hand
reconstruction with a special interest in joint replacement surgery,
and has published over 100 articles. Dr. Weiss attended medical
school and completed his orthopaedic residency at Johns Hopkins
medical school in Baltimore, and then completed his fellowship
in hand surgery at the Indiana Hand Center under the tutelage of
Dr. James Strickland. He is currently the R. Scot Sellers Scholar
of Hand Surgery, Professor of Orthopaedics and Associate Dean
of Medicine at Brown University. He also serves as the Director
of the Microvascular Surgery Laboratory. He was Editor-inChief of the Journal of the American Society for Surgery of the
Hand and is currently an Associate Editor of the Journal of Hand
Surgery. As the James B. Wray lecturer, he presented a paper
entitled, Wrist Arthritis & Instability.
Caption: Drs. Sanders, Anglen, and Weiss at 2010 GarceauWray Lectureship
12
Volume 4 – 2010
We gratefully acknowledge contributions from the following companies in support of the Garceau-Wray Lectureship:
CLARIAN HUMAN MOTION INSTITUTE
STRYKER ORTHOPAEDICS
ZIMMER MIDWEST
SMITH & NEPHEW
DEPUY ORTHOPAEDICS
ORTHOFIX
PFIZER, INC.
MEDTRONIC SPINAL AND BIOLOGICS
BIOMET HEARTLAND ORTHOPAEDICS, INC.
ANGIOTECH
BIOMED
DJO GLOBAL
In 30 years, I still plan to be hitting the trail
The LEGION™ CR knee with VERILAST™ Technology has been
lab tested for 30 simulated years of wear performance.
This revolutionary implant was lab tested more than twice as
long as other knee replacements.
It’s hypoallergenic and lighter weight – weighing 20% less
than traditional knee technology. And it substantially reduces
wear – a leading cause of knee replacement failure.
It’s time to put a stop to your chronic knee pain. Ask for the
only knee lab tested for 30 years of wear performance.
Rediscover your go with VERILAST Technology.
Go to RediscoverYourGo.com today to find a
surgeon who specializes in VERILAST Technology.
There are potential risks with knee replacement surgery such as loosening, fracture, dislocation, wear and infection that may result in the need for additional surgery.
Do not perform high impact activities such as running and jumping unless your surgeon tells you the bone has healed and these activities are acceptable. Early device failure,
breakage or loosening may occur if you do not follow your surgeon’s limitations on activity level. Early failure can happen if you do not guard your knee joint from overloading
due to activity level, failure to control body weight or accidents such as falls. Knee replacement surgery is intended to relieve knee pain and improve knee functions. Talk to your
doctor to determine what treatment may be best for you. Additional information available at www.RediscoverYourGo.com or 888-825-2062.
™Trademark of Smith & Nephew. Certain marks Reg US Pat. & TM Off.
VERILAST_Full Color_8.5x5.5.indd 1
13
8/3/2010 2:36:22 PM
Volume 4 – 2010
3rd Annual Lindseth Lectureship
November 5, 2010
Dr. James R. Gage,
2010 Lindseth Lecturer
8am - 5pm
6pm - Cocktail Reception and Dinner
University Place Conference Center & Hotel
850 W. Michigan Street
Indianapolis, Indiana
The Department of Orthopaedic Surgery at Indiana University School of Medicine is pleased to
present the 3rd Annual Lindseth Lectureship through the generosity of the Orthopaedic Residency
Alumni. The Lectureship will consist of a full day of talks and case presentations on pediatric
orthopaedics presented by the pediatric faculty of Indiana University and other distinguished
academic pediatric orthopaedists.
In addition to several invited speakers who are pediatric orthopaedic specialists, it is our honor to
welcome Dr. James R. Gage of Gillette Children‛s Hospital, St. Paul, Minnesota as the third annual
Lindseth Lecturer in Pediatric Orthopaedics. Dr. Gage is the former Medical Director of Gillette
Children‛s Specialty Healthcare and Professor Emeritus at the University of Minnesota. The title
of his presentation is ‘The Evolution of Treatment of Ambulatory Cerebral Palsy‛.
Registration fee for this program is $50, which includes conference materials, continental breakfast,
break refreshments, and lunch. Reservations for the dinner may be purchased at an additional $30.
Residents-in-training may attend the meeting and dinner free of charge; however, registration is
required for all attendees. On line registration is available at http://cme.medicine.iu.edu. After
November 3, 2010 please register at the door.
IU School of Medicine – 2010 Mark Brothers Lectureship Award
Dr. and Mrs. Guey C. Mark created the endowed Mark Brothers Lectureship to recognize nationally and internationally renowned medical scientists of Asian descent. The Mark Brothers
Lectureship has been awarded for outstanding biomedical and clinical research since its origin in 1999. The winners have had long,
distinguished careers, many holding endowed chairs. Several have
had significant leadership roles in their medical schools and departments, or directed research institutes such as those at the NIH or
major universities.
This year Dr. Freddie Fu was received this honor from the IU
School of Medicine. Dr. Fu is Distinguished Service Professor and
David Silver Chair of Orthopaedics at University of Pittsburgh, with
joint appointments in Physical Therapy, Mechanical Engineering,
and Health & Physical Activity. He serves as head team physician
for the Pittsburgh Department of Athletics, and company physician
for the Pittsburgh Ballet, as well as multiple professional sports
teams. He is the founding medical director of the UPMC Center
for Sports Medicine, former President of the AOSSM, and current
President of the International Society of Arthroscopy, Knee Surgery,
and Sports Medicine. He is an NIH funded clinicain-scientist who
has received over 170 professional awards and honors, published
over 350 papers and edited 28 major textbooks.
Dr. Jeff Anglen, Chair, Department of Orthopaedic Surgery, Laurie Mark,
4th year medical student and granddaughter of Dr. Guey Mark, and
Dr. Freddie Fu, 2010 Mark Brothers award recipient.
The IU School of Medicine maintains an archive of award presentations through Media Viewer. If you would like to learn more
about Dr. Guey Mark and view Dr. Fu’s lecture, entitled Anatomic
ACL Reconstruction: A Change in Paradigms, use the following
link: http://bit.ly/bSKrLE.
14
Volume 4 – 2010
An Interview with Bill Capello
JOA: Bill, you recently made an extremely generous bequest
to our department by endowing the Bill and Louise Capello Chair in
Orthopaedics. This kind of support shows great confidence in IU
Orthopaedics, and demonstrates great leadership that I’m hoping will
kick off alumni support for our most recent project, the drive to get an
arthroscopy simulator.
WC: I was happy to do it, and I think it’s nice if you can use it to
stimulate additional support. I was recently at a social event and ran into
Jim Steichen, who was a hand surgeon with the Indiana Hand Center,
retired now, an emeritus professor. He happened to be sitting at my
table and he made a point, during the night, to come over and sit down
directly beside me and mention this whole thing and tell me how he was
impressed with that kind of gesture. I never realized that the word is out
so to speak.
Dr. William and the late Louise Capello
JOA: We announced it at the IU AAOS reception in New Orleans,
and recently sent a letter to the alumni about it. I think it means a lot to people when a faculty member shows that kind of
support. I wanted to share with our alums a little about you and how you got to where you are today. Did you come from a
medical family?
WC: No, I was actually the first one in my family to graduate from college. All four of my grandparents came from
northern Italy. My father was a house painter, who went into business for himself and became sort of a contractor for little
homes. I went to work in the summers when I was 10 and worked as a carpenter during the summers through medical school.
My father and my grandfather, his dad, believe it or not, took night courses at Carnegie Tech, Carnegie Mellon, in chemistry.
They both loved chemistry. They didn’t get degrees, but my granddad had this chemistry lab in his garage. He would do
experiments. My grandfather had a couple of patents. He was a very interesting guy.
JOA: Where’d you grow up?
WC: In western Pennsylvania, in a coal mining town. There were probably 800 people in the town. The towns were all
named after mines. I didn’t realize I was from Pittsburgh until I went to college, and after I had to take a half an hour to explain
it, and they finally said “Well, you’re from Pittsburgh.” So, it was only 15 miles away but in another world.
JOA: What about college?
WC: I went to Rutgers on a football scholarship. Back then, colleges had a lot of interest in kids from western Pennsylvania.
They produced a lot of decent ball players over the years. Joe Montana, Dan Marino, Mike Ditka - they were all from that area.
I was fortunate enough to play at a very small school as a halfback and did well. I had full scholarship offers to Notre Dame,
, Miami (FL), Arizona State, Minnesota, and Navy.
JOA: But you picked Rutgers.
WC: Well, I picked Rutgers because by that time I had decided to go into medicine. I wrote away to five of the schools
that I was seriously considering, Notre Dame was one of them, and simply asked them “If I complete your pre-med program,
what are my chances of getting into medical school?” which I thought was a reasonable question. I only got two responses, one
from Notre Dame, which said “We don’t know” and one from Rutgers that said “100%.”
JOA: Sounds like the pre-med program might have been pretty tough. What was your major at Rutgers?
WC: I majored in biological sciences in the School of Liberal Arts. I wound up taking no less than 19-21 credits per
semester. There was a committee of one, one guy, Ralph DeFalco, was your advisor, and he would sit you down and he would
say “Where do you want to go to medical school? “ I wanted to go to Pittsburgh. He said “Good! Because no one wants to go
to Pittsburgh.” He wrote all your evaluation letters, long hand, and he got over 100 guys into medical school that year.
JOA: That’s pretty cool.
WC: I have a good friend, Jim D’Antonio, who’s an orthopedist in Pittsburgh now. We’ve written several papers together.
Jim was also from western Pennsylvania, on the Rutgers football team, and a fraternity brother of mine. Another guy, Andy
15
Volume 4 – 2010
An Interview with Bill Capello (continued)
Carollo, was another friend of ours, three Italians. Carollo was fullback and Jim and I were the halfbacks on the freshman
football team. And we’re all three orthopaedic surgeons today.
JOA: Do you guys get together at all now?
WC: Well, Jim and I see each other routinely, and we see Andy from time to time. He still lives in New Jersey.
JOA: How did you get interested in Orthopaedics?
WC: Initially I wanted to be a GP, but Pitt wasn’t turning out any GPs. If you were in the top 15% of the medical school
class or so, you would go into Internal Medicine. So that’s where I went. I wanted to be a neurologist.
JOA: Really?
WC: Yes. So I interviewed at the University of Virginia and was accepted into the Neurology program there. It was a
pretty decent program at the time. But, that was to occur after my internship, so I applied for a straight medical internship and
I got one at the University of Pittsburgh. It was every other night call for a year, and it was during that year I realized a bunch
of things. One, I wasn’t cut out to be an internist. I’d had a bad experience on Orthopaedics as a student, but when I got into it
as a house officer, you kind of know everybody, and there was no question that the guys I really enjoyed were the Orthopods. I
kind of felt like they were normal people. So I decided, what the heck, I’m going to become an orthopaedic surgeon.
JOA: Where did you train?
WC: I wanted to stay at Pitt. I picked up the phone, like within 10 minutes of getting my Berry Program deferment letter,
called Al Ferguson up, who was the Chairman at Pitt, and I said, “Dr. Ferguson, I just got this deferment. Do you have a spot
for me?” He said, “I just gave the last one away this morning to Jim D’Antonio.” I decided to look around, but everywhere I
called was full. Finally, I called Iowa. Iowa was in the matching program, but the match had fallen apart. Iowa was one of the
only major programs that still hadn’t committed because they were in the match. Well, I did get in, I don’t know how. But it
was the only place I applied. That was good. Then I went in the Army after that.
JOA: After the residency?
WC: Yes, that’s how I got here.
JOA: Oh, is that right? I was wondering what your connection was to Indiana.
WC: I have to tell you, I was really disappointed.
JOA: In coming to Indianapolis?
WC: Oh yeah. I had originally been assigned
to Fort McPherson in Atlanta, and my wife and
I were so excited about going to Atlanta. Well, I
got bumped. So then I said I’d go to Fort Eustis,
VA, which was open, outside of DC. Same thing
happened! And they finally said, “Well, we’re
going to put you at Fort Benjamin Harrison”
and I told my wife that we’d better accept this,
otherwise we could wind up some place in
Louisiana.
JOA: It’s getting worse and worse, better
take this one. When did you get married?
WC: I got married in 1965, when I was a
sophomore in medical school.
JOA: How’d you guys meet?
WC: Her brother and I played American
Legion baseball together. He was a couple of
years older than I was. He was a good player.
16
Volume 4 – 2010
Anyhow, I remember him saying that he was a senior in high school and he had gotten a football scholarship to Rutgers.
So a couple of years later, there I am in the same spot, so I decided to call him up just to see how Rutgers was. I went down
to meet him and who answers the door but my future wife. She was the same age I was, we were seniors in high school at that
time. So that’s how we started dating.
JOA: And so did you guys date all the way through college and medical school?
WC: Yes, and then got married while I was in medical school.
JOA: So you guys came to Indianapolis and spent two years here in the Army.
JOA: When did you start to develop an interest in arthroplasty?
WC: Oh, that was when I came here. I got a phone call from Don Kettlekamp, who had been on the faculty at Iowa when
I was a resident. He had just taken the job here. I remember the exact conversation we had. He called me up and said “Bill,
what are you doing?” I said “Nothing yet. I don’t have a job.” He said “Well, we’re desperate here. It was going to be Paul
DeRosa, Dick Lindseth and me with Ray Pierce over a Wishard. We don’t have anybody here doing any adult stuff. We need
help. You want a job? You got a job.” I told him that I’d come down for a year.
So I came here and he said to me, “I don’t care what else you do but you gotta do hips. I said “Well, Don, let me tell
you something. When I was a resident, I did two total hips. And I’ve been in the service for two years and I haven’t even seen
one.” I went over to the VA and looked over the resident’s shoulders, and they thought I was a great faculty member because
I wasn’t bothering them.
I remember Don called me in his office and said, “Look, you’ve got to do me a favor. This old man here in town, this
old orthopaedist is driving me crazy. He’s insisting that I send over a young guy. I’ve tried to get Merrill Ritter to go but he
said, “I’m not going!” He said “Would you consider going over there?” I said, “Well, I don’t care. I’ve got nothing else to
do.” So, I go to Winona Hospital, where I met Palmer Eicher.
JOA: That was up on Meridian?
WC: Yes. He seemed ancient at the time, and he was a crusty guy. He takes me in his office and shows me this little cup.
“You just put it on top of the bone, you don’t cut the bone off, you just put it on top, put a piece of plastic in and you’re done.
I’m going to do one tomorrow. Come over here tomorrow and I’ll show you how to do it.” Within a matter of probably two
weeks, I was doing the surgery, and he was helping me.
JOA: Really?
WC: Yes, on his patients. So I got pretty proficient operating, and he got to trust me. Then he retired. He basically said,
“Look, I’m old. I’m retiring and I like the way you handle people. I’d be happy if you took over my practice. “ So he shipped
patients over here, gave me all his charts, and he said, “By the way, here. If you want to play around with this thing, go ahead.”
It turned out to be the Indiana Conservative Hip.
JOA: And so did he just make it himself?
WC: DePuy made it for him in Warsaw. Anyway, I was invited to be part of a hip symposium at the AAOS meeting where
I also met Dr. Frank Stinchfield founder of both the Hip Society and the International Hip Society, One the plane ride home I
sat next to Dr. Drennan Lowell, a professor at Harvard who, a month later, invited to give Grand Rounds at Harvard. My first
paper was on the conservative hip, and was an invited paper to CORR at the request of Dr. Michael Freeman. I began to see
some failures and report them, which was unusual – a lot of people didn’t report failures. With the help of a resident named
Nancy Wilson, I wrote a paper on bone scanning of surface replacements. It turns out you can predict which ones will fail based
on the scan. That paper won the Hip Society’s Charnley Award.
JOA: You have had a great career here at IU over 30+ years. Did you ever think about going anywhere else?
WC: I had some offers. Paul Curtis was chair at Ohio State, and he recruited me shortly after I came here. Tom Mallory,
who is a well known, high volume hip surgeon in Columbus called me up a while after that, and I went to look there. I had
been to Italy to learn osteotomies from Bombelli, and was interested in that stuff. Well, Tom was doing total hips and whoever
worked with Tom was going to do total hips. He’s such a nice guy, but he was very clear that you had to turn out a certain
volume or else you weren’t worth much.
17
Volume 4 – 2010
I can remember talking to his business manager. I’ll never forget that conversation. The guy says “What do you charge
for a total hip in Indiana?” And I said, “Like $3,000.” He said, “How’d you arrive at that?” I said, “I don’t have a clue!” He
said, “You don’t know why you charge that amount?” I said, “Not really.” He said “How much does it cost you to do it there?”
I said, “I have no idea.” “He said, “Well, we can tell you exactly how much it costs and know the clear cost of a total hip, we
have a certain amount of evidence that will support our charges. If anybody ever asks us, we can defend exactly what we are
charging.” Anyhow, he offered me more money to start than I’ve ever made. He said, “Then after a year or so you’ll start
making some real money.”
Also, Gus Sarmiento called me up when he took the job as Chair in LA. He called Leo Whiteside at the same time, too.
He wanted both of us to come out there and join his faculty. And I thought that if I were going to go anywhere, that’s probably
where I’d go. So then he called me back and said “I’m just going out there, give me a chance.” And you know he ran into some
real political problems out there.
JOA: Yeah, I know Gus and have a copy of his book, “Bare Bones”. It’s an interesting book.
WC: After he got there, he called me and said “Look Bill, this is probably not the place for you. And that was about it. I
never really looked around after that. I’d been here about 10 years, so I decided to stay.
JOA: You liked it and things were going well. You could stay in one place, focus on one thing and really take care of
business. You’ve seen some significant ups and downs for this Department over the time that you’ve been here.
WC: I have. When I came here, we had a pretty simple compensation plan. I mean everybody made the same, basically.
Whatever was made was put into a pot and divided up equally among all of us, allowing a couple of thousand dollars for
different academic ranks, but basically that was it. It allowed you to kind of do what you wanted to do and, you know, if my
partner gave me a hip to do, it didn’t hurt his income. So we could kind of super-specialize there without taking a financial hit
getting started. So that was kind of a good thing. I recognized the fact that the guys working at Riley and Wishard were working
hard and not making any money because the patients didn’t pay. My overhead was about 85%. That never bothered me, it
didn’t have a bearing on me. I was making enough money.
JOA: What do you think are the biggest changes you’ve seen in the residency program over the 30+ years that you’ve been
here?
WC: Well, I think, in general terms, we’re training high quality people in our program. We’ve always had high quality
people. but we had a bigger spectrum early on.
JOA: Do you think the applicant pool has just gotten better and better?
WC: That, and I think it also reflects the fact that the institution has got a better name, and we attract better people. I really
think that the educational program we offer the residents, with the curriculum we put together, is really first rate and a marked
improvement over what it was for me when I came here. I think in general the residents seem much happier, and there’s a much
better team approach than I’ve ever seen which is really rewarding for me.
JOA: Do you think residents coming out today will have as good a career as we’ve had during our careers? And the same
opportunities? Will there be innovators like yourself and Palmer Eicher?
WC: I still think there are going to be guys who are going to excel, develop new things either in the lab or at the bedside. I
still think we attract the kinds of individuals who are capable of doing that. It may not be quite as easy, but in my mind, they’ve
always been rare.
JOA: What do you hope to accomplish by endowing the professorship?
WC: My goal is to support our ability to have people here who will continue the great work that the Department has done
in teaching, research and service. I’d like to see them continue on with clinical research, because that’s such an important part
of how we learn, how we advance our profession. I hope to make it easier for IU Orthopaedics to continue the tradition of
excellence that my friends and colleagues have built here over the years. It would be very rewarding to do that.
JOA: Bill, I think I can speak for the whole IU Orthopaedic family, three decades worth of residents, fellows, students and
faculty, when I say thank you for your service and loyalty.
WC: It has been an honor and a pleasure.
18
Volume 4 – 2010
Volunteer Orthopaedic Experience in South India
Alexander D. Mih, MD
Associate Professor, Department of Orthopaedic Surgery
Orthopaedic surgeons in the United States have numerous
opportunities to volunteer their services both at home and
abroad. The American Academy of Orthopaedic Surgery and
the American Society for Surgery of the Hand are actively
involved in numerous national and international programs
providing opportunities for both service and teaching.
Likewise, the Indiana University School of Medicine has
strong ties to overseas medical centers in a variety of locations
around the world. The need for contemporary medical care in
developing countries is great, especially in areas far removed
from large population centers. Matching medical volunteers
to appropriate opportunities can be difficult due to problems
with facilities, support systems and language/cultural
differences.
One program that has been active in bridging the gap
between medical volunteers and the unique needs of a
population in a developing country has been the medical
program of the South India Church of Christ Mission (SICCM).
The Mission has been meeting needs in the Indian state of
Tamil Nadu since the 1950‘s, bringing medical treatment to
this population in a variety of fields from immunizations,
well baby/maternal care, and the treatment of orthopaedic
disorders. In the 1970’s, the program treated several thousand
patients with leprosy annually and served as one of the district
hospital centers attended by the late Dr. Paul Brand, one of
the pioneers in the field of reconstructive surgery for this and
other disorders. As effective chemotherapy was developed
for leprosy, the need for reconstructive surgery was greatly
reduced.
Image 1: Girl with polio and severe atrophy of arm
motor atrophy can be addressed through appropriate tendon
transfer with a resultant significant improvement in function.
(IMAGE 1) Leprosy is rarely seen in the U.S., with almost
all cases involving contact with the nine-banded armadillo
in the Gulf coast area. The nerve damage inflicted by this
disorder preferentially affects the ulnar nerve leading to the
classic claw position of the hand in the setting of impaired
sensation. (IMAGE 2)
In 1996, a group of Orthopaedic Surgeons and Physiatrists
from Indiana University traveled to Tamil Nadu to initiate a
program with SICCM focusing on polio and other childhood
disorders. Following this original encounter, additional
orthopaedic medical trips were undertaken to treat patients in
this developing area. This area has been largely agricultural,
although recent development has led to the addition of some
manufacturing.
The focus of the medical program has largely been
on disorders of the upper extremity. Numerous conditions
are encountered on a regular basis and include congenital
disorders, nerve palsy secondary to infectious causes such
as polio and leprosy, burn scar contracture, and the residual
effects of trauma. The goal has been to improve the upper
extremity function of those afflicted with these disorders with
an emphasis on the needs of daily living and employment
Surgery in the developing world often exposes the
surgeon to conditions not frequently encountered. While
rarely encountered in the West, polio remains a significant
problem in many areas of the world. Massive efforts by both
governmental and non-governmental organizations (NGO’s)
toward immunization have been successful in reducing the
incidence of the viral disease, yet new cases continue to
emerge each year. The resulting nerve palsy with profound
19
Image 2: Claw deformity from leprosy secondary to ulnar
nerve palsy
Open flame cooking is the normal mode of meal
preparation leading to frequent accidental burns. The lack
of early and effective burn care may result in profound
deformities that often require staged reconstructive efforts.
(IMAGE 3) Combinations of contracture release, skin
grafting and therapy measures can greatly improve hand
function. (IMAGE 4)
Volume 4 – 2010
Volunteer Orthopaedic Experience in South India (continued)
the world. The residency program at that institution has
welcomed lecturers from the Indiana University Department
of Orthopaedic Surgery, and faculty visits between institutions
have encouraged academic exchange and collaboration.
Image 3: Longstanding burn scar contracture
Image 5: Resident Lonnie Davis with medical student
Damian Harris, and faculty member, Jeff Greenberg
Image 4: Result after surgical release of burn scar
contracture
The goal of this program has been to bring contemporary
treatment to patients without access to medical care. A
dedicated effort has been put forth in securing appropriate
operating conditions, anesthesia service, and aftercare. A
large number of individuals trained in everything from
preoperative screening to vocational training have been a
vital link in the overall success of the medical program. A
fruitful partnership between both secular and faith-based
organizations has developed bringing restorative surgery to
over 1000 patients in south India.
The role of medical education is fundamental to the
ultimate success of any volunteer program. Faculty from
Indiana University, as well as from other US medical centers,
has participated in a vast array of educational conferences
including several National Hand Surgery Courses at the
Christian Medical College of Vellore, Tamil Nadu. The open
exchange of information, technical training and research into
these disorders has been beneficial to attendees from around
Image 6: Resident Kurt Martin examining hand pre-op
20
Volume 4 – 2010
Volunteer Orthopaedic Experience in South India (continued)
Image 7: Resident Matt Welsch with patient and Michigan State faculty member, Jeff King
The Indiana University Orthopaedic Surgery Department
has provided enthusiastic support for resident involvement in
this overseas project. Since 1997, 14 residents and medical
students have participated in this project as have six faculty
members. (IMAGES 5, 6, 7) Over 15 nurses, therapists
and other personnel have also provided service with several
individuals making multiple trips. Orthopaedic implant and
equipment companies have provided significant monetary
21
and material support. Resident physicians are involved
in every aspect of patient care from initial evaluation and
recommendations through surgery and recovery under direct
supervision of Indiana University faculty. A log of procedures
and activity is kept by residents during their time in India.
For further information regarding this program please contact
Alexander D Mih, MD by email: amih@iupui.edu.
Volume 4 – 2010
Charles H. Turner, Ph.D.
1961 - 2010
The Department of Orthopaedic Surgery lost a great leader
and the Director of Orthopaedic Research on July 16, 2010, when
Dr. Charles H. Turner passed away at home, with his family, in
Indianapolis, Indiana. He is survived by his two children, Jeff and
Emily; his parents, Bob and Mary Turner; and his siblings Robert,
David, and Anne Marie.
Dr. Turner was born November 29, 1961 in Roswell, New
Mexico. He earned his B.S. in mechanical engineering from Texas
Tech University in 1983 and his Ph.D. in biomedical engineering
from Tulane University in 1987. He joined the faculty on the Indiana
University-Purdue University Indianapolis (IUPUI) campus in 1991
after four years with the Osteoporosis Research Center at Creighton
University. During his tenure at IUPUI, Charles rose to the ultimate
ranks of Chancellor’s Professor and Associate Director within
the Department of Biomedical Engineering (Purdue University),
and Professor and Director of Orthopaedic Research within the
Department of Orthopaedic Surgery (Indiana University School of
Medicine).
Dr. Turner was an internationally renowned expert in musculoskeletal biomechanics and bone biology,
with particular interests in how bone responds to mechanical loading and skeletal genetics. He published more
than 250 scientific papers and gave over 100 invited presentations worldwide. He received numerous awards
and honors for his contributions to the field, including receiving the prestigious Fuller Albright Award from the
American Society for Bone and Mineral Research in 2001; elected as a Fellow of the American Institute for
Medical and Biological Engineering in 2001; the Abraham M. Max Distinguished Professor Award from the
Purdue School of Engineering and Technology in 2006; and being named a Chancellor’s Professor at IUPUI in
2008. He also won numerous grants from the National Institutes of Health and served as an expert consultant
for many agencies including the National Institutes of Health, National Science Foundation, National Research
Council, National Aeronautics and Space Administration, Food and Drug Administration, Canadian Institutes
of Health Research, Swiss National Science Foundation, Austrian Science Fund, Israel Science Foundation
and the Wellcome Trust.
Throughout his career, Dr. Turner showed dedication to the training of young engineers and scientists at
all levels. Many of these individuals were awarded prestigious young investigator awards while under Dr.
Turner’s tutelage and have since gone on to successful careers in academia and industry.
Dr. Turner was one of the world’s leaders in bone biomechanics research. He was a distinguished scientist
and engineer, teacher, colleague, mentor, and friend, and he will be sorely missed.
A funeral service for Dr. Turner was held on July 20th at the Second Presbyterian Church in Indianapolis.
To honor his memory, the family would like contributions to be made out to the Charles H. Turner Young
Investigator Bone Research Award. This award will be presented annually to a pre-doctoral student or postdoctoral fellow on the IUPUI campus who will present their bone-related research at an annual meeting.
Donations can be made out to Indiana University Foundation-Charles H. Turner Young Investigator Bone
Research Award and sent to Indiana University Foundation, P.O. Box 660245, Indianapolis, IN 46266-0245
using the enclosed donation card. If you would like to make a donation using a credit card please visit the
following secure website: www.medgifts.iu.edu/tribute.
22
Volume 4 – 2010
Opportunity for Financial Support of the IU Residency Program
Arthroscopy Skills Trainer (ArthroSim)
Residents and residency programs today face challenges which we never imagined, from mastering the exploding
knowledge in our field to increasing regulatory burdens from government and society. As if learning to do a good
history and physical exam weren’t hard enough, the incorporation of rapidly changing technologies into orthopaedic
practice and training is a constant struggle, and makes achieving competence a moving target. It is increasingly
expensive to provide training, and, at the same time, resources to provide the training are being squeezed tighter
and tighter.
Because we believe all orthopaedic surgeons share an interest in, and commitment to training the next generation
of our profession, we increasingly turn to our alumni and friends who may not be in full time academic practice to
help with this important activity. Many of our local alumni provide career mentoring, clinical rotations, research
opportunities, and participate in selection of students for residency positions. Likewise, faculty and alumni have
been very generous in providing philanthropic financial support to help with the increasing costs of providing a first
rate education to IU’s current orthopaedic residents. Dozens of alumni and faculty responded to our fund-raising
project two years ago, and we were able to open the George Rapp Orthopaedic Library and Media Center for
orthopaedic residents to bring state-of-the-art computer learning resources to our residency training program.
After many years of development, there is now a useful and realistic surgical simulator for arthroscopic training.
You may have read about this in the October 2009 AAOS NOW (http://www.aaos.org/news/aaosnow/oct09/cover2.
asp). ArthroSim is the result of collaboration between the American Academy of Orthopaedic Surgeons (AAOS),
the Arthroscopy Association of North America (AANA), the American Board of Orthopaedic Surgeons (ABOS)
and Touch of Life Technologies (ToLTech). Obtaining an arthroscopy simulator would facilitate the training of our
residents and keep IU Orthopaedics at the forefront of residency training, It also fits in well with the IU School of
Medicine’s new simulation center, one of the areas in which IU SOM is a true leader in medical education. The goal
of this new campaign is to bring our orthopaedic alumni together to raise funds for the purchase of the arthroscopy
simulator. If you have any questions about this project or the equipment, please do not hesitate to contact Dr. Anglen or any of the current Orthopaedic faculty.
We realize that times are tight
for everyone, however we would
hope that all of you appreciate
the importance your orthopaedic
residency training played in your
own success and ability to provide
outstanding care to your patients. I
hope you will join with your fellow
IU Ortho classmates and support this
campaign. We are asking our alumni
who are interested in advancing
the training of current orthopaedic
residents to donate to this project
through the IU Foundation. A
donation card is enclosed in this
Journal for your ease in making a
tax-deductible donation. Thank you
in advance for your support of this
project.
23
Volume 4 – 2010
Picnic to Welcome New Residents
Residents, Drs. Jon Wilhite,
Justin W. Miller, and Larry
Martin enjoying the picnic
Dr. Jeff Anglen enjoying
conversation with Meredith Hole,
Department Administrator,
and Dr. Bill Capello, Professor
Emeritus, at the annual summer
picnic
Anglen Residence
Hostess, Diane Anglen (standing)
with Dr. and Mrs. Mark Webster
Indiana Alumni Reception – AAOS Annual Meeting
Dr. Gary Moore (class of
1985), Dr. Rick Eaton (class
of 1983), Dr. Mark O’Meara
(class of 1982) reminisce at
the Indiana Alumni Reception
at the annual AAOS meeting
New Orleans
Dr. Wes Mesko (class of 1986)
in discussion with Dr. Jeff
Anglen at the reception
Dr. David Foulk and his wife,
Mary, with Dr. Matt Welsch
and his wife, Tammy meet
in their first year as resident
alumni (class of 2009)
24
Dr. Jerry Mackel (class of 1974) and his
wife, Dr. Barry Callahan (class of 1995) and
his wife, with Pat Price from the Indiana
Orthopaedic Society
Volume 4 – 2010
Garceau-Wray
University Place Conference Center
Dr. Christine Caltoum with speaker, Dr. Matt Dobbs from
Washington University
Dr. Kirk Reichard, PGY-5 resident, receiving the George
Alavanja award for Orthopaedic Professionalism and
Fellowship from Dr. Anglen
Dr. Jeff Anglen with Dr. Twee Do, pediatric specialist
and speaker at the Lindseth Lectureship
Residents, Drs. Chad Turner and Matt Abbott, chat with
Ryan Elpers, Stryker Rep, in the vendor’s area during a
break in the meetings
Dr. Richard Lindseth, speaker, Dr. Scott Mubarek from
the University of California, San Diego, and Dr. Jeff
Anglen
Lindseth Lectureship
Dr. Jon Wilhite, PGY-4 resident, receiving the Best
Resident Research Paper taward from Dr. Anglen
University Place Conference Center
25
Diane Anglen, Dr. Brian Mullis, April Sasso, Dr. Rick Sasso,
and Dr. Anglen at the annual holiday party
Volume 4 – 2010
Dr. Larry Martin, PGY-5 resident with his wife, Jermeliah
Holiday Party
Columbia Club
Dr. Kirk Reichard, PGY-5 resident, with his wife, Julie, and
baby daughter, Emma, Dr. Joe Bellamy, PGY-4 resident, and Dr.
Susan McDowell, PGY-3 resident
Dr. Chris Vincent, PGY-2 resident, and his wife, Jenni, with Dr.
Justin A. Miller, PGY-4 resident, and his wife, Meredith enjoying
the holiday party
Dr. Christine Caltoum arriving at the party
26
Volume 4 – 2010
Residency Program Alumni
Class of 1974
Colin W Hamilton, MD
Jerry L Mackel, MD
Class of 1956
Joseph C Randolph, MD
Robert J. Burkle, MD
Thomas W Marshall, MD
Class of 1958
Class of 1975
Gerald H. Weiner, MD
Ronald G Bennett, MD
Kenneth L Bussey, MD
Class of 1961
Ronald G. Kleopfer, MD (deceased) Milton R Carlson, MD
William H Couch, MD
Class of 1962
Robert L Forste Jr, MD
John M Miller, MD
Alfred E Kristensen, MD
George F Rapp, MD
Class of 1976
John G Suelzer, MD
James E. Albright, MD
Class of 1963
James R. Dashiell, MD
Donald F Hodurski, MD
Alois E Gibson, MD
John L Reynolds, MD
Class of 1964
Peter C. Weber, MD
Walter E Badenhausen, MD
Class of 1977
Ronald M Gilbert, MD
Robert T Clayton, MD
Class of 1965
Charles E Jordan, MD
William O Irvine, MD
Stephen G Powell, MD
Wilbur G Sandbulte, MD
Class of 1967
John F Showalter, MD
Peter C Boylan, MD
Leo Stelzer, Jr., MD
Class of 1968
Class of 1978
Steven R Glock, MD
David L Bankoff, MD
George E Reisdorf, MD
Edward Dykstra, MD
James W Strickland, MD
Philip M Faris, MD
Class of 1969
James Heinrich, MD
Philip H Ireland, MD
Bennett J. Cremer, MD
David F Mackel, MD
Ronald P Pavelka, MD
David A Tillema, MD
Class of 1979
Larry T Johnson, MD
Class of 1970
Philip W Pryor, MD
Wheeler T Daniels, MD
Theodore L Stringer, MD
G Paul DeRosa, MD
Terry R Trammell, MD
William J Sabo, MD
Class of 1980
Class of 1971
Michael M Durkee, MD
William A Atz, MD
James P Pemberton, MD
Kyu Sop Cho, MD
Class of 1981
Pedro Musa-Ris, MD
George W Lane, MD
Keith D Sheffer, MD
K Donald Shelbourne, MD
Willard G Yergler, MD
Franklin D Wilson, MD
Class of 1972
David A Yngve, MD
Anthony J Arnold, MD
Class of 1982
Robert E Cravens, MD
John G Crane, MD
Alan J Habansky, MD
Eric S Leaming, MD
Charles J Holland, MD
Mohammed R Nekoomaram, MD
James B Steichen, MD
Mark T. O’Meara, MD
John P. Vincent, MD
Dennis C Stepro, MD
Class of 1973
Class of 1983
John Howard Avery, MD
Karen S Duane, MD
John M Gossard, MD
Richard W Eaton, MD
John C Klein, MD
Gary W Misamore, MD
Robert L Thornberry, MD
William B LaSalle, MD
Thomas M Trancik, MD
Wade Rademacher, MD
Class of 1955
Edward V Schaffer, MD
Class of 1984
Steven K Ahlfeld, MD
Frank Johnson, Jr., MD
John K Schneider, MD
Christopher Stack, MD
Phillip L Stiver, MD
Class of 1993
Paul M Keller, MD
Michael L Kramer, MD
Daniel E Lehman, MD
Lynn M. Nelson, MD
Peter Sallay, MD
Class of 2002
Robert O Anderson, MD
Timothy G Berney, MD
Joseph G Jerman, MD
Chad E Mathis, MD
Lance A Rettig, MD
Class of 1985
John M Ambrosia, MD
Louis Angelicchio, MD
Vincent L. Fragomeni, MD
John O. Grimm, MD
Gary R Moore, MD
Class of 1994
Karl M Baird M.D.
David A Goertzen, MD
Stephen L Kollias, MD
Scott A Lintner, MD
Dean W Ziegler, MD
Class of 2003
Cary M Guse, MD
Daniel W Hanson, MD
Adelbert (AJ) J Mencias, MD
Mark C Page, MD
Todd R Wurth, MD
Class of 1986
Jack Farr II, MD
Michael S Green, MD
J Wesley Mesko, MD
Richard D Schroeder, MD
Charles D Van Meter, MD
Class of 1995
Barry S Callahan, MD
Carey A Clark, III MD
James E Goris, MD
Kosmas J Kayes, MD
John I Williams, MD
Class of 2004
Kevin E Julian, MD
Aaron LeGrand, MD
Kurt R Martin, MD
John T Pinnello, MD
Timothy L Walker, MD
Class of 1987
Joseph Baele, MD
Richard G Buch, MD
Robert A Czarkowski, MD
David A Fisher, MD
Donna P Phillips, MD
Class of 1988
Frederick E Benedict, MD
Gregory Graziano, MD
Michael F Kaveney, MD
Delwin E Quenzer, MD
H Jeffery Whitaker, MD
Class of 1989
Andrew Combs, MD
P Kevin Gerth, MD
Robert J Huler, MD
Class of 1990
Jeffrey A Clingman, MD
Dean C Maar, MD
Keith A Miller, MD
Richard Mullins, MD
William B Rozzi, MD
Carlos K Woodward, MD
Class of 1996
James S Kapotas, MD
Karen J McRae, MD
P Andrew Puckett, MD
Nirmal (Nimu) K Surtani, MD
Peter Tang, MD
Class of 1997
Joseph F Bellflower, MD
Thomas W Kiesler, MD
Scott A Magnes, MD
Paul S Nourbash, MD
James R Post, MD
Class of 1998
Rick Ahmad, MD
William P Didelot, MD
Jarvis Earl, MD
David B Fulton, MD
Thomas J Puschak, MD
Class of 1999
Vivek Agrawal, MD
Dale Dellacqua, MD
Mark B Durbin, MD
Colin G Sherrill, MD
Marshall L Trusler, MD
Class of 1991
Mark J Conklin, MD
Steven E Fisher, MD
Gregory T Hardin, MD
Bruce T Rougraff, MD
Jeffrey D Webster, MD
Class of 2000
George Alavanja, MD
Patrick K Denton, MD
Brett F Gemlick, MD
Steven B Smith, MD
Anton A. Thompkins, MD
Class of 1992
David Brokaw, MD
Richard V Davis, MD
Norman Mindrebo, MD
Jonathan H Phillips, MD
John C Pritchard, MD
Class of 2001
Jamie Kay, MD
Euby Kerr, MD
Kevin E Klingele, MD
Christopher R Price, MD
Kirnjot (KJ) Singh, M.D.
27
Class of 2005
Lonnie D Davis, MD
Jedediah W Jones, MD
Michael J Sukay, MD
Marcus A. Thorne, MD
Class of 2006
C Noel Henley, MD
Ari J Kaz, MD
Brian J. Kerr, MD
G. Peter Maiers, MD
Aaron J Mast, MD
Alex Meyers, MD
Class of 2007
Brady P. Barker, MD
Padraic Obma, MD
Michael J. Rusnak, MD
Bret W. Winter, MD
Jeffrey Wu, MD
Class of 2008
Ben J. Garrido, MD
Sean M. Garringer, MD
Kevin J. Lemme, MD
John W. Powell, MD
Class of 2009
Gregory Dikos, MD
David Foulk, MD
Karl Shively, MD
Matthew Welsch, MD
Ripley Worman, MD
Class of 2010
Megan Brady, MD
Conor Dwyer, MD
Larry Martin, Jr, MD
Justin W Miller, MD
A Kirk Reichard, MD
Volume 4 – 2010
Alumni News
Class of 1956
Robert J. Burkle, M.D. is practicing as a board-certified orthopaedic surgeon and is an active staff member at Terre Haute Regional
Hospital in Terre Haute, IN. He also serves as courtesy staff at
Union Hospital in Terre Haute and at Greene County Hospital in
Linton, IN. He is an active member of the Vigo Medical Society,
ISMA, AMA, Indiana Bone & Joint Club, and the Indiana Orthopaedic Society. He has 5 grown children and 7 grandchildren.
Class of 1961
Ronald G. Kleopfer, MD, died 7-22-09 in Cody, Wyoming at the
age of 79.
Class of 1970
G. Paul DeRosa, MD has retired from operative orthopaedics but
continues to be a consultant to the ABOS as Executive Director
Emeritus. He is also Emeritus Professor of Orthopaedics at Duke
University and maintains a consultant firm for orthopaedic graduate medical education, primarily for programs that have difficulties
with the ACGME. He and his wife, Mary Ann, live in Durham, NC,
and are busy with a growing family. Their son, James and his wife,
Molli, are expecting their first child in January and that will be the
13th grandchild!
He has three grown daughters – Rachel, who is an Emergency
Medicine physician in New Hampshire; Sarah, who is an archaeologist with the National Forest Service in New Hampshire; and Laura,
who is a professor of marine biology presently working in Woods
Hole, Mass. He and his wife. Cheryl, live in Geneva, New York.
Class of 1986
Wes Mesko, MD sent the following in response to our request for
alumni news:
Thanks to Indiana University department of Orthopedics for
reinstating me as a 1986 alumni in this year’s edition (Editor’s note:
Sorry, Wes). I was encouraged when Judy told me that I was not
the only person who noticed I was not in the list. I know I learned
my lesson to never be late in sending my annual donation to the
Department again, and I never again will throw away an unopened
letter from IU. It took me six months to convince the hospital at
re-credentialing time that I had, indeed, finished an orthopedic residency. Thankfully, all is well now.
Judy asked me for a brief profile. As the years pass, my gratitude increases toward Indiana University Department of Orthopedic
Surgery with its attending surgeons, staff, nurses, and fellow residents who gave me the opportunity to train to become an Orthopedic Surgeon. I am especially grateful to Bill Capello and Dave Heck
who let me take a 2nd bite at the apple of training to be one of his
first total joint fellows after I had completed my HPSP pay back to
the Air Force.
Now in my 21st year in Lansing, Michigan, I find my occupation has been a most enjoyable and rewarding ride. Dave Heck’s
role model for data collection motivated me from Day #1 to create a
personal registry that now includes over 8000 joints. I was selected
this year to be a board member of the American Joint Replacement
Registry (AJRR) to get America on board in the vital area of an
implant registry. International medicine has remained a vital part
of my career, as I have participated in providing orthopedic care in
short-term mission trips to Haiti, Nicaragua, Vietnam, and Kenya.
I am grateful for the multi-year donations of total hip and knee implants and instrumentation from the Stryker Corporation, as I have
led annual week-long teams to Tenwek Hospital in Kenya to do over
60 joints in the last 4 years.
G. Paul DeRosa and family at his 70th birthday party
Class of 1977
Charles E Jordan, MD retired from active orthopaedic surgery
practice in 2004, sold his office building, and now does part-time
Independent Medical Examinations. This allows plenty of time for
travel and his passport is nearly full with trips to China, Africa, India, Egypt, Russia, Germany, France, Switzerland, England, Peru,
Ecuador, Costa Rica, Netherlands, Scandinavia, Turkey, Greece, the
Caribbean and all over the US and Canada.
Chuck and Cheryl Jordan traveled to Africa, France, and China in
the past year.
This photo was taken by Wes Mesko’s son, Daniel, from about 10
yards away in a safari vehicle – with the driver ready to hit the gas
should the lions decide we looked like we’d make a good meal.
28
Volume 4 – 2010
Alumni News (continued)
to work at ‘Double Harvest’, an agricultural outreach in Haiti that also
supported two operating suites.
Dr. Mindrebo is the father of four students – one an undergraduate, two graduate students, and one who just started medical school
at IU this fall. He is also a grandfather of two. Working in underserved areas has become part of the children’s lives and their
vocational goals.
Class of 2001
Kevin Klingele, MD has been the attending surgeon at Nationwide
Children’s Hospital in…since 2002 and is currently the Program
Director for Orthopaedic Education and Clinical Research and
Surgical Director of Sports Medicine. He and his wife, Molly, have four
children: Nathan (8), Andrew (6), Luke (4), and Emma (2). Kevin’s
email address is: Kevin.Kingele@nationwhidechildrens.org.
Class of 2007
Michael Rusnak, MD is doing orthopaedic trauma in Fort Collins, Colorado, with the Orthopaedic Center of the Rockies.
Jeff Wu, M.D. is practicing at the Cleveland Clinic in Florida and recently married his wife, Melissa, a former staff member at Riley Hospital, in Maui.
This was our team in from Tenwek hospital in Bomet, Kenya in May,
2009 where we did 18 joints in a 4-day stint. Standing - Nathan
Mesko (MD); Viki Watkins (Scrub Tech); Meshack (RN); Daniel
Mesko (Med Student); Elliot (Med Student); David (Anesthetist);
Kneeling - J. Wesley Mesko (MD); Paul (Anesthetist).
My wife, Kathy, and I have been blessed with good health, and have
enjoyed seeing our three sons grow up - one in Orthopedic Residency,
one in Med School contemplating Orthopedic Surgery, and #3 finishing
college with a business degree bound and determined to maneuver himself into a position to make the rules of how his brothers will get paid.
I thank Judy for the invitation for a brief Bio, and look forward to
reading others in the future. In reality, I want to know if Mike Green and
Rich Schroder of the class of 1986 are still alive and well, about whom
I have not heard any reliable news and precious little rumors since we
finished. I nominate both of them to be featured in the next edition.
Class of 1992
Norman Mindrebo, MD started his practice, New Hope Orthopaedics
and Sports Medicine in Indianapolis in 1998. His undergraduate studies
in third world development and his deep interest in world events empowered he and his wife to travel to Haiti following the recent earthquake
Jeff and Melissa Wu at their wedding this past year in Maui
Norm Mindrebo with colleagues in Haiti following the earthquake
29
The Alumni News has been a popular section in the IOJ, but we need
you to provide us with the content each year. If you’d like to report some
news, personal or professional, we’d love to publish your info next year.
If you notice that you or any of your classmates’ names are missing from
our alumni list, let us know as well. Please email Donna Roberts (danders@iupui.edu) where you’re working, any awards you’ve won, how
many kids you have, any interesting travels, or anything else you think
your fellow alumni would be interested in reading about. Don’t forget
to attach a photo or two. Thanks!!!
Volume 4 – 2010
An Invitation To Get Involved
I recently came across the following Native American proverb:
“Tell me and I’ll forget. Show me, and I may not remember. Involve me, and I’ll
understand.”
The proverb applies to so many life experiences including family, work, involvement
in the community and our professional organizations. How many of us take the time to
really get involved? I know that many of you who are still practicing in Indiana have been
members of the Indiana Orthopaedic Society and have attended our annual meetings
held throughout the state. I also know that during the past 54 years of its existence several
have dropped their membership due to lack of interest or retirement. Also a few have
begged financial difficulties believing that the dues of $250 is excessive and more than
they are willing pay (IOS has not raised dues in 17 years). I encourage you to return to our society and become
members of IOS, and above all, participate in our annual meetings.
During the past three years attendance at our annual meetings has increased to 120 attendees on average which
is roughly one third of our membership. According to statistics that is a significant number of participants. Our
exhibitors have contributed over $55,000 annually to support IOS through meeting exhibits, grants and sponsorships.
Our recent April meeting in Indianapolis at the Conrad Hotel was another successful event which included a reception
in the new Lucas Oil Stadium Quarterback Club. Our Keynote speakers included Butler University basketball coach
Brad Stevens, son of orthopedist Mark Stevens. He spoke to a standing room only crowd and his message was one
of empowerment, involvement, and commitment.
U.S. Senator John Barrasso, also a keynote speaker from Casper, Wyoming, where he
practiced for 24 years as an orthopedic surgeon, and elected to the Senate in 2008, shared his
prospective on Washington and the Health Care Reform was enlightening and surprising.
Here is a brief look at what IOS has to offer.
IOS has introduced a recent technologic improvement to our meetings using Audience
Response systems. And to make our meetings more appealing to all specialties we have added
breakout sessions targeting subspecialties such as Total Joint, Sports Medicine, Trauma, Spine
and Hand. New this year was a breakout session pertaining to Medical Legal Issues which will
continue to be a part of our programming.
Annual Meeting – Save The Date May 13-14, 2011
Join us May 13-14, 2011, at the French Lick Resort and West Baden Hotel. Our Presidential
speakers are Dr. James Andrews of Birmingham, Alabama, and Dr. Richard J. Hawkins of
Greenville, South Carolina.
Dr. Andrews is Senior Orthopaedic Consultant for the Washington Redskins football
team and Medical Director for the Tampa Bay Rays baseball team. He is the team physician
for the Birmingham Barons Double A baseball team, an affiliate of the Chicago White Sox.
Dr. Andrews is also the Co-Medical Director of the Ladies Professional Golf Association.
Previously, Dr. Andrews has been a member of the Sports Medicine Committee affiliated with
the United States Olympic Committee . He has served on the NCAA Competitive Safeguards in Medical Aspects
of Sports Committee.
Dr. Richard J. Hawkins practices orthopedic surgery in Greenville, South Carolina and Spartanburg, South
Carolina. Dr. Hawkins specializes in shoulder, elbow and knee reconstructive surgery and sports medicine. A
renowned shoulder surgeon, he has authored textbooks on shoulder surgery that are used throughout the world. Dr.
Hawkins is a founding member of the American Shoulder and Elbow Surgeons Society and is team physician for
the Denver Broncos and the Colorado Rockies. He also is a clinical professor at the University of South Carolina
School of Medicine.
30
Volume 4 – 2010
An Invitation To Get Involved (continued)
IOS President Dr. Gary Misamore and his committee are developing plans for a great
meeting you do not want to miss.
IOS Leadership: IOS Board members include President Gary Misamore, Vice President Dan
Lehmen, Secretary Treasurer, Peter Maiers, Membership Chairman Joe Randolph, Members at
Large, Chris LaSalle, Scott Karr and Molly Weiss, BOC representatives, Dave Bankoff and Eric
Monesmith, Immediate Past President Tom Woo, Legislative Chair Bob Hagen, Jeff Anglen, IU
Program Chair, and Executive Director Patricia K Price, a recipient of the AAOS 2009 Executive
Director of the Year. This honor acknowledges the excellency of our programs and is a primary
reason to join and actively participate in our society.
IOS PAC: The state PAC focuses on those in the House and Senate who have significant roles in health related
issues. Your PAC money plays an important part in raising awareness about the issues important to orthopaedic
surgeons around the state. PAC donations are $100.
IOS Foundation: The Foundation is an independent organization that raises funds to support resident education
and involvement in related activities including participation at the National Orthopaedic Leadership Conference.
Grants have also been made to Special Olympics, IU Alumni “Project Operation” and the Indiana Chapter of
Arthritis Foundation, plus a Orthopaedic Resident 2009 Mission trip to Kenya. Foundation contributions are $100.
Donations over $100 are appreciated.
IOSociety.org: IOS web site has updated information regarding board members, annual meeting information,
membership applications, a career center, membership dues a newsletter and a variety of interesting topics. Just log
on and search our site for other hot links to the AAOS and our popular “Contact Congress” tab.
Physician Assistants and Nurse Practioners: IOS has created a new membership category “associate
membership” for orthopaedic PAs and NPs. We encourage your PAs and NPs to attend our annual meeting and
become active members. At the 2011 meeting, we will be inviting Practice Administrators.
IOS NEWS Publication
Our newsletter, published three times a year, incorporates items related to Board of Councilors activities,
meeting updates and medical-legal issues.
Get Involved!
On behalf of the IOS Board of Directors I invite you to become an active member of IOS, if you have been a
previous member in good standing consider rejoining. Applications are available on our web site iosociety.org.
The truth of the proverb is as you get involved you will understand the importance of IOS membership, the
importance of time commitment and energy to help us achieve our goals.
• To remain as politically unbiased as possible while still supporting those issues important to the Indiana
Orthopaedic Society membership and our patients.
• To enhance our commitment to stay abreast of current information and advancements in the dynamic practice
of modern orthopaedic surgery.
• To be part of a proactive cutting-edge society to preserve our optimal environment in the practice of
Orthopaedics.
• To address those issues pertinent to the practice of Orthopaedics.
• To achieve our vision to be a collegial group of orthopaedic surgeons with united voice for quality orthopaedic
care.
See you in French Lick!!
Patricia K. Price
Executive Director -Indiana Orthopaedic Society
31
Volume 4 – 2010
Adult Trauma: Getting Through the Night
An Instructional Course Lecture, American Academy of Orthopaedic Surgeons
By Andrew H. Schmidt, MD, Jeffrey Anglen, MD, Arvind D. Nana, MD, and Thomas F. Varecka, MD
© 2010 The Journal of Bone and Joint Surgery, Inc. Reprinted from the Journal of
Bone and Joint Surgery American, Volume 92, pp. 490-505, with permission.
There has been a dramatic change in the approach to the treatment of acute musculoskeletal injuries over the past decade. The
previous emphasis on socalled ‘‘early total care,’’ which advocated
immediate definitive repair of all injuries, has shifted to an approach emphasizing ‘‘damage control orthopaedics’’ for a multiply
injured patient. In this new paradigm, definitive repair of fractures
is delayed until the patient is stabilized physiologically, associated
soft-tissue injuries (if present) have healed, and optimum resources
are available. However, there remain situations in which immediate treatment may be needed, such as in a patient with a pelvic ring
injury and hemodynamic instability, a compartment syndrome, or
an irreducible joint dislocation with associated neurovascular compromise. In these circumstances, there may not be time to safely
transfer the patient to a specialized center, and emergent treatment
directed at the specific problem must be provided. Emergent treatment of open fractures, compartment syndrome, and hemodynamic
instability in a patient with a pelvic fracture as well as damage control in multiply injured patients should be understood by all who
treat musculoskeletal injuries. Finally, a less-often discussed but no
less important aspect of surgical care that may affect initial treatment decisions and outcome is sleep deprivation and fatigue of the
members of the surgical team.
Open Fractures
Traditionally, the initial management of open fracture wounds
was débridement within six hours after the injury to prevent infection. That guideline was based on animal experiments performed in
the 1890s and is not supported by modern human clinical studies.
The LEAP study, a prospective multicenter investigation of severe
open lower-extremity fractures, showed no relationship between
the time from the injury to the surgery and subsequent infection1.
Multiple retrospective series of open fractures have also failed to
support the ‘‘six-hour rule,’’2-4 and recent literature reviews have
revealed scant support for emergency surgical débridement of open
fractures5,6. The current consensus favors prudent early surgery
within the first twenty-four hours.
The initial surgical procedure for an open fracture is débridement and irrigation of the open wound. The purpose of débridement
is to remove foreign material, contaminating pathogens, and devitalized host tissue. The principles of the surgical procedure include (1)
extension of the traumatic wound longitudinally, with the surgeon
being careful to consider options for future closure and proceeding
systematically through each tissue layer from superficial to deep;
(2) careful inspection of surfaces, with preservation of critical tissue such as skin and articular surfaces when possible; and (3) thorough removal of foreign material and dead tissue. Doing this well
requires attention, patience, and surgical judgment. Tissue viability
is dynamic, and initially it is not possible to determine precisely
which tissue will survive. Usually, repeat examination is necessary
to ensure adequate removal of dead tissue. Open wounds do not necessarily adequately decompress tissue compartments, and compartment syndrome is a risk with many high-energy fractures. Irrigation
of open fracture wounds cleans the wound by removing additional
debris and lowering the bacterial load. The irrigation volume, pressure, mode of delivery, and additives are all of potential importance,
but little information is available about these parameters. Animal
studies suggest that increasing the volume of fluid improves removal of particulate debris and bacteria up to a point7, but there are
no clear clinical guidelines regarding this parameter. Although there
are no specific data to support this recommendation, we suggest an
empiric protocol of using 9 L (three 3-L bags) of fluid for Gustilo
type-III open fracture wounds, 6 L (two bags) for a type-II wound,
and 3 L for a type-I wound. High-pressure irrigation has been shown
to drive contamination into the tissue, damage bone, delay healing,
and impair infection resistance in animal models and in vitro experiments8. Pulsatile delivery of fluid has no proven advantage9.
Irrigation-fluid additives have included antiseptics, antibiotics, and
soaps. Antiseptics such as Betadine (povidoneiodine) or hydrogen
peroxide are toxic to host immune cells and should not be used;
antibiotics are of no proven value in open fracture wounds. Soap
solutions help to remove dirt and bacteria through disruption of the
hydrophobic and electrostatic forces that bind them to surfaces. In
one prospective clinical study, soap solution was compared with antibiotic solution for open fracture wounds and soap was found to
have an advantage10.
Traditional teaching dictates that open fracture wounds should
not be closed; however, low-energy wounds that have been adequately débrided and cleaned can be closed safely, if closure can
be done without tension. If these conditions cannot be met, the fracture wound should be covered, within a week, by delayed primary
closure, skin-grafting, rotational flaps, or free tissue transfer. During the time before definitive coverage, the wound tissues should
be protected from desiccation with appropriate dressing techniques.
Two methods in use are the antibiotic bead-pouch technique and the
Vacuum Assisted Closure device (wound V.A.C.; KCI, San Antonio, Texas). The antibiotic bead-pouch technique is a simple method
in which handmade polymethylmethacrylate beads are placed on a
strand of heavy suture or 18-gauge surgical wire and placed into the
wound; the wound is covered with an occlusive adhesive barrier
such as OPSITE Post-Op (Smith and Nephew, Memphis, Tennessee) or Ioban (3M, St. Paul, Minnesota).
Stabilizing open fractures promotes healing and infection
resistance. The choice and timing of fixation strategy depends on
the characteristics of the patient, the injury, the surgeon, and the
operating room resources. In general, immediate plate fixation of
open fractures of the lower extremity should be avoided because
of an increased risk of infection, although immediate plate fixation
32
Volume 4 – 2010
Adult Trauma: Getting Through the Night (continued)
of upperextremity open fractures can often be done safely. Acute
intramedullary nail fixation of open fractures of the lower extremity
can be acceptable, provided that a clean wound with viable bone and
soft tissues is achieved with irrigation and débridement. Temporary
external fixation, often spanning injured joints, is a useful strategy to
protect soft tissues, allow adequate time for planning, and avoid performing complex procedures in the middle of the night. When done
for a severely, multiply injured patient with unresolved physiologic
issues, this strategy is known as ‘‘damage control orthopaedics.’’11
Antibiotic treatment is one of the most important aspects of
open fracture care. Traditionally, cephalosporin antibiotics were
used for three days. For type-III open fractures, aminoglycosides
were added and treatment was extended to five days. It has been
suggested that penicillin be added to the regimen for agricultural
injuries with soil contamination because of the risk of clostridial
infection. However, these recommendations are based on poorly
designed studies done more than twenty years ago12,13. More recent
data support a shorter duration (twenty-four to forty-eight hours)
of first-generation cephalosporin antibiotics and no additional drugs
for coverage of gramnegative or clostridial organisms14,15.
Compartment Syndrome
Acute compartment syndrome can complicate any extremity
injury, but it is most common in patients with tibial fracture, especially in men under the age of thirty-five years16. Patients with forearm fracture are the second most common group. Although acute
compartment syndrome occurs as a result of the initial injury, it is
important to remember that acute surgical stabilization can increase
the risk of the syndrome17,18. The diagnosis can be difficult, and it
should be considered for all patients with an extremity injury. Acute
compartment syndrome is a surgical emergency because a delay in
treatment may be associated with substantial short and long-term
morbidity related to the degree of muscle necrosis that occurs. In
the early phase, morbidity is related to potential renal impairment
from rhabdomyolysis, whereas long-term disability is related to
the degree of functional impairment caused by muscle fibrosis and
neural dysfunction. Not surprisingly, delayed diagnosis of acute
compartment syndrome is a common reason for litigation against
physicians19,20.
Clinical Diagnosis of Compartment Syndrome
Acute compartment syndrome is typically diagnosed on clinical grounds. The ‘‘classic’’ symptoms of acute compartment syndrome are known as the ‘‘five P’s’’—pain, pallor, pulselessness, paresthesia, and paralysis—but these are late findings. Escalating pain,
pain with passive stretch of the involved muscle, and numbness are
the clinical clues of an acute compartment syndrome. These criteria are subjective and may be attributed to the associated fracture.
This diminishes their diagnostic value. Avoiding regional anesthetic
blockade and patient-controlled analgesia, which can completely
mask the pain that occurs with acute compartment syndrome, is recommended21. Peripheral nerves are sensitive to ischemia; therefore,
hypoesthesia in the distribution innervated by a peripheral nerve located within the involved compartment is an important early finding
in acute compartment syndrome22,23. However, neurologic deficits
33
may be due to the initial trauma and are therefore not specific.
The variability in the clinical signs and symptoms of acute compartment syndrome makes the accuracy of clinical diagnosis poor,
and the sensitivity and positive predictive value of clinical findings
are low24. In contrast, the specificity and negative predictive value of
clinical signs are high, meaning that the absence of clinical findings
associated with compartment syndrome of the leg is more useful for
excluding the diagnosis than the presence of findings is for confirming the diagnosis24. Given the uncertainty in the clinical diagnosis
of acute compartment syndrome, a high index of suspicion must be
maintained when caring for patients at risk.
Measurement of Intramuscular Pressure
By definition, intramuscular pressure is elevated in cases of
acute compartment syndrome, but, because there is wide variation
in intramuscular pressure among patients with tibial fractures and
since many patients without compartment syndrome can have intramuscular pressures exceeding 30 mm Hg, the direct measurement
of intramuscular pressure is not diagnostic25. Intramuscular pressure
measurement is an adjunct to the clinical examination and is indicated for any patient with equivocal findings; no reliable diagnostic
threshold has yet been described26-28. Intramuscular pressure measurement is the sole means of diagnosis for patients for whom a clinical examination is not possible, such as those who are intoxicated
or have a head injury or those who are already intubated. Typically,
intramuscular pressure is measured in the anterior, lateral, and deep
posterior compartments of the leg with use of either a commercially
available device such as the Stryker Intra- Compartmental Pressure
Monitor System (Stryker, Kalamazoo, Michigan) or an arterial line
manometer. Both techniques have acceptable accuracy29. Intramuscular pressures vary within each compartment, with measurable differences occurring at distances as close as 5 cm from the site at
which the highest pressure was recorded30. Intramuscular pressures
are also influenced by the position of the adjacent joints31.
The most well-supported threshold for fasciotomy appears to
be a perfusion pressure of <30 mm Hg32-34. The perfusion pressure
(DP, or ‘‘delta P’’) is equal to the diastolic blood pressure minus
the intramuscular pressure. When the perfusion pressure is ‡30 mm
Hg, it is safe to assume that the patient does not have an acute compartment syndrome. Conversely, when DP is <30 mm Hg for a sustained period of time, compartment syndrome may be present and
fasciotomy is recommended.
To improve the diagnosis of compartment syndrome and eliminate the need to perform multiple serial intramuscular pressure measurements, continuous intramuscular pressure monitoring has been
advocated33,35. McQueen et al. demonstrated that continuous pressure monitoring of the anterior compartment of the leg in a cohort
of patients with a tibial fracture in whom a compartment syndrome
developed led to a marked reduction in the sequelae of acute compartment syndrome, presumably because the diagnosis was made
earlier33. One important benefit of continuous monitoring is that the
time trend of intramuscular pressure is an important variable that
cannot be assessed on the basis of a single measurement. Prayson et
al. reported that 53% of the patients in their series had at least one
intramuscular pressure measurement that was within 40 mm Hg of
Volume 4 – 2010
their mean arterial pressure (an alternative definition of a borderline perfusion pressure), yet none had signs of sequelae of compartment syndrome25. Thus, a rising or sustained elevated pressure (or
inadequate perfusion pressure) is a more important indication of an
acute compartment syndrome and a better indicator of the need for
fasciotomy than is a single pressure.
How to accurately assess perfusion pressure in patients who are
under anesthesia is not known.While a patient is under anesthesia,
the blood pressure may be artificially low, leading to an inaccurately
small perfusion pressure, and to unneeded surgery if that pressure
is used to decide whether a patient needs a fasciotomy. Kakar et al.
recorded blood pressures in a series of patients undergoing tibial
nail fixation36. Diastolic blood pressure during surgery was lower
than that either before or after surgery, but the postoperative diastolic blood pressure was predicted by the preoperative blood pressure. Therefore, a more accurate measurement of an anesthetized
patient’s perfusion pressure should be based on the preoperative
diastolic pressure rather than the intraoperative pressure. The only
caveat to this is that, if the patient is to remain under anesthesia for
some time, the intraoperative blood pressure should be used.
Surgical Treatment of Compartment Syndrome
Once identified, compartment syndrome must be treated with
prompt fasciotomy. Early diagnosis of acute compartment syndrome
and prompt fasciotomy have been shown to lead to more rapid union
and improved function in patients with a tibial fracture32,33. In contrast, if fasciotomy is done too late, the procedure may have little
benefit and may actually be harmful37. Fasciotomy that is performed
after myonecrosis has occurred exposes the necrotic tissue and
can lead to bacterial colonization and infection. Finkelstein et al.
reviewed the cases of five patients in whom fasciotomy had been
performed more than thirty-five hours after the injury. Of these five
patients, one died of multiple organ failure and the others had amputation of the limb37.
Technique of Fasciotomy
The fasciotomy is done by making a longitudinal skin and fascial incision over the entire compartment with release of all constricting tissues. An inadequate skin incision can contribute to persistent elevation of intramuscular pressure38. The precise incisions
to be made and the structures that require release vary depending
on the situation.
Two-incision fasciotomy of the leg: Fasciotomy of the leg can
be done safely and easily with use of two incisions: one lateral and
one medial. The anterior and lateral compartments are released
separately through the lateral incision. The superficial posterior
compartment may be released through either incision. The deep
posterior compartment is released through the medial incision. The
intervening skin flap is at risk for necrosis if there has been damage to the anterior tibial artery. Therefore, when the anterior tibial
artery is known to be or suspected of being injured, a singleincision
four-compartment release from a lateral approach is recommended.
To perform a two-incision fasciotomy, initially a lateral incision is
made midway between the fibula and the anterior crest of the tibia.
The skin is gently retracted anteriorly and posteriorly to expose the
fascia of the anterior and lateral compartments, respectively. The
lateral intermuscular septum that divides the anterior and lateral
compartments and the superficial peroneal nerve are identified.
The peroneal muscle fascia is usually released first. Finally, the anterior compartment fascia is completely released. Alternatively, the
fascia overlying one compartment can be released, followed by division of the intermuscular septum to decompress the other compartment. However, iatrogenic injury to the superficial peroneal nerve
may be more likely with this technique39. Next, the medial incision
is made 1 cm posterior to the posteromedial border of the tibia. The
saphenous vein and nerve should be identified. The fascia of the
gastrocnemius-soleus complex should be completely released. Distally, the soleus bridge (representing the condensation of the anterior and posterior investing fibers of the soleus muscle) should be
specifically released from the posterior aspect of the tibia in order
to completely decompress the flexor digitorum longus and tibialis
posterior muscles.
Single-incision fasciotomy of the leg: To perform a single-incision fasciotomy, a single lateral incision, extending from the neck of
the fibula to the lateral malleolus, is made. Fibulectomy is not necessary39. The anterior and lateral compartments are released in the
manner described for the two-incision fasciotomy. The superficial
posterior compartment (the gastrocnemius-soleus muscle complex)
is released by elevating the skin posteriorly. Finally, a parafibular
approach is used to decompress the deep posterior compartment.
The peroneal muscles are retracted anteriorly, and the dissection is
carried posteriorly to the fibula. With the lateral head of the gastrocnemiussoleus retracted posteriorly, the septum dividing the superficial and deep posterior compartments can be identified and released.
If access to the deep posterior compartment is difficult, a medial
incision can always be made as described above.
Upper-extremity fasciotomy: The muscles of the entire upper
extremity can be decompressed with use of an extended anterior
incision extending from the shoulder to the wrist. In the upper arm,
anterior release of the biceps and brachialis can be extended across
the elbow and incorporated into a volar fasciotomy of the forearm. In
turn, the volar forearm release can be extended into the palm of the
hand to release the median (carpal tunnel) and ulnar nerves (Guyon
canal). Beginning with the upper arm, an anterior incision is made
along the medial edge of the biceps. The fascia of the biceps and
underlying brachialis are released. The incision is extended across
the flexion crease of the elbow in a zigzag fashion in order to avoid
later contracture, and then it is continued distally along the volar
aspect of the forearm as needed. Although rarely necessary, the triceps can be decompressed with use of a separate posterior incision.
Adequate decompression of the forearm requires release of a number of potential sites of compression, including the lacertus fibrosus,
all muscle fascia, and the flexor retinaculum. First, the incision is
continued along the medial border of the mobile wad, consisting of
the brachioradialis and radial wrist extensors, which are released.
The fascia of the digital flexors, supinator, and pronator quadratus is
released as needed. Rarely, a separate dorsal forearm fasciotomy is
needed. Finally, a standard carpal tunnel release is performed at the
wrist, with the incision again crossing the wrist flexion crease in a
zigzag fashion to avoid contracture. Injury to the palmar cutaneous
branch of the median nerve must be avoided. If the hand is also involved, release of the thenar, hypothenar, and interosseous muscles
34
Volume 4 – 2010
of the hand is performed separately with use of longitudinal dorsal
incisions between the second and third metacarpals and between the
fourth and fifth metacarpals.
Management of fasciotomy wounds: An advance in the management of fasciotomy wounds is the wound V.A.C. device. When
applied at the time of fasciotomy, the wound V.A.C. device may
allow earlier closure of the fasciotomy site and a decreased need for
skingrafting40. Closure of the fasciotomy site before five days is not
recommended and can be associated with recurrent compartment
syndrome41. Skin-grafting is associated with fewer complications
than is either primary or delayed wound closure42.
Damage Control Orthopaedics
The understanding of the role of orthopaedic resuscitation in
the overall management of multiply injured patients has changed
dramatically in recent years. The potential benefits of optimal fracture care in this patient population include (1) facilitating overall
patient care, (2) controlling bleeding, (3) decreasing additional softtissue injury, (4) avoiding further activation of the systemic inflammatory response, (5) removal of devitalized tissue, (6) prevention of
ischemia/ reperfusion injury, and (7) pain relief.
Until recently, appropriate fracture care in a multiply injured
patient was considered to be fixation of all fractures as soon as possible. This was thought to decrease the inflammatory load through
stabilization of bone and soft tissue, and all long-bone fractures
were definitively stabilized within twenty-four hours (or as soon as
possible) so that the patient could be positioned upright for adequate
pulmonary toilet. The paradigm at the time was ‘‘This patient is too
sick not to be treated surgically.’’ In a landmark study, Bone et al.
showed that this type of management resulted in fewer days of ventilator treatment, fewer days in the intensive-care unit, and lower
prevalences of multiple organ failure and mortality43.
About fifteen years ago, published reports began to suggest
that, in some cases, this aggressive initial management might be
harmful44. The term ‘‘damage control’’ was originally coined by the
United States Navy to describe the repair of damaged sea vessels
in combat to allow continued use. An approach best described as
‘‘damage control surgery’’ was reported by Rotondo et al., who used
rapid but nondefinitive control of hemorrhage to avoid the lethal
triad of acidosis, hypothermia, and coagulopathy in patients exsanguinating from penetrating abdominal trauma45. In 1993, the report
by Pape et al. of increased pulmonary complications in multiply injured patients undergoing immediate femoral nailing44 ushered in
the era of ‘‘damage control orthopaedics,’’ and the new paradigm
is best described as ‘‘optimal surgery’’ rather than ‘‘maximal surgery.’’
In the past decade, substantial work has been done to define
which group of patients can be safely treated with maximal fixation
and which should have damage control surgery only. In general, the
early death of a multiply injured patient is caused by primary brain
injuries and major blood loss, whereas late death is due to secondary brain injury and host defense failure46. The first ‘‘hit’’ (initial
trauma) results in hypoxia, hypotension, organ and soft-tissue injuries, and fractures. The second and subsequent ‘‘hits’’ (surgical
procedures and sepsis) lead to hypoperfusion, hypoxia/ischemia,
reperfusion, blood loss due to acute endothelial injury, and tissue
35
damage causing local necrosis, inflammation, and acidosis. Any
type of surgical procedure that induces substantial bleeding and/or
soft-tissue damage can be sufficiently traumatic to the patient to represent a ‘‘second hit.’’
Damage control orthopaedics is defined as the provisional stabilization of musculoskeletal injuries in order to allow the patient’s
overall physiology to improve. The primary tactic of damage control orthopaedics is to use traction or external fixation as the means
of provisional stabilization. The purpose of damage control orthopaedics is to avoid the worsening of physiologic parameters related
to the second hit of a major orthopaedic procedure by delaying definitive fracture repair until the patient’s physiology is optimized.
In this approach, the focus is on controlling the bleeding, managing
the injuries to the soft tissues, and achieving provisional fracture
stability.
Pathophysiology of Trauma
Cytokines, leukocytes, the vascular endothelium, and endothelialleukocyte interactions are the key determinants of the response
to injury. Typical physiologic changes that occur after trauma are
increased capillary permeability in the lung, gut, blood vessels, and
muscle. The lung parenchyma is most affected in trauma patients.
The largest capillary bed in the body is found in the lung, and pulmonary edema is a frequent sign of increased pulmonary permeability. As is the case in the lung, increased permeability of the blood
vessels leads to movement of fluid into the third space. Increased tissue permeability also results in translocation of bacteria in the gut.
In muscle, edema and bleeding can lead to compartment syndrome.
The inflammatory response to injury (first hit or second hit)
includes the systemic inflammatory response syndrome, which is
mediated by proinflammatory cytokines, arachidonic acid metabolites, proteins of the acute phase/coagulation systems, complement
factors, and hormonal mediators. Systemic inflammatory response
syndrome can lead to adult respiratory distress syndrome and/or
multiple organ failure. Simultaneous with the onset of systemic
inflammatory response syndrome is the counter-regulatory anti-inflammatory response syndrome, which can cause immunosuppression and subsequent infection. The counter-regulatory antiinflammatory response syndrome is described as endothelial cell damage,
accumulation of leukocytes, disseminated intravascular coagulopathy, and microcirculatory imbalances that lead to apoptosis and necrosis of parenchymal cells.
Measurement of specific markers can help to quantify the inflammatory responses. These markers include base deficit or serum
lactate, soluble thrombomodulin, polymorphonuclear elastase, interleukin (IL)-6, IL-10, and human leukocyte antigen (HLA) DR
(Table 1). Genetic influences have also been shown to play a role
with IL-6, IL-10, tumor necrosis factor (TNF), and HLA-DR47. A
base deficit or elevated serum lactate level is considered evidence of
continued metabolic acidosis. A serum lactate level of >2.5 mmol/L
can indicate occult hypoperfusion and can be used to judge a patient’s suitability for surgery. Crowl et al. showed that, when a nail is
used to stabilize a femoral fracture within twenty-four hours after the
injury, there is a twofold higher incidence of postoperative complications if the serum lactate level is >2.5 mmol/L48. Four hours after
femoral nailing (with or without reaming), markers associated with
Volume 4 – 2010
Table 1. Specific Markers and Mediators of
Damage Control Surgery
Base deficit or serum lactate (hypovolemic shock)
Soluble thrombomodulin (endothelial injury)
Polymorphonuclear elastase (tissue injury)
Interleukin-6 (pro-inflammatory cytokine)
Interleukin-10 (anti-inflammatory cytokine)
Human leukocyte antigen DR (resistance to infection)
the systemic inflammatory response are elevated49. Waydhas et al.
demonstrated that patients with a high polymorphonuclear elastase
level combined with a high C-reactive protein level and thrombocytopenia have a 79% incidence of lung, liver, or kidney failure50.
IL-6 concentration has also been shown to be a reliable index of
the magnitude of injury (burden of trauma) and of the ‘‘second hit’’
produced by the surgical procedure49. If the initial IL-6 level is >500
pg/dL (>5 mg/L), then definitive surgery should be delayed for at
least four days after provisional stabilization surgery51. Patients with
a high Injury Severity Score52 have an elevated IL-6 level for more
than five days. The potent anti-inflammatory cytokine IL-10 also
inhibits TNF-a and IL-1 expression and negatively regulates HLADR expression. Giannoudis et al. showed that elevated initial and
persistently elevated IL-10 levels correlate with sepsis53. HLA-DR
is an indicator of resistance to infection and is expressed by circulating monocytes. It is required for antigen presentation and helper Tlymphocytes and thus plays a central role in the immune response to
infection. Diminished HLA-DR expression is associated with sepsis
and death54.
Timely analysis of specific markers and factors may not be
possible in many facilities. In the absence of precise biomarker data,
the orthopaedic surgeon may have to rely on physiologic and clinical parameters to guide decision-making (Table 2). The following
injuries are usually best managed with the damage control ortho-
paedic protocol: femoral shaft fracture in a multiply injured patient,
pelvic ring injuries with substantial hemorrhage, and polytrauma in
a geriatric patient. Pape et al. described the criteria for implementing
the damage control orthopaedic protocol to include a serum lactate
level of >2.5 mmol/L, a base excess of >8 mmol/L, a pH of <7.24,
a temperature of <35C, surgical time of more than ninety minutes,
coagulopathy, and transfusion of more than ten units of packed red
blood cells55. When damage control orthopaedic protocols are followed, initial stabilization of fractures is achieved with minimal
blood loss, fluid shifts, hypothermia, or prolonged surgical time.
Options for fracture stabilization in damage control orthopaedic
protocols include skeletal traction, splints or casts, intramedullary
nail fixation, conventional plates, minimally invasive plates, and
external fixation. External fixation is the preferred method of initial stabilization because it can be done quickly with minimal blood
loss. Nana and Kessinger showed that use of spanning external fixation for complex distal tibial fractures that are treated immediately
improves skin perfusion56.
After provisional stability has been obtained, definitive surgery
is considered only after the patient has been adequately resuscitated.
End points for resuscitation with use of damage control principles
are outlined in Table 3. A simplified guideline is to proceed with
definitive surgery when fluid balance is negative.
Hemodynamic Instability in Patients with a Pelvic
Ring Injury
Up to 40% of patients with an unstable pelvic ring injury die
from their injuries, and hemodynamic instability is the main predictor of death. The initial management of patients with a pelvic ring
injury, including the assessment and management of hemodynamic
instability and acute (rather than definitive) stabilization of the pelvic injury, is critical. There are several key points to remember:
1. Pelvic ring injuries are markers of violent injury and are associated with life-threatening hemorrhage and injuries to other organs and sites, including the abdominal viscera and genitourinary
system. It should not be assumed that the pelvis is the source of
bleeding in an unstable patient.
Table 2. Parameters to Consider When Deciding to Implement Damage Control Orthopaedic Protocol
Polytrauma with Injury Severity Score of >20 points and additional thoracic trauma (Abbreviated Injury Scale score83 of >2 points)
Polytrauma with abdominal and pelvic injuries and hemorrhagic shock (systolic blood pressure of <90 mm Hg)
Injury Severity Score of ≥40 points without additional thoracic injury
Initial pulmonary artery pressure of >24 mm Hg
Increased pulmonary artery pressure of >6 mm Hg during intramedullary nailing
Difficult resuscitation
Platelet count <90,000/μL (<90 109/L)
Hypothermia (e.g., temperature of <35˚C)
Transfusion of >10 units of blood
Bilateral lung contusion on initial chest radiograph
Multiple long-bone fractures and truncal injury
Prolonged duration of anticipated surgery (>90 min)
36
Volume 4 – 2010
2. Although the anatomic and mechanistic classifications of
pelvic ring injuries are useful, they are not perfectly predictive of
the risk of bleeding.
3. Pelvic ring compression with sheets is a simple and effective
treatment for immediate management of bleeding in patients with
an open-book injury.
4. The role of immediate angiography instead of operative exploration remains controversial and probably varies depending on
institutional resources and injury patterns.
5. The key to the correct initial assessment of a pelvic ring
injury is careful evaluation of the radiographs for evidence of deformity and instability.
Assessment of Pelvic Ring Injury
The physical examination of patients with a pelvic ring injury
is primarily aimed at defining the neurovascular status of the lower extremities. The motor function and the sensation in the lower
extremities should be documented. The examiner should look for
asymmetry and/or deformity of the iliac crest, limb-length inequality, and skin lesions (including any open wounds and areas of closed
degloving). Every patient should have a rectal examination, the
prostate should be examined in males, and the vagina should be examined in females, as lacerations in these locations may be the site
of an open pelvic fracture.
Standard imaging of the pelvic ring includes both plain radiographs and computed tomography scans. Radiographs should include anteroposterior, inlet, and outlet views. A cystogram should
be done in all patients, and a retrograde urethrogram should be perTABLE 3. End Points for Damage Control Resuscitation
Giannoudis84
Stable hemodynamics
Stable oxygen saturation
Lactate level of <2 mmol/L
No coagulopathy
Normal temperature
Urinary output of >1 mL/kg/hr
No inotropic support
formed in male patients prior to passage of a Foley catheter. Computed tomography is done primarily to define the posterior part of
the pelvic ring; axial views best demonstrate sacroiliac joint injuries and sacral fractures. Vertical displacement is underestimated on
anteroposterior radiographs and cannot be measured on axial computed tomography cuts. Vertical displacement can be determined on
the inlet and outlet radiographs of the pelvis.
Deformity and instability should be established when radiographs of an injured pelvis are evaluated. Deformity is assessed on
the basis of the relative degree of internal or external rotation of the
iliac wing as well as anteroposterior and/or vertical displacement of
the posterior aspect of the pelvis. A pelvic fracture is considered to
be unstable when there is symphysis diastasis of >2.5 cm, >1 cm of
displacement of the posterior part of the pelvis, complete widening
of the posterior sacroiliac joint, and/or any neurologic injury.
Classification of Pelvic Ring Injuries
A fracture classification system should group together fractures
that have a similar injury pattern, treatments, potential complications, and sequelae. With pelvic fractures, all of these are primarily
related to the condition of the posterior aspect of the pelvic ring
because stability, neurologic injury, pelvic asymmetry, limb-length
inequality, and persistent lumbosacral pain are determined by the
extent of injury to the posterior aspect of the pelvic ring.
Tile Classification
Pennal, Tile, and colleagues classified injuries into three types57.
Type-A injuries are stable with an intact posterior arch. Type-B injuries are rotationally unstable, with incomplete disruption of the posterior arch. These are subdivided into open-book or external rotation
injuries (Type B1), lateral compression or internal rotation injuries
(Type B2), and bilateral injuries (Type B3). Finally, Type-C injuries
are both rotationally and vertically unstable, and they are subdivided
into different types depending on the nature of the posterior injury.
Young-Burgess Classification
Tscherne et al.85
No increasing infiltrate on chest radiograph
Balanced or negative fluid balance
PaO2/FiO2 (arterial oxygen tension/fraction of inspired
oxygen) of >250
Pulmonary artery pressure of <24 mm Hg
Maximal inspiratory airway pressure of <35 cm H2O
Platelet count of >95,000/μL (>95 10˚/L)
White blood-cell count of <12,000/μL (>12 10˚/L)
Intracranial pressure of <15 cm H2O
37
Young, Burgess, and colleagues proposed a mechanistic classification of pelvic ring injury, noting a correlation between the
mechanism of injury and associated complications58. They proposed
four types of injuries: anteroposterior compression (APC), lateral
compression (LC), vertical shear (VS), and combined. Each of these
major groups is further subtyped on the basis of the degree of displacement, deformity, and instability.
Hemodynamic Instability
Hemodynamic instability is defined by shock (low blood pressure), metabolic parameters (base deficit), and the need for blood
products. The risk of bleeding is correlated with the fracture pattern,
but hemodynamic instability can occur with any pelvic fracture59.
Anteroposterior compression (APC) pelvic injuries are more likely
to be associated with posterior bleeding, whereas lateral compression injuries are more often associated with anterior vessel injury.
Volume 4 – 2010
Sarin et al. reviewed the cases of 283 patients with a pelvic ring
injury who were in shock (a systolic blood pressure of <90 mm Hg)
at the time of presentation60. Thirteen percent required embolization because of persistent hypotension. In that series, the fracture
pattern and orthopaedic management did not differ between the
stable patients and those needing angiography. Advanced age was
significantly correlated with an increased need for embolization
in women only (the mean age of the women who needed embolization was fifty-five years compared with forty years for women not
needing embolization), while the Injury Severity Score correlated
with the need for embolization in men but not in women60.
Treatment Options
Fluid replacement is the initial treatment for a patient with a
pelvic ring injury who is hemodynamically unstable. Fluid replacement alone can increase bleeding in some instances and should be
used judiciously. If the patient does not respond to fluid replacement, or initially responds but becomes hypotensive again, the
source of bleeding should be found. Ultrasonographic examination
of the abdomen and pelvis and computed tomographyangiography are the most common and expeditious means with which to
evaluate bleeding. If there are no other sources of bleeding except
the pelvic fracture, angiography, circumferential compression (by
means of a sheet, pelvic binder, or external fixation), or an exploratory laparotomy with vascular repair and packing of the pelvis are
three ways to control the bleeding. The most appropriate choice is
institution and/or physician-dependent, and the options have not
been standardized.
Angiography has a limited role in the management of patients with pelvic ring injuries. Most bleeding after a pelvic ring
injury is venous, and embolizable arterial lesions are uncommon.
Large-vessel embolization has also been shown to cause extensive necrosis of the hip abductor muscles61. Balogh et al. reported
increased adherence to the key steps of the guidelines and better
clinical outcomes after institution of evidencebased practice guidelines that included abdominal clearance with diagnostic peritoneal
aspiration/lavage or ultrasound (FAST [Focused Assessment with
Sonography in Trauma] examination), noninvasive pelvic binding within fifteen minutes after presentation, pelvic angiography
within ninety minutes after admission, and pelvic external fixation within twenty-four hours62. In the period after the guidelines
were instituted, the transfusion of packed red blood cells in the first
twenty-four hours decreased from 16 ± 2 units to 11 ± 1 units and
the mortality rate decreased from 35% to 7% (p < 0.05).
Fangio et al. used angiography in thirty-two patients with an
average Injury Severity Score of 39 points who remained hypotensive despite controlled fluid resuscitation (500 mL of normal saline
solution) and dopamine infusion and who did not have thoracic and
abdominal bleeding, cardiac tamponade, or tension pneumothorax63. Twenty-five patients had positive results on angiography
and underwent embolization. There was no relationship between
the presence of an arterial lesion and the pelvic fracture pattern; in
fact the only significant differences between those with and those
without a lesion on angiography were the initial blood pressure
(65 compared with 78 mm Hg) and the amount of blood products
received. Thirteen patients had a laparotomy because of expanding
intraabdominal fluid; three of six laparotomy procedures that were
done before angiography revealed negative findings, whereas only
one of seven done after angiography revealed negative findings.
Twenty-five patients underwent embolization; pelvic arterial bleeding was stopped in twenty-four (96%) of them and was followed by
hemodynamic improvement in twentyone (84%)63.
Cook et al. reviewed the cases of twenty-three patients with a
pelvic fracture who underwent angiography and found that the fracture morphology was not predictive of the location of the vascular
injury64. Six of ten patients who died had had angiography as the
first therapeutic intervention. Five of the ten patients had a fracture
pattern that produced an increase in pelvic volume (APC or VS pattern), and two of those patients died during angiography. Cook et al.
believed that these patients would have been better treated with external fixation before the angiography. Shapiro et al. demonstrated
that repeat pelvic angiography might be necessary in patients with
persistent hypotension after previous angiography, whether or not
arterial bleeding was identified during the initial session65.
Circumferential compression, external fixation, and pelvic
packing to control pelvic stability are valuable methods to help control bleeding. They reduce bleeding, lessen pain, and allow the patient to be mobilized. Pelvic stability should be achieved as soon as
possible after the injury and initial assessment. Simple wrapping of
the pelvis with a sheet is now commonplace in the United States for
any patient suspected of having a pelvic ring injury. It is cheap and
simple, and it can be very effective.
Bottlang et al. investigated stabilization of pelvic ring fractures
with slings in cadavers66. They demonstrated that circumferential
compression with a noninvasive pelvic sling is an effective and
safe method for reducing and stabilizing open-book pelvic fractures (Young-Burgess APC II, APC III, and LC II) at an emergency
scene66. Provisional pelvic external fixation as an initial method of
controlling bleeding works but has a 21% rate of complications,
which consist mostly of pin-track infections without sequelae67. Cothren et al. reported a reduction in blood product requirements and
no deaths due to bleeding after instituting a protocol of preperitoneal
pelvic packing and pelvic external fixation68.
Recommended Algorithm for Treatment of Bleeding in Patients
with Pelvic Ring Injury
All patients identified with a pelvic ring injury during initial
resuscitation should be treated with a pelvic binder and a Foley catheter (after a retrograde urethrogram and cystogram), and additional
pelvic radiographs including inlet and outlet views and a pelvic
computed tomography scan should be obtained. Fluid resuscitation
is given with continuous monitoring of urine output, the base deficit,
hemoglobin levels, and coagulation function. Mechanical instability
of the pelvis is determined and, in patients with persistent hypotension, subsequent management depends on the fracture pattern:
Rotationally unstable injuries: Patients with these fracture patterns may respond to wrapping of the pelvis with a sheet or application of a binder. If appropriate resources and expertise are available,
anterior pelvic external fixation or symphyseal plate fixation can
be done. Plate fixation is performed if the patient undergoes a lapa
38
Volume 4 – 2010
rotomy; otherwise, an external fixator is applied. Some apparent
open-book injuries include vertically unstable posterior injuries for
which posterior iliosacral fixation is also warranted. The challenge
is to identify these.
Lateral compression injuries: These are more stable, and early pelvic fixation is not beneficial. If these patients remain hemodynamically unstable, angiography or laparotomy is indicated.
Rotationally and vertically unstable injuries: Rarely, posterior
pelvic clamping in the operating room is done after angiography if
the patient is persistently hemodynamically unstable.
Lower-Extremity Emergencies
Orthopaedic conditions in the lower extremity that are emergent problems include hip dislocation, displaced femoral neck fracture in any patient in whom femoral head salvage is desirable (most
patients less than sixty-five years of age), knee dislocation, talar
neck fracture with displacement, and subtalar dislocation.
Dislocation of the hip joint is usually a high-energy injury that
can interrupt the blood supply to the femoral head and cause cartilage necrosis. Relocation should be done emergently to prevent
irreversible damage to the joint, although reported time guidelines
Upper-Extremity Emergencies
The one absolute, nondeferrable, middle-of-the-night upperextremity surgical emergency procedure is the attempted replantation of an amputated finger or limb. While a lengthy discussion of
this subject is beyond the scope of this review, it is important to
bear in mind that replantation is time-sensitive. Restoration of arterial inflow and venous outflow is vital for the successful salvage of
the amputated part and recovery of as much function as possible.
Infectious processes require early, if not immediate, intervention. Infection causes fibrosis, adhesions, edema, stiffness, and
other detrimental effects that adversely affect the normal sliding
and excursion of delicate hand and upper-extremity structures.
Immediate evacuation of pus and surgical control of infection are
mandatory as soon as they are feasible. Suppurative tenosynovitis
and septic arthritis caused by human bites, animal bites, or other
penetrating injuries need immediate surgical treatment and antibiotic coverage with a third-generation cephalosporin. Ceftriaxone,
or a similar antibiotic, should be used until specific culture and
sensitivity results are available. An infectious disease consultation
should be considered.
Deteriorating neurologic function is an indication for at least
provisional, if not definitive, stabilization of an upper-extremity
fracture (Figs. 1-A, 1-B, and 1-C). A distal radial fracture due to a
high-energy injury is particularly noteworthy, if not notorious, in
this regard, with respect to median nerve compromise. There are
three possible situations that can arise after distal radial fracture
that may lead to acute dysfunction of the median nerve:
1. The median nerve is found to be impaired or nonfunctional
at the time of presentation. Under such circumstances, the nerve
was probably injured at the time of impact, by stretch or laceration
(uncommon), and immediate or early intervention will not change
the natural history of the nerve’s recovery. Emergent surgery is not
warranted.
2. The neurologic function deteriorates during the process of
examination, initial treatment, or early observation. This is essentially an impending compartment syndrome of the carpal tunnel
and requires emergent carpal tunnel decompression (Figs. 2-A and
2-B). Fracture reduction alone can result in adequate ‘‘decompression’’ of the median nerve (in cases in which neurologic compromise is caused by pressure from a displaced bone fragment).
3. Nerve function changes over a period of several days or weeks.
This most likely represents alteration in nerve physiology secondary
to inflammation, hematoma organization, or accumulation of acute
phase mediators. Nerve decompression and irrigation are indicated,
but this should be done on an urgent, not an emergent, basis.
39
Fig. 1-A A severely displaced distal radial fracture, which was
associated with evolving median nerve symptoms.
Fig. 1-B The wrist after immediate temporary treatment with an
external fixator.
Volume 4 – 2010
formation of a tense hemarthrosis may compress the blood vessels
supplying the femoral head. In that setting, an open or percutaneous capsulotomy may improve the blood flow to the head, although
this remains unproven. However, there are risks to this procedure,
including damage to those very same blood vessels.
Dislocation of the knee joint (that is, the femorotibial articulation, as opposed to the patellofemoral articulation) is a high-energy
injury and can be limb-threatening because of associated vascular
Fig. 1-C After definitive fixation with a volar plate.
in the literature range from six to twenty-four hours. There are conflicting and strong opinions from various experts, but good data are
lacking69. Theoretically, an associated acetabular fracture changes
the urgency by decompressing both the soft-tissue tension and the
hematoma. An expeditious relocation of the dislocated hip makes
sense, if only from the point of view of reducing the patient’s pain.
Certainly, patients should not be transferred to other centers with a
hip that is still dislocated.
Fig. 2-A A high-energy distal radial fracture with acute carpal
tunnel syndrome caused by a displaced volar fragment that was
not reducible by closed means (arrow).
A variety of reduction maneuvers have been described, including the Allis, Bigelow, Stimson, and East Baltimore lift70
maneuvers. Adequate pain control, relaxation, and assistance are
required. If one or two gentle and controlled attempts at reduction are unsuccessful, additional treatment should be carried out
in an operating room with the patient under general anesthesia and
with the facilities available for open reduction. Repeated, forceful attempts are ill-advised. The inability to reduce a dislocation is
often due to interposed fragments from the femoral head or from
the acetabulum, and such a dislocation should be treated in the operating room, where trochanteric osteotomy may be necessary to
facilitate reduction71,72. If a patient has an unstable closed reduction
or a dislocation with interposed fragments, skeletal traction should
be used until definitive surgical treatment is accomplished.
A femoral neck fracture in a young patient requires emergent
reduction and fixation to protect the blood supply to the femoral
head, and a controllable factor in outcome is the quality of the reduction. An anatomic reduction is recommended even if it must be
performed in an open fashion. Fixation with three screws placed
peripherally in an inverted-triangle configuration provides good
stability. The necessity for a capsulotomy to release the hemarthrosis is controversial. In a young patient with a nondisplaced or minimally displaced fracture, the capsule may be competent and the
Fig. 2-B Immediate open reduction and volar plate fixation with
carpal tunnel release was performed.
40
Volume 4 – 2010
injury. If there is an abnormality of the pulses or of perfusion in the
limb, emergent evaluation and treatment are indicated. If the pulses
can be palpated and are clinically normal, and the anklebrachial
index is >0.9, arteriography is not necessary. If the limb is obviously not perfused, arteriography also is not necessary because the
patient should be taken directly to the operating room for vascular
exploration and repair. Delay of the vascular repair is an important
risk factor for subsequent amputation73-75.
The knee should be gently reduced and stabilized with a splint
or external fixation to allow close monitoring of the neurovascular
status and compartment pressures. There is no advantage to emergent ligament repair. Rarely, the dislocation is irreducible by closed
means. This is usually due to the medial femoral condyle tearing
through the capsule and becoming button-holed, with capsularligamentous tissue being caught in the intercondylar notch. If the
patient is neurovascularly intact, this situation is not necessarily an
emergency, but the patient should be monitored closely and taken
on an urgent basis to the operating room for an open reduction.
Talar neck fracture is considered an emergency by some because of the tenuous nature and retrograde flow of the blood supply
to the talar dome, but emergent reduction and fixation have not
been shown to improve outcomes76-78. However, if the displacement
compromises the skin, as evidenced by tight blanched medial skin
without capillary refill, the patient should be treated emergently to
save the skin from dying. The same principle holds true for subtalar dislocation. If the skin is compromised, emergent reduction
is warranted. Reduction can usually be accomplished in a closed
fashion, but occasionally a surgical procedure is required if there is
interposition of tendons.
Surgeon Performance and Fatigue
As with any orthopaedic emergency, the timing of the definitive procedure depends on multiple factors: availability of a
suitable operating room, availability and operational integrity of
appropriate equipment, availability of experienced assistants and
Fig. 3-A A comminuted
femoral fracture presenting late in the evening.
scrub personnel, and other factors. Often overlooked, however, is
the state of readiness of the surgeon. When deciding whether surgical treatment should be done in the middle of the night, surgeons
are not always the most reliable judges of their own capabilities.
Fatigue and sleeplessness have subtle but real negative influences
on surgeons’ performances79.
Because of the similar types of responsibilities and decisionmaking involved with their jobs, surgeons are often compared with
airline pilots with respect to performance accuracy and performance
deterioration as fatigue comes into play. Sexton et al. reported that
>70% of surgeons refused to admit to fatigue-induced deterioration
in performance as compared with only 23% of airline pilots80. Like
surgery, flying airplanes requires a coordinated and skilled team.
Over 90% of pilots were able to relinquish some authority and responsibility when they were overly fatigued, as opposed to about
55% of surgeons. Our medical colleagues do a much better job of
recognizing fatigue; anesthesiologists are much better at preserving cohesiveness and team function when they are fatigued, doing
almost twice as well as surgeons in these performance domains.
Even residents and house officers far surpass us80. Fischer et al.
studied petrochemical shift workers and found work performance
and alertness were markedly impaired when they worked the nighttime shift81. Not surprisingly, these parameters showed a marked
tendency to worsen further as the nocturnal work shift passed. Bartel et al. evaluated a cohort of anesthesiologists before and after a
twentyfour-hour period of call82. The study group was tested for
their ability to accurately complete a set of increasingly complex
psychomotor tests. After a night on call, 30% of the doctors showed
more than a 15% increase in simple-task reaction time and more
than one-half showed similar increases in reaction times for more
complex tasks.
Surgeons are not the only ones affected by fatigue-induced
deficits in accuracy and performance; however, we tend to be much
less likely to recognize and acknowledge the fatigue effect.
Fig. 3-B Immediate nailing was done during the
middle of the night. Postoperative radiographs revealed a missed distal interlocking screw (arrow).
41
Fig. 3-C Revision surgery was required to replace the
distal interlocking screw.
Volume 4 – 2010
Unfortunately, errors of commission probably take center
stage more frequently than do most other errors when late-night
or middle-of-the-night procedures are undertaken. Fatigue and accompanying decreases in decision-making accuracy and deterioration in motor skills can lead to imprecise reductions, inaccurate
fixation, and incomplete treatment. Such circumstances often lead
to poor outcomes and, worse, the need for revision surgery (Figs.
3-A through 4-B). Complex articular reconstructions are best deferred until the entire surgical team is well rested and ready to undertake these orthopaedic challenges.
Fig. 4-A Postoperative
anteroposterior radiograph of
a malreduced bicondylar tibial
plateau fracture, with unacceptable residual articular step-off
(arrow).
Fig. 4-B Anteroposterior
radiograph after revision
fixation showing anatomic
reduction of the articular
surface.
References
1. Webb LX, Bosse MJ, Castillo RC, MacKenzie EJ; LEAP Study Group. Analysis of surgeon-controlled
variables in the treatment of limb-threatening type-III open tibial diaphyseal fractures. J Bone Joint Surg
Am. 2007;89:923-8.
2. Charalambous CP, Siddique I, Zenios M, Roberts S, Samarji R, Paul A, Hirst P. Early versus delayed
surgical treatment of open tibial fractures: effect on the rates of infection and need of secondary surgical
procedures to promote bone union. Injury. 2005; 36:656-61.
3. Khatod M, Botte MJ, Hoyt DB, Meyer RS, Smith JM, Akeson WH. Outcomes in open tibia fractures:
relationship between delay in treatment and infection. J Trauma. 2003;55:949-54.
4. Spencer J, Smith A, Woods D. The effect of time delay on infection in open long-bone fractures: a 5-year
prospective audit from a district general hospital. Ann R Coll Surg Engl. 2004;86:108-12.
5. Crowley DJ, Kanakaris NK, Giannoudis PV. Debridement and wound closure of open fractures: the
impact of the time factor on infection rates. Injury. 2007;38:879-89.
6. Werner CM, Pierpont Y, Pollak AN. The urgency of surgical debridement in the management of open
fractures. J Am Acad Orthop Surg. 2008;16:369-75.
7. Gainor BJ, Hockman DE, Anglen JO, Christensen G, Simpson WA. Benzalkonium chloride: a potential
disinfecting irrigation solution. J Orthop Trauma. 1997;11:121-5.
8. Bhandari M, Schemitsch EH, Adili A, Lachowski RJ, Shaughnessy SG. High and low pressure pulsatile
lavage of contaminated tibial fractures: an in vitro study of bacterial adherence and bone damage. J Orthop
Trauma. 1999;13:526-33.
9. Owens BD, White DW, Wenke JC. Comparison of irrigation solutions and devices in a contaminated
musculoskeletal wound survival model. J Bone Joint Surg Am. 2009;91:92-8.
10. Anglen JO. Comparison of soap and antibiotic solutions for irrigation of lower-limb open fracture wounds.
A prospective, randomized study. J Bone Joint Surg Am. 2005;87:1415-22.
11. Bose D, Tejwani NC. Evolving trends in the care of polytrauma patients. Injury. 2006;37:20-8.
12. Patzakis MJ, Wilkins J, Moore TM. Use of antibiotics in open tibial fractures. Clin Orthop Relat Res.
1983;178:31-5.
13. Patzakis MJ, Wilkins J, Moore TM. Considerations in reducing the infection rate in open tibial fractures.
Clin Orthop Relat Res. 1983;178:36-41.
14. Hauser CJ, Adams CA Jr, Eachempati SR; Council of the Surgical Infection Society. Surgical Infection Society guideline: prophylactic antibiotic use in open fractures: an evidence-based guideline. Surgical
Infect (Larchmt). 2006;7:379-405.
15. Gosselin RA, Roberts I, Gillespie WJ. Antibiotics for preventing infection in open limb fractures. Cochrane Database Syst Rev. 2004;1:CD003764.
16. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk?
J Bone Joint Surg Br. 2000;82:200-3.
17. Kenny C. Compartment pressures, limb length changes and the ideal spherical shape: a case report and in
vitro study. J Trauma. 2006;61:909-12.
18. Nassif JM, Gorczyca JT, Cole JK, Pugh KJ, Pienkowski D. Effect of acute reamed versus unreamed
intramedullary nailing on compartment pressure when treating closed tibial shaft fractures: a randomized
prospective study. J Orthop Trauma. 2000;14:554-8.
19. Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment syndrome. J Bone Joint Surg
Am. 2004;86:864-8.
20. Templeman D, Varecka T, Schmidt R. Economic costs of missed compartment syndromes. Read at 60th
Annual Meeting of the American Academy of Orthopaedic Surgeons; 1993 Feb; San Francisco, CA. Paper
no. 212.
21. Richards H, Langston A, Kulkarni R, Downes EM. Does patient controlled analgesia delay the diagnosis
of compartment syndrome following intramedullary nailing of the tibia? Injury. 2004;35:296-8.
22. Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am. 1983;63:539-65.
23. Rorabeck CH. The treatment of compartment syndromes of the leg. J Bone Joint Surg Br. 1984; 66:93-7.
24. Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive
of the disorder? J Orthop Trauma. 2002; 16:572-7.
25. Prayson MJ, Chen JL, Hampers D, Vogt M, Fenwick J, Meredick R. Baseline compartment pressure
measurements in isolated lower extremity fractures without clinical compartment syndrome. J Trauma.
2006;60:1037-40.
26. Janzing HM, Broos PL. Routine monitoring of compartment pressure in patients with tibial fractures:
beware of overtreatment! Injury. 2001;32: 415-21.
27. Ovre S, Hvaal K, Holm I, Strømsøe K, Nordsletten L, Skjeldal S. Compartment pressure in nailed tibial
fractures. A threshold of 30 mmHg for decompression gives 29% fasciotomies. Arch Orthop Trauma Surg.
1998;118:29-31.
28. Wall CJ, Richardson MD, Lowe AJ, Brand C, Lynch J, de Steiger RN. Survey of management of acute,
traumatic compartment syndrome of the leg in Australia. ANZ J Surg. 2007;77:733-7.
29. Boody AR, Wongworawat MD. Accuracy in the measurement of compartment pressures: a comparison of
three commonly used devices. J Bone Joint Surg Am. 2005;87:2415-22.
30. Heckman MM, Whitesides TE, Grewe SR, Rooks MD. Compartment pressure in association with closed
tibia fractures. The relationship between tissue pressure, compartment, and the distance from the site of the
fracture. J Bone Joint Surg Am. 1994;76:1285-92.
31. Kumar P, Salil B, Bhaskara KG, Agrawal A. Compartment syndrome: effect of limb position on pressure
measurement. Burns. 2003;29:626.
32. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold
for decompression. J Bone Joint Surg Br. 1996;78: 99-104.
33. McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg Br. 1996;78:95-8.
34. White TO, Howell GE, Will EM, Court-Brown CM, McQueen MM. Elevated intramuscular compartment pressures do not influence outcome after tibial fracture. J Trauma. 2003;55:1133-8.
35. McQueen MM, Christie J, Court-Brown CM. Compartment pressures after intramedullary nailing of the
tibia. J Bone Joint Surg Br. 1990;72: 395-7.
36. Kakar S, Firoozabadi R, McKean J, Tornetta P 3rd. Diastolic blood pressure in patients
with tibia fractures under anaesthesia: implications for the diagnosis of compartment syndrome.
J Orthop Trauma. 2007;21:99-103.
37. Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syndrome: course after delayed fasciotomy. J Trauma. 1996;40:342-4.
38. Cohen MS, Garfin SR, Hargens AR, Mubarak SJ. Acute compartment syndrome. Effect of dermotomy
on fascial decompression in the leg. J Bone Joint Surg Br. 1991;73:287-90.
39. Tornetta P 3rd, Templeman D. Compartment syndrome associated with tibial fracture. Inst Course Lect.
1997;46:303-8.
40. Yang CC, Chang DS, Webb LX. Vacuum-assisted closure for fasciotomy wounds following compartment
syndrome of the leg. J Surg Orthop Adv. 2006;15: 19-23.
42
Volume 4 – 2010
41. Wiger P, Tkaczuk P, Styf J. Secondary wound closure following fasciotomy for acute compartment
syndrome increases intramuscular pressure. J Orthop Trauma. 1998;12:117-21.
42. Johnson SB, Weaver FA, Yellin AE, Kelly R, Bauer M. Clinical results of decompression dermotomy—
fasciotomy. Am J Surg. 1992;164:286-90.
43. Bone LB, Johnson KD, Weigelt J, Scheinberg R. Early versus delayed stabilization of femoral fractures.
A prospective randomized study. J Bone Joint Surg Am. 1989;71:336-40.
44. Pape HC, Auf’m’Kolk M , Paffrath T, Regel G, Strum JA, Tscherne H. Primary intramedullary femur
fixation in multiple trauma patients with associated lung contusion—a cause of posttraumatic ARDS? J
Trauma. 1993;34:540-8.
45. Rotondo MF, Schwab CW, McGonigal MD, Phillips GR 3rd, Fruchterman TM, Kauder DR, Latenser BA, Angood PA. ‘Damage control’: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma. 1993;35: 375-83.
46. Keel M, Trentz O. Pathophysiology of polytrauma. Injury. 2005;36:691-709.
47. Hildebrand F, Pape HC, van Griensven M, Meier S, Hasenkamp S, Krettek C, Stuhrmann M. Genetic predisposition for a compromised immune system after multiple trauma. Shock. 2005;24:518-22.
48. Crowl AC, Young JS, Kahler DM, Claridge JA, Chrzanowski DS, Pomphrey M. Occult hypoperfusion is associated with increased morbidity in patients undergoing early femur fracture fixation. J Trauma.
2000;48:260-7.
49. Giannoudis PV, Smith RM, Bellamy MC, Morrison JF, Dickson RA, Guillou PJ. Stimulation of the
inflammatory system by reamed and unreamed nailing of femoral fractures. An analysis of the second hit.
J Bone Joint Surg Br. 1999;81:356-61.
50. Waydhas C, Nast-Kolb D, Trupka A, Zettl R, Kick M, Wiesholler J, Schweiberer L, Jochum M.
Posttraumatic inflammatory response, secondary operations, and late multiple organ failure. J Trauma.
1996;40:624-31.
51. Pape HC, van Griensven M, Rice J, Gänsslen A, Hildebrand F, Zech S, Winny M, Lichtinghagen
R, Krettek C. Major secondary surgery in blunt trauma patients and perioperative cytokine liberation:
determination of the clinical relevance of biochemical markers. J Trauma. 2001;50:989-1000.
52. Baker SP, O’Neill B, Haddon W Jr, Long WB. The injury severity score: a method for describing
patients with multiple injuries and evaluating emergency care. J Trauma. 1974;14:187-96.
53. Giannoudis PV, Smith RM, Perry SL, Windsor AJ, Dickson RA, Bellamy MC. Immediate IL-10 expression following major orthopaedic trauma: relationship to anti-inflammatory response and subsequent
development of sepsis. Intensive Care Med. 2000;26: 1076-81.
54. Ditschkowski M, Kreuzfelder E, Rebmann V, Ferencik S, Majetschak M, Schmid EN, Obertacke
U, Hirche H, Schade UF, Grosse-Wilde H. HLA-DR expression and soluble HLA-DR levels in septic
patients after trauma. Ann Surg. 1999;229:246-54.
55. Pape HC, Giannoudis PV, Krettek C, Trentz O. Timing of fixation of major fractures in blunt polytrauma: role of conventional indicators in clinical decision making. J Orthop Trauma. 2005;19:551-62.
56. Nana A, Kessinger S. Improved soft-tissue perfusion following application of temporizing external fixation in complex distal tibia fractures. Presented as a poster exhibit at the Annual Meeting of the Orthopaedic Trauma Association; 2008 Oct 15-18; Denver, CO. Poster no. 99.
57. Pennal GF, Tile M, Waddell JP, Garside H. Pelvic disruption: assessment and classification. Clin Orthop Relat Res. 1980;151:12-21.
58. Young JW, Burgess AR, Brumback RJ, Poka A. Pelvic fractures: value of plain radiography in early
assessment and management. Radiology. 1986; 160:445-51.
59. Metz CM, Hak DJ, Goulet JA, Williams D. Pelvic fracture patterns and their corresponding angiographic sources of hemorrhage. Orthop Clin North Am. 2004;35:431-7.
60. Sarin EL, Moore JB, Moore EE, Shannon MR, Ray CE, Morgan SJ, Smith WR.
Pelvic fracture pattern does not always predict the need for urgent embolization. J Trauma.
2005;58:973-7.
61. Yasumura K, Ikegami K, Kamohara T, Nohara Y. High incidence of ischemic necrosis of
the gluteal muscle after transcatheter angiographic embolization for severe pelvic fracture.
J Trauma. 2005;58: 985-90.
43
62. Balogh Z, Caldwell E, Heetveld M, D’Amours S, Schlaphoff G, Harris I, Sugrue M.
Institutional practice guidelines on management of pelvic fracture-related hemodynamic instability: do they
make a difference? J Trauma. 2005;58:778-82.
63. Fangio P, Asehnoune K, Edouard A, Smail N, Benhamou D. Early embolization and vasopressor administration for management of life-threatening hemorrhage from pelvic fracture.
J Trauma. 2005;58: 978-84.
64. Cook RE, Keating JF, Gillespie I. The role of angiography in the management of haemorrhage from major
fractures of the pelvis. J Bone Joint Surg Br. 2002;84:178-82.
65. Shapiro M, McDonald AA, Knight D, Johannigman JA, Cuschieri J. The role of repeat angiography in
the management of pelvic fractures. J Trauma. 2005;58: 227-31.
66. Bottlang M, Krieg JC, Mohr M, Simpson TS, Madey SM. Emergent management of pelvic ring fractures
with use of circumferential compression. J Bone Joint Surg Am. 2002;84 Suppl. 2:43-7.
67. Mason WT, Khan SN, James CL, Chesser TJ, Ward AJ. Complications of temporary and definitive
external fixation of pelvic ring injuries. Injury. 2005; 36:599-604.
68. Cothren CC, Osborn PM, Moore EE, Morgan SJ, Johnson JL, Smith WR. Preperitonal pelvic packing
for hemodynamically unstable pelvic fractures: a paradigm shift. J Trauma. 2007;62:834-9.
69. Bhandari M, Matta J, Ferguson T, Matthys G. Predictors of clinical and radiological outcome in patients
with fractures of the acetabulum and concomitant posterior dislocation of the hip. J Bone Joint Surg Br.
2006;88:1618-24.
70. Schafer SJ, Anglen JO. The East Baltimore Lift: a simple and effective method for reduction of posterior
hip dislocations. J Orthop Trauma. 1999; 13:56-7.
71. Anglen JO, Hughes M. Trochanteric osteotomy for incarcerated hip dislocation due to interposed posterior
wall fragments. Orthopedics. 2004;27: 213-6.
72. Moed BR, WillsonCarr SE, Watson JT. Results of operative treatment of fractures of the posterior wall of
the acetabulum. J Bone Joint Surg Am. 2002;84: 752-8.
73. Hollis JD, Daley BJ. 10-year review of knee dislocations: is arteriography always necessary? J Trauma.
2005;59:672-5.
74. Klineberg EO, Crites BM, Flinn WR, Archibald JD, Moorman CT 3rd. The role of arteriography in
assessing popliteal artery injury in knee dislocations. J Trauma. 2004;56:786-90.
75. Mills WJ, Barei DP, McNair P. The value of the ankle-brachial index for diagnosing arterial injury after
knee dislocation: a prospective study. J Trauma. 2004;56:1261-5.
76. Vallier HA, Nork SE, Barei DP, Benirschke SK, Sangeorzan BJ. Talar neck fractures: results and outcomes. J Bone Joint Surg Am. 2004;86:1616-24.
77. Patel R, Van Bergeyk A, Pinney S. Are displaced talar neck fractures surgical emergencies? A survey of
orthopaedic trauma experts. Foot Ankle Int. 2005; 26:378-81.
78. Lindvall E, Haidukewych G, DiPasquale T, Herscovici D Jr, Sanders R. Open reduction and stable fixation of isolated, displaced talar neck and body fractures. J Bone Joint Surg Am. 2004;86: 2229-34.
79. Rothschild JM, Keohane CA, Rogers S, Gardner R, Lipsitz SR, Salzberg CA, Yu T, Yoon CS, Williams DH, Wien MF, Czeisler CA, Bates DW, Landrigan CP. Risks of complications by attending physicians after performing nighttime procedures. JAMA. 2009;302; 1565-72.
80. Sexton JB, Thomas EJ, Helmreich RL. Error, stress, and teamwork in medicine and aviation: cross sectional surveys. BMJ. 2000;320:745-9.
81. Fischer FM, de Moreno CR, Notarnicola da Silva Borges F, Louzada FM. Implementation of 12-hour
shifts in a Brazilian petrochemical plant: impact on sleep and alertness. Chronobiol Int. 2000;17: 521-37.
82. Bartel P, Offermeier W, Smith F, Becker P. Attention and working memory in resident anaesthetists after
night duty: group and individual effects. Occup Environ Med. 2004;61:167-70.
83. Committee on Injury Scaling. The Abbreviated Injury Scale (AIS) 1990—Update 98. Des Plaines, IL:
Association for the Advancement of Automotive Medicine; 1998.
84. Giannoudis PV. Surgical priorities in damage control in polytrauma. J Bone Joint Surg Br. 2003; 85:47883.
85. Tscherne H, Regel G, Pape HC, Pohlemann T, Krettek C. Internal fixation of multiple fractures in patients with polytrauma. Clin Orthop Relat Res. 1998;347;62-78.
Volume 4 – 2010
Current and Future Trend in Articular Cartilage Restoration
Jack Farr, MD
Cartilage Restoration Center of Indiana – OrthoIndy, Indianapolis, IN
Introduction
Cartilage restoration has evolved from the very limited
use of fresh osteochondral allografts by a few centers (e.g.,
Gross, Convery, and Meyers) to the widespread use of
marrow stimulation today and the lower volume techniques
of osteochondral autograft and cultured chondrocyte
implantation. While the scientific goal of articular cartilage
restoration is to recreate normal hyaline cartilage at the site
of a cartilage defect, at present this has only been achieved
through osteochondral transfer, noting that limitations of
autograft and allograft implants preclude widespread use.
While hyaline-like tissue properties may be demonstrated using
cell therapy alone, the tissue lacks the natural stratification
of normal hyaline cartilage. However, the clinical goal in
each of these cartilage surgeries is pain free normal function
with a durable implant. With increased emphasis on costs, it
may not be necessary for all techniques to yield hyaline like
cartilage, but rather to satisfy patient goals. That is, while
laudable, stratified hyaline cartilage may not be necessary
to meet these goals. In fact, currently when evaluating new
clinical cartilage restoration techniques, the FDA does not
request biopsies for histomorpholgy, but rather they require
patient reported outcomes as the primary endpoint. This is
typically pain or, when there are co-primary endpoints, the
endpoints are pain and functional activity level. Therefore,
as one explores future trends in the technique of cartilage
restoration, the demand match approach is useful; applying
the optimal technique to benefit the specific cartilage lesion
of a specific patient in a cost efficient manner.
Osteochondral Allograft
Bugbee et al1 recently reported the largest series of
osteochondral allograft (OCA) with follow up as long as
19.5 years. The PROs (patient reported outcomes) results for
monopolar OCA continue to be approximately 76% good/
excellent, while bipolar typically in the range of 50% positive.
The number of transplants per year has been relatively stable
in the range of 1-2,000/year as surgical challenges limit the
number of interested surgeons and availability continues to
be a limiting factor. Currently, extensive testing necessitates
a delay of 10-14 days from harvest to availability for
transplant. As the chondrocyte viability decreases with
storage time, most tissue banks expire the tissue at 28 days.
To extend the shelf life, various alternative medias have been
tried and most recently, Bugbee et al2 showed improved
chondrocyte viability of OCA stored at 37º Centigrade
instead of the classic 4º Centigrade. At the time of transplant,
the chondrocytes are vulnerable to impaction forces and may
be easily die with standard levels of impaction. The trend
is to use thin (6-8 mm) composites that are beveled and
use only finger pressure to press-fit the plug in the socket.
This thinner construct also speeds the time of incorporation
through creeping substitution by requiring less allograft bone.
Williams et al3 showed viability is also affected negatively
during the post operative environment (hemarthrosis) and
this may be an area for optimization. To expand availability, a
variety of freezing techniques have been tried, but even those
with cryo-preservation have not yielded consistent outcomes.
That led to a search for other ways to preserve the tissue. One
approach is to stabilize the matrix and allow all the cells to
die. In one example of this technique, the matrix is stabilized
by cross linking with methylene blue. Animal studies are
promising and human trials are to begin shortly.
It is typically stated that OCA are immune-privileged, yet
a percentage of patients become antibody positive after OCA
transplantation4. When Bugbee et al4 compared PROs, those
that were antibody positive had less favorable outcomes than
those that are antibody negative. This antibody response is
primarily to the boney portion of the graft--probably the soft
tissue remnants within the subchondral bone. Thus, the thin
OCA constructs noted above that allow pulsatile irrigation to
more thoroughly clean the bone, may decrease the extent of
an immunogenic response. Carried to the extreme, removal
of all bone would negate immunogenic response, yet pure
cartilage shells do not integrate with host bone. However,
if the cartilage is particulated, the chondrocytes escape,
multiply and form new matrix. While this has been shown to
occur in the animal model, the Cartilage Restoration Center
of Indiana has submitted for publication the first prospective
case series using this technique: DeNovo NT (IsTo St. Louis
MO and Zimmer, Warsaw IN)
Marrow Stimulation
Marrow stimulation is the generic term for the techniques
that allow marrow cells to enter from the subchondral bone.
The goal for the “marrow derived cells” is to create hyalinelike cartilage when exposed to the appropriate post operative
mechanical environment (continuous passive motion and
protected weight bearing). This term may be a misnomer
as there is typically little or no red marrow in subchondral
knee bone. Rather, most of the pluripotential cells in the
clot are probably similar in origin to any other clot that
occurs throughout the body—blood derived and local tissue
derived. Regardless, numerous studies show a wide range
of fibrocartilage to hyaline-like cartilage with this technique.
The preservation of the mechanical and biologic integrity
of the subchondral bone plate is important for clinical
success. As it is technically difficult to reproducibly “lightly
burr” the subchondral plate without weakening it, drilling
and microfracture, as popularized by Steadman5, are more
commonly used than abrasion arthroplasty technique. One of
the reported advantages of marrow stimulation over drilling
was that microfracture would not cause the thermal necrosis
thought possible with drilling. However, this concern is
being challenged by Buschmann et al6 as they demonstrated
in an animal model that drilling does not cause thermal injury
44
Volume 4 – 2010
Current and Future Trend in Articular Cartilage Restoration (continued)
and that the drill holes allow more consistent channels for
cell migration compared to microfracture. Regardless of
whether the technique is drilling or microfracture, the ease
of performing an all-arthroscopic inexpensive “marrow
stimulation” procedure and the acceptable results in small
to medium sized cartilage lesions has resulted in this being
the most widely used cartilage restoration procedure in the
United States.
Expanding on marrow stimulation, the goals are to
improve the hyaline-like characteristics and durability of
the resultant tissue. One option is to increase the number
of available adult stem cells using true hemopoetic marrow
harvested from the iliac crest. The marrow or concentrated
stem cells are then transferred to a microfracture-prepared
bed. Another approach is to apply an acellular scaffold
for cells to organize (autologous membrane induced
chondrogenesis or AMIC). There are many scaffold variants
ranging from a true physical membrane to a biphasic liquid
hydrogel that congeals in situ. Finally, it may be possible to
further influence the pluripotential cells with growth factors,
such as reported with OP-1.7
Osteochondral Autografts
Morgan (United States) and Bobic (United Kingdom)8
developed the technique of harvesting moderate sized
osteochondral (OC) plugs (8-12 mm) and transferring them
to focal cartilage defects. During the same time period,
Hangody (Hungary)9 used smaller OC plugs (4-8mm) to
create a mosaicplasty at the recipient site. Currently, efforts
are directed at diminishing harvest site morbidity (pain and
hemarthrosis) by back filling the harvest sites and using
laboratory data to select the harvest site. Cole10 demonstrated
there is less stress at the intersection of the trochlea and
the medial femoral condyle than the site of classic harvest
laterally. When harvest sites are unknown, there are subsets
of patients who experience pain at these sites.
Science will continue to guide optimization of the
technique. For example, to avoid chondrocyte death minimal
force is applied to the cartilage to seat the plug. The plug needs
to be flush with the surrounding cartilage to avoid increased
stress on the opposing articular surface. Expanding on this
concept, synthetic plugs may have the capacity to reform bone
and cartilage in the defects (see cell free scaffolds below).
Cultured Chondrocyte Implantation
The rapidly exploding field of cell therapy to treat article
cartilage defects is based on the pioneering work of Dr. Lars
Peterson. The basics of the technique are still used today
and for the foreseeable future. As a two-stage technique, the
first stage is a biopsy of healthy articular cartilage harvested
arthroscopically from a low load area of the knee. The
matrix is enzymatically degraded to release the chondrocytes.
The chondrocytes expand in a monolayer culture (where
they dedifferentiate into spindle cells) creating more than
10 million cells from only the few hundred thousand cells
in the original biopsy. The cell suspension is then injected
45
beneath a periosteal patch or collagen substitute11, where
they differentiate to chondrocytes and produce matrix.
Two companies now assay the cells to assure this potential
(Genzyme VIP and Tigenix ChondroSelect). Since the work
of Peterson, there have been many modifications for the use
of autologous chondrocyte implantation (ACI).
The timing and action of the cells in culture may be
modified with various factors. For example, fibroblast growth
factor (FGF) is used by Prochon which requires fewer cells
at harvest and less time to implantation while maintaining a
higher chondrocytic phenotype. This is just the start of cell
manipulation during culturing with the end goal of creating
cells that reproducibly form hyaline cartilage. Using this
same technique, it is possible to use allograft cells. With one
product, DeNovo NT, infantile chondroctyes have a robust
cell and matrix response. The chondrocytes are so robust
that disks of neocartilage are formed without the need for a
scaffold. The safety and feasibility has been shown clinically
in a three center (the Cartilage Restoration Center of Indiana
[CRCI] being one such center) Phase I-II study of DeNovo
ET (IsTo, St. Louis MO and Zimmer, Warsaw, IN).
The original technique used autologous periosteum to
form a water tighter cover over the chondrocyte suspension.
This often resulted in periosteal overgrowth, which required
subsequent surgery (usually chondroplasty). To obviate this
problem, a variety of scaffolds have been used in place of the
periosteum with clinical outcomes similar to ACI. Initially,
these largely collagen membranes (C-ACI) were used in the
same manner as the periosteum and thus the term CollagenACI or C-ACI originated. This technique was then modified
by Steinwach12 who seeded the cell suspension on the scaffold.
After cell adherence the patch is implanted. Finally, many
companies are providing a construct that result from seeding
the cells onto a scaffold during the culturing process. This
allows a physically robust chondrocyte/scaffold construct
that allows arthroscopic implantation.
Converting this two-stage procedure to a one-stage
procedure is appealing to patients and insurance companies
alike. As with the DeNovo NT mentioned above, it is possible
to mince autologous cartilage at the time of surgery, implant
it and have it grow “new cartilage” as reported at ICRS
Poland in 2007 by CRCI13. A prospective properly powered
randomized control phase 3 trial is now under way to evaluate
clinical efficacy of this technique (Cartilage Autologous
Implant System CAIS). Future modifications of each of these
techniques will focus on arthroscopic applications, efficacy
and cost effectiveness.
Scaffold Use in Cartilage Restoration
Scaffolds are currently not approved for cartilage
restoration in the United States for clinical use outside of
FDA approved trials. Outside the US, scaffold use in cartilage
surgery is more prevalent than the original cell suspension
ACI technique. Scaffolds are often categorized by their
structure (monophasic, biphasic, multiphasic, etc.) and/or if
they are used “with” or “without” cells. To be clear as to the
Volume 4 – 2010
US clinically available scaffolds. For detailed information of
the basic science and clinical applications please refer to the
chapter by Gomoll and Farr.14
mechanism of action, the term should be “scaffolds without
cells at implantation,” as these scaffolds function by providing
structural guidance for endogenous pluripotential cells, which
rapidly populate them. Tables 1-3 list the preclinical and non-
Table 1
Scaffolds Without Cells At Time of Implantation (Host Cell Source)
Scaffold Type
Product Name
Manufacturer
Autologous Matrix Induced Chonrogenesis
AMIC®
Geistlich Biomaterials15
Matrix modulated marrow stimulation
BST CarGel™
BioSyntech16
GelrinC™
Regentis Biomaterials17
PGA, Hyaluronan, Autologous Serum
(combination)
ChonDux™
Cartilix18 (subsidiary of Biomet)
TRUFIT◊ CB Plug™
Smith & Nephew19
MaioRegen®
Finceramica20
Chondromimetic™
Orthomimetics21
CR-Plug®
RTI Biologics22
ASEED® Scaffold
Interface Biotech23
Multiphase scaffold to fill osteochondral defect
Table 2
Scaffolds With Seeded Cells (Single-Stage)
Product Type
Product Name
Manufacturer
Collagen patch seeded
ACT-Cs: ACT (Autologous Chondrocyte Transplant)
(combination)
Cartilage Autograft Implant System
CAISTM
DePuy/Mitek, Inc.24
Cell replacement technology
Cell Replacement Technology™ (CRT) Instruct ™ Products
CellCoTecTM25
Table 3
Scaffolds With Cells Cultured On/Within Scaffold (Two-Stage)
Product Name
Manufacturer
MACI ™ (Matrix Associated ACI)
Genzyme26
CartiGro® ACT on Chondro-Gide
Stryker27/Geistlich Surgery15
NeoCart™
Histogenics28
CaRes®
ArthroKinetics29
Hyalograft C™ (Hyaff-11 HA Polymer)
Fidia Farmaceutici S.p.A.30
Bioseed C®
BioTissue Technologies GmbH31
Cartipatch®
TBF Banque de tissues32
Novocart 3D®
TETEC® Tissue Engineering Technologies AG33
The BioCart™
ProChon Biotech, LTD34
Cartilink®-3 for Autologous Chondrocyte Implantation (ACI)
Interface Biotech23
46
Volume 4 – 2010
References
Selected Reading in Cartilage Restoration
1. Farr J, Yao J. Chondral defect repair with particulated
juvenile cartilage allograft. Cartilage. Submitted 2010.
2. Farr J. Allograft particulate cartilage transplantation:
DeNovo® Natural Tissue Graft in Cartilage SurgeryAn Operative Manual. Submitted 2010.
3. Maj. Slabaugh MA, Capt. Hess DJ, Bajaj S, Farr J, Cole BJ.
Management of chondral injuries associated with patellar
instability. Op Tech Sports Med. Submitted 2009.
4. Farr J, Cole B, Salata M, Collarile M, Bajaj S. Cartilage
restoration in the patellofemoral joint in Anterior Knee
Pain and Patellar Instability, 2nd ed. (Sanchis-Alfonso, ed.).
London: Springer-Verlag; Submitted 2009 (ahead of print).
5. Farr J, Gomoll AH. Articular cartilage repair with
bioscaffolds. In Insall & Scott, Surgery of the Knee. 5th ed.
(Diduch, ed.). 2009 (ahead of print).
6. Gomoll AH, Farr J. Future developments in cartilage repair.
In Biologic Joint Reconstruction: Alternatives to Joint
Arthroplasty (Cole BJ and Gomoll AH, eds). Thorofare, NJ:
SLACK Inc; 2009.
7. Gomoll AH, Probst C, Farr J, Cole BJ, Minas T. Use of a type
I/III bilayer collagen membrane decreases reoperation rates
for symptomatic hypertrophy after autologous chondrocyte
implantation. Am J Sports Med. 2009; 37:20S-23S.
8. Zaslav K, Cole BJ, Brewster R, DeBarardino T, Farr J,
Fowler P and Nissen C. A prospective study of autologous
chondrocyte implantation in patients with failed prior
treatment for articular cartilage defect of the knee: results of
the study of the treatment of articular repair (STAR) clinical
trial. Am J Sports Med. 2009; 37:42-55.
9. Farr J. Specific considerations for patellofemoral chondral
disease. In Biologic Joint Reconstruction: Alternatives
to Joint Arthroplasty (Cole BJ and Gomoll AH, eds).
Thorofare, NJ: SLACK Inc; 2009.
10. Farr J. Autologous chondrocyte implantation and
anteromedialization in the treatment of patellofemoral
chondrosis. Orthop Clin N Am. 2008; 39:329-35.
11. Farr J. Autologous chondrocyte implantation improves
patellofemoral cartilage treatment outcomes. Clin Orthop
Rel Res. 2007; 463: 187-94.
12. Gomoll AH, Minas T, Farr J, Cole BJ. Treatment of
chondral defects in the patellofemoral joint. J Knee Surg.
2006;19:285-95.
13. Farr J. Patellofemoral articular cartilage treatment. AAOS
Monograph Series 29: Common patellofemoral problems.
2005 ; 85-99.
14. Cole BJ, Farr J. Putting it all together. Op Tech Orthop.
2001; 11:151-4.
47
1. Görtz S, De Young AJ, Bugbee WD. Fresh osteochondral allografting for steroid-associated
osteonecrosis of the femoral condyles. Clin Orthop Rel Res. In press.
2. Pallante AL, Bae WC, Chen AC, Görtz S, Bugbee WD, Sah RL. Chondrocyte viability is
higher after prolonged storage at 37 degrees C than at 4 degrees C for osteochondral grafts. Am J
Sports Med. 2009; 37 Suppl 1:24S-32S.
3. Pylawka TK, Wimmer M, Cole BJ, Virdi AS, Williams JM. Impaction affects cell viability in
osteochondral tissues during transplantation. J Knee Surg. 2007; 20:105-10.
4. Sirlin CB, Brossmann J, Boutin RD, Pathria MN, Convery FR, Bugbee W, Deutsch R,
Lebeck LK, Resnick D. Shell osteochondral allografts of the knee: comparison of MR imaging
findings and immunologic responses. Radiology. 2001; 219:35-43.
5. Steadman JR, Rodkey WG, Briggs KK. Microfracture to treat full-thickness chondral defects:
surgical technique, rehabilitation, and outcomes. J Knee Surg. 2002; 15:170-6.
6. Chen H, Sun J, Hoemann CD, Lascau-Coman V, Ouyang W, McKee MD, Matthew S,
Buschmann MD. Drilling and microfracture lead to different bone structure and necrosis during
bone-marrow stimulation for cartilage repair. J Orthop Res. 2009; 27:1432-38.
7. Huang Z, Ryu W, Ren P, Fasching R, Goodman SB. Controlled release of growth factors on
allograft bone in vitro. Clin Orthop Rel Res. 2008; 466:1905-11.
8. Vladimir Bobic, Craig Morgan, Thomas Carter. Osteochondral autologous graft transfer. Op
Tech Sports Med. 2000; 8:168-78.
9. Hangody L, Füles P. Autologous osteochondral mosaicplasty for the treatment of full-thickness
defects of weight-bearing joints: ten years of experimental and clinical experience. J Bone Joint
Surg Am. 2003; 85-A Suppl 2:25-32.
10. Garretson R, Katolik L, Verma N, Beck P, Bach B, Cole B. Contact pressure at osteochondral
donor sites in the patellofemoral joint. Am J Sports Med. 2004; 32:967-74.
11. Gomoll A, Probst C, Farr J, Cole B, Minas T. Use of a Type I/III Bilayer Collagen Membrane
Decreases Reoperation Rates for Symptomatic Hypertrophy After Autologous Chondrocyte
Implantation. Am J Sports Med. 2009; 37:205-35.
12. Steinwachs M. New technique for cell-seeded collagen-matrix-supported autologous
chondrocyte transplantation. Arthroscopy. 2009; 25:208-11.
13. Farr J, Binnete F, Hwang J, Cook S, Smith T. The Cartilage Autograft Implantation System
(CAIS) is being investigated in the US as a primary surgical treatment of articular cartilage
lesion(s) located on the femur (medial and lateral condyles or trochlea). In: Proceedings of the
International Cartilage Restoration Society; Oct. 1, 2007; Warsaw, Poland.
14. Farr J, Cole B. Articular Cartilage Repair with Bioscaffolds. In: Diduch D, eds. Insall & Scott
Surgery of the Knee. Elsevier; 2010 (ahead of print).
15. Geistlich Group. Geistlich Surgery. Available at: http://www.geistlich.com/?dom=3&rub=1477.
Accessed March 30, 2010.
16. BioSyntech. BST-CarGel for Cartilage Repair. Available at: http://www.biosyntech.com/en/
expertise/orthopedics/?BST=CarGel. Accessed March 30, 2010.
17. Regentis Biomaterials. GelrinC. Available at: http://gelrin.com/product.asp?ID=1. Accessed
March 30, 2010.
18. Biomet. Biomet Orthopedics. Available at: http://www.biomet.com/orthopedics/. Accessed
March 30, 2010.
19. Smith & Nephew. TruFit Plug. Available at: http://global.smith-nephew.com/us/product23822.
htm. Accessed March 30, 2010.
20. Finceramica. Finceramica Biomedical Solutions. Available at: http://www.finceramica.it/view.
jsp?s=10&p=1. Accessed March 30, 2010.
21. Orthomimetics. Chondromimetic. Available at: http://www.orthomimetics.com/chondromimetic.
htm. Accessed March 30, 2010.
22. RTI Biologics. RTI Biologics. Available at: http://www.rtix.com/. Accessed March 30, 2010.
23. Interface Biotech. Interface Biotech. Available at: http://www.interfacebio.com/index.php?aci_
physicians. Accessed March 30, 2010.
24. Johnson & Johnson. DePuy Mitek Inc. Available at: http://www.depuymitek.com/. Accessed
March 30, 2010.
25. CellCoTec. CellCoTec: A revolutionary approach to cartilage repair. Available at: http://www.
cellcotec.com/. Accessed March 30, 2010.
26. Genzyme. Matrix-induced Autologous Chondrocyte Implantation (MACI). Available at: http://
www.genzyme.com.au/prod/maci/au_p_hcp_bio-maci.asp. Accessed March 30, 2010.
27. Stryker. Stryker. Available at: http://www.stryker.com/en-us/index.htm. Accessed March 30,
2010.
28. Histogenics. NeoCart autologous engineered neocartilage. Available at: http://www.histogenics.
com/neocart.html. Accessed March 30, 2010.
29. ArthroKinetcs. ArthroKinetics. Available at: http://www.arthro-kinetics.com/. Accessed March
30, 2010.
30. Fidia Farmaceutici S.P.A. Fidia Farmaceutici S.P.A. Available at: http://www.fidiapharma.com/
files/index.cfm. Accessed March 30, 2010.
31. BioTissue Technologies. Bioseed C Introduction. Available at: http://www.biotissue-tec.com/enProductsPatientsBioSeedCIntroduction.html. Accessed March 30, 2010.
32. TBF Tissue Engineering. Cartipatch. Available at: http://www.tbf-lab.com/ortho/index.
php?option=com_content&view=article&id=76&Itemid=38&lang=fr. Accessed March 30,
2010.
33. TETEC. What is NOVOCART 3D? Available at: http://www.tetec-ag.de/en/physicians/products/
novocart_3d.htm. Accessed March 30, 2010.
34. ProChon Biotech L. The Product BioCart Overview. Available at: http://www.prochon.com/.
Accessed March 30, 2010.
Volume 4 – 2010
Minimum 10-Year Results after Anterior Cruciate Ligament
Reconstruction: How the Loss of Normal Knee Motion
Compounds Other Factors Related to the Development
of Osteoarthritis after Surgery
K. Donald Shelbourne, MD, Tinker Gray, MA
This report is a summary of a paper that was previously published in
the American Journal of Sports Medicine and received the 2010 Hughston Award for the most outstanding article in AJSM for 2009. Citation:
Shelbourne KD, Gray T. Minimum 10-year Results after Anterior Cruciate
Ligament reconstruction: How the Loss of Normal Knee Motion Compounds
other Factors Related to the Development of Osteoarthritis after Surgery.
Am J Sports Med. 2009;37:471–480. Reprinted with permission.
Introduction
There are very few studies reporting the results of ACL
reconstruction at 10 years or more after surgery. Some studies
have shown that patients who have meniscus loss, articular
cartilage damage, or both, have lower subjective scores and
more radiographic evidence of arthritis when compared to
patients who have very little joint damage at the time of ACL
reconstruction.
Few studies have examined how the loss of range
of motion (ROM) affects the long-term results of ACL
reconstruction. The purpose of this study was to examine
how the loss of normal knee hyperextension, flexion, or both,
affected the results of ACL reconstruction at longer than
10-year follow-up.
Methods
The study group included patients who underwent ACL
reconstruction with an ipsilateral patellar tendon graft between
1982 and 1994. Patients were evaluated objectively according
to the International Knee Documentation Committee (IKDC)
criteria including evaluation of ROM, isokinetic strength
scores, KT-1000 stability testing, and radiographs. Using
the IKDC criteria for grading ROM, knee extension was
considered normal if it was within 2˚ of the normal knee, and
knee flexion was considered normal if it was within 5˚ of
the normal knee. Patients were evaluated subjectively using
a modified Noyes knee questionnaire. Regression analysis
was performed to determine what factors affected subjective
scores.
Regression analysis showed that loss of normal knee
extension was the most significant factor relating to lower
subjective scores (p<.001); loss of normal knee flexion was
also significant (p=.0034).
The overall IKDC objective grade was normal in 48%,
nearly normal in 42%, abnormal in 9%, and severely abnormal
in 0.5%. Most patients (73%) had normal knee ROM at
long-term follow-up, while 10% of patients demonstrated
loss of normal extension alone, 11% demonstrated loss of
normal flexion alone, and 6% demonstrated loss of both knee
extension and flexion. Of the 502 patients in the study, 367
(73%) had normal knee extension and flexion, and 135 (27%)
had less than normal extension or flexion. In the group of
patients who had normal knee extension and flexion, 29%
had less than normal radiographic ratings. By comparison, in
the group of patients who had less than normal ROM, 71%
had less than normal radiographic ratings. (p<.001)
Current literature theorizes that the development
of osteoarthritis leads to a loss of ROM. However, the
percentage of patients who were lacking ROM at ≥ 10 years
after surgery was not statistically significantly different than
what was observed at the 2 and 5 years post-operative times.
Therefore, the results from this study indicate that a loss of
ROM may contribute to the development of osteoarthritis.
When looking at the group of patients who had intact menisci,
normal articular cartilage, and normal knee extension and
flexion, 98% of them had normal radiographs.
Patients who had normal knee extension and flexion had
significantly higher modified Noyes scores than patients who
lacked knee ROM. (p<.001) (Figure 1)
Results and Discussion
Objective follow-up was obtained on 502 patients
at a mean of 14.1 ± 3.4 years (range 10.0-24.3 years)
postoperatively, and subjective follow-up was obtained on
1113 patients at a mean of 15.9 ± 3.6 years (range 10.0-24.0
years) postoperatively. Subjective scores were not statistically
significantly different between patients who returned for
objective follow-up and those who returned a survey only.
(p=.4747)
Figure 1. Patients who had normal knee hyperextension and
flexion had significantly higher modified Noyes knee questionnaire
scores than patients who lacked normal knee ROM.
48
Volume 4 – 2010
Minimum 10-Year Results after Anterior Cruciate Ligament Reconstruction:
How the Loss of Normal Knee Motion Compounds Other Factors Related to
the Development of Osteoarthritis after Surgery (continued)
Patients who had meniscectomy or articular cartilage
damage had significantly lower subjective survey scores if
they also had less than normal ROM. Patients with intact
menisci and loss of ROM had statistically significantly lower
subjective scores than patients with intact menisci and normal
ROM. However, patients who had meniscectomy but were
able to maintain normal ROM fared just as well. (Figure 2)
When patients have normal ROM, their subjective scores
remain high even if articular cartilage damage is present at the
time of surgery. However, subjective scores are significantly
lower when ROM is less than normal. (Figure 3)
Conclusions
• At an average of 14.1 years after ACL reconstruction,
90% of patients had an overall IKDC grade of normal or
nearly normal.
• Even 3° to 5° of knee extension loss compared with the
opposite knee can cause adverse symptoms, especially
when other damage is present in the knee
Figure 2. Modified Noyes knee questionnaire scores based
on ROM and meniscus status. Patients who had less than
normal ROM had statistically significantly lower modified
Noyes scores.
• Patients who had normal knee extension and flexion had
significantly better survey scores than patients who had
ROM loss
Patients who had a loss of normal ROM had worse
results and more radiographic evidence of osteoarthritis.
Almost all patients (98%) who had intact menisci, normal
articular cartilage, and normal knee extension and flexion
had normal radiographs at follow-up. Although the surgeon
and patient cannot control the damage sustained to the knee
joint after ACL injury, results following ACL reconstruction
can be maximized by ensuring that full ROM is achieved
and maintained. By having patients achieve full, symmetric
ROM compared to the opposite knee before and after ACL
reconstruction, we may be able to prevent the development
of osteoarthritis, especially in patients with meniscus or
cartilage damage.
49
Figure 3. Modified Noyes knee questionnaire scores based
on ROM and articular cartilage status at the time of surgery.
Patients with normal ROM have high subjective scores even
if articular cartilage damage is present; however, subjective
scores are significantly lower when ROM is less than
normal.
Volume 4 – 2010
The Use of Implantable Bone Stimulators in Nonunion Treatment
Michael S. Hughes, MD, Department of Orthopaedic Surgery, University of Missouri-Columbia
Jeffrey O. Anglen, MD, Department of Orthopaedic Surgery, Indiana University
Copyright © SLACK Incorporated. This article originally published at:
www.orthosupersite.com/view.aspx?rid=61003. Reprinted with permission.
Abstract
Background: Delayed or failure of bone healing in fracture,
osteotomy, and arthrodesis patients continues to be a clinical
dilemma. Electromagnetic stimulation is one modality demonstrated
in many studies to aid bone healing, however relatively few studies
depict the use and complications associated with direct current
implantable bone stimulators (IBS).
Methods: Over a 9 year period, we studied a consecutive series of
120 adult patients who underwent implantation of a direct current
bone stimulator. The goals of this study were to determine the time
until healing, the presence of infection, and the need for additional
nonunion surgery or salvage procedure following internal bone
stimulator placement for nonunion treatment.
Results: Of the factors affecting the time until healing, tobacco
smoking was a significant factor associated with increased time
until healing. Tobacco smoking and duration of nonunion prior to
implantable bone stimulator placement were both significant factors
in the need for revision nonunion surgery or salvage procedure after
IBS placement. Deep soft tissue infection or osteomyelitis was a
significant factor predicting prolonged time to healing, subsequent
infection following IBS placement, and the need for revision or
salvage surgery.
Conclusion: There are several studies detailing the beneficial effects
of electromagnetic stimulation in the peer reviewed literature.
With the relative lack of complications directly attributable to
electromagnetic implantable bone stimulators, their use may be an
effective adjuvant to stable internal fixation and autogenous bone
grafting in healing nonunions. However, the use of IBS in nonunion
patients with prior deep soft tissue infection or osteomyelitis
exhibited an increased rate of post-operative infection in this series.
Level of Evidence: Therapeutic Level I
Introduction
In 2004, an estimated 15 million fractures occurred in the
United States.1 A report from five years earlier estimated that 5-10%
of fractures resulted in delay or failure of fracture union.2 Because
recent data indicates that a fracture requiring hospitalization costs an
average of $27,000 and results in an average of 27 days out of work,
it is obvious that recalcitrant fracture healing may have significant
impact on patients and health care resources.1 The importance of
this clinical dilemma continues to prompt basic science and clinical
research to improve methods of fracture repair. This includes
research into devices that generate physical forces in the form of
electric or ultrasonic fields to stimulate fracture healing.
The utilization of electricity as a treatment for fracture nonunions
is thought first to have been described in 1814 by Boyer, but little
scientific evidence beyond case reports were initially published.3,4
The discovery of piezoelectric potentials by Fakuda and Yasuda in
1957 and further study of the relationship between electrical fields
and mechanical stress in bone by Bassett prompted a resurgence
of interest in bone-healing stimulation therapies.5-7 Several clinical
and laboratory studies followed, demonstrating a positive effect of
electrical stimulation on bone healing. There are several methods of
delivering electrical stimulation including direct current, inductive
coupling, and capacitive coupling.8-11 One common pathway through
which these methods of electrical stimulation delivery appear to
exert their effects involves increasing cytosolic calcium ions and
increasing activated cytoskeletal calmodulin.12
Despite hundreds of articles in the literature describing the effects of electromagnetic stimulation on bone healing, there are few
blinded, randomized controlled clinical trials detailing its use in delayed bone healing.4,11,13,14 A meta-analysis of these trials was unable
to determine the impact of electrical stimulation based on pooled
analysis of available data, and its appropriate role in orthopaedic
surgery continues to be debated 15 This study retrospectively examines a single surgeon’s cohort of patients who underwent surgical
implantation of direct current electric bone stimulators for nonunion
of fractures, arthrodesis or osteotomies in an effort to delineate the
duration of time until healing of the nonunion occurred. The presence of infection or other implant related complications following
implantable bone stimulator placement and the need for additional
nonunion surgery or salvage procedure to address recalcitrant nonunion were also investigated.
Materials and Methods
A retrospective study of consecutive patients treated by a
single surgeon (JOA) with an implantable bone stimulator (IBS) as
an adjunct for achieving osseous union was performed. A total of
121 internal bone stimulators were placed in 120 patients, as one
patient had 2 separate stimulators for two different locations of
nonunion, by the senior author between the dates of 1995 to 2004
at a tertiary hospital with an established nonunion referral practice.
Indications for internal bone stimulator placement included fracture
nonunion (105), arthrodesis nonunion (4), osteotomy nonunion (3),
malunion osteotomy (5), and primary fixation of open fractures with
large segmental bony defects (4).
Nine subjects within the primary fracture and malunion
osteotomy groups were excluded from the statistical analysis to
reduce the heterogeneity of indications of internal bone stimulator
placement. Two fracture nonunion patients had a second internal
stimulator placed due to serial need for nonunion fixation
secondary to early hardware failure but for statistical purposes the
total duration of IBS placement was recorded. One patient in the
fracture nonunion group had two separate stimulators placed for
two different locations of fracture nonunion and this patient was
included twice in the statistical analysis. One elderly patient in the
fracture nonunion group died in the post-operative period from a
pulmonary embolus and was excluded from the analysis. Thus,
statistical analysis included a total of 111 patients undergoing IBS
placement for nonunion treatment.
50
Volume 4 – 2010
The Use of Implantable Bone Stimulators in Nonunion Treatment (continued)
The diagnostic criterion for a bony nonunion is variable
throughout the literature, and for the purposes of this study the
definition was derived in part from the U.S. Food and Drug
Administration’s definition.16 In this study a nonunion was
diagnosed when there was a lack of progression in radiographic and
clinical healing after a three month period, necessitating clinical
intervention. Fracture, arthrodesis, and osteotomy nonunions were
categorized as atrophic, hypertrophic, or oligotrophic.17 A healed
nonunion was determined by the presence of at least three cortices
with bridging callus and absence of significant pain or instability
with weightbearing activities.
Patient demographics collected included age, medical
comorbidities (diabetes, rheumatoid arthritis, peripheral
vascular disease, hypothyroidism) and patient use of drugs that
have demonstrated effects on bone healing (nonsteroidal antiinflammatory drugs, corticosteroids, tobacco and alcohol).18 The
anatomic site of internal bone stimulator placement was categorized
using the AO/OTA fracture classification.19 The Gustilo classification
was used to classify open fractures and the number of irrigation and
debridements performed for initial treatment were recorded.20,21 The
occurrence of superficial cellulitis, osteomyelitis, pin site and deep
soft tissue infections at any time in the history was recorded.
For the purposes of this paper an “intervention” is considered any
procedure performed or treatment provided in the attempt to achieve
osseous union. “Operative interventions” include external fixation,
intramedullary nail dynamization, internal fixation, autogenous
bone grafting, allograft or synthetic bone use, recombinant growth
factors, or osteotomies. “Nonoperative interventions” include
bracing, casting, external ultrasound, or external electric bone
stimulators. Additionally, the number of trips to the operative suite
needed to facilitate fracture healing were documented and referred
to as “operative periods.”
The number of fracture interventions and operative periods
performed were recorded and divided into one of three chronological
groups for further analysis. These included those interventions and
surgical trips during initial fracture fixation, nonunion treatment
prior to implantable bone stimulator, and nonunion treatment
simultaneous with the placement of the IBS. A salvage procedure
was defined as an amputation, arthrodesis, or joint arthroplasty
indicated for failed bone union or progressive infection.
The Osteogen® implantable direct current bone growth
stimulator (Biomet Trauma, Parsippany, NJ) was used in each case.
The Osteogen has the anode directly on the battery and a single or
double titanium cathode wire, which is implanted at the nonunion
site. Patients were counseled preoperatively that the battery would
be removed approximately one year after implantation. The cathode
wire was coiled into the nonunion gap and buried into host bone and/
or bone graft, usually with the ends anchored into 2.0 mm drill holes
in living bone. Care was taken to avoid cathode contact with metal
implants. The battery was placed in an extrafascial, subcutaneous
pocket in each of the 121 cases. The removal of the bone stimulator
battery and its duration of implantation were recorded. Complications
that could be directly attributable or even remotely linked to the
implantable bone stimulator placement including infection, implant
failure, point tenderness at the battery site, and neurologic deficit
were recorded.
51
Statistical analysis was performed on the remaining 111 bone
nonunion subjects with SAS v9 software (SAS Institute Inc., Cary,
NC, USA). To evaluate the time until healing of the nonunion, the
variable lengths of follow-up between the patients that healed their
nonunion and those that had a persistent nonunion were addressed,
as those subjects with longer follow-up are more likely to have
healing take place or a complication to occur. Thus, survival
analysis methods using the LIFETEST procedure and the PHREG
procedure for Cox Proportional Hazards model analysis were
utilized. Evaluation of post-implantable bone stimulator infection
and need for post-implantable bone stimulator nonunion surgery
or salvage procedure included use of a Poisson distribution and a
generalized linear model (GENMOD in SAS). Significance was set
at an alpha level of 0.05. One subject was excluded from the analysis
secondary to death from a medical complication in the immediate
postoperative period. This investigation was approved by our local
Institutional Review Board.
Source of Funding
None of the authors received payments or other benefits
or a commitment or agreement to provide such benefits from a
commercial entity. A commercial entity (EBI/Biomet) paid or
directed, or agreed to pay or direct, benefits less than $10,000 to a
research fund, foundation, educational institution, or other charitable
or nonprofit organization with which the authors are affiliated or
associated.
Results
In the 111 patients analyzed who underwent IBS for nonunion
following fracture, osteotomy, or arthrodesis, the average age was
47 years. Forty-four percent of patients smoked cigarettes, with an
average of 1.08 packs per day (Table 1). The duration of follow-up after
initial fracture or index procedure was 45.1 months (range, 7-182).
The mean duration of time that the patient had an ununited bone
prior to IBS implantation was 17.9 months (range, 3-137). The mean
follow-up time after IBS placement in the 105 patients that returned
for a three- month postoperative visit was 28.7 months (range, 3-141).
TABLE 1. Demographic Data for fracture,
osteotomy, or arthrodesis nonunion subjects
Parameter
Age
Mean
(range or percentage)
47.4 mths (18-69)
Tobacco smoking
49 (44%)
Chronic Medical Illness
33 (30%)
Prescription medications that
affect bone healing
22 (19%)
Follow-up duration after index
procedure or fracture
45.1 mths (7-182)
Duration of unhealed fracture,
osteotomy or arthrodesis
17.9 mths (3-137)
Volume 4 – 2010
TABLE 2. Nonunion Characteristics for fracture,
osteotomy, or arthrodesis nonunions
Parameter
N = (mean or percentage)
Open fracture (n = 104 fracture nonunions)
36 (35%)
Atrophic nonunion
Initial interventions prior to IBS
- Operative fixation
Nonunion interventions prior to IBS
- Hardware exchange with repeat fixation
- Bone autografting of nonunion
Initial and nonunion operative periods prior to IBS
History of any infection prior to IBS
History of deep infection (deep soft tissue or osteomyelitis)
Iliac crest bone grafting intervention prior to IBS
Interventions simultaneous to IBS
Iliac crest bone grafting intervention simultaneous to IBS
78 (69%)
159 (1.43)
108 (68%)
152 (1.36)
94 (62%)
35 (23%)
185 (1.66)
22 (20%)
13 (12%)
34 (31%)
253 (2.3)
103 (93%)
A total of 94 patients (85%) healed their nonunion after IBS
placement at a mean time of 7.1 months (range, 3-35). Additional
nonunion characteristics are outlined in Table 2 and radiographs are
presented in Figure 1. The locations of the nonunions and open fractures
according to the AO/OTA fracture classification are reported in
Table 3. Complications directly associated with IBS placement
included three asymptomatic cathode wire breakages (2.7%) and
one patient with tenderness at the site of the battery (0.9%). PostIBS placement complications in which bone stimulator culpability
could not be clearly excluded consisted of three transient nerve
palsies (2.7%) and 11 infections (9.9%). The infections involved the
fracture or nonunion site and not the subcutaneous site of the IBS
battery. To our knowledge only 65 patients (59%) had their battery
removed at an average of 10.9 months after placement.
Results of the survival analysis for nonunion time to healing
in the subjects with nonunions revealed that tobacco smoking
was a significant covariate for continued nonunion or need for a
salvage procedure to address the nonunion. (p=0.013) (Figure 2)
The history of a deep infection, consisting of either a deep soft
tissue infection requiring surgical treatment or osteomyelitis, was a
significant factor contributing to recalcitrant nonunion. (p= 0.0336)
Additionally, the femur and hip location of nonunion compared to
1A
upper extremity and leg/ankle regions locations was a statistically
significant covariate for continued nonunion following bone
stimulator placement. (p=0.0367) Patient age, medical comorbidity,
use of autogenous bone graft, and history of active infection during
the nonunion treatment were not statistically significant factors
contributing to healing time.
The presence of an infection following implantation of the bone
stimulator was statistically similar when compared to age, tobacco
smoking, medical illness, and area of implantation. However, just as
seen with analysis of nonunion time to healing, the history of deep
soft tissue infection or osteomyelitis was a statistically significant
factor contributing to an infection following IBS placement.
(p=0.0275, 95% C.I.= 0.165-2.8)
Analysis of the need for revision nonunion surgery or a salvage
procedure following the bone stimulator placement revealed that the
duration of the nonunion prior to IBS placement was a significant
factor. (p=0.0041, 95% C.I.= 0.0067- 0.0356) The longer the
nonunion had been present prior to IBS implantation, the higher the
likelihood of needing a revision or salvage procedure. The presence
of tobacco smoking not only affected the outcome of time to healing
but also had a significant impact on the need for revision or salvage
procedure. (p=0.0293, C.I.= 0.134- 2.53) Similarly, the history of a
1B
1C
1D
1E
Figure 1. Case #90 with distal femur nonunion (A) and postoperative radiographs following hardware removal, blade plating, iliac crest
bone grafting and IBS placement (B,C). Radiographs at time of 7-month follow-up with fracture consolidation and patient with clinical signs
of healing (D,E)
52
Volume 4 – 2010
AO/OTA location
Number of
nonunions
Number of open
fractures
8
11
12
13
21
22
31
32
33
41
42
43
44
62
Total
1
1
12
5
1
2
17
14
4
11
21
18
2
2
111
0
0
0
3
0
1
0
3
0
4
15
10
0
0
36
deep infection or osteomyelitis was a significant factor leading to
nonunion revision or salvage procedure. (p=0.0037, C.I.=0.57- 2.98)
However, the age of the patient, history of an active infection during
the nonunion treatment, or the presence of an atrophic nonunion
were not statistically significant covariates in the risk of requiring
revision or salvage procedures.
Based on the survival analysis data, with outcome being any
complication (direct or indirect), it is estimated that 17% of the
patients will have a complication within the first 12 months after
IBS placement (95% C.I.= 9-30%). There was a significantly higher
proportion of patients undergoing iliac crest bone grafting at the time
of IBS placement (93%) than during previous nonunion surgeries
(31%). (p<0.0001 using McNemar’s test)
Discussion
Fracture nonunion is a dilemma that consumes considerable
resources and can cause significant patient disability. Electromagnetic
and ultrasound bone stimulators have been have been studied as
adjuncts for fracture healing. Numerous basic science studies have
detailed the effects that electromagnetic stimulation has on biological
pathways. At a cellular level, electromagnetic stimulation has been
shown to increase production of bone morphogenetic protein 2,
alkaline phosphatase, cytosolic calcium, and activated cytoskeletal
calmodulin. 12,22,23 Capacitative coupled electromagnetic stimulation
has also been shown to increase osteoprogenitor cell proliferation,
osteoblast proliferation and differentiation, increased arteriolar
vasodilation and neoangiogenesis, and modulate bone resorption.24-27
Additionally, there are several clinical studies describing the use of an
implantable bone stimulator as an adjunct to achieve primary spinal
and foot fusions as well as congenital pseudarthrosis unions.28-31
To the best of our knowledge there is only one cohort of
patients identified in the literature that describes the use of an
53
implantable bone stimulator for recalcitrant nonunions. Paterson et
al. published a prospective multicenter trial almost three decades
ago using a implantable direct current stimulators in 84 nonunions
and a subsequent report on the same group which had a 10 year
average follow-up of those patients.32 They found that the use of
a bone stimulator led to an 84% rate of union and that there were
zero complications associated with the implanted stimulator. Of
considerable note is that nearly 50% of their patient had undergone
no previous surgeries, and 81% had only one prior surgical procedure
performed to achieve union prior to IBS placement. Our patients had
considerably more previous interventions and trips to the operating
room than those of Patterson et al. prior to the implantation of the
bone stimulator (mean of 1.66 operative period and 2.82 operative
and nonoperative interventions). Unfortunately their study did not
utilize a concomitant comparison group, which is a weakness of our
study as well.
The survival analysis including an adjustment for duration of
follow-up revealed that tobacco smoking had a significant effect on
time to healing as well as need for revision surgery or a salvage
procedure. Tobacco smoking has had a long association with wound
and fracture healing problems so this data further reiterates smoking
as a risk factor and the possible benefits in smoking cessation.33,34 An
important finding of this study is that a deep soft tissue infection or
osteomyelitis was a significant factor predicting prolonged time to
healing, subsequent infection following IBS placement, and the need
for revision or salvage surgery. Both actively draining and indolent
infections of long bones have been associated with the presence
of nonunion and the appropriate diagnosis and management is a
challenging clinical problem.35-37
One of the components in determining the utility of the IBS
as a modality is the potential complications that could result with
the intervention. Survival analysis demonstrated a 17% rate of
complications at the 12-month interval. Our cohort revealed three
cathode wire breakages that, although asymptomatic, did create
a potential for harm, or at least ineffective treatment. Though
symptoms of tenderness at the site of the generator can be directly
attributable to the implantation of the stimulator, the three postoperative nerve palsies and eleven cases of post-operative infection
cannot be directly attributed to the implant. It is plausible that the
increased rate of post IBS infection in patients with a history of deep
1.00
Survival Distribution Function
TABLE 3. Distribution of Nonunion
location and open fracture location
0.75
0.50
0.25
0.00
0
5
10
15
20
25
30
35
Time
No tabacco use
Tobacco use
Figure 2. Time from IBS placement to nonunion healing versus
tobacco smoking
Volume 4 – 2010
infection was due in part to the additional cathode wires and anode
battery pack serving as a foreign body to facilitate the infection.
However, due to this study’s design infection cannot be directly
attributed to the presence of the internal bone stimulator. We believe
it is unlikely that the stimulator placement itself had a significant
effect on the incidence of infection or on the nerve palsies, as they
were placed in conjunction with more significant and risky operative
manipulations: removal of broken or failed hardware, correction of
deformity, bone grafting and repeat fixation.
This study serves well at presenting the potential complications
that implantation of direct current bone stimulators. The use of a
single surgeon in this investigation as opposed to 30 surgeons in the
study by Paterson et al. may well serve as a constant factor when
treating the often heterogenous problem of nonunions.
A significant limitation with a retrospective cohort study is the
inability to draw conclusion regarding treatment effectiveness, due
to lack of a comparable control group. This study in no way can
determine whether implantable bone stimulators are a factor that
contribute to nonunion healing directly, however it does identify the
direct and possible indirect complications that additional implanted
hardware may cause. As in many studies of fracture and nonunion
patients, the group was highly heterogenous with regard to both
patient and injury factors. Because most of these patients were
referral patients to a tertiary center, the variable lengths of followup may underestimate the complications that occur and would be
discovered with longer duration of follow-up. Future investigations
are needed with control groups to determine efficacy of the internal
bone stimulators to heal nonunion. However, with the largely
supportive foundation of evidence that currently exists regarding
the electromagnetic stimulation in the literature and the relative lack
of direct complications, implantable bone stimulators may be an
effective adjuvant to stable internal fixation and autogenous bone
grafting in healing fracture, osteotomy, and arthrodesis nonunions.
References
1. Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic
Cost. 1st ed. Rosemont, IL: American Academy of Orthopaedic Surgeons, 2008.
2. Praemer A, Furner S, Rice D. Musculoskeletal Conditions in the United States. Rosemont, IL:
American Academy of Orthopaedic Surgeons, 1999, p. 182.
3. Peltier, LF. A brief historical note on the use of electricity in the treatment of fractures. Clin
Orthop Relat Res. 1981; 161:4-7.
4. Scott G, King JB. A prospective, double-blind trial of electrical capacitive coupling in the
treatment of non-union of long bones. J Bone Joint Surg Am. 1994; 76(6):820-6.
5. Fukada E, Yasuda I. On the piezoelectric effect of bone. J Phys Soc Japan. 1957; 12: 1158-1162.
6. Bassett CA, Becker RO. Generation of electric potentials by bone in response to mechanical
stress. Science. 1962; 137:1063-4.
7. Bassett CA, Pawluk RJ, Becker RO. Effects of Electric Currents on Bone in Vivo. Nature.
1964; 204:652-4.
8. Brighton CT, Black J, Friedenberg ZB, et al. A multicenter study of the treatment of non-union
with constant direct current. J Bone Joint Surg Am. 1981; 63(1):2-13.
9. Baranowski TJ Jr, Black J, Brighton CT, et al. Electrical osteogenesis by low direct current. J
Orthop Res, 1983; 1(2):120-8.
10. Rubinacci A, Black J, Brighton CT, et al. Changes in bioelectric potentials on bone associated
with direct current stimulation of osteogenesis. J Orthop Res. 1988; 6(3):.335-45.
11. Sharrard, WJ. A double-blind trial of pulsed electromagnetic fields for delayed union of tibial
fractures. J Bone Joint Surg Br. 1990; 72(3):347-55.
12. Brighton CT, Wang W, Seldes R, et al. Signal transduction in electrically stimulated bone cells.
J Bone Joint Surg Am. 2001. 83(10):1514-23.
13. Barker AT, Dixon RA, Sharrard WJ, et al. Pulsed magnetic field therapy for tibial non-union.
Interim results of a double-blind trial. Lancet. 1984; 1(8384):994-6.
14. Simonis RB, Parnell EJ, Ray PS, et al. Electrical treatment of tibial non-union: a prospective,
randomised, double-blind trial. Injury. 2003; 34(5):357-62.
15. Mollon B, da Silva V, Busse JW, et al. Electrical stimulation for long-bone fracture-healing: a
meta-analysis of randomized controlled trials. J Bone Joint Surg Am, 2008; 90(11):2322-30.
16. Health, U.S.F.a.D.A.C.f.D.a.R. Guidance document for industry and CDRH staff for the
preparation of investigational device exemptions and premarket approval applications for bone
growth stimulator devices. Rockville, MD: U.S. Department of Health and Human Services,
1998.
17. Weber B, Czech O. Pseudarthrosen. Wien, Germany: Bern Stuttgart, 1973.
18. Gaston MS, Simpson AH. Inhibition of fracture healing. J Bone Joint Surg Br, 2007;
89(12):1553-60.
19. Fracture and dislocation compendium. Orthopaedic Trauma Association Committee for
Coding and Classification. J Orthop Trauma/ 1996; 10 Suppl 1:v-ix, 1-154.
20. Gustilo RB. Anderson JT. Prevention of infection in the treatment of one thousand and twentyfive open fractures of long bones: retrospective and prospective analyses. J Bone Joint Surg Am.
1976; 58(4):453-8.
21. Gustilo RB, Mendoza, RM, Williams DN. Problems in the management of type III (severe)
open fractures: a new classification of type III open fractures. J Trauma, 1984; 24(8):742-6.
22. Aaron RK, Boyan BD, Ciombor DM, et al. Stimulation of growth factor synthesis by electric
and electromagnetic fields. Clin Orthop Relat Res. 2004; 419:30-7.
23. Wang Q, Zhong S, Ouyang J, et al. Osteogenesis of electrically stimulated bone cells mediated
in part by calcium ions. Clin Orthop Relat Res. 1998; 348:259-68.
24. Chang K, Chang WH, Huang S, et al. Pulsed electromagnetic fields stimulation affects
osteoclast formation by modulation of osteoprotegerin, RANK ligand and macrophage colonystimulating factor. J Orthop Res, 2005; 23(6):1308-14.
25. Tsai MT, Chang WH, Chang K, et al. Pulsed electromagnetic fields affect osteoblast proliferation
and differentiation in bone tissue engineering. Bioelectromagnetics, 2007; 28(7):519-28.
26. Smith TL, Wong-Gibbons, D, Maultsby J. Microcirculatory effects of pulsed electromagnetic
fields. J Orthop Res, 2004; 22(1):80-4.
27. Yen-Patton GP, Patton WF, Beer DM, et al. Endothelial cell response to pulsed electromagnetic
fields: stimulation of growth rate and angiogenesis in vitro. J Cell Physiol, 1988; 134(1):37-46.
28. Paterson DC, Simonis RB. Electrical stimulation in the treatment of congenital pseudarthrosis
of the tibia. J Bone Joint Surg Br, 1985; 67(3):454-62.
29. Kane WJ. Direct current electrical bone growth stimulation for spinal fusion. Spine, 1988;
13(3):363-5.
30. Saxena A, DiDomenico LA, Widfelt A, et al. Implantable electrical bone stimulation for
arthrodeses of the foot and ankle in high-risk patients: a multicenter study. J Foot Ankle Surg,
2005; 44(6):450-4.
31. Donley BG, Ward DM. Implantable electrical stimulation in high-risk hindfoot fusions. Foot
Ankle Int. 2002; 23(1):13-8.
32. Paterson DC, Lewis GN, Cass CA. Treatment of delayed union and nonunion with an implanted
direct current stimulator. Clin Orthop Relat Res. 1980; 148:117-28.
33. Castillo RC, Bosse MJ, MacKenzie EJ, et al. Impact of smoking on fracture healing and risk of
complications in limb-threatening open tibia fractures. J Orthop Trauma. 2005; 19(3):151-7.
34. Porter SE, Hanley EN Jr. The musculoskeletal effects of smoking. J Am Acad Orthop Surg.
2001; 9(1):9-17.
35. Jain AK, Sinha S. Infected nonunion of the long bones. Clin Orthop Relat Res. 2005; 431:57-65.
36. Motsitsi NS. Management of infected nonunion of long bones: the last decade (1996-2006).
Injury. 2008; 39(2):155-60.
37. Struijs PA, Poolman RW,Bhandari M. Infected nonunion of the long bones. J Orthop Trauma.
2007; 21(7):507-11.
54
Volume 4 – 2010
Pediatric Diaphyseal Femur Fractures:
A Comparison of Flexible Versus Rigid Intramedullary Nailing
Daniel J. Cuttica, DO, Doctors Hospital, Columbus, OH; Allan C. Beebe, MD, Nationwide Children’s Hospital, Columbus,
OH; John R. Kean, MD, Nationwide Children’s Hospital, Columbus, OH; Jan E. Klamar, MD, Nationwide Children’s
Hospital, Columbus, OH and Kevin E. Klingele, MD, Nationwide Children’s Hospital, Columbus, OH
Introduction
Corresponding Author:
Fractures of the femoral shaft are common injuries in the
pediatric population, with a reported incidence of 19 per 100,000.1
The etiology of these fractures varies. Causes include: child abuse,
motor vehicle collisions, motor vehicle-pedestrian accidents, falls,
and other high-energy injuries.
Kevin E. Klingele, MD
Department of Orthopedics
Nationwide Children’s Hospital
700 Children’s Drive, Suite A-2630
Columbus, OH 43205-2696
T: 614-722-3393
F: 614-722-3373
Email: Kevin.Klingele@nationwidechildrens.org
No financial support or funding was received for this work.
Background: Fractures of the femoral shaft are common injuries
in the pediatric population. Multiple treatment options for
these fractures exist. In the older child or adolescent who is not
skeletally mature, two common treatment methods include flexible
intramedullary nailing and rigid intramedullary nailing. The purpose
of this study is to compare the outcomes of pediatric diaphyseal
femur fractures managed via intramedullary nailing in skeletally
immature patients aged eight years or older.
Multiple treatment options for these fractures exist, such as
closed reduction with immediate or delayed spica casting, external
fixation, open or submuscular plate fixation, and intramedullary
nailing. Patient age, fracture location and pattern, and experience
and surgeon preference are all factors to consider when choosing a
particular treatment.
Methods: A comparative, retrospective chart and radiographic
review of skeletally immature patients aged eight and older who were
treated by flexible or rigid intramedullary nails were performed. A
minimum of 12-week follow-up was required. Outcomes evaluated
included time to union, incidence of malunion, time to full weightbearing, residual limp, limb length discrepancy, presence of
heterotopic ossification, avascular necrosis, infection, and painful
hardware or nail tip irritation.
In the older child or adolescent who is not yet skeletally mature,
two common treatment methods include flexible intramedullary
nailing and rigid intramedullary nailing. Each method has its
advantages and disadvantages. Reported advantages of flexible
intramedullary nailing include rapid fracture stabilization and patient
mobilization, metaphyseal entry with avoidance of the physis, small
incisions, and short hospital stays.2-8 Disadvantages include soft tissue
irritation by the nail tip and loss of reduction in unstable fractures or in
large children.2,4,8-12 Rigid intramedullary nailing also allows for rapid
patient mobilization, but has the advantage of increased stability.
This aids in the prevention of angular and rotational malalignment
and shortening at the fracture site.2,8,13-16 In the past, a piriformis entry
point was commonly used for rigid, antegrade intramedullary nailing
of pediatric femur fractures. This technique has been shown to have
an incidence of avascular necrosis (AVN) of the femoral head.13,17-19
A trochanteric starting point has lessened the risk of AVN, but several
case reports of AVN do still exist.20,21
Results: There were a total of 77 fractures in 75 patients included in
the study. There were 43 fractures treated with flexible nails (Group
F) and 34 fractures treated with rigid nails (Group R). There was
no difference between the two groups in time to union, residual
limp, or limb length discrepancy. Group R had a significantly
shorter time to full weight-bearing and a significantly greater
incidence of heterotopic ossification. Group F had a significantly
greater incidence of malunion (p = 0.022) and hardware irritation
(p = 0.008). No cases of avascular necrosis were identified.
The purpose of this retrospective review is to compare the outcomes of pediatric diaphyseal femur fractures treated by flexible intramedullary nailing to those treated via rigid, antegrade intramedullary nailing using a trochanteric entry point in skeletally immature
patients aged eight years and older. Outcomes include: time to union
(including incidence of delayed union and nonunion), incidence of
malunion, time to full weight-bearing, incidence of residual limp
and deformity, limb shortening, incidence of heterotopic ossification, and incidence of painful hardware or nail tip irritation.
Conclusion: Rigid intramedullary nailing of pediatric femur
fractures through a trochanteric starting point has a lower incidence
of malunion, shorter time to full weight-bearing, and decreased
incidence of hardware-related complications compared to flexible
intramedullary nailing of pediatric femoral shaft fractures in children
aged eight years and older. There is a higher incidence of heterotopic
ossification at the proximal end of the femur with this method,
however its effects clinically are negligible. Future prospective
studies are necessary to further compare these methods.
Level of Evidence: Level III, retrospective, comparative study
55
Approval from the Institutional Review Board at our hospital
was obtained prior to initiating this study. We retrospectively reviewed
consecutive femoral shaft fractures treated by intramedullary nailing
at our institution from January 1, 2001 to August 1, 2006. 101 patients
were initially identified. Inclusion criteria included: patients treated
with either a flexible titanium nails or stainless steel Enders nails or
with a rigid antegrade trochanteric entry rod; skeletal immaturity with
a minimum age of eight years; and a minimum follow-up of 12 weeks.
Exclusion criteria included: nails using a piriformis starting point,
age less than eight years, skeletal maturity (closed femoral physes),
Volume 4 – 2010
Pediatric Diaphyseal Femur Fractures: A Comparison of Flexible Versus Rigid
Intramedullary Nailing (continued)
and follow-up less than 12 weeks. After applying our inclusion
and exclusion criteria, a total of 77 fractures in 75 patients were
identified. There were 43 fractures treated by flexible intramedullary
nailing (Group F) and 34 fractures were treated by antegrade, rigid
intramedullary nailing with a trochanteric starting point (Group R).
All patients had preoperative anteroposterior and lateral
radiographs of the femur identifying the fracture. Fractures were
classified as transverse, short oblique, long oblique, or comminuted.
All patients were followed at regular intervals with clinical
and radiographic evaluations, and charts and radiographs were
retrospectively reviewed. Clinical outcome measures included time
to full weight-bearing, incidence of residual limp, incidence of
clinically detectable limb length discrepancy, incidence of painful
hardware or nail tip irritation, and incidence of postoperative
infection. Radiographic evaluation included assessment of time
to union, incidence of delayed union and nonunion, incidence of
malunion, incidence of heterotopic ossification, and incidence
of avascular necrosis of the femoral head. Union was defined as
bridging callus across three cortices. Delayed union was defined
as lack of complete healing at 12 weeks. Nonunion was defined as
absence of complete healing at six months. Malunion was defined
as angulation in the coronal plane greater than 5 degrees and in the
sagittal plane greater than 10 degrees at the time of union.22
Treatment group comparisons for categorical outcomes were
statistically evaluated using Fisher’s exact test. For the time to event
outcomes, Kaplan-Meier methods were used to estimate survival
probabilities. Survival curves were compared using the log-rank test.
Results
A total of 77 fractures in 75 patients were treated. Average
patient age was 11.6 years old (range, 8-16 years). Average followup was 47.5 weeks (range. 13-177 weeks). There were 43 fractures
treated with flexible intramedullary nailing (Group F), including 27
fractures treated with stainless steel Enders nails and 16 fractures
treated with titanium flexible nails. There were 34 fractures treated
with a rigid, antegrade, trochanteric intramedullary nail (Group R).
In Group F, fractures were classified as transverse in 27 patients,
short oblique in eight patients, long oblique in five patients, and
comminuted in three patients. In Group R, fractures were classified
as long oblique in 12 patients, transverse in nine patients, short
oblique in seven patients, and comminuted in six patients. As shown
in Table 1, there was a statistically significant association between
treatment and fracture pattern (p=0.006), with a greater proportion
of transverse fractures treated with flexible nails.
The median time to full weight-bearing for Group F was 12
weeks (range, 6-26 weeks). In Group R the median time to full
weight-bearing was 10 weeks (range. 4-13 weeks). The estimated
survival curves were significantly different (log-rank p = 0.0013).
In Group F there were six patients with a residual limp at final
follow-up. Two of these patients had a malunion of their fracture,
while one other patient had a malunion and limb length discrepancy.
Postoperative radiographs were not available for one of these
patients. The final two patients in Group F with a residual limp
had an otherwise uncomplicated course. In Group R, there were
nine patients with a residual limp at final follow-up. Five of these
patients had associated polytrauma, one with a gunshot wound to
the thigh. There were two cases of clinically detectable limb length
discrepancy on physical exam in both groups.
In Group F, there were 13 occurrences of hardware irritation,
all occurring at the nail tip insertion sites, including seven treated
by stainless steel Enders nails and six treated by flexible titanium
nails. Removal of the nails after fracture union provided relief of
symptoms in all 13 patients. In Group R there were two instances
of hardware irritation. In one patient, there was pain at a prominent
distal locking screw. The prominent screw was removed after
fracture union and provided relief of symptoms. The second patient
had persistent anterior thigh pain after fracture union. Removal of
the nail relieved the patient’s symptoms. There was a significantly
greater incidence of hardware-related symptoms in Group F. (p =
0.008)
A total of 64 fractures were available for the radiographic
review. All fractures in both groups went on to union. In Group F the
median time to union was 7 weeks (range, 4-13 weeks). A delayed
union occurred in one patient, which healed uneventfully at 13
weeks. In Group R, the median time to union was 7 weeks (range,
3-13 weeks). A delayed union occurred in one patient, which healed
uneventfully at 13 weeks. There was no statistically significant
difference in the time to union outcome between the two groups.
There were nine malunions in Group F. Four of these malunions
had valgus angulation (range, 7-15 degrees) (see Figure 1), four had
varus angulation (range, 6-9 degrees), and one had apex anterior
angulation (12 degrees). Five of these fractures were classified as
transverse, two were short oblique, one was comminuted, and one
was long oblique. In Group R there were two malunions, both with
valgus angulation (7 and 10 degrees). One fracture was classified
as short oblique and the other as comminuted. The incidence of
malunion was significantly greater in Group F (p = 0.022). These
results are summarized in Table 2.
TABLE 1. Comparison of Fracture Pattern and Procedure
Fracture pattern
Comminuted
Long oblique
Short oblique
Transverse
Total
Flexible nail
Troch nail
Total
3
5
8
27
43
6
12
7
9
34
9
17
15
36
77
56
Volume 4 – 2010
Heterotopic ossification did not occur in any patient in Group
F. In Group R, heterotopic ossification occurred in 12 patients. This
difference was statistically significant. (p < 0.001)
No cases of avascular necrosis were identified in either group.
There was one case of postoperative wound infection in Group R,
which was successfully treated with irrigation and debridement and
antibiotics.
Discussion
In the older child or adolescent who is not yet skeletally
mature, two commonly used treatment methods of femur fracture
stabilization include flexible intramedullary nailing and rigid,
antegrade intramedullary nailing via a trochanteric entry point.
Reported advantages of flexible intramedullary nailing include
rapid fracture stabilization and patient mobilization, metaphyseal
entry with avoidance of the physis, small incisions, and short
hospital stays.2-8 There have been several studies demonstrating the
effectiveness of flexible intramedullary nailing. Heinrich et al, in a
prospective analysis, noted favorable results with flexible nailing as
well as shorter hospital stays and less disruption to family life when
compared to nonoperative treatment methods.6 In a multicenter
study on the early use of flexible titanium nails, excellent to
satisfactory results were seen in 57 of the 58 cases, with the most
common complication being soft tissue irritation at the nail tip.3
Flynn et al compared titanium elastic nailing to traction and spica
Figure 1. A. Initial postoperative radiographs of an 8-year-old
male with a comminuted femoral shaft fracture treated by titanium
flexible intramedullary nailing.
57
Figure 1. B and C. Five and 11 weeks post- op radiographs,
respectively, demonstrating increased valgus angulation.
Volume 4 – 2010
motion, and to return to school than the external fixation group with
fewer complications.23
Rigid intramedullary nailing also allows for rapid patient
mobilization and aids in the prevention of angular and rotational
malalignment and fracture shortening.2,8,13-16 The major reported
complication of this treatment method has been avascular necrosis
of the femoral head, related to a piriformis starting point. The use
of this entry point is believed to be responsible for disruption of the
blood supply to the femoral head. 13.17-19 The use of an entry point
at the tip of the greater trochanter, or lateral to the tip of the greater
trochanter, can help to decrease the risk of this complication.20,21
There has been concern over growth disturbances of the
proximal femur, particularly coxa valga, due to disruption of the
greater trochanter apophysis when a trochanteric entry point has been
used.24 Gage et al demonstrated that arrest of the greater trochanter
apophysis after age eight years had no effect on trochanteric growth.
A more recent radiographic review following intramedullary nailing
via trochanteric entry in pediatric patients with a mean age of 10
years demonstrated no clinically significant proximal femoral
changes. The authors concluded that intramedullary nailing through
a trochanteric starting point in children age nine and older does not
produce a clinically significant proximal femoral deformity.26
Figure 1. D. Six-months post-op radiograph.
casting in a prospective cohort study. The group treated with flexible
nailing had a shorter hospital stay, walked sooner with and without
support, and returned to school earlier than the spica casting group.
Both groups had similar complication rates.4 In a prospective,
randomized study, Bar-On et al compared flexible intramedullary
nailing to external fixation in pediatric femoral shaft fractures. The
authors found a shorter time to full weight-bearing, to full range of
Multiple studies have shown the efficacy of rigid nailing
using a trochanteric starting point.15,16,27 Townsend and Hoffinger
reported satisfactory results in their series of 34 patients, who were
between the ages 10-17 years. All fractures went on to union, and
no infections, rotational deformities, implant failures or avascular
necrosis occurred.16 Momberger et al reported on 50 patients, age
range of 10-16 years, treated with a rigid intramedullary nail through
a trochanteric starting point. No patient had angular or rotational
deformities, avascular necrosis, or proximal femoral deformities.27
In another series, favorable outcomes in 20 patients with an age
range of 11-16 years were reported, with all fractures healing and all
patients returning to pre-injury function.15 However, malunion was
not defined in these three studies.
TABLE 2. Comparison of Malunions
Patient
Age
Height
(cm)
Weight
(kg)
Fracture
type
1
2
3
4
5
6
12
8
12
10
10
9
142
126
168
NR
140
NR
30
23
50
50
50
35
Transverse Proximal 1/3
Short oblique Middle 1/3
Transverse Proximal 1/3
Transverse
Middle 1/3
Transverse
Middle 1/3
Transverse
Middle 1/3
7
8
9
10
11
12
8
8
15
11
152
132
140
NR
159
52
34
22
110
81
Comminuted
Long oblique
Short oblique
Comminuted
Short oblique
NR = not recorded
58
Fracture
location
Middle 1/3
Middle 1/3
Middle 1/3
Distal 1/3
Middle 1/3
Treatment
Deformity
Enders
Titanium
Enders
Enders
Titanium
Enders
9˚ Varus
15˚ Valgus
6˚ Varus
7˚ Varus
10˚ Valgus
12˚ Apex
anterior
8˚ Varus
7˚ Valgus
10˚ Valgus
10˚ Valgus
7˚ Valgus
Enders
Titanium
Enders
Troch nail
Troch nail
Volume 4 – 2010
The purpose of this study was to compare the clinical and
radiographic outcomes of flexible intramedullary nailing to rigid
intramedullary nailing through a greater trochanteric starting point
in the treatment of pediatric diaphyseal femur fractures. We found
a significantly higher incidence of hardware irritation and malunion
in those patients treated with flexible rods. There was a significantly
increased incidence of heterotopic ossification and shorter time to
full weight-bearing in those managed with rigid nails. There was no
significant difference in time to union, residual limp, or shortening
between the two groups.
Hardware irritation from the nail tips is the most commonly
reported complication in flexible intramedullary nailing of pediatric
femur fractures, with an incidence of 7-51% reported.2-5,10-12 An
incidence of 30 percent was found in our study, which is consistent
with previous studies. All of these patients had relief of the symptoms
after nail removal. The incidence of hardware related symptoms was
significantly less in Group R.
Angular deformity is another complication that has been
reported with flexible nailing. Factors associated with an increased
risk of angular deformity include length, unstable fractures,
mismatched nails, and larger patient size.10-12 A recent biomechanical
analysis of titanium elastic nail fixation in pediatric femur fractures
demonstrated an increased risk for loss of reduction in patients
weighing more than 40 to 45 kg.28 In our study, there was a 29
percent (nine fractures) incidence of malunion in Group F and only
a six percent (two fractures) incidence in Group R. In Group F, two
of these malunions occurred in length unstable fractures. Also, there
were three malunions in patients weighing more than 45 kgs in Group
F, one of which was associated with a length unstable fracture. Six of
these malunions occurred in patients treated by stainless steel Enders
nails, while three occurred in patients treated by flexible titanium
nails. Of the three malunions in Group F in patients weighing more
than 45 kgs, all were treated by Enders nails. Of the length unstable
fractures in Group F that went on to malunion, one was treated by
Enders nails and one was treated by flexible titanium nails. Based
on these results, there did not appear to be an association between
malunion and the type of flexible nail used in our study. Finally,
there were no cases of mismatched flexible nails.
A lower incidence of malunion was seen in Group R. All nails
were either statically- or dynamically-locked based on the fracture
pattern, resulting in more stability and increased resistance to length,
angular, and rotational forces.
Of the malunions in Group F, seven fractures progressed from
a well-aligned position to a malaligned position over time, while
two were malaligned after initial treatment. Both of the fractures in
Group R that went on to malunion were stabilized in a malaligned
position and did not progress as in Group F.
There are several limitations of the current study. These include
the retrospective design and variable length of follow-up. However,
this reflects what is seen in the clinical setting,as many patients
with femoral shaft fractures in this age group return to preoperative
function by 12 weeks postoperatively and are subsequently lost
to follow-up. Finally, not all patients had radiographs available
for follow-up, as only 64 of 77 fractures were available for the
radiographic review.
In summary, we conclude that rigid intramedullary nailing
of pediatric femur fractures through a trochanteric starting point
59
has a lower incidence of malunion, shorter time to full weightbearing, and decreased incidence of hardware related complications
compared to flexible intramedullary nailing of pediatric femoral
shaft fractures in children aged eight years and older. There is a
higher incidence of heterotopic ossification at the proximal end
of the femur with this method, however, its effects clinically are
negligible. Future prospective studies are necessary to further
compare these methods.
References
1. Hinton RY, Lincoln A, Crockett MM, et al. Fractures of the femoral shaft in children: Incidence,
mechanisms, and sociodemographic risk factors. J Bone Joint Surg Am. 1999; 81:500-9.
2. Anglen JO, Choi L. Treatment options in pediatric femoral shaft fractures. J Orthop Trauma.
2005; 19:724-33.
3. Flynn JM, Hresko T, Reynolds RA, et al. Titanium elastic nails for pediatric femur fractures:
A multicenter study of early results with analysis of complications. J Pediatr Orthop. 2001;
21:4-8.
4. Flynn JM, Luedtke LM, Ganley TJ, et al. Comparison of titanium elastic nails with traction and
a spica cast to treat femoral shaft fractures in children. J Bone Joint Surg Am. 2004; 86:770-7.
5. Flynn JM, Schwend RM. Management of pediatric femoral shaft fractures. J Am Acad Orthop
Surg. 2004; 12:347-59.
6. Heinrich SD, Drvaric DM, Darr K, et al. The operative stabilization of pediatric diaphyseal
femur fractures with flexible intramedullary nails: A prospective analysis. J Pediatr Orthop.
1994; 14:501-7.
7. Rathjen KE, Riccio AI, De La Garza D. Stainless steel intramedullary fixation of unstable
femoral shaft fractures in children. J Pediatr Orthop. 2007; 27:432-41.
8. Routt ML, Schildhauer TA. Fractures of the Femoral Shaft. In: Green NE, Swiontkowski MF.
Skeletal Trauma in Children. 3rd ed. Saunders; 2003:407-38.
9. Ho CA, Skaggs DL, Tang CW, et al. Use of flexible intramedullary nails in pediatric femur
fractures. J Pediatr Orthop. 2006; 26:497-504.
10. Luhman SJ, Schootman M, Schoenecker PL, et al. Complications of titanium elastic nails for
pediatric femoral shaft fractures. J Pediatr Orthop. 2003; 23:443-7.
11. Narayanan UG, Hyman JE, Wainwright AM, et al. Complications of elastic stable
intramedullary nail fixation of pediatric femoral fractures, and how to avoid them. J Pediatr
Orthop. 2004; 24:363-9.
12. Sink EL, Gralla J, Repine M. Complications of pediatric femur fractures treated with titanium
elastic nails: A comparison of fracture types. J Pediatr Orthop. 2005; 25:577-80.
13. Beaty JH, Austin SM, Warner WC, et al. Interlocking intramedullary nailing of femoral shaft
fractures in adolescents: preliminary results and complications. J Pediatr Orthop. 1994; 14:178-83.
14. Galpin RD, Willis RB, Sabano N. Intramedullary nailing of pediatric femoral fractures. J
Pediatr Orthop. 1994; 14:184-9.
15. Kanellopoulos AD, Yiannakopoulos CK, Soucacos PN. Closed, locked intramedullary nailing
of pediatric femoral shaft fractures through the tip of the greater trochanter. J Trauma. 2006;
60:217-23.
16. Townsend DR, Hoffinger S. Intramedullary nailing of femoral shaft fractures in children via the
trochanter tip. Clin Orthop. 2000; 376:113-8.
17. Astion DJ, Wilber JH, Scoles PV. Avascular necrosis of the capital femoral epiphysis after
intramedullary nailing for a fracture of the femoral shaft: A case report. J Bone Joint Surg Am.
1995; 77:1092-4.
18. O’Malley DE, Mazur JM, Cummings RJ. Femoral head avascular necrosis associated with
intramedullary nailing in an adolescent. J Pediatr Orthop. 1995; 15:21-3.
19. Thometz JG, Lamdan R. Osteonecrosis of the femoral head after intramedullary nailing of
a fracture of the femoral shaft in an adolescent: A case report. J Bone Joint Surg Am. 1995;
77:1423-6.
20. Sanders JO, Browne RH, Mooney JF, et al. Treatment of femoral fractures in children by
pediatric orthopedists: Results of a 1998 survey. J Pediatr Orthop. 2001; 21:436-41.
21. Stans AA, Morrissy RT, Renwick SE. Femoral Shaft Fracture Treatment in Patients Age 6 to 16
Years. J Pediatr Orthop. 1999; 19:222-8.
22. Kasser JR, Beaty JH. Femoral Shaft Fractures. In: Beaty JH, Kasser JR eds. Rockwood and
Wilkins’ Fractures in Children. 6th ed. Lippincott, Williams & Wilkins; 2006:893-936.
23. Bar-On E, Sagiv S, Porat S. External fixation or flexible intramedullary nailing for femoral shaft
fractures in children: A prospective, randomized study. J Bone Joint Surg Br. 1997; 79:975-8.
24. Raney EM, Ogden JA, Grogan DP. Premature greater trochanteric epiphysiodesis secondary to
intramedullary rodding. J Pediatr Orthop. 1993; 13:516-20.
25. Gage JR, Cary JM. The effects of trochanteric epiphysiodesis on growth of the proximal end
of the femur following necrosis of the capital femoral epiphysis. J Bone Joint Surg Am. 1980;
62:785-94.
26. Gordon JE, Swenning TA, Burd TA, et al. Proximal femoral radiographic changes after
lateral transtrochanteric intramedullary nail placement in children. J Bone Joint Surg Am. 2003;
85:1295-301.
27. Momberger N, Stevens P, Smith J, et al. Intramedullary nailing of femoral fractures in
adolescents. J Pediatr Orthop. 2000; 20:482-4.
28. Li Y, Stabile KJ, Shilt JS. Biomechanical analysis of titanium elastic nail fixation in a pediatric
femur fracture model. J Pediatr Orthop. 2008; 28:874-8.
Volume 4 – 2010
Slipped Capital Femoral Epiphysis
Associated With Consumer Products
From the
Department of Orthopaedic Surgery, Indiana School of Medicine, Indiana University,
and the James Whitcomb Riley Children’s Hospital, Indianapolis, Indiana
Address all correspondence to:
Riley Children’s Hospital, Room 4250
702 Barnhill Drive
Indianapolis, Indiana 46202
317-278-0961
FAX 317-274-7197
rloder@iupui.edu
This research was supported in part by the Garceau
Professorship Endowment, Indiana University, Department
of Orthopaedic Surgery, and the Rapp Pediatric Orthopaedic Research Endowment, Riley Children’s Foundation,
Indianapolis, Indiana.
Abstract
Background: Children with slipped capital femoral epiphysis
(SCFE) frequently present to the emergency department (ED).
It was the purpose of this study to review those SCFEs that
present to the ED due to consumer product events using the
National Electronic Injury Surveillance System database.
Materials and Methods: ED visits 2002 through 2006
involving the lower trunk, pubic region, and upper leg were
analyzed. A p < 0.05 was considered statistically significant.
Results: Of 20,594 ED visits for children 9-16 years old,
33 had a diagnosis of SCFE. Those with a SCFE were more
frequently male (78% vs. 61.6%) and more often admitted
to the hospital (85% vs. 7.6%). Race was known for 25
children; there were 19 (63%) White; 5 (28%) Black, and 1
(9%) Amerindian child. With 19 White children, the expected
number of Blacks and Amerindian children would be 33 and
7, respectively, based on prior demographic distributions
of children diagnosed with SCFE. (p = 0.001) The average
incidence was 8.7/100,000 children 9-16 years, with an increase
over time: 2.7/100,000 in 2002 increasing to 13.0/100,000 in
2006 (p = 0.015). The consumer products associated with the
SCFE children were sports and recreational equipment in 27
and falls in 6. The most frequent sports related activity was
basketball in 11 (33%) children, higher than the control group
of children of the same age without SCFE in the database
(6.7%). (p = 1 x 10-6).
Conclusions: There was an increasing incidence of SCFE over
the 5-year study period. SCFE associated with presentation
to the ED with an injury related to consumer products was
higher than expected in White children. The sport most
frequently associated with injuries in children with SCFE
was basketball (33%). The proximal femoral physis seems to
be very vulnerable to biomechanical stresses in basketball.
Level of Evidence: Level II
Slipped capital femoral epiphysis (SCFE) is a common
adolescent hip disorder, and children with this disorder
frequently present to the emergency department (ED). The
child’s onset of symptoms may be associated with a particular
event, such as a sporting/recreational activity or a fall
involving a particular product. The National Electronic Injury
Surveillance System (NEISS) collects patient information
from the NEISS hospitals for all ED visits associated with
consumer products. Since sporting/recreational activities
and falls often involve a consumer product, cases of SCFE
associated with such products will be identified by the
NEISS. It was the purpose of this study to review cases of
SCFE presenting to the ED associated with consumer product
events using the NEISS database.
The detailed NEISS data for ED visits for the 5-year
period, 2002 through 2006, involving the lower trunk, pubic
region, and upper leg (NEISS body part codes 79, 38, and 81)
were downloaded from the NEISS website. Further details
regarding the acquisition of NEISS data is in Addendum I.
Three data columns (those titled diag_other and narr1 and
narr2 [narrative columns describing the details for each ED
visit]) were searched for the following terms: epiphysis,
epiphysiolysis, SCFE, slipped epiphysis, slipped capital
femoral epiphysis. When encountered, the narrative columns
were specifically read to confirm the diagnosis of SCFE.
These cases were considered to be SCFEs; the others were
considered not to be SCFEs and comprise the control group.
The data was then analyzed by gender, race, where the injury
occurred, associated consumer product (for SCFE cases),
and disposition from the ED. Race was classified according
to Eveleth and Tanner1 as White, Black, and Amerindian
(Hispanic and Native American). This study was determined
to be exempt by the local Institutional Review Board.
Statistical Analyses
Continuous data are reported as the mean ±1 standard
deviation. Discrete data are reported as frequencies and
percentages. Analyses between groups of continuous data
60
Volume 4 – 2010
Slipped Capital Femoral Epiphysis Associated With Consumer Products (continued)
were performed with the Student’s t-test (2 groups) or
ANOVA (3 or more groups). Differences between groups of
discrete data were analyzed by the Pearson’s χ2 test. Statistical
analyses were performed with Systat 12 software� (San Jose,
CA, 2007). A p < 0.05 was considered to be statistically
significant.
Results
All cases of SCFE were between the ages 9 – 16 years.
There were 20,594 ED visits for children ages 9-16 years
involving the lower trunk, pubic region, and upper leg; 33
had a diagnosis of SCFE and 20,561 without SCFE. Those
children with a SCFE were more frequently male (78 vs.
61.6%) and admitted to the hospital (85% vs. 7.6%). There
were no differences between those with and without SCFE
by age, race, or where the injury occurred (Table I). There
was a significant increase in SCFE cases over the 5 year span
compared to the non SCFE cases (Cochran’s linear trend, χ2
= 5.87, df = 1, p = 0.015) (Figure 1).
Table 1
Children Presenting To The Ed For Injuries Involving
The Trunk, Pelvis, And Upper Leg:
Those With And Without A SCFE
Variable
Age (yrs)
Gender
M
F
Race
Amerindian
Black
White
ED Disposition
Admit
Release
Injury Location
Home
Public Property
School
With SCFE
12.6 + 1.6
Without SCFE
12.6 + 2.2
26 (79)
7 (21)
12667
7886
1 (9)0
5 (28)
19 (63)
1457 (9.2)0
4413 (28.0)
9913 (62.8)
28 (85)
5 (15)
1543 (7.6)0
18865 (92.4)
6 (30)
11 (55)
3 (15)
6542 (43.8)
5023 (33.6)
3364 (22.5)
Figure 1: The changing incidence of SCFE in children presenting
to the emergency department due to consumer products for injuries
involving the lower trunk, pelvis, and upper leg. The open black box
represents the annual number of SCFE cases and the closed black
rhomboids represent the annual incidence of SCFE in this study.
The solid black line represents the incidence of SCFE in the study
of Lehmann et al. (2), the short hatched black line the incidence in
the study of Kelsey (3), and the long hatched black line the average
incidence in the present study over the 5 year span. The increasing
incidence of SCFEs was statistically significant (Cochran’s linear
trend, χ2 = 5.87, df = 1, p = 0.015).
p value
0.92
average incidence was 8.7/100,000 children ages 9-16.
There was a rapid increase between 2002 (2.7/100,000) and
2006 (13.0/100,000) (Table II, Figure 1). This increase was
statistically significant (Cochran’s linear trend, p = 0.015).
0.03
Discussion
0.37
< 10
Several interesting findings were noted in this study.
Although the average incidence was 8.7/100,000 children ages
9 through 16, similar to the 10.8 and 10.08 in the studies of
-6
Table 2
Changing Incidence Of SCFE Cases
Presenting To The Emergency Department
And Associated With Consumer Products
0.13
The consumer products associated with the 33 SCFEs
were sports and recreational equipment in 27 and falls in 6.
The sports and recreational activities were basketball in 11,
gymnastics in 2, skateboards in 2, bicycles in 2, and band,
dancing, football, kickball, playground equipment, scooter,
skiing, sledding, trampoline, and wrestling in one each. The 6
falls were associated with crutches in 3, with one fall each in
the shower, off a porch, and off a couch. All the falls occurred
in males, although this was not statistically significant (Fisher
exact test, p = 0.30).
The entire number of ED visits for the years 2002 through
2006 for children 9-16 years old was used to calculate the
annual and 5-year average incidence of SCFE. The 5-year
61
Year
Number ED visits
ages 9 through 16
years
# SCFE cases
Incidence per
100,000
2002
75414
2
2.7
2003
76016
5
6.6
2004
75826
7
9.2
2005
73996
9
12.2
2006
77220
10
13.0
Total
378472
33
8.7
Volume 4 – 2010
Lehmann (2) and Kelsey (3), there was about a 5-fold increase
in incidence over the 5-year study period. The numbers in this
study are small and a limitation of this study, yet this increase
was statistically significant. This differs when comparing the
incidence between the 30-year time span before 2000. The
incidence of SCFE for children ages 9 through 16 in 1970 (3)
was 10.08/100,000 and 10.8/100,000 in 2000 (2). Reasons
for the increase is not known but could possibly be due to
better or more accurate coding in the database.
The racial composition of the SCFE children was
different when compared to other studies. SCFEs are more
prevalent in Black and Amerindian children2-5, yet in this
study 76% of the SCFEs were in White children with 28% in
Black and 9% in Amerindian children. The racial composition
of the SCFE group and control group was not statistically
different (9913 White - 62.8%, 4413 Black – 28.0%, 1457
Amerindian – 9.2%) (p = 0.37) and similar to the general US
population < 18 years of age in the year 2000 (67.3% White,
14.8% Black, and 17.9% Amerindian when excluding other
racial groups for the purposes of comparison).6 Using the
racial prevalence for SCFE2 of 1.0 for White, 3.94 for Black,
and 2.53 for Hispanic children, the expected number of Black
and Amerindian SCFE patients for a group of 19 White SCFE
patients in a population having the same racial proportion as
the control group is 33 Black and 7 Amerindian children,
statistically different than the 5 Black and 1 Amerindian child
in this study (χ2 = 13.60, df = 2, p = 0.001). (Figure 2) These
differences will require further investigation.
Figure 2: Observed and expected differences in the racial
proportions of SCFE in children presenting to the emergency
department associated with consumer products.
There was a high association of SCFE with sports injuries;
27 of 33 (81%). The stresses placed across the physis with
these activities are likely a causative factor of SCFE. The
contribution of physical activity to SCFE has been previously
noted, where the stress imposed on the proximal femoral
physis in an obese running adolescent is sufficient to result
in a SCFE.7 Most interesting was that 33% of the consumer
products associated with SCFE was basketball, significantly
greater than the 6.7% in the non-SCFE control group (Fisher
exact test, p = 1 x 10-6).
It could be postulated that football and bicycling would
also induce SCFE due to the significant vertical stresses
placed on the proximal femoral physis during biking and
the impacts on the knees during football. However, there
was no difference in the proportion of children in the nonSCFE NEISS group involved in football when compared to
the SCFE group (11.l% [2282/20561] vs. 3% [1/33], Fisher
exact test, p = 0.086) or in biking (10.1% [2073/18488] vs.
6% [2/31], Fisher exact test, p = 0.77). Thus the proximal
femoral physis seems to be remarkably vulnerable to slipping
when exposed to the biomechanical stresses from basketball.
We postulate that the three-dimensional force vector(s) in
basketball compared to other sports are particularly likely
to result in physeal failure. Basketball involves significant
running and twisting of the trunk and lower extremities,
and perhaps the proximal femoral physis is more sensitive
to this combination of vertical and rotational forces. This
may support the concept (8) that SCFE is not a true slipping
but rather a rotational displacement of the proximal femoral
physis.
The relationship between athletic activities and SCFE
was studied by Murray and Duncan (9), who reviewed three
groups of English males aged 17 to 21 years old. Group A
consisted of 94 males from a boarding school with a strong
emphasis on sports; group B consisted of 77 males from a
boarding school with a stronger emphasis on academics
compared to sports; and group C consisted of 80 males from
public schools where sporting activities were voluntary.
Evidence of SCFE in adolescence, defined as a tilt deformity
of the femoral head, was noted in 24% (23 boys) of group
A, 9% (7 boys) of group B, and 15% (12 boys) of group
C. These differences were statistically different. There was
a suggestion that jumping activities were more frequent
in those with a tilt deformity compared to other athletic
activities. Since basketball was not one of the English sports,
no comparisons can be made between this study and that of
Murray (9).
There are limitations in this study. The first is the small
number of SCFE cases. Another is the absence of other
demographic data commonly reviewed in SCFE studies:
symptom duration, nature of SCFE (stable vs. unstable), body
weight / height / body mass index, laterality, and unilateral/
bilateral nature. However, the strong association between
SCFE and basketball in this study suggest further areas for
investigation.
Addendum 1
The NEISS, operated by the US Consumer Product Safety
Commission (USCPSC), is a probability sample of hospitals
in the U.S. and its territories that have at least six beds and an
emergency department (ED). The sample is stratified based
on ED size and geographic location. Patient information is
collected daily from each NEISS hospital for every patient
62
Volume 4 – 2010
treated in the ED due to an injury associated with consumer
products. National estimates are made of the total number of
product-related injuries treated in U.S. hospital EDs based
on the NEISS data collected from these hospitals. These
estimates can be tailored by year of injury, product involved
in the injury, gender and age of the injured patient, diagnosis,
disposition, location and mechanism of injury, and body part
injured. This data base is in the public domain and can be
found at www.cpsc.gov/library/neiss.html. Further details
regarding NEISS, the sample design, and the coding manual
are available at the same web site.
Detailed injury data, available from 2002 on, gives
a narrative description of each case, allowing for specific
analyses of the injuries. The data is given in codes, with
detailed descriptions at the NEISS web site. The NEISS
codes for the geographical location of the injury are 1
(home), 2 (farm), 4 (street or highway), 5 (other public
property), 6 (mobile home), 7 (place of industry), 8 (school),
9 (recreational or sporting facility), or 0 (unknown). Codes 1,
2, 4, and 6 were grouped into the home group, codes 5 and 9
into the public property group, and 8 as school. Code 7 was
ignored due to the extremely small number in that group. The
NEISS codes for emergency room disposition are 1 (treated
and released), 2 (treated and transferred to another hospital
for admission), 4 (treated and admitted), 5 (observed), 6 (left
without being seen), and 8 (fatality). Codes 2, 4, and 5 were
grouped together as an admission, and code 1 was considered
a release.
63
References
1. Eveleth PB, Tanner JM. Worldwide variation in human growth. 2nd ed. Cambridge: University
Press, 1990.
2. Lehmann CL, Arons RP, Loder RT, Vitale MG. The epidemiology of slipped capital femoral
epiphysis: an update. J Pediatr Orthop. 2006; 26:286-290.
3. Kelsey JL, Keggi KJ, Southwick WO. The incidence and distribution of slipped capital femoral
epiphysis in Connecticut and southwestern United States. J Bone Joint Surg AM. 1970; 52A:1203-1216.
4. Kelsey JL. The incidence and distribution of slipped capital femoral epiphysis in Connecticut. J
Chron Di.s 1971; 23:567-578.
5. Loder RT, and 47 coinvestigators from 33 orthopaedic centers and 6 continents. The
demographics of slipped capital femoral epiphysis. An international multicenter study. Clin
Orthop. 1996; 322:8-27.
6. US Census Bureau. Quick Tables - American Fact Finder. In:: Census 2000 Summary File 2,
Matrices PCT3 and PCT4; 2000. Accessed March 4, 2008.
7. Pritchett JW, Perdue KD. Mechanical factors in slipped capital femoral epiphysis. J Pediatr
Orthop. 1988; 8:385-388.
8. Tayton K. Does the upper femoral epiphysis slip or rotate? J Bone Joint Surg Br. 2007; 89B:1402-1406.
9. Murray RO, Duncan C. Athletic activity in adolescence as an etiological factor in degenerative
hip disease. J Bone Joint Surg Br. 1971; 53-B:406-419.
Volume 4 – 2010
Valgus Slipped Capital Femoral Epiphysis:
Prevalence, Presentation, and Treatment Options
Craig F. Shank, MD,* Eric J. Thiel, MD,* and Kevin E. Klingele, MD†
© 2010, Wolters Kluwer Health/ Lippincott, Williams, & Wilkins.
Shank CF, Thiel EJ, Klingele KE. Valgus Slipped Capital Femoral Epiphysis: Prevalence,
Presentation, and Treatment Options. J Pediatr Orthop. 2010; 30(2):140-146.
Background: Valgus slipped capital femoral epiphysis
(SCFE), defined as posterolateral slippage of the proximal
femoral epiphysis on the metaphysis, is an uncommon
occurrence. The purpose of this study was to review our
institution’s experience with valgus SCFE to better describe
its prevalence, clinical presentation, and treatment.
Methods: Radiographs of patients undergoing treatment of
SCFE between 1996 and 2008 were reviewed. Valgus SCFE
was identified by increased prominence of the lateral femoral
epiphysis relative to the lateral femoral neck and an increased
anteroposterior physis shaft angle. We identified 12 patients
(16 hips) with valgus SCFE and compared them with 123
cases identified as classic posteromedial SCFE.
Results: The prevalence of valgus SCFE at our institution
was 4.7% (12 of 258 patients). Significant differences
between patients with valgus SCFE and those with classic
SCFE were found for age at presentation (mean 1.1 y younger,
P = 0.033), sex (58% female vs. 28% male, P = 0.044), and
classification as atypical SCFE (42% vs. 3%, P < 0.001),
respectively. Four patients in the valgus group had pituitary
and growth hormone dysfunction, and 1 was diagnosed with
Stickler syndrome. Hips of valgus patients had a significantly
higher mean femoral neck shaft angle (154.3 degrees)
as compared with classic SCFE patients (140.5 degrees)
(P < 0.001). Difficulty placing hardware for in situ fixation
was noted in 5 of 11 valgus cases, with 1 case complicated by
articular surface penetration and chondrolysis.
Conclusions: Valgus displacement often presents with a
relatively normal appearance on anteroposterior radiographs.
Valgus SCFE may be associated with obesity, coxa valga,
hypopituitarism, and Stickler syndrome. Posterolateral
displacement of the femoral epiphysis makes in situ fixation
of valgus SCFE more difficult, due to the necessity of a more
medial starting point.
Level of Evidence: Case series, Level IV.
Key Words: slipped capital femoral epiphysis, valgus
(J Pediatr Orthop 2010;30:140–146)
Slipped capital femoral epiphysis (SCFE) is a common
disorder of the adolescent hip. Failure of the proximal femoral physis results in a deformity classically characterized as
medial and posterior displacement of the proximal femoral
epiphysis on the metaphysis. However, as the femoral epiphysis is relatively confined within the acetabulum, the deformity can also be described as displacement of the distal
femur on the proximal epiphysis. In the majority of cases,
the distal fragment is found in varus, extension, and external
rotation relative to the proximal fragment.1 In 1926, Muller2
described a case of lateral and posterior displacements of the
femoral epiphysis on the metaphysis, which has been termed
as valgus SCFE. Since then, at least 26 cases of valgus SCFE
have been described in the orthopaedic literature.3-5 The purpose of this study was to review our institution’s experience
with valgus SCFE to better define its prevalence, clinical presentation, and treatment.
Methods
After approval by the institutional review board, a retrospective radiographic review was performed for all children undergoing operative treatment of SCFE from 1996 to
2008. The SCFE cases were classified as classic (varus) or
valgus based on preoperative and intraoperative radiographs.
Cases with inadequate radiographs for classification were
excluded. No clear criteria defining valgus SCFE could be
found in prior published reports. For the purpose of this study,
a valgus SCFE was defined as apparent posterolateral
slippage of the proximal femoral epiphysis in relationship to
the femoral neck. A unilateral valgus SCFE was defined as
a displaced, painful slip demonstrating: (1) increased prominence of the lateral femoral epiphysis in relation to the lateral
femoral neck (Klein’s line) on an anteroposterior (AP) radiograph and (2) an increased AP physis shaft angle compared
to the contralateral hip (Fig. 1). Bilateral valgus SCFE were
defined by both apparent lateral displacement of the femoral
epiphysis on the femoral neck as well as obvious prominence
of the lateral femoral epiphysis compared to Klein’s line.
Displaced SCFE that did not meet these criteria were classified
as classic, or varus SCFE.
For hips classified as valgus SCFE, measurements
of proximal femoral geometry were made as described by
Yngve et al.5 Measurements were based on the preoperative
AP pelvis and lateral films; AP measurements are illustrated
in Figure 2. Films demonstrating clear rotational differences
64
Volume 4 – 2010
Valgus Slipped Capital Femoral Epiphysis: Prevalence, Presentation,
and Treatment Options (continued)
Statistical Analyses
For statistical calculations, each patient was counted
only once except for radiographic measurements, which
included both hips of bilateral cases. Statistical analyses
were performed with the assistance of Microsoft Excel
(Microsoft Corporation, Redmond, WA) and Statistics
Online Computational Resource (UCLA, Los Angeles, CA).
Continuous variables are reported as the mean ± 1 standard
deviation. Differences between groups of continuous data were
analyzed using both the Student t test and the Wilcoxon
rank-sum test. The results of the nonparametric statistical
method are reported for groups with 10 cases. Comparisons
between affected hips and contralateral unaffected hips were
analyzed using paired tests. Groups of discrete data were
analyzed for differences using the Fischer exact test.
Results
Between 1996 and 2008, 305 patients underwent
treatment of SCFE at the authors’ institution. Radiographs
allowing reliable classification as classic or valgus SCFE were
available for 258. From this group, 12 patients (16 hips) were
defined as valgus SCFE, yielding a prevalence of 4.65%.
Clinical parameters for the classic and valgus SCFE
groups are summarized in Table 1. Statistically significant
differences between the children with valgus and classic
SCFE were found for sex (58.3% female vs. 27.5% male,
P = 0.044), classification as an atypical SCFE (41.7 vs. 3.1%
P = 0.013), and age at presentation (11.6 ± 3.1 vs. 12.7 ± 1.6 y,
FIGURE 1. AP (A) and frog lateral (B) pelvis radiographs of a 10year-old female with a mild right valgus SCFE. Bilateral coxa valga
and increased prominence of the right femoral epiphysis relative to
the lateral femoral neck are demonstrated on the AP view. AP indicates anterioposterior; SCFE, slipped capital femoral epiphysis.
between the extremities were excluded from measurement.
Hospital and outpatient records were reviewed to record
demographic, clinical, and follow-up information for each
patient. Hip stability was determined by ability to bear
weight, and atypical SCFE was defined as SCFE associated
with endocrinopathy or syndrome. For comparison purposes,
a retrospective review of hospital records and radiographs
was performed for classic SCFE cases (n = 123) treated
between November 2002 and December 2008, when a single,
computerized hospital record system began in our institution.
Radiographic measurements, as well as demographic and
clinical information, were recorded in the same manner as
for the valgus patients.
65
FIGURE 2. Illustration of measurements of proximal femoral geometry on anteroposterior (AP) view. Note the increased AP physis
shaft angle on right valgus SCFE versus unaffected contralateral
hip. a = neck shaft angle, b = neck physis angle, g = AP physis shaft
angle, y = AP physeal tilt. SCFE indicates slipped capital femoral
epiphysis.
Volume 4 – 2010
TABLE 1. Clinical Characteristics of Slipped Capital Femoral Epiphysis
Parameter
Classic SCFE (n = 123)
Valgus SCFE (n = 12)
87/33
68/43
19/49
15/28
73/37
72/21
98/3
12.7 ± 1.6
3.3 ± 4.3
160 ± 11.3
73.7 ± 20.6
28.8 ± 7.3
5/7
8/4
5/3
3/1
6/5
10/1
7/5
11.6 ± 3.1
1.8 ± 1.4
156.4 ± 10.8
67.7 ± 20.2
28.7 ± 6.1
Sex (male/female)
Unilateral/bilateral
Side (right/left)
Simultaneous/sequential
Race (white/black)
Stable/unstable
Typical/atypical presentation
Age at presentation (y)
Symptom duration (months)
Height (cm)
Weight (kg)
Body mass index (kg/m2)
P
0.044
0.76
0.10
0.15
0.51
0.45
< 0.001
0.033
0.28
0.37
0.36
0.97
SCFE indicates slipped capital femoral epiphysis.
P = 0.033). Four patients in the valgus group were diagnosed
with endocrine abnormalities before or after developing
SCFE. All 4 had panhypopituitarism resulting in deficiencies
of growth hormone and thyroid hormone, whereas 1 had
adrenal insufficiency and renal failure, as well. A fifth atypical
patient in the valgus group had been diagnosed with hereditary progressive arthroophthalmopathy (Stickler syndrome).
Three of the valgus SCFE patients presented with bilateral
slips, and 1 patient developed a sequential SCFE, also valgus
in nature.
A summary of the radiographic measurements of
proximal femoral geometry for the classic and valgus groups
is presented in Tables 2 and 3 and illustrated in Figure 2. On
the basis of the posterior physeal tilt (Southwick angle), the
SCFE groups demonstrated similar slip severity (33.7 vs. 30
degrees, P = 0.30). For unilateral classic SCFE, the mean
AP physis shaft angle (γ) was 49.7 degrees in the affected
hip versus 60.4 degrees in the unaffected hip (P<0.001,
Table 3). This difference represents an apparent varus
angulation of 10.7 degrees. As expected, the affected side in
unilateral valgus SCFEs demonstrated a significant increase
in the AP physis shaft angle versus the normal side (84.9 vs.
70.4 degrees, P = 0.012), giving a mean valgus angulation of
14.5 degrees.
The mean AP femoral neck shaft angle (α) was
approximately 13 degrees greater in the valgus SCFE group
than the classic SCFE group (154.3 vs. 140.5 degrees). This
difference is statistically significant (P<0.001) and also was
noted in unaffected hips (153 vs. 141.2 degrees, P<0.001).
There was no significant difference in mean AP neck shaft
angle between SCFE hips and unaffected hips (classic
P<0.76, valgus P<0.50), between male and female hips
(P<0.38), or between atypical and idiopathic valgus SCFE
hips (P<0.33). Mean femoral geometry measurements were
not significantly different between the unilateral and bilateral
SCFEs within either group.
Eleven of 12 valgus SCFE patients were treated with
in situ fixation using 6.5 or 7.3 mm cannulated screws. Ten
hips (7 patients) were treated by percutaneous in situ fixation
through the anterior femoral neck, as described by Lindaman
et al6 (Fig. 3). Four valgus hips (4 patients) were pinned
using an open approach to the proximal femur with screws
placed through the anterolateral femoral cortex, according
to the preference of 1 surgeon at our facility. No significant
intraoperative complications were noted in the records.
However, during a number of valgus SCFE cases, surgeons
encountered diffculty achieving fixation perpendicular to
the physis and central in the epiphysis. One case required
placement of a second guidewire and 2 cases required
placement of a second screw to achieve adequate fixation.
In 2 other cases, diffculty placing fixation was noted in the
operative report, and final screw placement was not central on
TABLE 2. Radiographic Measurements of Proximal Femoral Geometry—All Slipped Capital Femoral Epiphysis
Measurement
Posterior physeal tilt (Southwick angle), ϕ
AP physis shaft angle, γ
Neck physis angle, β
Physeal tilt angle, θ
Neck shaft angle, α
33.7 ± 12.6
50.6±10
– 0.4±10
39.8±10
140.5±7.7
Valgus SCFE (n = 16)
30 ± 12.9
84.9±12.4
20.5±10.7
6.9±10.2
154.3±7
AP indicates anterioposterior; SCFE, slipped capital femoral epiphysis.
66
P
0.3
<0.001
<0.001
<0.001
<0.001
Volume 4 – 2010
TABLE 3. Radiographic Measurements of Proximal Femoral Geometry—Unilateral Slipped Capital Femoral Epiphysis
Measurement
Posterior physeal tilt (Southwick angle), ϕ
AP physis shaft angle, γ
Neck physis angle, β
Physeal tilt angle, θ
Neck shaft angle, α
34.2 ± 12.4
49.7 ± 9.50
– 2.5 ± 10.5
40.8 ± 10.0
141.5 ± 7.70
Contralateral Hips
11.1 ± 6.9
60.4 ± 7.1
9.3 ± 5.1
26.8 ± 7.3
141.2 ± 7.3
Valgus SCFE (n = 8) Contralateral Hips
25.9 ± 9.2
84.9 ± 8.7
19.3 ± 8.9
7.7 ± 6.8
155.5 ± 9.1
9.4 ± 5.9|
70.5 ± 8.1|
6.1 ± 4.8|
19.1 ± 8 | |
153.1 ± 5.9|
AP indicates anterioposterior; SCFE, slipped capital femoral epiphysis.
both AP and lateral views. One patient with bilateral, stable,
severe valgus SCFE was managed with staged, surgical hip
dislocations and subcapital osteotomy.
The average length of follow-up for valgus SCFE
patients was 14.4 months (range, 1.8-44 mo). Three patients
developed minor postoperative complications (periincisional numbness, superficial wound dehiscence, minor
leg length discrepancy). No valgus patient developed loss
of fixation, slip progression, or neurovascular injury. Two
patients experienced major complications. The single patient
who managed with staged, subcapital osteotomies developed
segmental osteonecrosis of 1 hip requiring hardware
removal. At the latest follow-up, the patient was ambulatory
without substantial hip stiffness and only occasional pain.
One case of atypical, stable, valgus SCFE that was managed
using an open anterolateral approach required placement
of 2 screws due to difficulty placing fixation lateral enough
in the epiphysis. At the first postoperative visit, the patient
was noted to have severe hip pain, stiffness, and joint-space
narrowing. A computed tomographic (CT) scan showed
evidence of chondrolysis and intra-articular hardware
placement requiring revision of fixation. No other patient in
the valgus group developed radiographic or clinical evidence
of chondrolysis or osteonecrosis. At the latest follow-up,
5 of the remaining 10 patients reported no pain and 5 reported
mild or occasional pain. None were noted to have significant
restrictions in hip range of motion.
Discussion
In the majority of SCFE cases, the capital femoral
epiphysis is displaced posterior and medial relative to the
femoral neck. Muller2 was the first to describe a case of
posterior and lateral displacement and to give the term valgus
SCFE. At least 26 cases have been reported subsequently in
the orthopaedic literature.3–5 Previous case reports and case
series do not describe specific criteria used to identify a
valgus slip on plain radiographs. We chose to define valgus
SCFE by posterior slippage associated with both accentuation
of the lateral epiphysis relative to Klein’s line and increased
lateral tilt of the epiphysis relative to the femoral shaft
(Figs. 1, 2). These criteria were chosen because they have
notable implications regarding the diagnosis and management
of valgus SCFE. Failure of Klein’s line to intersect a
substantial portion of the lateral epiphysis is often advocated
67
to help practitioners recognize SCFE on an AP radiograph.
However, hips with valgus SCFE will appear normal by this
criterion, underscoring the importance of obtaining lateral
and contralateral comparison views in children with hip pain.
Lateral tilt of the epiphysis relative to the femoral shaft is also
an important feature of valgus SCFE because it influences the
optimal trajectory for in situ fixation.
Twelve patients (16 hips) were classified as valgus
SCFE, representing a 4.7% prevalence of SCFE cases at
our institution. Loder and colleagues4 recently reported a
similar prevalence of 4% among 105 children with idiopathic
SCFE. The authors also reviewed prior case reports of valgus
SCFE, calculating an incidence of 1.6% among 757 SCFEs.
Thus, it appears that although valgus displacement occurs
in a minority of SCFE, it is not particularly rare. In fact, it
is probable that clinicians who frequently evaluate children
with hip pain will encounter valgus SCFE. Awareness of its
existence and differences from the classic varus form may
help avoid errors in diagnosis and treatment.
In most cases, the epidemiology of the valgus SCFE
group was quite similar to the group of classic patients studied.
Statistically significant differences between the children with
classic SCFE and those with valgus SCFE were found only
for age at presentation, patient sex, and proportion of atypical
slips. The mean age at presentation (11.6 y) was 1.1 years
younger in the valgus group (P = 0.033). This finding may
be due, in part, to the higher proportion of females among
the valgus patients. Loder et al4 also compared epidemiologic
data of varus and valgus SCFE patients and found a younger
mean age for 4 idiopathic valgus SCFEs at their institution.
However, this was not statistically significant (P = 0.09) and
the average age for all valgus SCFEs reported in the literature
was 12.4 years,4 higher than the average age reported in
1 large SCFE study (12.2 y).7 A male predominance has been
noted in reports of the epidemiology of SCFE,1,7 and this
finding was confirmed among classic SCFE patients at our
institution (72.5% male). However, valgus SCFE patients
at our institution were more likely to be females (58.3%,
P = 0.044). This is consistent with prior reports, in which 19
of 26 cases of valgus SCFE were females (72%).3–5
The etiology of SCFE is not fully understood, but a
number of biomechanical and biochemical factors play
important roles in its development. Obesity, endocrine
changes, collagen abnormalities within the physis, as well
Volume 4 – 2010
as increased obliquity and retroversion of the femoral physis
have all been implicated in the pathogenesis of SCFE.1
Likewise, valgus SCFE has been associated with a number of
potential etiologies. It has been suggested that the appearance
of a varus or valgus SCFE is simply radiographic parallax
caused by variable rotation of the proximal femur. Under
this theory, external rotation of a posteriorly displaced
epiphysis causes the apparent varus displacement observed
in most SCFE cases. Rarely, internal rotation results in a
valgus appearance.8,9 Like Yngve et al,5 we did not observe
rotational differences in trochanter prominence between
classic and valgus slips. Furthermore, 3-dimensional imaging
has confirmed true medial or lateral epiphyseal displacement
in a number of reports on SCFE.3,10–12 In our study, 3 patients
underwent 3-dimensional CT imaging allowing confirmation
of true valgus and posterior displacement. In 1 of these
patients, the deformity was further established by direct
inspection during open surgical hip dislocation.
The impact of patient size on the risk of SCFE is well
established. From our data, it appears likely that obesity
plays a role in the valgus slip, as well. Despite a younger
age and more atypical slips, the mean height, weight, and
body mass index (BMI) of the valgus group did not differ
significantly from the classic group. Furthermore, the
means were quite high (>95th percentile) given the group’s
average age.13 Endocrine changes are also recognized to be
FIGURE 3. AP pelvis (A) and frog lateral (B) radiographs of a
left, valgus SCFE managed with percutaneous, in situ fixation. AP
(C) and frog lateral (D) radiograph status postsingle screw fixation.
AP indicates anterioposterior; SCFE, slipped capital femoral
epiphysis.
an important factor in the pathogenesis of SCFE. Reviews
of the prior literature on valgus SCFE have not noted
endocrine dysfunction to be common in this condition.3,4
Only Yngve et al5 noted an association with endocrinopathy,
reporting 2 patients with underdeveloped genitalia and 1 with
panhypopituitarism in a series of 7 valgus patients. Four of
the 12 valgus patients in our study had endocrine disorders;
all 4 patients suffered from panhypopituitarism resulting in
growth hormone deficiency and hypothyroidism. Both growth
hormone deficiency and hypothyroidism are associated with
an increased risk of SCFE,1,14,15 but we are unaware of any
suggested association with either coxa valga or valgus SCFE.
Interestingly, Docquier et al,15 in a review of orthopaedic
complications of growth hormone therapy, present 1 case of
bilateral coxa valga and valgus SCFE. We also encountered
1 case of valgus SCFE in a patient with Stickler syndrome, a
collagen disorder. An increased incidence of both coxa valga
and SCFE has been found in patients with this condition.16,17
Furthermore, 1 case of posterolateral SCFE has been reported
in a review of orthopaedic manifestations of this condition.17
Although further investigation is necessary, the above data
suggest that both hypopituitarism and Stickler syndrome may
be associated with valgus SCFE.
Structural differences in the proximal femur have been
postulated to contribute to SCFE by increasing shear forces
across the growth plate. Imaging studies of SCFE patients
have demonstrated decreased femoral anteversion as well as
increased slope of the physeal plate in the sagittal and coronal
planes.12,18–20 Biomechanical models have confirmed that these
changes could elevate shear forces beyond the strength of the
proximal femoral physis.21–23 Structural abnormalities have
also been postulated to contribute to valgus SCFE. Previous
authors have suggested that increased femoral anteversion
is associated with valgus SCFE, which could help explain
the female predominance in this condition.4,10 Radiographic
or range of motion data were not available to allow
evaluation of this factor in the present study. Most reports of
valgus SCFE have noted an association with bilateral coxa
valga.3–5,10 Barrios et al18 did not find an association between
classic varus SCFE and neck diaphysis angle, finding an
average neck shaft angle of 141.8 degrees in both SCFE
and control hips.8 In contrast, we found an average neck
shaft angle (α) of 154.3 degrees in valgus SCFE hips (vs.
140.5 degrees in varus hips, P<0.001). This mean angle is
very similar to those observed by Yngve et al (155 degrees)5
and Loder et al (153 degrees).4 Yngve et al5 performed
a biomechanical analysis based on the proximal femoral
geometry of their valgus patients. They calculated that the
combination of coxa valga, lateral physeal tilt, and posterior
tilt could produce posterolateral shear stresses high enough to
cause growth-plate failure, particularly in obese patients.5 Our
analysis of unaffected hips showed that valgus patients have
a decreased medial physeal slope relative to the pelvis (θ) and
femoral shaft (γ) compared with classic patients. However,
this is likely secondary to the increased neck shaft angle in
the valgus group. We did not find significant differences in
AP physeal slope relative to the femoral neck (neck physis
68
Volume 4 – 2010
angle β, P = 0.12) or in posterior physeal slope (Southwick
angle ϕ, P = 0.43) between the unaffected hip groups.
Our review of surgical treatment of valgus SCFE at our
institution found evidence of diffculty placing in situ screw
fixation. Previous authors have noted that central screw
positioning perpendicular to the laterally displaced physis
requires a more medial soft-tissue approach and cortical
entry point than the classic, varus SCFE.3–5,10 This trajectory
makes percutaneous guide wire placement challenging and
may even endanger the femoral neurovascular bundle.4,10 As
a result, Segal et al10 recommend a limited open anteromedial
approach for fixation of valgus SCFE with identification and
protection of the neurovascular structures. In the present
series of 16 hips, no neurovascular complications were noted.
However 2 of the 4 hips in which an open approach was used,
experienced diffculty with screw positioning, 1 resulting in
joint penetration and chondrolysis. Percutaneous fixation did
not result in major complications, but difficulty with screw
positioning was still encountered in 3 of these 10 hips.
Our experience with treatment of valgus SCFE
underscores the importance of recognition of this variant
for the purpose of preoperative planning. Preoperative
3-dimensional imaging should be considered, along with
postoperative CT if doubts exist regarding screw position.
With caution regarding the location of the neurovascular
bundle, percutaneous fixation appears to be safe and effective.
Limited follow-up data indicate that valgus SCFE patients
have a good short-term prognosis, as long as major surgical
complications are avoided. The use of surgical hip dislocation
and corrective osteotomy may play a role in the more severe,
valgus SCFE cases.
The findings of this study must be tempered by
its limitations. The study design was retrospective and
information was not available for all patients for some
clinical and radiographic data points. The small number of
patients in the valgus group limits the statistical power of
the study. We attempted to define specific inclusion criteria
for the valgus group. The criteria are relatively objective in
the case of unilateral slips but, unfortunately, identification
of mild bilateral valgus slips remains quite subjective. We
avoided radiographic classification or measurements based
on films with obvious rotational abnormalities and found few
trochanteric or neck shaft angle differences between affected
and unaffected hips. However, radiographic measurements
of the proximal femur in 2 planes are affected by technique,
patient positioning, and deformity secondary to SCFE.24
Plain radiograph measurements of SCFE geometry have
been shown to overestimate or underestimate some values
compared with CT measurements.25
In conclusion, valgus displacement of the proximal
femoral physis is an unusual presentation of SCFE but occurs
in as many as 4.7% of SCFE patients. Valgus SCFE may
be difficult to identify on the AP radiographic view due to
accentuation of the lateral epiphysis relative to Klein’s line.
Thus, lateral and contralateral hip views are critical to the
radiographic evaluation of adolescent hip pain. Valgus SCFE
69
patients present at a slightly younger age and are more likely
to be female. We found an association between valgus SCFE
and panhypopituitarism, as well as a potential association
with Stickler syndrome. Valgus SCFE was associated
with a significantly increased AP neck shaft angle, which
could increase lateral shear forces on the epiphysis. When
combined with other risk factors such as obesity, endocrine
dysfunction, or collagen abnormalities, physeal failure and
posterolateral displacement can occur. This deformity may
make screw placement for in situ fixation technically difficult.
We recommend thorough preoperative evaluation of the
deformity followed by cautious percutaneous in situ fixation
for mild-to-moderate valgus SCFE. Severe displacement
may make screw placement difficult and increase the risk
of neurovascular injury if done through a percutaneous or
limited open approach. Satisfactory short-term results can be
expected if surgical complications are avoided.
References
1. Aronsson DD, Loder RT, Breur GJ, et al. Slipped capital femoral epiphysis: current concepts.
J Am Acad Orthop Surg. 2006;14: 666–679.
2. Muller W. Eie engstehung von coxa valga durch epiphysenverschiebung. Beitr Z Klin Chir.
1926;137:148–164.
3. Shea KG, Apel PJ, Hutt NA, et al. Valgus slipped capital femoral epiphysis without posterior
displacement: two case reports. J Pediatr Orthop B. 2007;16:201–203.
4. Loder RT, O’Donnell PW, Didelot WP, et al. Valgus slipped capital femoral epiphysis. J
Pediatr Orthop. 2006;26:594–600.
5. Yngve DA, Moulton DL, Evans EB. Valgus slipped capital femoral epiphysis. J Pediatr Orthop
B. 2005;14:172–176.
6. Lindaman LM, Canale ST, Beaty JH, et al. A fluoroscopic technique for determining the
incision site for percutaneous fixation of slipped capital femoral epiphysis. J Pediatr Orthop.
1991;11:397–401.
7. Lehmann CL, Arons RR, Loder RT, et al. The epidemiology of slipped capital femoral
epiphysis: an update. J Pediatr Orthop. 2006; 26:286–290.
8. Griffth MJ. Slipping of the capital femoral epiphysis. Ann R Coll Surg Engl. 1976;58:34–42.
9. Nguyen D, Morrissy RT. Slipped capital femoral epiphysis: rationale for the technique of
percutaneous in situ fixation. J Pediatr Orthop. 1990;10:341–346.
10. Segal LS, Weitzel PP, Davidson RS. Valgus slipped capital femoral epiphysis. Fact or fiction?
Clin Orthop Relat Res. 1996;322:91–98.
11. Shanker VS, Hashemi-Nejad A, Catterall A, et al. Slipped capital femoral epiphysis: is the
displacement always posterior? J Pediatr Orthop B. 2000;9:119–121.
12. Kordelle J, Millis M, Jolesz FA, et al. Three-dimensional analysis of the proximal femur
in patients with slipped capital femoral epiphysis based on computed tomography. J Pediatr
Orthop. 2001;21:179–182.
13. National Center for Health Statistics, Center for Disease Control. Growth charts. 2000. Available
at http://www.cdc.gov/growthcharts. Accessed March 5, 2009.
14. Loder RT, Wittenberg B, DeSilva G. Slipped capital femoral epiphysis associated with
endocrine disorders. J Pediatr Orthop. 1995;15:349–356.
15. Docquier PL, Mousny M, Jouret M, et al. Orthopaedic concerns in children with growth
hormone therapy. Acta Orthop Belg. 2004; 70:299–305.
16. Rose PS, Ahn NU, Levy HP, et al. The hip in Stickler syndrome. J Pediatr Orthop. 2001;21:657–663.
17. Bennett JT, McMurray SW. Stickler syndrome. J Pediatr Orthop. 1990;10:760–763.
18. Barrios C, Blasco MA, Blasco MC, et al. Posterior sloping angle of the capital femoral physis: a
predictor of bilaterality in slipped capital femoral epiphysis. J Pediatr Orthop. 2005;25:445–449.
19. Mirkopulos N, Weiner DS, Askew M. The evolving slope of the proximal femoral growth plate
relationship to slipped capital femoral epiphysis. J Pediatr Orthop. 1988;8:268–273.
20. Pritchett JW, Perdue KD, Dona GA. The neck shaft-plate shaft angle in slipped capital femoral
epiphysis. Orthop Rev. 1989;18: 1187–1192.
21. Gómez-Benito MJ, Moreo P, Pérez MA, et al. A damage model for the growth plate: application
to the prediction of slipped capital epiphysis. J Biomech. 2007;40:3305–3313.
22. Fishkin Z, Armstrong DG, Shah H, et al. Proximal femoral physis shear in slipped capital
femoral epiphysis—a finite element study. J Pediatr Orthop. 2006;26:291–294.
23. Litchman HM, Duffy J. Slipped capital femoral epiphysis: factors affecting shear forces on the
epiphyseal plate. J Pediatr Orthop. 1984;4:745–748.
24. Gekeler J. Radiology of adolescent slipped capital femoral epiphysis: measurement of epiphyseal
angles and diagnosis. Oper Orthop Traumatol. 2007;19:329–44.
25. Richolt JA, Hata N, Kikinis R, et al. Quantitative evaluation of angular measurements on plain
radiographs in patients with slipped capital femoral epiphysis: a 3-dimensional analysis of computed
tomography-based computer models of 46 femora. J Pediatr Orthop. 2008;28:291–296.
Volume 4 – 2010
Outpatient Microdiscectomy for Lumbar Disc Herniation in
Adolescent Patients: Long-Term Follow-up Study
Natalie M. Best MD, Rick C. Sasso MD
Indiana Spine Group and
Indiana University School of Medicine, Indianapolis, IN
Abstract
Study Design: Data collected prospectively were reviewed
for patients aged 19 years or younger who had a discectomy
procedure without arthrodesis as an outpatient.
Objective: The purpose of our article is to investigate the
clinical outcome of discectomy on the lumbar spine in adolescent patients.
Summary of Background Data: Standard discectomy has
been proven to be effective in adult patients and can be done
successfully as an outpatient. Controversy remains over the
best surgical solution for adolescent patients with lumbar disc
herniation. Some have advocated fusion along with discectomy.
Methods: Standard discectomy has been proven to be effective in adult patients and can be done successfully as an outpatient. Controversy remains over the best surgical solution
for adolescent patients with lumbar disc herniation. Some
have advocated fusion along with discectomy.
Results: No patients were hospitalized following the procedure. Two patients (6.5%) had complications. One had a postoperative hematoma, and the other had a recurrent herniation
requiring a subsequent operation. Patient reported outcomes
were favorable with 84.6% stating a good or better outcome.
Conclusions: Results have confirmed favorable results
following lumbar decompression without arthrodesis in adolescent patients for disc herniation. Few required subsequent
operations or had recurrent herniations.
Introduction
Standard discectomy has been routinely performed by
surgeons since it was first used by Mixter and Barr in 1934.1
Microlumbar discectomy (MLD) has since become a standard procedure to decompress the nerve resulting in relief of
many of the common symptoms of leg pain, numbness, and
weakness. Many studies have justified the use of discectomy
without arthrodesis in adult patients for the treatment of lumbar disc herniations.2-11 However, there has been controversy
over the procedure for lumbar herniation in the adolescent
spine due to reports of poor results prompting some to recommend simultaneous arthrodesis.12-22
The incidence of lumbar herniation in pediatric patients
is relatively rare, and the exact number has been debated.
In adolescent patients presenting with back pain, 3-3.7%
have been reported to have a disc herniation.12,14,17,20 Out of
the total population of discectomy procedures, 0.4-3% have
been reported to be on adolescent patients,12,15,16,20,21 and up to
15.4% in a study out of Japan.18 Although not common, the
prevalence of lumbar disc herniation in adolescent patients
remains, along with the difficulty in determining the correct
course of action for these patients. This study aims to validate
the efficacy of outpatient discectomy without arthrodesis in
adolescent patients.
Patient Population
From February, 1992 to August, 2001, 1377 decompression procedures on the posterior lumbar spine without fusion
were retrospectively studied. Thirty-one of these procedures
(2.3%) were performed on teenage patients 19 years of age or
younger. All were performed by one spine surgeon at one of
four facilities. The two main facilities were suburban teaching hospitals. The other facilities were suburban surgery
centers. The demographics of the patients were largely
suburban, mid-to large metropolitan US city residents.
Patients were all diagnosed with herniated nucleus pulposus (HNP), which required the decompression procedure
due to unsatisfactory non-operative treatment. Patients with
structural abnormalities or previous instrumentation were
excluded from the study. All procedures were performed on
one level. Specifically, decompression procedures included
microdiscectomy. Most patients had a unilateral hemilaminotomy. General anesthesia was used on all procedures.
Each procedure was counted separately. There were no exclusions due to sex or medical condition.
Data Collection
A retrospective review was done on all patients by examining their medical records. A comprehensive study was done
recording demographic information, diagnosis, preoperative
visual analog scale (VAS) score (recorded by the patient on
a scale of 1-10 at their pre-operative appointment 3-4 weeks
prior to surgery), level of surgery, and any complications
including recurrence. In addition, it was noted whether the
surgery was done as an inpatient and if so, for what reason.
A procedure was considered outpatient if the patient left the
hospital the same day of surgery, without being hospitalized.
Patients were then contacted by either telephone or mail in
70
Volume 4 – 2010
Outpatient Microdiscectomy for Lumbar Disc Herniation in Adolescent Patients:
Long-Term Follow-up Study (continued)
order to complete an outcome questionnaire. This questionnaire was developed by the principal investigator and
evaluated patient satisfaction with the procedure. An
unbiased observer not involved in the surgical procedures
made the follow-ups 2.5-7.8 years following their surgical
procedure. A minimum follow-up of 2.5 years was chosen
in order to capture all of the complications directly resulting
from the surgery as well as to rate patient satisfaction with the
procedure. Follow-up was first attempted by the telephone.
If the patient could not be reached, a questionnaire was sent
to the patient with the same wording as what was said over
the telephone. VAS scores were done on a scale of 1-10, 10
described as the worst pain imaginable. On the mailed questionnaire, this was done by circling one number from 1-10.
Statistical Methods
Descriptive statistics (number, mean/frequency, standard deviation/percentage, and range) were provided for age,
gender, previous surgery, and pre-operative VAS score for
pain. Summary statistics were listed for both the total patient
population and the patients with post-operative follow-up.
Frequency tables were provided for each of the categorical
variables (number of hospitalizations, number of inpatient
conversions, number of complications, surgical outcome,
and whether the procedure would be repeated). The primary
outcome measurement in this study was conversion to an
inpatient procedure. A Wilcoxon matched pairs test was used
to test for the mean difference between pre-operative and
post-operative VAS scores.
Results
Study Population
In the final study population, 31 consecutive
procedures on patients aged 19 or younger were included.
Thirteen (42%) had a minimum 2.5 year follow-up. The
demographic information for these patients is presented in
Table 1. Eighteen (58%) of the total 31 patient population
were male. Mean age was 17.2. No cases were worker’s
compensation patients, and none were taking part in litigation in relationship to their injury. All procedures were done
on one level. All 31 procedures were done on an outpatient
basis. The average follow-up time was 4.6 years (range 2.57.8 years, SD=1.6). The demographic data for the follow-up
population are in Table 2. Follow-up questionnaires were not
completed due to incorrect contact information, inability to
reach, or refusal to participate. Due to the age of the patients
included in this population, it was difficult to find accurate
contact information two years following their surgery. Many
had moved away or likely changed names due to marriage.
For the patients who did complete the questionnaire, 5 of the
13 (38.5%) were male; the mean age was 17.3. The overall
demographic characteristics of all patients and patients with
follow-ups are similar, except for a lower percentage of male
patients in the follow-up population.
Table 1. Demographic Information
Total Population
N
Mean/ Frequency
Std Dev/ Percent
Minimum
Maximum
Age
31
17.2
1.6
14
19
Gender - Male
31
18
58.1%
Previous Surgery
31
0
0.0%
Pre-Operative VAS (Pain)
28
8.2
1.9
1
10
Table 2. Demographic Information in Follow-up Population
Follow-Up Population
N
Mean/ Frequency
Std Dev/ Percent
Minimum
Maximum
Age
13
17.3
1.7
14
19
Gender - Male
13
5
38.5%
Previous Surgery
13
0
0.0%
Pre-Operative VAS (Pain)
11
8.7
1.4
5
10
71
Volume 4 – 2010
Table 3: Complication Rates, Patient Reported Outcomes
Patients Age 14-19
N
Frequency
Percentage
Inpatient Procedures
31
0
0.0%
Unplanned Inpatient Procedures
31
0
0.0%
Complications
31
2
6.5%
Outcome of Good-Excellent
13
11
84.6%
Would Repeat Procedure
13
10
76.9%
Inpatient Procedures
Reasons for hospitalization were identified from the
operative notes, discharge summaries, and medical charts.
Out of the 31 procedures, none were hospitalized. This information is detailed in Table 3. All of the patients reported that
they were able to leave the same day as the procedure.
Complications
Two of the 31 patients (6.5%) had a complication.
One patient had a recurrent HNP, and the other had a postoperative hematoma. The one patient who had a recurrent
herniation (3.2%) underwent a revision laminectomy at the
same level 4.5 years later. This was the only patient with a
revision in this population. The complication rate is listed in
Table 3.
Patient Reported Outcome
Surgical outcome was reported as excellent, very good,
good, fair or poor by all 13 follow-up participants. Eleven
of the13 patients (84.6%) stated that their surgical outcome
was good or better, and one (7.7%) reported a poor outcome.
When asked whether they would repeat the procedure again
as an outpatient, 10 (76.9%) stated that they would.
Based on patients who had both pre-operative and postoperative pain VAS scores, a calculated mean difference
between these scores was determined. The mean difference
was 6.8 ( p<.001). All patient-reported outcome results are
detailed in Table 3.
Discussion
Recent studies have shown favorable results for discectomy in adolescent patients.16,17,20 However, the debate over
whether a fusion is necessary in such patients remains. A
2008 study by Dewing reported that young, active patients
do well following lumbar microdiscectomy without arthrodesis.3 Many returned to unrestricted active military duty
and had high satisfaction with their outcome. Recurrent her-
niation rate was 3% with four
out of the six requiring additional surgery. Patients included
in that particular study were
between the ages of 19-46 years
with a mean age of 27 years. In
our study, the age was restricted
to patients aged 14-19. Our recurrent HNP rate was 3.2%,
which was similar to the above
study with older patients.
The age restriction for adolescent patients has not been
consistent. When looking at the literature, there was no consensus on what the restriction should be. For this study, we
chose the age of 19 years or younger. Due to the inconsistency of age limitation, it is difficult to compare incidence rates,
and there has been some debate about what the true incidence
is. In this study, 2.3% of all patients who underwent a discectomy were aged 19 years or younger. This is comparable to
other published rates of 0.4% to 3%.12,15,16,20,21 Less than
1% of the total population were 16 years of age or younger,
which is also within the published range.
One difference in this study compared to many of the
other studies on adolescent patients is that we excluded all
patients with structural abnormalities and those who had previous instrumentation. This would likely affect the results as
some patients might have required instrumentation and fusion as well as hospitalization following their procedure. In
this population, all patients received only a microdiscectomy.
In a study by Parisini, he showed worsened results in followup.21 One reason for a difference is that his study included 40
cases of 129 (31%) with structural abnormalities, and four
patients (2.3%) had a fusion done. In long-term follow-up,
10% had reintervention. His study was also conducted on patients who had their surgery between the years of 1975-1991,
which was earlier than all patients in our study. Operative
techniques likely improved following that time period.
Numerous studies have attempted to evaluate treatment
of lumbar herniation in adolescent patients. Some studies
have recommended conservative therapy while others have
stated surgery is necessary in many of these patients due to
conservative therapy resulting in unsatisfactory results. Recent studies have shown favorable results in lumbar surgery
in adolescent patients for HNP.12,13,16-18,20,22 The debate has
been over the necessity of fusing such patients. Most of the
studies done have included patients who had instrumentation
or fusion done. This has resulted in varying results. Some
have recommended the use of fusion, and have shown better
follow-up results with less reinterventions.12,16 Other studies
have stated that fusion is not necessary and that laminotomy
72
Volume 4 – 2010
without fusion is the best option.17,18,20,22 In order to make a
uniform study population, this study only included patients
who did not have fusion or instrumentation. All patients were
therefore able to have the procedure as an outpatient and did
not necessitate hospitalization.
One criticism of performing discectomy procedures on
adolescent patients is the high incidence of reoperation and
recurrent herniations. In this study, only one patient needed
a revision. Higher rates of reoperations have been reported,
ranging from 24-28% of all adolescent patients requiring a
subsequent operation.12,13,20 Our experience has been more favorable with only one patient needing a revision. Certainly,
these patients are susceptible to having a subsequent herniation, but with adequate follow-up, there does not appear to
be worse results following discectomy alone without arthrodesis.
To compare these results with results of the total population would better characterize whether adolescent patients
should be treated similarly to adult patients. A study published
by the above authors showed that microlumbar discectomy
could be performed successfully and safely in patients on an
outpatient basis.2 That study had a complication rate of 8.6%
and a recurrent herniation rate of 6.4%. The rates in this study
are lower. Although this study population is much smaller,
patients did as well as the older patient population. And, the
adolescent patients also had their operations performed on an
outpatient basis with no readmissions or hospitalizations in
the total population. Patients were satisfied with their operation and would have the operation again as an outpatient.
For young patients with disc herniation, outpatient microlumbar discectomy without arthrodesis is a good surgical solution with a low complication rate and high patient
satisfaction. Patients will continue to need follow-up for
recurrent herniation or involvement of another level, but as
these results show, patients do very well following this initial
operation.
73
References
1. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N
Engl J Med. 1934; 211:210-5.
2. Best NM, Sasso RC. Success and safety in outpatient microlumbar discectomy. J Spinal Disord.
2006; 19(5):334-7.
3. Dewing CB, Provencher MT, Riffenburgh RH, et al. The outcomes of lumbar microdiscectomy in a young, active population: correlation by herniation type and level. Spine. 2008;
33(1):33-8.
4. Findlay GF, Hall BI, Musa BS, et al. A 10-year follow-up of the outcome of lumbar microdiscectomy. Spine. 1998; 21:1168-71
5. Hansraj KK, Cammisa FP, O’Leary PF, et al. Decompressive surgery for typical lumbar stenosis. Clin Orthop. 2001; 384:10-7.
6. Iguchi T, Kurihara A, Nakayama I, et al. Minimum 10-year outcome of decompressive
laminectomy for degenerative lumbar spinal stenosis. Spine. 2000; 25:1754-9.
7. Postacchini F. Management of herniation of the lumbar disc. J bone Joint Surg. Br 1999; 81:56776.
8. Silvers HR, Lewis PJ, Asch HL. Decompressive lumbar laminectomy for spinal stenosis. J
Neurosurg. 1993; 78(5)695-701.
9. Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical vs nonoperative treatment for lumbar
disk herniation: the Spine Patient Outcomes Research Trial (SPORT): a randomized trial. JAMA.
2006; 296:2441-50.
10. Weinstein JN, Tosteson TD, Lurie JD, et al. Surgical vs nonoperative treatment for lumbar disk
herniation: the Spine Patient Outcomes Research Trial (SPORT) observational cohort. JAMA.
2006; 296:2451-9.
11. Williams RW. Microlumbar discectomy: a conservative surgical approach to the virgin herniated
disc. Spine. 1978; 3:175-82.
12. DeOrio JK, Bianco AJ. Lumbar disc excision in children and adolescents. J bone Joint Surg Am.
1982; 64:991-6.
13. Durham SR, Sun PP, Sutton LN. Surgically treated lumbar disc disease in the pediatric population: an outcome study. J Neurosurg. 2000; 92(1 suppl): 1-6.
14. Ebersold MJ, Quast LM, Bianco AJ Jr. Results of lumbar discectomy in the pediatric patient.
J Neurosurg. 1987; 67(5):643-7.
15. Ewald W, Eberhardt C, Scholrling S, et al. J Bone Joint Surg Br. 2001; 83(Suppl 2):140-1.
16. Isihara H, Matsui H, Hirano N, et al. Lumbar intervertebral disc herniation in children less
than 16 years of age: Long-term follow-up study of surgically managed cases. Spine. 1997;
22:2044-9.
17. Kumar R, Kumar V, Das NK, et al. Adolescent lumbar disc disease: findings and outcome.
Childs Nerv Sys. 2007; 23:1295-9.
18. Kurihara A, Kataoka O. Lumbar disc herniation in children and adolescents: a review of 70
operated cases and their minimum 5-year follow-up studies. Spine. 1980; 5:443-51.
19. Mayer HM, Brock M. Percutaenous diskectomy in the treatment of pediatric lumbar disk disease. Surg Neuro.l 1988; 29:311-4.
20. Papagelopoulos PJ, Shaughnessy WJ, Ebersold MJ, et al. Long-term outcome of lumbar discectomy in children and adolescents sixteen years of age or younger. J Bone Joint Surg Am. 1998;
80:689-98.
21. Parisini P, Di Silvestre M, Greggi T, et al. Lumbar disc excision in children and adolescents.
Spine. 2001; 26(18):1997-2000.
22. Shillito J Jr. Pediatric lumbar disc surgery: 20 patients under 15 years of age. Surg Neurol. 1996;
46(1):14-8.
Volume 4 – 2010
Clinical Outcomes of Scaphoid and Triquetral Excision With
Capitolunate Arthrodesis Versus Scaphoid Excision and
Four-Corner Arthrodesis
R. Glenn Gaston, MD, Jeffrey A. Greenberg, MD, Robert M. Baltera, MD, Alex Mih, MD, Hill Hastings, MD
© 2009, The Journal of Hand Surgery - American, Volume 34:1407-1412, 2009.
Reprinted with permission, Elsevier Limited, Oxford, United Kingdom
Purpose: To compare the clinical outcomes of scaphoid and
triquetral excision combined with capitolunate arthrodesis
versus 4-corner (capitate, hamate, lunate, triquetrum)
intercarpal arthrodesis.
Methods: We retrospectively identified 50 patients with
scapholunate advanced collapse wrist changes who had
4-corner arthrodesis. Thirty-four patients were able to return
and complete all follow-up evaluations. Patient demographics
were similar between the 2 groups. Follow-up evaluation
included radiographs, wrist range of motion (flexionextension, radial-ulnar deviation, and pronation-supination);
grip strength; visual analog scale (VAS); and Disabilities
of the Arm, Shoulder, and Hand (DASH) questionnaire.
Complications of nonunion, hardware migration, conversion
to wrist arthrodesis or arthroplasty, and pisotriquetral arthritis
were recorded.
Results: Sixteen patients had capitolunate arthrodesis, and 18
patients had a 4-corner arthrodesis. There was no statistical
difference in radial-ulnar deviation, pronation–supination,
grip strength, VAS, or DASH scores between groups. There
was a slight increase in flexion–extension in the 4-corner
group. There were 2 nonunions in the 4-corner group and none
in the capitolunate group. Five patients in the capitolunate
group required screw removal secondary to migration. Three
patients in the 4-corner group required a subsequent pisiform
excision.
Conclusions: Capitolunate arthrodesis compares favorably
to 4-corner arthrodesis at an average 3-year follow-up in this
series with respect to range of motion, grip strength, DASH
scores, and VAS. Advantages of capitolunate arthrodesis
include a lessened need for bone graft harvesting while
maintaining a similarly low nonunion rate, easier reduction
of the lunate following triquetral excision, and avoiding
subsequent symptomatic pisotriquetral arthritis. Screw
migration, however, remains a concern with this technique.
(J Hand Surg 2009;34A:1407–1412. © 2009 Published by
Elsevier Inc. on behalf of the American Society for Surgery
of the Hand.)
From OrthoCarolina, Charlotte, NC; Indiana Hand Center, Indianapolis, IN.
Received for publication December 1, 2007; accepted in revised form May 27, 2009.
No benefits in any form have been received or will be received related directly or
indirectly to the subject of this article.
Corresponding author: R. Glenn Gaston, MD, OrthoCarolina,1025 Morehead Med
Dr., Suite 300, Charlotte, NC 28204; e-mail: glenngaston@hotmail.com.
0363-5023/09/34A08-0005$36.00/0
doi:10.1016/j.jhsa.2009.05.018
Type of Study/Level of Evidence: Therapeutic III.
Key Words: Arthrodesis, capitolunate, fusion, limited,
wrist.
Traditionally, 4-corner arthrodesis has been the recommended motion-sparing procedure for scapholunate advanced collapse (SLAC) wrist based on the large surface area
available for bony union and the proven track record in published series. In Watson’s original article on the management
of SLAC wrist, 3 of the reported 16 patients who had limited
wrist arthrodesis had a capitolunate (CL) arthrodesis with results similar to the patients who had 4-corner arthrodesis.1 In
an earlier work of Watson’s on limited wrist arthrodesis, 3
of 26 patients had CL arthrodesis with favorable results, including 1 patient who “rode 4,753 miles on a bike with hand
brakes.”2 Capitolunate arthrodesis was first reported in 1966
for Kienböck’s disease,3 and early applications of this technique to the SLAC wrist were met with poor outcomes secondary to a high nonunion rate.4,5 The current 4-corner arthrodesis technique advocated by Watson arose from the desire
to increase the surface area for bony union when compared
to CL arthrodesis. Technical refinements of CL arthrodesis
(specifically changing fixation from K-wires to compression
screws) have greatly decreased the incidence of nonunion.
The need for a bone graft is lessened or eliminated, and excising the triquetrum eases lunate reduction and eliminates
pisotriquetral arthritis as a complication.6–8 Although recent
studies have demonstrated improved efficacy of CL arthrodesis, we could find no previous articles that directly compared
a single institution’s experience with CL arthrodesis to the
traditional 4-corner arthrodesis.
The null hypothesis of our study is that no difference
exists in clinical outcomes of 4-corner and capitolunate arthrodesis.
Fifty-seven patients with SLAC deformities who had
4-corner or CL arthrodesis over the last 10 years were identified retrospectively at our institution. Following institutional
review board approval, patients were contacted by phone and
mail to participate in the study. Thirty-one patients had been
treated with 4-corner arthrodesis, and 26 patients had capitolunate arthrodesis. Five patients who had 4-corner arthrodesis using a circle plate were excluded to avoid potential
74
Volume 4 – 2010
Clinical Outcomes of Scaphoid and Triquetral Excision With Capitolunate
Arthrodesis Versus Scaphoid Excision and Four-Corner Arthrodesis (continued)
Table 1. Patient Demographics
Characteristic
4-Corner Arthrodesis
Capitolunate Arthrodesis
SD
P Value
48 y (18-73)
57 y (48-86)
14.1
.04
Male gender
81%
88%
Workers’ compensation
13%
28%
0.4
.10
Smoking history
44%
42%
0.51
.83
High demand
65%
75%
0.46
.47
Age (mean) (range)
device-related confounding complications, as recent studies
have found this technique to have a higher risk of complications than other techniques.9,10 One patient had died of unrelated causes, and 1 patient was incarcerated at the time of the
study. The remaining 50 patients were contacted to participate, of whom 34 were able to return to the office and complete follow-up evaluations. The mean follow-up time of all
patients was 35.5 months (range, 4–110 months). The mean
time of follow-up was 31.0 months for the CL patients and
39.0 months for the 4-corner patients. This difference was not
statistically significant (p = .45). Of the patients who completed follow-up, 16 had CL arthrodesis and 18 had 4-corner
arthrodesis.
The 2 cohorts were similar with respect to patient age,
gender, workers’ compensation status, smoking history, and
level of activity (Table 1). Objective measurements made by
blinded, senior certified hand therapists included range of
motion and grip strength. Subjective patient outcome measures used were the visual analog scale (VAS) and the Disabilities of the Arm, Shoulder, and Hand (DASH) scores. The
incidence of fracture union, hardware migration, conversion
to wrist arthrodesis or arthroplasty, and pisotriquetral arthritis
were recorded. Union was determined based on physical examination findings of absence of tenderness directly over the
arthrodesis site as well as radiographic evidence of bridging
trabeculae at all arthrodesis sites.
loidectomy (12 patients), posterior interosseous neurectomy
(7 patients), carpal tunnel release (3 patients), cubital tunnel
release (1 patient), and carpometacarpal arthroplasty (1 patient). Radial styloidectomy was performed in cases in which,
with radial deviation, there was contact or notable tightness
between the styloid and the trapezium. Autologous bone graft
was harvested from the distal radius in 7 patients and from
the iliac crest in 1 patient to augment the CL likelihood of fusion. In the remaining 8 patients, bone graft was not used.
The same dorsal approach was used for patients having
4-corner arthrodesis. In all cases, the scaphoid was excised.
The lunate extension was corrected, and the lunate, capitate,
hamate and triquetrum were temporarily pinned with 1.14mm (0.45-in) K-wires. Next, their articular cartilage and
subchondral bone was removed with rongeurs and curettes.
Statistical analysis was performed using 2-tailed t-tests
and Fisher’s exact tests with statistical software (SAS software, version 9.1, Carey, NC).
Surgical Technique
The surgical technique for CL arthrodesis was performed
as described by Calandruccio et al., using Accutrak antegrade
compression screws (Accumed Inc., Beaverton, OR) in all
cases (Fig. 1).6 In the majority of cases, the triquetrum was
excised; however, in 4 cases it was retained based on the
treating surgeon’s discretion. We found triquetral resection
to improve the ease of correcting lunate extension. A total
of 24 additional procedures were performed in conjunction
with CL arthrodesis in 15 of 16 patients including radial sty-
75
FIGURE 1: Wrist posteroanterior radiograph following CL
arthrodesis.
Volume 4 – 2010
(1 patient). Autologous bone graft was used in all cases; it
was harvested from the distal radius in 12 cases and from the
iliac crest in 6 cases.
Postoperative management was similar among all patients, consisting of a postoperative splint for 2 weeks followed by 1 month of cast immobilization. K-wires were
only used in the 4-corner patients (9 of these) and they were
removed after clinical and radiographic evidence of healing
was present, typically around 3 months after surgery. Active
and active-assisted range of motion exercise was instituted
at the 6-week postoperative mark with passive range of motion and strengthening exercise commenced at 8 to 12 weeks
based on radiographic and clinical determination of healing.
Results
FIGURE 2: Wrist posteroanterior radiograph following 4-corner
arthrodesis.
Hardware used for 4-corner arthrodesis included K-wires (9
patients), compression screws (6 patients, of whom 5 patients
had compression screws (Accutrak) and 1 had 1.5-mm AO
screws), and compression staples (1 patient) (Fig. 2). A total
of 17 concomitant procedures were performed in 12 of the 18
patients. These included radial styloidectomy (11 patients),
posterior interosseous nerve resection (4 patients), carpal
tunnel release (1 patient), and carpometacarpal arthroplasty
The results are summarized in Table 2. Wrist range of
motion was similar between the 2 groups. The flexion–extension arc averaged 58% of the contralateral side for 4-corner
patients and 48% of the contralateral side for CL patients.
The mean difference between the 2 techniques in terms of
flexion–extension arc was 10.3% (95% CI 0.1, 20.5) and was
slightly statistically significant (p.0477). Radial-ulnar deviation averaged 70% of the contralateral side for 4-corner patients and 60% of the contralateral side for CL patients. The
mean difference between techniques was 9.7% (95% CI 11.7,
31.1) and not statistically significant (p = .35). Pronation–supination arc averaged 98% of the contralateral side in patients
with 4-corner arthrodesis and 99% of the contralateral side in
patients with isolated CL arthrodesis. This small difference
in pronation–supination means of 1.5% was not statistically
significant (p = .56).
Similarly, there was no statistically or clinically significant difference in grip strength between the 2 groups (p = .31,
95% CI -25.5, 8.3). Patients in the 4-corner cohort averaged
78% of the contralateral side, and the CL cohort averaged
70% of the contralateral side. Neither VAS nor DASH was
statistically or clinically different between groups.
With respect to the need for bone graft, only 50% of
CL arthrodesis patients (8 of 16) had bone graft used, versus 100% of 4-corner patients (18 of 18), with a union rate
of 100% in CL patients and 89% in 4-corner patients. This
Table 2. Results
Outcome Measure
4-Corner Arthrodesis
Capitolunate Arthrodesis
P Value
95% CI
Flexion-extension
73˚
63˚
.048
0.1, 20.5
Radial-ulnar deviation
38˚
32˚
.35
11.7, 31.1
Pronation-supination
162˚
167˚
.56
Grip strength
27 kg
23 kg
.31
-25.5, 8.3
VAS
1.1
1.4
.54
-0.84, 1.7
DASH
22
17
.39
-17.1, 6.9
76
Volume 4 – 2010
reliable means of treating SLAC wrist.4,6,7,11 Our treatment
has come full circle since Watson’s original description of
this condition. In his original article, he reports patients having CL arthrodesis. Over the years, 4-corner arthrodesis has
become the limited wrist arthrodesis of choice for most surgeons because of the higher surface area available for fusion
and the high nonunion rate associated with CL arthrodesis. It
is now thought that this high incidence of nonunion in earlier
studies was likely due to inadequate fixation techniques.4,5
Recent studies using compression techniques have demonstrated markedly lower nonunion rates that are equal to or
lower than that reported for 4-corner arthrodesis.6,7
FIGURE 3: A Wrist posteroanterior radiograph following CL
arthrodesis. B Wrist posteroanterior radiograph demonstrating
proximal screw migration.
difference in union rate was not statistically significant (p =
.49). Of patients with nonunion, 1 had fixation with K-wires
and 1 with compression screws.
Five patients in the CL group required removal of their
screws, with 2 patients requiring concomitant wrist arthrodesis. Figures 3A and 3B show the screws to be more prominent
at later follow-up, with erosion into the lunate facet of the
distal radius in Figure 3B. The radiographs are slightly projectionally different; however, these screws had been placed
with direct visualization of them seated beneath the subchondral bone of the lunate at the time of surgery and were noted
to protrude from the subchondral bone and be prominent at
the time of revision surgery. Of the 4 patients who had retention of the triquetrum, 3 required screw removal secondary to
migration. Three of the patients who required screw removal
secondary to migration had bone graft used at the index procedure and 2 did not. All patients who had K-wires placed
for 4-corner arthrodesis had the pins removed electively (8
patients). One patient in the 4-corner group required staple
removal for dorsal impingement.
Two patients in each group had a subsequent revision to
total wrist arthrodesis, and 1 patient in the CL group had conversion to wrist arthroplasty. Three patients in the 4-corner
cohort required a subsequent pisiform excision for pisotriquetral arthritis (3 of 18) versus none in the CL group but this
was not statistically significant (p = .23). The overall number
of revision surgeries, not including elective K-wire removal,
was 5 of 16 patients for CL and 6 of 18 for 4-corner patients.
The rate of revisions was not statistically significant between
groups (p = .897).
When our results are compared with previous reports
on CL arthrodesis, several observations can be made.4,6
Range of motion and grip strength are similar between studies (Figs. 4, 5). The flexion–extension arc has been shown
to be 53%, 48%, and 48% of the contralateral extremity by
Kirschenbaum, Calandruccio, and our study, respectively.4,6
Radial-ulnar deviation has been found to be 60%, 45%, and
60%, respectively, by the same studies. Grip strength has
been shown to be 61%, 70%, and 70% by the same authors,
FIGURE 4: Comparison of wrist range of motion following CL
arthrodesis.
Discussion
Numerous treatment options exist for the management
of SLAC wrist. Recently, CL arthrodesis, combined with
scaphoid and triquetral excision, has been advocated as a
77
FIGURE 5: Comparison of grip strength following CL arthrodesis.
Volume 4 – 2010
VAS. Advantages of 4-corner arthrodesis include a statistically significant improved arc of flexion–extension of 10° and
avoidance of screw back-out. Advantages of CL arthrodesis
include a lessened need for bone graft harvesting while maintaining a similarly low nonunion rate, achieving easier reduction of the lunate following triquetral excision, and avoiding
subsequent symptomatic pisotriquetral arthritis. Triquetral
excision can be particularly beneficial in aiding lunate reduction in the presence of a type II lunate, where colinearity of
the lunate and capitate axes can be challenging to establish
owing to the presence of a hamate facet on the lunate.
FIGURE 6: Comparison of nonunion rates following CL arthrodesis.
References
respectively. However, a marked difference is seen with respect to nonunion rate (Fig. 6). Earlier reports by Krakauer
and Kirschenbaum, using staples and K-wires, had nonunion
rates of 50% and 33%, respectively.4,5 Using newer compression techniques, the rate has been lowered to 18%,6 8%,7 and
ultimately 0% in this study. The nonunion rate for 4-corner
arthrodesis was 11% in our study, which is consistent with
the 4% to 18% rate reported in the literature.12,13
Although many of our outcome measurements had similar means between the 2 groups and were not statistically
significant, the confidence intervals are large, reflecting the
rather small sample size. For example, with respect to grip
strength, the means of the 2 groups were 78% and 72% of
the contralateral limb, a seemingly small difference. The 95%
confidence intervals, however, were -25.5 to -8.6, meaning
that a difference of up to 25% could theoretically exist between the 2 groups, although the difference was not found in
our study.
We found comparable results of CL fusions and 4-corner
fusions at an average 3-year follow-up in this series with respect to range of motion, grip strength, DASH scores, and
1. Watson HK, Ballet FL. The SLAC wrist: scapholunate advanced collapse pattern of degenerative arthritis. J Hand Surg 1984;9A:358–365.
2. Watson HK, Goodman ML, Johnson TR. Limited wrist arthrodesis. Part II: Intercarpal and
radiocarpal combinations. J Hand Surg 1981; 6:223–233.
3. Graner O, Lopes EI, Carvalho BC, Atlas S. Arthrodesis of the carpal bones in the treatment of
Kienböck’s disease, painful unfused fractures of the navicular and lunate bones with avascular
necrosis and old fracture-dislocations of carpal bones. J Bone Joint Surg 1966; 48A:767–774.
4. Kirschenbaum D, Schneider LH, Kirkpatrick WH, Adams DC, Cody RP. Scaphoid excision
and capitolunate arthrodesis for radioscaphoid arthritis. J Hand Surg 1993;18A:780–785.
5. Krakauer J, Bishop A, Cooney W. Surgical treatment of scapholunate advanced collapse.
J Hand Surg 1994;19A:751–759.
6. Calandruccio JH, Gelberman RH, Duncan SF, Goldfarb CA, Pae R, Gramig W. Capitolunate arthrodesis with scaphoid and triquetrum excision. J Hand Surg 2000;25A:824–832.
7. Goubier JN, Teboul F. Capitolunate arthrodesis with compression screws. Tech Hand Upper
Extrem Surg 2007;11:24 –28.
8. Gaston RG, Lourie GM, Floyd WE, Swick M. Pisotriquetral dysfunction following limited
and total wrist arthrodesis. J Hand Surg 2007;32A:1348–1355.
9. Vance MC, Hernandez JD, Didonna ML, Stern PJ. Complications and outcome of four corner
arthrodesis: circular plate fixation versus traditional techniques. J Hand Surg 2005;30A:1122–
1127.
10. Shindle MK, Burton KJ, Weiland AJ, Domb BG, Wolfe SW. Complications of circular plate
fixation for four corner arthrodesis. J Hand Surg 2007;32B:50 –53.
11. Duteille F, Rehart S, Dautel G, Merle M. Capitolunate arthrodesis: the lateral approach. Tech
Hand Upper Extrem Surg 2001;5:212–215.
12. Seigel JM, Ruby LK. A critical look at intercarpal arthrodesis: review of the literature. J Hand
Surg 1996;21A:717–722.
13. Wyrick JD, Stern PJ, Kiefhaber TR. Motion-preserving procedures in the treatment of scapholunate advanced collapse wrist: proximal row carpectomy versus four-corner arthrodesis.
J Hand Surg 1995; 20A:965–970.
78
Volume 4 – 2010
Arthroscopic Coracoclavicular Ligament Reconstruction Utilizing a
Semitendinosis Graft and Titanium Flip Button Tension Band Construct
Vivek Agrawal, MD
The Shoulder Center, PC, Carmel, IN
Correspondence:
Vivek Agrawal MD
The Shoulder Center, PC
12188-A North Meridian Street
Suite 310
Carmel, IN 46032-4406
dragrawal@theshouldercenter.com
(317) 802-9686
Introduction
The surgical treatment of symptomatic complete or
high grade acromioclavicular (AC) joint disruptions remains
controversial with more than 60 published techniques.1
Concerns regarding strength of initial fixation, cyclic failure,
and inconsistent outcomes with techniques similar to the
coracoacromial (CA) ligament transfer first described by
Weaver and Dunn have been reported.2-5 Failure due to
synthetic material abrasion at the clavicle or coracoid as well
as cyclic failure of the synthetic material is a concern with
techniques utilizing a synthetic material construct alone.6, 7
Excellent biomechanical strength and clinical outcomes have
been recently reported with tendon graft coracoclavicular
(CC) reconstruction.8-10 This paper describes an arthroscopic
technique that is equally suitable to acute or chronic high
grade AC joint disruptions as well as previously failed CC
reconstructions. A tension band construct is created utilizing
a single titanium flip button device placed at the inferior
cortex of the coracoid (#7 PE ZipLoop Extended ToggleLoc;
Biomet. Warsaw, IN) combined with a Semitendinosis graft.
Along with offering the benefits of an arthroscopic approach,
the technique also offers the additional advantage of placing
no hardware at the superior aspect of the clavicle.
Figure 1a: Patient with symptomatic Right Grade IV AC Separation.
Figure 1b: Same patient positioned in the semi-lateral decubitus
position with portal sites and clavicle incision outlined.
Surgical Technique
the coracoid is then performed similar to the manner first
described by Wolf.11
After initially learning an arthroscopic AC reconstruction
technique in August 2000, as described by Wolf,11 we have
gradually modified our technique both to address potential
biomechanical and clinical limitations and to formulate the
most reliable technique with inherent applicability for the
broadest possible patient population.
The inferior and lateral aspect of the coracoid process is
clearly visualized followed by a 1.5cm incision in Langer’s
lines at the superior aspect of the clavicle (3cm incision if
also performing a distal clavicle resection). Subcutaneous
dissection is performed followed by subperiosteal elevation
of soft tissues to the anterior and posterior margins of the
clavicle. The periosteum anterior and inferior to the clavicle
is elevated to allow instrument passage to the coracoid.
The clavicular and coracoid tunnels are created utilizing an
arthroscopic ACL guide and a 2.4mm drill point guide wire
as previously described.11 (Figure 2) A 4.5mm cannulated
drill is utilized over the initial guide wire to create a 4.5mm
tunnel in the clavicle and coracoids. (Figure 3) The clavicular
tunnel is placed approximately 35mm proximal to the distal
clavicle, placing it between the trapezoid and conoid ligament
insertions.13, 14
We perform all shoulder arthroscopy procedures in the
modified lateral decubitus position utilizing 6-10 pounds of
counter-traction to suspend the arm. (Figure 1) For patients
that prefer an autograft, we recommend harvesting the
ipsilateral Semitendinosis graft with the patient initially in the
supine position.12 Glenohumeral and subacromial arthroscopy
for diagnosis and treatment is initially performed as required
for each unique patient circumstance. We prefer to address
all other concurrent pathology prior to proceeding with the
CC reconstruction. Visualization of the inferior aspect of
79
Volume 4 – 2010
Titanium Flip Button Tension Band Construct (continued)
The guide wire is removed leaving the cannulated drill in
place. After a pulling suture is passed through the cannulated
drill, superior to sub-coracoid, and retrieved via the anterior
cannula, the pulling suture is tied to the ToggleLoc passing
suture. The ToggleLoc device has two adjustable ZipLoops,
a passing suture loop, and a “zip suture” loop. (Figure 4)
With counter traction applied to the ZipLoops to ensure the
ToggleLoc does not flip prematurely, the ToggleLoc device is
pulled down through the clavicle and coracoid tunnels until
it is clearly visualized inferior to the coracoids. (Figure 5)
The ToggleLoc device is now allowed to flip and engage the
inferior coracoids. (Figure 6)
Figure 4: #7 PE ZipLoop Extended ToggleLoc; Biomet. Warsaw, IN.
Figure 2: Sawbones model demonstrating placement of 2.4mm
drill point guide wire.
Figure 3: Arthroscopic view of 4.5mm cannulated drill over the
initial guide wire at inferior aspect of coracoid.
The “zip suture” loop and one of the ZipLoops is
retrieved anterior to the clavicle leaving one ZipLoop within
the clavicular tunnel and one anterior to the clavicle. (Figure
7) The Semitendinosis graft is passed through the anterior
ZipLoop to create two equal limbs. The appropriate limb
of the “zip suture” loop is pulled to shorten this anterior
ZipLoop, pulling the Semitendinosis graft to the coracoid
tunnel. The ToggleLoc can be rotated or adjusted under direct
visualization, utilizing a probe via the anterior cannula, prior
to fully reducing the anterior ZipLoop. The anterior ZipLoop
is reduced fully, firmly approximating the midpoint of the
Semitendinosis graft to the superior aspect of the coracoid
and fixing the position of the ToggleLoc at the inferior
coracoids. (Figure 8)
One limb of the Semitendinosis graft is now passed
posterior to the clavicle and medial to the clavicular
tunnel to mimic the conoid ligament. With one limb of
the Semitendinosis posterior to the clavicle and the other
anterior, the limbs are passed through the remaining ZipLoop
in the clavicle tunnel. A surgeon’s knot is utilized to tie the
80
Volume 4 – 2010
Figure 5a: ToggleLoc device is pulled down through the clavicle
and coracoid tunnels.
Figure 5b: ToggleLoc device engaged at inferior aspect of
coracoid.
The passing suture is removed from the ToggleLoc
device. Next, the two limbs of “zip suture” are separated and
tied, sliding the knot to the superior aspect of the coracoid
utilizing standard arthroscopic techniques. The excess ends
of the graft are trimmed and the incision is closed in layers
(fascia, subcutaneous, skin). The portals are closed with
simple sutures. The patient wears a simple sling for one
month postoperatively, performing Codman and supine range
of motion exercises daily. Active motion and activities are
gradually increased with most patients returning to all regular
activities at 12-16 weeks postoperatively. We encourage
patients to wait at least 6 months to return to contact sports
(football, rugby, hockey, etc.) and Olympic style lifts (Dead
lift, Snatch, Clean and Jerk). 15
Discussion
Figure 6: Arthroscopic view of ToggleLoc device engaged at
inferior aspect of coracoid.
two limbs of the graft over the clavicle while the clavicle
is held in a reduced position with the arm traction released.
A running locking suture (MaxBraid, Biomet) is utilized to
suture the two limbs together. The “zip suture” is now pulled
to shorten the clavicular ZipLoop until it is shortened as
much as possible. This ZipLoop compresses the graft to the
superior aspect of the clavicle, while also creating a construct
to maintain tension in the graft. (Figure 9)
81
Of the multiple techniques previously described for
high grade AC disruptions, arthroscopic CC reconstruction
has only been described recently.11, 16-21 Although many
techniques focus on transfer of the CA ligament with or
without augmentation, we prefer to avoid utilizing the CA
ligament because the CA ligament may play an important
role in shoulder function.5 Strength of initial fixation, cyclic
failure, and inconsistent outcomes with techniques similar
to the coracoacromial CA ligament transfer first described
by Weaver and Dunn are also of potential concern.3-6, 9,
22
Techniques utilizing only a synthetic material or rigid
fixation to maintain the relationship between the clavicle
and coracoid are inherently reliant on the biologic healing
Volume 4 – 2010
Figure 7: The “zip suture” loop and one of the ZipLoops is retrieved
anterior to the clavicle leaving one ZipLoop within the clavicular
tunnel and one anterior to the clavicle.
Figure 8: The anterior ZipLoop is reduced fully, firmly approximating the
midpoint of the Semitendinosis graft to the superior aspect of the coracoid
and fixing the position of the ToggleLoc at the inferior coracoid.
potential of the patient’s disrupted CC ligaments and may
not be appropriate for chronic AC disruptions or previously
failed reconstructions. The biomechanical and functional
limitations of these techniques have also been studied.4,
6, 7, 23
Recent work focusing on reconstruction of the CC
ligaments with biologic tissue (allograft or autograft) has
shown promising biomechanical and clinical results.8, 10, 13, 20,
22, 24, 25
Our technique builds on and differs from previously
reported open and arthroscopic biologic CC reconstruction
techniques:
• Placing the graft at the superior cortex of the coracoid
more accurately reproduces the anatomic location of the
native CC ligaments and avoids the possibility of anterior
clavicle translation with passage of the graft around the
clavicle.14, 28, 29
• An arthroscopic technique potentially offers reduced
morbidity, improved cosmesis, and the ability to address
concurrent shoulder pathology.11, 16
• The lack of superior hardware placement avoids the potential
for hardware loosening, irritation, or prominence.
• A single 4.5mm tunnel in the clavicle and coracoid instead
of larger or multiple tunnels help reduce the risk of
subsequent fracture.26, 27
• The continuous suture loops placed through the coracoid
and clavicle provide uniform compression of the graft at
the coracoid and clavicle. Rather than relieve load from
the graft, they create a tension band construct to maintain
graft tension and position.
• The risk of neurovascular injury to structures medial to the
coracoid is reduced as no dissection medial to the coracoid
is required.
• The placement of a single drill hole in the clavicle at 35mm
medially allows the two limbs of the graft to reproduce the
anatomic course and function of the Trapezoid and Conoid
ligaments.14
• The #7 Adjustable Loop ToggleLoc Device has an average
peak load of 1664.1N, 374.1lbs with 0mm cyclic loading
slippage under testing resulting in the highly desirable
likelihood of failure of the Semitendinosis graft rather
than at the points of fixation similar to the open technique
described by Lee et al (Biomet Sports Medicine, data on
file).9
• Minimal preparation of the graft is required reducing
operative time.
• The technique utilizes readily available implants and
instruments, familiar to many arthroscopic surgeons,
making it relatively simple to learn.
82
Volume 4 – 2010
patients prospectively for longer term outcomes. In summary,
we present a strong and reliable arthroscopic technique for
anatomic CC reconstruction as an option for significantly
symptomatic high grade acute and chronic AC disruptions as
well as failed CC reconstructions.
References
Figure 9a: Graft passed and tied through clavicular ZipLoop.
Figure 9b: Ziploops fully reduced fixing tension and position of graft.
Figure 9c: Postoperative radiograph of arthroscopic CC reconstruction
technique.
As of January 2010, we have performed the technique
in six patients. All patients had high grade AC disruptions
with disabling symptoms secondary to high energy injuries
(motor vehicle accident, recreational vehicle accident,
bicycle accident, contact sports, or industrial accident). All
six patients also had concurrent shoulder pathology treated
arthroscopically at the same operation (rotator cuff tear-2,
anterior instability-1, posterior instability-1, SLAP Lesion-4)
highlighting the benefits and advantages of an arthroscopic
approach. With an admittedly short follow-up, we have had
no complications or failures to date and find the technique
highly satisfactory for our patients. We continue to follow our
83
1. Rockwood CAJ, Williams, G.R. Jr., Young, D.C. Disorders of the acromioclavicular joint. In:
Rockwood CAJ, Matsen, F.A. III, ed. The Shoulder. 2 ed. Philadelphia: Saunders; 1998:483553.
2. Weaver JK, Dunn HK. Treatment of acromioclavicular injuries, especially complete
acromioclavicular separation. J Bone Joint Surg Am. Sep 1972; 54(6):1187-1194.
3. Harris RI, Wallace AL, Harper GD, Goldberg JA, Sonnabend DH, Walsh WR. Structural
properties of the intact and the reconstructed coracoclavicular ligament complex. Am J Sports
Med. Jan-Feb 2000; 28(1):103-108.
4. Jari R, Costic RS, Rodosky MW, Debski RE. Biomechanical function of surgical procedures
for acromioclavicular joint dislocations. Arthroscopy. Mar 2004; 20(3):237-245.
5. Lee TQ, Black AD, Tibone JE, McMahon PJ. Release of the coracoacromial ligament can lead
to glenohumeral laxity: a biomechanical study. J Shoulder Elbow Surg. Jan-Feb 2001; 10(1):6872.
6. Kippe MA, Demetropoulos CK, Baker KC, Jurist KA, Guettler JH. Failure of coracoclavicular
artificial graft reconstructions from repetitive rotation. Arthroscopy. Sep 2009; 25(9):975-982.
7. Lim YW, Sood A, van Riet RP, Bain GI. Acromioclavicular Joint Reduction, Repair and
Reconstruction Using Metallic Buttons-Early Results and Complications. Techniques in Shoulder
& Elbow Surgery. 2007; 8(4):213-221
8. Nicholas SJ, Lee SJ, Mullaney MJ, Tyler TF, McHugh MP. Clinical outcomes of
coracoclavicular ligament reconstructions using tendon grafts. Am J Sports Med. Nov 2007;
35(11):1912-1917.
9. Lee SJ, Nicholas SJ, Akizuki KH, McHugh MP, Kremenic IJ, Ben-Avi S. Reconstruction
of the coracoclavicular ligaments with tendon grafts: a comparative biomechanical study. Am J
Sports Med. Sep-Oct 2003; 31(5):648-655.
10. Jones HP, Lemos MJ, Schepsis AA. Salvage of failed acromioclavicular joint reconstruction
using autogenous semitendinosus tendon from the knee. Surgical technique and case report. Am
J Sports Med. Mar-Apr 2001; 29(2):234-237.
11. Wolf EM, Pennington WT. Arthroscopic reconstruction for acromioclavicular joint dislocation.
Arthroscopy. May 2001; 17(5):558-563.
12. Wolf EM. Arthroscopic Anterior Cruciate Ligament Reconstruction: TransFix Technique. In:
Chow JCY, ed. Advanced Arthroscopy. New York: Springer-Verlag; 2001:449-450.
13. Mazzocca AD, Santangelo SA, Johnson ST, Rios CG, Dumonski ML, Arciero RA. A
biomechanical evaluation of an anatomical coracoclavicular ligament reconstruction. Am J
Sports Med. Feb 2006; 34(2):236-246.
14. Rios CG, Arciero RA, Mazzocca AD. Anatomy of the clavicle and coracoid process for
reconstruction of the coracoclavicular ligaments. Am J Sports Med. May 2007; 35(5):811-817.
15. Clayer M, Slavotinek J, Krishnan J. The results of coraco-clavicular slings for acromioclavicular dislocation. Aust N Z J Surg. Jun 1997;.67(6):343-346.
16. Laurent L, Gloria PB, Jan L. Arthroscopic Treatment of Acute and Chronic Acromioclavicular
Joint Dislocation. Arthroscopy. 2005; 21:8(1017):e1-e8.
17. Hosseini H, Friedmann S, Troger M, Lobenhoffer P, Agneskirchner JD. Arthroscopic
reconstruction of chronic AC joint dislocations by transposition of the coracoacromial ligament
augmented by the Tight Rope device: a technical note. Knee Surg Sports Traumatol Arthrosc. Jan
2009; 17(1):92-97.
18. Tomlinson DP, Altchek DW, Davila J, Cordasco FA. A modified technique of arthroscopically
assisted AC joint reconstruction and preliminary results. Clin Orthop Relat Res. Mar 2008;
466(3):639-645.
19. Scheibel M, Ifesanya A, Pauly S, Haas NP. Arthroscopically assisted coracoclavicular ligament
reconstruction for chronic acromioclavicular joint instability. Arch Orthop Trauma Surg. Nov
2008; 128(11):1327-1333.
20. Pennington WT, Hergan DJ, Bartz BA. Arthroscopic coracoclavicular ligament reconstruction
using biologic and suture fixation. Arthroscopy. Jul 2007; 23(7):785 e781-787.
21. Wolf EM, Fragomen, A.T. Arthroscopic reconstruction of the coracoclavicular ligaments for
acromioclavicular joint separations. Oper Tech Sports Med. 2004; 12:49-55.
22. Lee SJ, Keefer EP, McHugh MP, et al. Cyclical loading of coracoclavicular ligament
reconstructions: a comparative biomechanical study. Am J Sports Med. Oct 2008; 36(10):19901997.
23. Costic RS, Labriola JE, Rodosky MW, Debski RE. Biomechanical rationale for development
of anatomical reconstructions of coracoclavicular ligaments after complete acromioclavicular
joint dislocations. Am J Sports Med. Dec 2004; 32(8):1929-1936.
24. Wellmann M, Kempka JP, Schanz S, et al. Coracoclavicular ligament reconstruction:
biomechanical comparison of tendon graft repairs to a synthetic double bundle augmentation.
Knee Surg Sports Traumatol Arthrosc. May 2009; 17(5):521-528.
25. Grutter PW, Petersen SA. Anatomical acromioclavicular ligament reconstruction: a
biomechanical comparison of reconstructive techniques of the acromioclavicular joint. Am J
Sports Med. Nov 2005; 33(11):1723-1728.
26. Nalla RK, Stolken JS, Kinney JH, Ritchie RO. Fracture in human cortical bone: local fracture
criteria and toughening mechanisms. J Biomech. Jul 2005; 38(7):1517-1525.
27. McBroom RJ, Cheal EJ, Hayes WC. Strength reductions from metastatic cortical defects in
long bones. J Orthop Res. 1988; 6(3):369-378.
28. Salzmann GM, Paul J, Sandmann GH, Imhoff AB, Schottle PB. The coracoidal insertion of
the coracoclavicular ligaments: an anatomic study. Am J Sports Med. Dec 2008; 36(12):23922397.
29. Morrison DS, Lemos MJ. Acromioclavicular separation. Reconstruction using synthetic loop
augmentation. Am J Sports Med. Jan-Feb 1995; 23(1):105-110.
Volume 4 – 2010
Metastatic Disease of the Extremities: Tips for Management
Daniel Wurtz M.D. and Judd Cummings M.D.
Section of Orthopaedic Oncology
Indiana University Department of Orthopaedic Surgery
Introduction
Advances in the systemic treatment of patients with
metastatic carcinoma and multiple myeloma have improved
survival rates in patients with these diseases. Consequently,
metastatic involvement of the skeleton has become more
common as patient lives are prolonged, and they essentially
live with various degrees of systemic disease. While these
patients are rarely cured of their disease once metastatic,
they require a multidisciplinary team approach to optimize
treatment. The orthopaedic surgeon is an integral member of
this team. Our role in this scenario isn’t to affect a cure, but
to work with other members of the team to reduce pain and
improve the quality of life in these patients. This discussion
will provide some guidelines to orthopaedic surgeons for diagnosis and surgical management of patients with extremity
metastases.
bone disease to orthopaedic surgeons for immediate care
such as fracture fixation. Patients with destructive bone tumors without a diagnosis however need further work-up for
a specific diagnosis and determination of extent of disease
(staging) before surgical treatment is rendered. Above all, the
orthopaedic surgeon should resist the temptation for early
operative intervention to stabilize an involved bone until sufficient work-up has been completed to confirm a diagnosis
of metastatic disease. This work-up may include a biopsy of
the bone lesion before a surgery is performed that may inadvertently contaminate anatomic compartments or neurovascular structures and prevent margin-free surgical resection if
needed for cure. This caution and thoroughness on the part
of the orthopaedic surgeon will help prevent inappropriate
surgical intervention with the unfortunate consequences of
compromised patient outcomes and avoidable litigation.
Current Concepts
Evaluation
The approach to the work-up and treatment of undiagnosed destructive bone lesions has been confusing to both patients and clinicians. Much of the published literature on this
topic covers the “how to’s” of management but fails to elaborate on the logic behind the accepted treatment approach. The
diagnostic possibilities for bone lesions with radiographic
evidence of bone destruction include benign aggressive, primary malignant (with or without distant metastatic disease),
and metastatic from carcinoma or myeloma. The implications
for patient survival for each of these categories of disease
are vastly dissimilar, and each should be handled differently
with its own algorithm. Obviously benign- aggressive (noncancerous) tumors such as giant cell tumor of bone, aneurysmal bone cyst, and chondroblastoma to name a few may
cause local bone destruction but are not life threatening. They
are usually treated with intralesional curettage without need
for aggressive margin-free surgery and systemic treatment is
not needed.
Work-up of patients with known or suspected metastatic bone disease (MBD) begins with a thorough history and
physical exam. Personal or family history of carcinoma in
any patient with musculoskeletal pain should alert the physician to the possibility of metastatic disease. Lung, thyroid,
breast, prostate, and renal carcinomas account for roughly
80% of skeletal metastases.1 Patients typically complain of
deep, aching pain experienced both at rest and with activity.
If a lesion is present at or near a joint, pain can often be elicited with range of motion testing.
Primary malignant bone tumors, on the other hand, are
cancers. Those that are high grade have a significant risk for
systemic metastasis. Prompt surgical treatment is needed to
remove these malignancies with surgical margins free of tumor. This surgery is performed as part of an overall approach
to cure these patients. Patients with metastatic carcinoma
and multiple myeloma are unlikely to be cured of their disease. These cancers have already spread beyond their site of
origin. Systemic treatment for these patients is rendered to
achieve the goals of prolonging survival rather than cure. Understandably, our role as orthopaedic surgeons as members
of the treatment team is to help with efforts for prolonging
survival, controlling pain, and preserving function. Medical
oncologists, emergency room physicians, and other clinicians
frequently refer patients with known diagnoses of metastatic
Laboratory studies can be a useful adjunct in patient
evaluation. While rarely diagnostic of the primary carcinoma, they can help rule out other potential sources for pain or
radiographic abnormality such as infection or diffuse marrow abnormalities (leukemia, myeloma). Routine blood work
should include CBC with differential, chemistry panel including ionized calcium and alkaline phosphatase, and CRP /
sedimentation rate (ESR). Serum protein electrophoresis and
PSA levels should be checked especially in cases of metastatic disease of unknown origin. Tumor serum markers such
as CEA, AFP, CA-125 are not routinely used due to their lack
of specificity.
Imaging studies are crucial to both diagnosis and treatment planning for patients with MBD. Plain radiographs
provide an abundance of information, and when combined
with laboratory and clinical exam findings should allow the
orthopedists to establish an accurate differential diagnosis in
the majority of cases. Metastatic lesions often appear as a
lucent or radiolytic lesion with ill-defined borders. Surrounding bone sclerosis or periosteal reaction is uncommon. Soft
tissue masses are seen infrequently. Some carcinomas, such
as breast and prostate, can present with a mixed or blastic
pattern of bone involvement. Overall, the spine is the most
84
Volume 4 – 2010
Metastatic Disease of the Extremities: Tips for Management (continued)
frequent site of MBD followed by the pelvis and long bones,
particularly the proximal femur and humerus. Acral metastases or metastatic lesions distal to the elbow or knee are rare
and usually herald a poor prognosis. Lung and kidney carcinoma are the most commonly seen cancers metastasizing to
these distant sites.
If a patient is suspected of having MBD by initial history, physical exam and imaging studies, whole body bone
scans are useful to gauge extent of disease. Previously asymptomatic lesions can be diagnosed, monitored, and treated
appropriately. Computed tomography (CT) imaging is useful
to evaluate lesions in the spine and pelvis where complex
anatomical structures are better visualized in three dimensions. Furthermore, CT scanning can assist in surgical planning where resection and arthroplasty reconstruction is being
considered such as the hip or proximal humerus. Finally, CT
scans of the chest, abdomen, and pelvis are useful in detecting a primary cancer when the patient has a presumed metastatic lesion of unknown origin. (Figure 1 A, B) Magnetic
resonance imaging (MRI) has limited utility for MBD. Except in cases with soft tissue extension or spinal lesions with
questionable cord or nerve root involvement, MRI is not routinely indicated.
Management
Key Principles
Management of MBD involves both operative and nonoperative measures. Ideally patients will be monitored by both
A
oncology and orthopedic specialists. Careful consideration of
the patient’s prognosis and expected survival should be made
to avoid placing a terminally ill patient at unnecessary surgical risk. This prognosis for survival depends to a large extent
upon the specific tissue diagnosis of origin for metastatic carcinoma and the extent or stage of disease. Keep in mind that
patients with metastatic carcinoma from breast and prostate
may survive their disease for many years. A collaborative effort between the orthopaedic surgeon and the medical oncologist is necessary in most cases for a meaningful assessment
of the patient overall prognosis. Unfortunately, we as orthopaedic surgeons often discuss our recommendations, but do
not give adequate time to patients with terminal illnesses to
understand their expectations and desires for continued treatment. Understandably, we cannot always predict the shortterm outcome of patients with MBD, but good communication between physicians and patients will help to avoid either
over or under treatment.
The assessment of impending pathologic fracture risk
especially for weight-bearing long bones is crucial to identify
those patients who would benefit from prophylactic stabilization. Scoring systems, while imperfect, have been published
to aid in the prediction of fracture risk.2 In general, those patients with destruction in a lower extremity bone, especially
about the hip, with a radiolytic process that are painful with
weight bearing are at highest risk.3
For those patients with a pathologic fracture due to
metastatic disease, any fixation construct or reconstruction
should allow the patient to bear weight immediately or have
B
Figure 1 (A) A 58-year-old man presented with left shoulder and arm pain without a history of trauma. This AP radiograph shows a
pathologic fracture of the proximal humerus with an unknown primary malignancy. (B) A subsequent work-up of this patient with an axial CT
scan of the abdomen shows the likely source of metastatic disease is from a renal carcinoma of the left kidney.
85
Volume 4 – 2010
functional use of the involved extremity without restriction
in the immediate post-operative period. For this reason, fixation should be as rigid and durable as possible. Usually this
goal is achieved best with careful planning for fixation or reconstruction that will survive much longer than the predicted
longevity of the patient. Protective fixation for the entire involved bone should be considered. The number of interlocking screws in medullary nails should be maximized to prevent
the occurrence of a painful nonunion. Often cement fixation
should be considered to augment fixation particularly when
large destructive tumor voids are present. The principles of
traumatic (non-pathologic) fracture treatment with fixation
do not apply to those that are pathologic. Unlike traumatic
fractures, pathologic fractures due to metastatic disease usually do not heal. Fracture non-unions due to a hostile bone
environment secondary to cancer, radiation, or chemotherapy
are the rule rather than the exception.
Any patient with metastatic disease of unknown origin or diagnosed primary carcinoma with suspected skeletal
metastasis requires biopsy to establish a diagnosis of metastatic carcinoma. In many cases, a biopsy can typically be
done at the time of definitive surgical management with a
frozen section analysis of tissue obtained during the same
anesthetic. The biopsy should be performed in a manner
consistent with recommended biopsy technique to avoid unnecessary contamination in the event the diagnosis proves to
be a primary malignant bone tumor. If the pathologist cannot confirm metastatic disease or if the tissue is not optimal
A
for frozen section analysis, then the surgeon should provide
enough representative tissue for permanent section analysis
and delay any further surgery until a definitive diagnosis is
confirmed. This approach of confirming a suspected carcinoma or myeloma immediately prior to definitive fixation
requires the availability of a competent pathologist, and ideally, the proximity of the lab facility to prepare this tissue in
a timely fashion. Proceeding with caution and the use of a
frozen section will help prevent the unfortunate instrumentation of a primary malignant bone tumor. (Figure 2 A, B,
C) Once MBD has been confirmed, surgical treatment can
be initiated.
Post-operative adjuvant radiation treatment of the metastatic lesion should be considered in all patients. Radiation
therapy should be administered after surgery, not before, to
avoid unnecessary wound healing complications. Consultation with the radiation oncologist is suggested.
Other nonsurgical modalities are available for treatment
of patients with MBD. Pain control efforts supported by a
pain management specialist may have a significant positive
impact on quality of life. Bisphosphonates, radiopharmaceuticals, chemotherapy or hormonal therapies are often
used depending on primary diagnosis and patient co-morbidities. These treatment modalities should be continually
managed by the medical oncology service in consultation
with the orthopaedic surgeon.
B
C
Figure 2 Postoperative radiograph (A) taken after internal fixation of an impending pathologic fracture of the proximal femur. Preoperative
staging studies were not performed. A subsequent biopsy confirmed chondrosarcoma rather than metastatic bone disease and a resection
was performed. (B) Resected proximal femur with initial fixation hardware. (C) Opened specimen shows chondroid tissue consistent with
chondrosarcoma.
86
Volume 4 – 2010
A
B
C
Figure 3 AP radiograph (A) of a 72-year-old with left hip pain. This study shows a lucency in the left acetabulum. (B) An axial CT scan
confirms a radiolytic left acetabulum lesion consistent with metastatic disease. Further staging studies confirmed metastatic lung carcinoma.
(C) A total hip arthroplasty was performed with an acetabular reconstruction using threaded pins and cement fixation.
Recommended Surgical Management by
Anatomic Region
Intertrochanteric Region
Lower Extremity
Femoral Head / Neck
While the spine is the most common site of MBD, lesions in the pelvis and lower extremities are often more debilitating. These areas are subjected to high physiologic stresses
and response to radiation therapy is less predictable. Femoral
head and neck lesions rarely heal and generally require resection and arthroplasty reconstruction.4 If the patient’s general
heath permits, hemi-arthroplasty or total hip arthroplasty is
recommended depending on the presence or absence of acetabular disease and/or arthritic changes. A CT scan of the
pelvis is particularly useful in this setting to evaluate the
hip joint, as acetabular MBD can go unrecognized in a large
percentage of patients.5 The decision to augment acetabular
fixation with screws or cement should be dictated by overall
bone quality and extent of metastatic disease. (Figure 3 A, B,
C) On the femoral side, cement fixation of the stem is generally recommended. This allows for immediate full weightbearing and eliminates the need for biologic fixation that may
be significantly impaired by adjuvant radiation treatment or
metastatic disease. (Figure 4 A, B) Whether to use a long or
conventional length stem is controversial and continues to
be debated. Proponents argue that long stemmed prosthesis
offer the advantage of prophylactically stabilizing the entire
femur in the event of disease progression. Those opposed to
this concept argue that the risk of pulmonary complications
from a large cement load outweigh the theoretic benefit of
a long stem in the absence of documented non-contiguous
metastatic lesions. Regardless of the stem chosen, serious
consideration should be given to cementing techniques that
avoid pressurization so as to avoid potentially life threatening
pulmonary complications.
87
Both impending and realized fractures in this location
can be treated with a variety of techniques including open
reduction and internal fixation (ORIF), use of an intramedullary device, or arthroplasty. The appropriate choice of technique depends on overall patient health and life expectancy,
size of the lesion, amount of fracture displacement, condition
of the hip joint, and experience of the treating surgeon.
Use of a dynamic hip screw and side plate (ORIF) requires medial cortical integrity to be a viable option. Debate
continues regarding the issue of tumor debulking and cement
A
B
Figure 4 AP radiograph (A) of a patient with right hip pain
showing an impending pathologic fracture of the femoral neck.
(B) Reconstruction of the same patient using a cemented long stem
hemiarthroplasty.
Volume 4 – 2010
Subtrochanteric Region
Compressive forces in this region can approximate four
to six times body weight. Both ORIF techniques such as dynamic hip screws or fixed angle devices and intramedullary
nails can be used for both impending and realized fractures.
Intramedullary nails have better success rates with the advantages cited previously. Arthroplasty is reserved for cases of
extensive bone loss or as salvage procedures for failed previous surgery. Proximal femur replacing components are commonly used and require either greater trochanteric osteotomy
or direct abductor repair.
Femoral Diaphysis
A
B
Figure 5 AP (A) and lateral (B) radiographs of a patient with
impending pathologic fracture of the intertrochanteric region of the
proximal left femur. (C) Cephalomedullary nail fixation is preferred
in this location over sliding hip screw and plate devices.
augmentation. Removing gross tumor at the fracture site has
the advantage of decreasing tumor burden but often necessitates a larger exposure and increased blood loss. The residual
tumor cavity should be packed with bone cement in conjunction with fracture reduction and fixation. Unfortunately, even
with cement augmentation, this technique has a moderate incidence of failure.
Intramedullary nail fixation is the treatment of choice for
both impending and realized fractures. Consideration should
be given for placement of reconstruction or cephalomedullary screws even in the absence of documented disease at the
proximal femur or femoral neck, especially for patients with
longer life expectancies. The largest diameter nail possible
should be used and the nail statically locked. Whether to debulk or curette the metastatic lesion and augment the bone
with cement depends on the size of the lesion. This issue may
be somewhat controversial but lesions that occupy greater
than one diaphyseal diameter in the proximal to distal plane
or that prevent cortical contact of at least two cortices may
benefit from cement stabilization.6
Intramedullary devices typically enjoy better success
rates than ORIF techniques in this anatomic location. Advantages include a shorter lever arm and the ability to stabilize
the entire femur. Reconstruction or cephalomedullary screws
should be used. Depending on fracture pattern and surgeon
experience, intramedullary devices can often be inserted with
less blood loss and operative time compared with ORIF techniques. (Figure 5 A, B) If treating an impending fracture with
this technique, the surgeon should be confident of the diagnosis before proceeding. If MBD has not been documented previously, intra-operative frozen sections should be obtained to
confirm metastatic carcinoma. If the diagnosis is uncertain,
additional tissue should be obtained and sent for permanent
analysis and further definitive surgery postponed. Primary
bone sarcomas, while much less common, can masquerade
as MBD and should be treated by an orthopedic oncologist
as shown above.
Arthroplasty can be used as a primary mode of treatment,
especially in cases of extensive bone loss or as a salvage procedure for failed ORIF or prophylactic stabilization. Consideration for use of a calcar replacement stem should be given.
Every effort should be made to preserve the greater trochanter and native abductor mechanism. If this cannot be done, a
proximal femoral replacement (PFR) prosthesis is indicated.
(Figure 6 A, B) Post-operative rehab and therapy must be tailored appropriately to allow for soft tissue healing.
A
B
Figure 6 AP radiograph (A) of the right hip in this patient with renal
cell carcinoma metastasis showing continued tumor progression
around the fixation device and impending implant failure. (B)
Resection of the proximal femur and reconstruction with a cemented
proximal femoral replacement.
88
Volume 4 – 2010
resection with ankle fusion if there is significant bone and
cartilage destruction.
Foot
MBD in the foot is uncommon and portends a poor prognosis. Lung and genitourinary carcinomas account for the
majority of acral metastatic disease. Reconstructive efforts
are difficult especially if there is extensive bony destruction.
Partial amputation or ray resection often provides a better
outcome and less morbidity in these patients whose expected
survival is generally less than one year.
Upper Extremity
A
B
Figure 7 Preoperative AP radiograph (A) in a patient with knee
pain secondary to an impending pathologic fracture from multiple
myeloma involvement in the distal femur near the femoral component
of his knee replacement. Postoperative AP radiograph (B) after
fixation was achieved with a looking plate and screw construct
using intramedullary cement.
Supracondylar Region
Lesions in this area are often difficult to treat secondary to comminution and/or poor bone stock. Fortunately, this
is a relatively uncommon area for MBD involvement. There
are limited studies that discuss optimum treatment strategies.
Generally, lesions are treated with tumor curettage and debulking followed by cement augmentation and ORIF. (Figure
7 A, B) Locked plate constructs can be helpful when host
bone is of poor quality and offer the advantage of unicortical
screw placement if a preexisting femoral stem or IMN is in
place. If the lesion involves the epiphysis or joint, conventional knee arthroplasty or distal femur replacement (DFR)
and hinged knee arthroplasty is chosen depending on the size
of the lesion. The use of a long stemmed tibial component in
this setting depends on surgeon preference and disease status
of the tibia.
In general, patients with metastatic disease of the upper extremity may be treated more conservatively than those
with lower extremity involvement because the problems of
patient immobility are less for this group. For example, patients with impending fracture of the humerus and forearm
may be treated with low profile functional braces or splints
and external beam radiation in the hope of improved pain
control and progress of bone consolidation. However, those
patients with a pathologic fracture rarely heal their fracture
without internal fixation. If these patients have a reasonable
longevity, then internal fixation is usually indicated for pain
control and improved function.
Humerus
The humerus has three regions that may be involved
with metastatic disease. Each is unique and requires consideration for different treatment. The proximal humerus is a
common site for metastatic disease. For those without high
risk for fracture, consideration should be given for radiation
and protection in a sling, and gentle motion with restricted
weight-bearing. Those at high risk for impending fracture
should be treated with adequate fixation that allows for early
motion to avoid problems of shoulder joint stiffness. Often
the region of the head and surgical neck requires plate and
screw fixation approached though a deltopectoral incision.
This fixation is generally more rigid than that achieved with
intramedullary nails with transfixation screws. (Figure 8 A,
B) Unfortunately, this proximal plate and screw constructs do
not protect the remainder of the humerus. Preoperative workup should therefore include radiographs of the entire bone.
Tibia
Fewer than 5% of metastatic lesions involve the distal
extremities or feet. Treatment principles based on anatomic
location are similar to the femur. Proximal, periarticular lesions are managed best with resection and arthroplasty. Metaphyseal lesions, both proximal and distal, can be treated with
curettage, cement, and ORIF techniques. Diaphyseal lesions
are treated with IMN with or without curettage and bone cement. Distal tibia lesions that involve the joint may require
89
A
B
Figure 8 AP radiograph (A) of the proximal humerus showing
a nondisplaced pathologic fracture in a patient with metastatic
carcinoma. Postoperative AP radiograph (B) showing rigid fixation
of the proximal humerus fracture with a locking plate and screw
construct using cement.
Volume 4 – 2010
occurs when surgeons fail to lock intramedullary humeral
nails both proximally and distally. Unfortunately an impending pathologic fracture may progress to a non-healing and
painful fracture due to lack of torsional fixation. Metastatic
disease involving the distal humerus or supracondylar region
should be treated with plate and screw fixation with early,
gentle elbow motion.
Forearm
MBD involving the forearm is much less common than
that found in the humerus. Those patients with fracture or
impending fracture should be treated with plate and screw
fixation.
Conclusion
Figure 9 AP radiograph (A) of the proximal left humerus of a 60year-old female with metastatic breast carcinoma and a pathologic
humerus fracture. Postoperative radiograph (B) showing fixation of
the humerus with a locking intramedullary nail. Note that this nail
construct has proximal and distal fixation screws to insure static
fixation and avoid torsional failure.
The finding of multifocal disease in the humerus warrants
the use of an intramedullary nail with transfixation screws.7
Occasionally patients may present with destruction of the humeral head and require a cemented hemiarthroplasty. Those
with severe destruction of the proximal humerus occasionally
require resection and reconstruction with a proximal humerus
replacement. Patients with disease of the humeral diaphysis
are best treated with locked medullary nails that span the entire length of the humerus. (Figure 9 A, B) A common pitfall
Patients with metastatic bone disease frequently require
orthopaedic intervention to insure improved quality of life
and pain control. While some patients may not need surgical
fixation of pathologic fractures or impending fractures, many
will require durable bone fixation or replacement. Thoughtful evaluation of these patients in concert with collaboration
with other members of the oncology team will help the surgeon optimize treatment for these patients.
References
1. Bauer HCF: Controversies in the surgical management of skeletal metastases. J Bone Joint Surg.
2005; 87B:608-17.
2. Mirels H. Metastatic disease in long bones. A proposed scoring system for diagnosing impending
pathologic fractures. Clin Orthop. 1989; 249:256-64.
3. Hipp JA, Springfield DS, Hayes WC. Predicting pathologic fracture risk in the management of
metastatic bone defects. Clin Orthop. 1995; 312:120-35.
4. Camnasio F, Scotti C, Peretti GM, et al. Prosthetic Joint Replacement for Long Bone Metastases: Analysis of 154 Cases. Arch Orthop Trauma Surg. 2008; 128(8):787-93.
5. Wunder JS, Ferguson PC, Griffin AM, Pressman A, Bell RS: Acetabular Metastases: Planning for Reconstruction and Review of Results. Clin Orthop. 2003; 415:187-97.
6. Harrington KD. Orthopaedic management of extremity and pelvic lesions. Clin Orthop. 1995;
312:136-47.
7. Redmond BJ, Biermann JS, Blasier RB. Interlocking intramedullary nailing of pathological
fractures of the shaft of the humerus. J Bone Joint Surg Am. 1996; 78:891-96.
90
Volume 4 – 2010
Advances in Orthopaedic Oncology for 2010
Corresponding Author:
8450 Northwest blvd
Indianapolis, IN 46278
brougraff@aol.com
(317)802-2451
Introduction
Early improvements in orthopedic oncology started
from recognizing and carefully diagnosing tumors in a
similar and reproducible way. Once standard diagnoses and
grade evaluations of these unusual tumors were established,
clinical outcomes could be addressed. Chemotherapy for bone
sarcomas was initially utilized in the 1960’s in combination
with radical amputation. In the 1970s, improvement in
survival was found with the use of chemotherapy for
Ewing’s sarcoma and osteosarcoma.. In the 1980s and 90s
the evolution of limb sparing operations for both bone and
sarcomas with adjuvant treatment became commonplace,
instead of amputations. Similarly, imaging studies became
much improved and refined with the use of three-dimensional
imaging technology. Thus, the multidisciplinary approach to
orthopedic oncologic problems became mainstream approach
to patients with sarcoma due to these improvements in
radiology, pathology and surgery.
From a surgical standpoint, most resection and
reconstruction techniques were developed by orthopaedic
surgeons who continue to treat the majority of sarcomas to
this day. In 2010, the greatest challenge for physicians treating
sarcoma patients is the early recognition and improved
treatment of metastatic disease. A great deal of research and
hope is placed in the future of directed therapy to attack
sarcomas from the widely expanding field of oncogenetics
and exploiting gene translocations associated with many
orthopedic oncologic tumors. Surgical reconstruction
techniques are likewise improving, and radiographic staging
studies improve as the role of modern radiographic studies
continues to evolve.
This review will discuss the most common bone and soft
tissue sarcomas, good and poor prognostic findings, relative
cure rates, and the near future improvements anticipated in
the treatment of these challenging patients.
Osteosarcoma
Osteosarcoma is the most common primary malignancy
of bone in children and represents 20% of all primary bone
sarcomas. The incidence of osteosarcoma is four or five cases
per million individuals per year which translates to about 1000
to 1500 newly diagnosed cases in the United States each year.
Osteosarcoma is a primary cancer of bone which is defined as
91
Figure1 A-B Radiograph and biopsy
example of a 26-year-old male with a
distal femoral osteosarcoma. He was
treated with pre-surgical chemotherapy,
followed by resection and metal
endoprosthesis reconstruction.
a malignant proliferation of cells that synthesize and deposit
bone matrix.1,2 A conventional osteosarcoma represents 75%
of all osteosarcoma cases and is manifested by an aggressive
lytic and sometimes a blastic bone lesion in the metaphysis
of long bones. (Figure 1A-B) It is most commonly seen the
distal femur and proximal tibia and less likely occurs in the,
proximal humerus, pelvis or other bone sites. There are several
subtypes of osteosarcoma, including Paget’s sarcoma which
has a very poor prognosis and develops in an area of previous
pagetoid bone. Parosteal and periosteal osteosarcomas are
lower grade variants that occur on the surface of bones, that
typically do not need chemotherapy and can be treated with
wide surgical resection and reconstruction.3 Conventional
osteosarcomas are more commonly seen in males than
females, typically occur in the second decade of life, and
present as a painful soft tissue and bone mass. Occasionally
the patient will present with a pathologic fracture through the
lesion, which carries a very poor prognosis.
There are typically no systemic symptoms associated
with osteosarcomas. Fevers, weight loss and general malaise
are not symptoms typically seen in patients diagnosed with
osteosarcoma. A painful firm, deep mass of the extremity or
pelvis are the most common presenting symptom. Laboratory
studies are nonspecific, although alkaline phosphatase may
be elevated. Typically, the diagnosis is made from the plain
radiograph of the involved extremity or bone site. Further
imaging with whole body bone scan, computed tomography
(CAT scan), and magnetic resonance imaging (MRI)
further defines the local and systemic extent of the disease.
A carefully placed biopsy must be carried out to finalize
the diagnosis. The placement of the biopsy is critical so
that the biopsy site can be resected at the same time as the
tumor resection. Contamination of neurovascular structures
or postoperative fractures can result in an amputation for
the patient. It is strongly recommended that the biopsy be
performed by someone who is well-versed in the treatment
of osteosarcomas. The biopsy of osteosarcoma will typically
show a malignant cells forming osteoid on Hematoxylin and
Eosin (H&E) staining. No specific genetic error is associated
with osteosarcoma, although multiple genetic alterations can
Volume 4 – 2010
Advances in Orthopaedic Oncology for 2010 (continued)
be seen at times with these patients. There are no known
environmental agents associated with the development of
osteosarcoma.
After establishing the diagnosis with biopsy, the initial
treatment for osteosarcoma is pre-surgical chemotherapy.
Surgical resection and reconstruction or amputation is
typically performed after two to three months of the
neoadjuvant chemotherapy. Patients with metastatic disease
at the time of diagnosis, which is usually found in the lung,
have much poorer survival rates. These patients are treated
with chemotherapy, surgical resection of the primary tumor,
and attempts at metastatectomy, if feasible. Chemotherapy
for osteosarcoma typically involves doxorubicin, high-dose
methotrexate, cisplatin and ifosfamide. Surgical resection
is required for cure. Various surgical reconstruction options
have improved over the last 20 years including allograft
reconstruction, prosthetic-allograft reconstruction, large
metal endoprosthetic reconstruction, rotationplasty, and
vascular bone graft reconstruction.
Good prognostic factors for conventional osteosarcoma
include a negative chest CAT scan at the time of diagnosis,
a primary tumor < 8 cm, resectable disease, chemotherapyinduced tumor necrosis of > 90%, and distal sites of disease.
Poor prognostic factors for conventional osteosarcoma
include skip marrow metastases, a positive chest CAT scan,
a primary tumor > 8 cm, and presentation with a pathologic
fracture. The overall five-year survival rate of patients with
non-metastatic conventional osteosarcoma treated with
chemotherapy and surgery is 65%.4 If the chest CAT scan
is positive for metastases at the time of diagnosis, only 20
to 25% of these patients will live five years. Osteosarcoma
patients have a longer length of survival with aggressive
metastatectomy and aggressive chemotherapy. The future
treatment for conventional osteosarcoma includes finding
more effective treatment for metastatic disease, improved
skeletal reconstruction, and techniques that find better limb
lengthening and equalization. Other future developments
will be looking for better identification of high-risk patients
and in improved delivery of chemotherapy in these high risk
patients.
Ewing’s Sarcoma
Ewing’s sarcoma accounts for 1% of all childhood
tumors. It is the second most common primary bone sarcoma
of childhood and adolescence.5-10 Most patients are between
five and 30 years of age at the time of diagnosis. The incidence
of Ewing’s sarcoma in the United States is two cases per
million per year. It is unusual in African-Americans and
also less likely in Asian-Americans than Caucasians. Unlike
osteosarcoma, the treatment of Ewing sarcoma with surgery
alone has a nearly fatal outcome. Ewing’s sarcoma, unlike
osteosarcoma, is radiosensitive. Like osteosarcoma, Ewing
sarcoma is chemotherapy-sensitive and typically presents
with a painful bone mass.
Laboratory evaluation for Ewing’s sarcoma should
include lactate dehydrogenase, which can be elevated and
is associated with a poor prognosis. A complete blood count
may reveal leukocytosis or anemia, which is also associated
with a poor prognosis. Elevated erythrocyte sedimentation
rate is found in about half of patients with Ewing’s sarcoma,
and can confuse the initial diagnosis as perhaps being a bone
infection. Ewing’s sarcoma of bone is most likely identified
in long bones, pelvis, vertebra, ribs, clavicle, and scapula.
Unfortunately, approximately one-fourth of patients with
Ewing’s sarcoma present with metastatic disease. The most
common location of metastatic disease is lung, followed by
other bones, lymph nodes, and the liver.
Like patients with osteosarcoma, imaging should be
were obtained before the biopsy of a suspected Ewing’s
sarcoma. A carefully planned surgical biopsy and bone
culture is necessary for diagnosis. The tumor is characterized
by sheets of monotonous, small, round the blue cells. These
cells are extremely homogenous in appearance and typically
have well-defined borders with indistinct cytoplasm. CD 99
is a commonly used immunohistochemistry stain which is
positive in almost all Ewing’s sarcomas. Cytogenetic testing
typically reveals a translocation between T11 and T22. 90%
of patients with Ewing’s sarcoma have a translocation and the
fusion gene called EWS which combines with a FLI1 gene.
In the future, directed therapy may be used against these
genetic alterations.
Chemotherapy for Ewing’s sarcoma has recently been
accelerated, in that treatment which was given every three
weeks is now given every two weeks with an improvement in
overall survival.7 Chemotherapy agents that have been shown
to be effective with Ewing’s sarcoma include cyclophosphide,
doxorubicin, vincristine, and actinomycin D. Local control
for Ewing’s sarcoma includes the use of surgery and radiation
treatment. Surgical resection can be used without radiation
treatment in expendable bones and sites of disease where
wide surgical resection is feasible. It is advised to completely
resect the entire initial portion of bone involved with the
Ewing’s sarcoma if radiation is not given. It is probable
that surgical resection with radiation results in better local
controll than radiation alone, although no randomized studies
have been performed to define that difference. Due to late
secondary malignancies, radiation-induced malignancies,
and significant lifelong morbidity from childhood radiation,
most centers try to avoid radiation in immature patients with
Ewing’s sarcoma.5
Poor prognostic features for Ewing’s sarcoma include
age > 14 years, elevated LDH at the time of presentation,
weight loss and fever at the time of presentation, a fusion
gene other than the EWS-FLI 1, pelvis location, and a positive
chest for metastatic disease. Good prognostic features for
Ewing’s sarcoma include age < 15 years, a primary tumor
of < 8 cm or tumor volume < 200 cc, female gender, distal
location, a negative chest CAT scan, and 100% necrosis after
chemotherapy.
The outcome for Ewing’s sarcoma is associated with a
60% cure rate for non-metastatic patients and a 25 to 30 per
cent five-year survival in patients with metastatic disease.
92
Volume 4 – 2010
The Children’s Cancer Study Group recently published their
results of an accelerated chemotherapy program and found a
70% five-year survival for non-metastatic Ewing’s sarcoma
patients.11 The future of Ewing’s sarcoma includes targeted
chemotherapy for improved treatment for metastatic disease.
Further delineation of the best local control option with
radiation surgical resection is needed.
Chondrosarcoma
Chondrosarcoma is a primary bone malignancy that
affects mostly adults. Chondrosarcoma is characterized
by cartilage-forming malignant cells which do not form
osteoid. They are subclassified by histologic and clinical
behavior.12 Secondary chondrosarcoma occur in areas
of previous ostechondroma and previous enchondroma.
Conventional chondrosarcoma occur in areas of otherwise
normal bone. Other subtypes of chondrosarcoma include
clear cell chondrosarcoma, mesenchymal chondrosarcoma,
dedifferentiated
chondrosarcoma,
and
periosteal
chondrosarcoma. Chondrosarcomas can be low-grade,
intermediate grade, or high grade. Chondrosarcoma respond
poorly to chemotherapy and radiation. Surgical resection
is therefore paramount for local control and cure of a
chondrosarcoma. (See Figure 2 A-C)
Good prognostic findings for chondrosarcoma include
low-grade histology, distal anatomic site such as the fingers
or toes, clear cell variant, periosteal variant, scapular location,
and a normal chest CAT scan at the time of diagnosis. Bad
prognostic signs for chondrosarcoma include mesenchymal
or dedifferentiated subtype, pelvis location, and metastatic
disease on chest CAT scan at the time of diagnosis. The
treatment for chondrosarcoma is a wide surgical resection.
Wide surgical resection is associated with a local recurrence
rate, typically under 10%. If there are positive margins with
the resection, local recurrence rate can be between 33 and
60%. Because chemotherapy and radiation are not effective,
they do not appear to change local control data. Grade I
chondrosarcoma is typically associated with a 95% cure rate.
Grade II chondrosarcoma have a 75% cure rate, and grade III
chondrosarcoma only a 50% cure rate.13
Soft Tissue Sarcoma
Soft tissue sarcomas have many histologic subtypes and
can be seen as low-grade, intermediate grade, or high-grade
lesions.13-16 The most common type of soft tissue sarcoma is
a pleomorphic sarcoma, formerly called malignant fibrous
histiocytoma. The second most common kind of soft tissue
sarcoma is a liposarcoma, followed by malignant peripheral
nerve sheath tumor, synovial sarcoma, epithelioid sarcoma,
and angiosarcoma. Good prognostic features in soft tissue
sarcoma included low-grade histology, a tumor < 5 cm,
a normal chest CAT scan at the time of diagnosis, and a
surgically resectable site. Poor prognostic features for soft
tissue sarcoma include tumors > 5 cm, metastatic disease,
high grade histology, synovial sarcoma histology, and round
cell liposarcoma histology.
93
Figure 2 A-C Radiograph, MRI, and pathology of a 45-year-old
man with a acetabular de-differentiated chondrosarcoma. Tumor
was resected and reconstructed with a massive pelvic allograft. He
did not receive chemotherapy and is alive six years from diagnosis.
At this time, there is no convincing evidence that
chemotherapy improves the five-year cure rate of soft tissue
sarcomas. It has been shown to increase the length of survival
but does not improve the overall cure rate.17 Radiation
treatment has been associated with improved local control rate
Volume 4 – 2010
in selected cases to enhance limb salvage surgery. Surgical
resection remains the mainstay treatment for soft tissue
sarcomas of all grades and histology. With adjuvant radiation
treatment surgical resection and limb sparing operations for
high grade, large, deep soft tissue sarcomas is indicated in
90-95% of all patients. Metastatectomy has been associated
with a longer life span after a diagnosis of metastatic disease.
However, patients with metastatic soft tissue sarcoma have
only a 10% five-year survival.17
Future developments in the treatment of soft tissue
sarcomas will include improved directed chemotherapy
based on genetic abnormalties found within some tumor
types. Improvements in imaging and detection of metastatic
disease, as well as improvements in definitions of surgical
margins and indications for radiation treatment, will be
improved in the near future.
References
1. Bacci G, Briccoli A, Longhi A, et al. Treatment and outcomes of recurrent osteosarcoma:
Experience at Rizzoli in 235 patients initially treated with neoadjuvant chemotherapy. Acta
Oncol. 2005; 44:748-55.
2. Mankin HJ, Hornicek FJ, Rosenberg AE, et al. Survival data for 648 patients with
osteosarcoma treated at one institution. Clin Orthop Relat Res. 2004; 429:286-91.
3. Campanacci M, Picci P, Gherlinzoni F, et al. Parosteal Osteosarcoma. J Bone Joint Surg Br.
1984; 66:313-21.
4. Goorin AM, Anderson JW: Experience with multiagent chemotherapy for osteosarcoma:
Improved outcome. Clin Orthop Relat Res. 1991; 270:22-8.
5. Fuchs B, Valenzuela RG, Petersen IA, et al. Ewing’s sarcoma and the development of
secondary malignancies. Clin Orthop Relat Res. 2003; 415:82-9.
6. Grier HE, Krailo MD, Tarbell NJ et al. Addition of ifosfamide and etoposide to standard
chemotherapy for Ewing’s sarcoma and primitive neuroectodermal tumor or bone. N Engl J Med.
2003; 348:694-701.
7. Marina NM, Pappo AS, Parham DM, et al. Chemotherapy dose-intensification for pediatric
patients with Ewing’s family of tumors and desmoplastic round cell tumor: A feasibility study at
St. Jude’s Children’s Research Hospital. J Clin Oncol. 1999; 17:180-190.
8. O’Connor MI, Pritchard DJ. Ewing’s sarcoma: Prognostic factors, disease control, and the
reemerging role of surgical treatment. Clin Orthop Relat Res. 1991; 262:78-87.
9. Pritchard DJ, Dahlin DC, Dauphine RT, et al. Ewing’s sarcoma: A clinicopathological and
statistical analysis of patients surviving 5 years or longer. J Bone Joint Surg Am. 1975; 57:1016.
10. Wunder JS, Paulian G, Huvos AG, et al. The histological response to chemotherapy as a
predictor of the oncological outcome of operative treatment of Ewing sarcoma. J Bone Joint Surg
Am. 1998;80:1020-33.
11. Italiano A, Penel N, Robin YM, et al. Neo/adjuvant chemotherapy does not improve outcome
in resected primary synovial sarcoma: a study of the French Sarcoma Group. Ann Oncol. 2009;
20(3):425-30.
12. Bertoni F, Bacchini P, Hogendoorn PCW: Chondrosarcoma, In Fletcher CD, Unni KK Mertens
F (eds): World Health Organisation Classification of Tumours: Pathology and Genetics of
Tumours of Soft Tissue and Bone. Lyon, France, IARC Press, 2002, pp. 247-251.
13. Dickey ID, Rose PS, Fuchs B, et al: Dedifferentiated chondrosarcoma: The role of chemotherapy
with updated outcomes. J Bone Joint Surg Am. 2004; 86:2412-8.
14. Czerniak B: Pathologic and molecular aspects of soft tissue sarcomas. Surg Oncol Clin N Am.
2003; 12:263-303.
15. Massi D, Beltrami G, Capanna R, Franchi A. Histopathological re-classification of extremity
pleomorphic soft tissue sarcoma has clinical relevance. Eur J Surg Onco.l 2004; 30:1131-6.
16. Randall RL, Schabel KL, Hitchcock Y, et al. Diagnosis and management of synovial sarcoma.
Curr Treat Options Oncol. 2005; 6:429-59.
17. Pisters PW, Leung DH, Woodruff J, et al. Analysis of prognostic factors in 1,041 patients with
localized soft tissue sarcomas of the extremities. J Clin Oncol. 1996; 14(5):1679-89.
Author Information
The Indiana Orthopaedic Journal is an annual publication of the Department of Orthopaedic
Surgery. The Journal has a limited paper circulation and may be accessed electronically via the
IU Department of Orthopaedic Surgery website (http://www.orthopaedics.iu.edu/). We invite
original research papers, case studies, and opinion pieces from our core faculty, volunteer faculty,
residents, and alumni. We will also accept for reprint a recent, previously published paper with
written permission to reprint from the publisher.
When preparing your original manuscript for submission, please follow this general format.
An abstract is optional, but, if included, it should be 250 words or less. For research papers,
there should be an Introduction, Methods, Results, and Discussion sections. References
should be listed in order of appearance in the paper. Tables should be in a separate Word file
and not imbedded in the text of the paper. Figures may be submitted in jpg format or within a
PowerPoint file. All figures will appear in black-and-white in the Journal. Each figure should
have a legend, and all references, tables, and figures should be cited in the text. Incomplete
manuscripts will be returned to the submitting author.
Please submit no more than two manuscripts, case studies, or opinion papers per first author per
year. Manuscripts will be solicited via an email call for papers sent out in early January. All
manuscripts must be submitted electronically. Submission deadlines are generally on or about
the end of March with anticipated publication in early September of each year. Due to limited
space, a manuscript may be held for publication in a subsequent issue or rejected.
94
Patient Fit
is now an option
The new Zimmer
Natural Nail System
®
™
features anatomic implants
and intuitive instrumentation
designed to help you restore
your patients naturally.
Cephalomedullary Nails
t Anatomic anterior bows
(1.3 to 1.5m)
t 4° proximal lateralization angle
t Instrumentation for use with
patients large or small
t Straightforward technique
t Fixed angle screw options
To learn more about the Zimmer Natural Nail
System, contact your Zimmer representative
or visit www.zimmer.com
© 2010 Zimmer, Inc.

Indiana Orthopaedic Journal - Department of Orthopaedic Surgery

Transcription

Similar documents

KKOH New Brochure - Krishnakumar Orthopaedic Hospital

PowerPoint Presentation - AO

our PDF brochure

The London Implant Retrieval Centre

Be treated well - Methodist Le Bonheur Healthcare

Summer 2013 - UCSF Medical Center

Layzie, Krayzie, Bizzy

Leaders in Sports Medicine - Decatur

Weekend Warrior Injuries

The Avars were a nomadic people from the Eurasian steppe. They