(Mebooksfree Net) Pos&Tra&Art&Dia&Man&Out&1st
(Mebooksfree Net) Pos&Tra&Art&Dia&Man&Out&1st
Arthritis
Diagnosis, Management
and Outcomes
Savyasachi C. Thakkar
Erik A. Hasenboehler
Editors
123
Post-Traumatic Arthritis
Savyasachi C. Thakkar
Erik A. Hasenboehler
Editors
Post-Traumatic Arthritis
Diagnosis, Management and Outcomes
Editors
Savyasachi C. Thakkar Erik A. Hasenboehler
Hip & Knee Reconstruction Surgery Department of Orthopaedic Surgery
Johns Hopkins Adult Trauma Service
Department of Orthopaedic Surgery The Johns Hopkins Medical Institution
Columbia, MD Baltimore, MD
USA USA
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
I would like to dedicate this book to my
parents Mrs. Heena C. Thakkar and Dr.
C.J. Thakkar for their dedicated upbringing
and commitment towards excellence in life. I
would also like to dedicate the book to my
wife Dr. Rashmi S. Thakkar and my children
Sahuri and Shaarav who have provided me
with untiring support, love and patience.
Without these individuals, I would not be
where I am today!
Savyasachi C. Thakkar, MD
vii
Acknowledgments
The creation of this book has been a collective effort of several professionals. First,
we would like to thank the authors who have provided us their invaluable time and
energy to assemble various surgical cases that highlight the sentinel principles of
post-traumatic arthritis. Second, we would like to acknowledge Ms. Meera
V. Shanbhag who has devoted her talents as a pre-medical student at Vanderbilt
University in reviewing manuscripts and collating the contents of this book.
Third, this book would not have been possible without the oversight and plan-
ning provided by Mr. Kristopher Spring and Ms. Abha Krishnan. Both of them have
provided us with tremendous resources to make this book a reality.
Finally, we would like to thank our families for providing us with incredible sup-
port and motivation to devote time to projects such as this.
ix
Contents
xi
xii Contents
Index�������������������������������������������������������������������������������������������������������������������� 219
Contributors
xiii
xiv Contributors
Andrew P. Harris, MD Warren Alpert Medical School of Brown University,
Providence, RI, USA
Erik A. Hasenboehler, MD Department of Orthopaedic Surgery, Adult Trauma
Service, The Johns Hopkins Medical Institution, Baltimore, MD, USA
Curtis M. Henn, MD Medstar Georgetown University Hospital, Department of
Orthopaedics, Washington, DC, USA
Stefanie Hirsiger, MD Division of Orthopaedic and Traumatology, Department of
Surgery, Geneva University Hospitals, Faculty of Medicine, University of Geneva,
Geneva, Switzerland
Nigel N. Hsu, MD Department of Orthopaedic Surgery, Johns Hopkins University,
Baltimore, MD, USA
Eric Huish, DO Stanislaus Orthopaedics & Sports Medicine Clinic,
Modesto, CA, USA
Richard Iorio, MD Brigham and Women’s Hospital, Member of the Faculty,
Harvard Medical School, Boston, MA, USA
Michael W. Kessler, MD Medstar Georgetown University Hospital, Department
of Orthopaedics, Washington, DC, USA
Kelvin Y. Kim, MD Department of Orthopaedic Surgery, UNLV School of
Medicine, Las Vegas, NV, USA
Thomas J. Kim, MD Brown University, Warren Alpert Medical School,
Providence, RI, USA
William J. Long, MD, FRCSC ISK Institute, Department of Orthopaedic Surgery,
NYU Langone Medical Center, Hospital for Joint Diseases, New York, NY, USA
Hermes H. Miozzari, MD Division of Orthopaedic and Traumatology, Department
of Surgery, Geneva University Hospitals, Faculty of Medicine, University of
Geneva, Geneva, Switzerland
Kevin O’Malley, MD Medstar Georgetown University Hospital, Department of
Orthopaedics, Washington, DC, USA
Karthikeyan Ponnusamy, MD Pinnacle Orthopaedics, Canton, GA, USA
Lew Schon, MD Department of Orthopaedic Surgery, Mercy Medical Center,
Baltimore, MD, USA
Babar Shafiq, MD Department of Orthopaedic Surgery, The Johns Hopkins
Medical Institutions, Baltimore, MD, USA
Uma Srikumaran, MD, MBA The Johns Hopkins University, Division of
Shoulder and Elbow Surgery, Columbia, MD, USA
Contributors xv
Gehua Zhen and Xu Cao
Key Points
• Osteoarthritis is a disease that affects the whole joint. Biochemical and
biomechanical interactions among different components within the joint
actively participate in and contribute to the development and progression
of the disease.
• TGF-β plays an important role in the pathogenesis of osteoarthritis.
Temporal and spatial regulation of TGF-β activity is critical for mainte-
nance of homeostasis of joint tissues.
• The effects of TGF-β differ according to tissue type within the joint and
may vary at different time points. Various tissue-specific treatments target-
ing TGF-β signaling may produce optimal therapeutic effects.
Introduction
Recently, patient-specific finite element stress analysis has been used to measure
cartilage stress from residual surface incongruity after traumatic joint injury.
However, factors that trigger stress alterations in cartilage are not limited to carti-
lage itself. As a functional unit, the joint involves constant interaction between vari-
ous tissues [5]. Because of the physical contact between cartilage and bone, the
1 The Role of TGF-β in Post-traumatic Osteoarthritis 5
TGF-β
systems [10]. On secretion, the homodimers of mature TGF-β peptide link nonco-
valently to latency-associated peptide (LAP), with LAP masking its receptor-
binding domains and rendering it inactive [11]. The small latent complex formed by
LAP and TGF-β further interacts with latent TGF-β binding protein in the extracel-
lular matrix and forms the large latent complex. Although TGF-β synthesis is wide-
spread, activation is localized to sites where TGF-β is released from latency.
Temporal-spatial regulation of TGF-® activation is crucial for appropriate function
of this cytokine, and the abundant latent TGF-®s that are deposited in the extracel-
lular matrix ensure that sufficient TGF-β can be activated when necessary. The
TGF-β activation mechanism is tissue-specific and cellular context-dependent [12].
For example, enzyme-mediated proteolytic cleavage has been reported to be the
dominant pathway for TGF-β to be activated in tumors or metastasis, whereas pul-
monary fibrosis is induced by integrin-mediated excessive TGF-β activation.
Multiple mechanisms of TGF-β activation may be used or switched from one to
another depending on the cellular context or environmental stimuli [11].
TGF-βs signal via the heteromeric complexes of two related transmembrane ser-
ine/threonine kinase receptors, TGF-β type I and type II receptors (TβR-I and
TβR-II). TβR-I is also termed activin receptor-like kinase (ALK). The dimeric
ligand of TGF-β binds to the extracellular domains of TβR-I and TβR-II, inducing
close proximity of the receptors. Unlike TβR-II, which is unique to its ligand, dis-
tinctive TβR-Is can be phosphorylated by TβR-II, which determines the specificity
of the downstream signaling pathway [13]. Smad2 and Smad3 are substrates of
ALK5, whereas ALK1 phosphorylates Smad1, Smad5, and Smad8. After phosphor-
ylation by the receptor, the phosphorylated receptor-regulated Smad forms a com-
plex with the common mediator Smad4 and translocates to the nucleus where they
interact with other transcription factors (cofactors) to regulate transcriptional
responses. In addition to the Smad-dependent canonical pathway, TGF-β also sig-
nals through the Smad-independent or noncanonical pathways. The tumor necrosis
factor receptor-associated factor 4 (TRAF4), TRAF6, p38 mitogen-activated pro-
tein kinase (p38 MAPK), TGF-β-activated kinase 1 (TAK1; also known as
MAP3K7), Ras homolog gene family, phosphoinositide 3-kinase (PI3K), protein
kinase B, extracellular signal-regulated kinase (ERK), JUN N-terminal kinase
(JNK), and nuclear factor-κB (NF-κB) have all been reported to mediate the TGF-β
signaling pathway [14].
its role in subchondral bone. For example, genetically deleting TβR-II or Smad3 in
chondrocytes resulted in early onset of osteoarthritis in animal models, as evidenced
by the hypocellularity and decreased matrix protein synthesis of chondrocytes [22].
The effects of TGF-β in stimulating chondrogenic condensation, proliferating chon-
droprogenitors, and inhibiting terminal differentiation of chondrocytes have been
evidenced in multiple in vitro studies. These findings suggest that TGF-β is critical
to maintaining articular cartilage’s functional and structural integrity [23]. The
abundant latent TGF-β storage (~300 ng/mL) in the extracellular matrix of cartilage
provides sufficient raw material for TGF-β activation [24]. In physiological condi-
tions, minimal amounts of active TGF-βs are needed for the maintenance of carti-
lage physiological function. In osteoarthritic cartilage, many mechanisms involved
in the process of TGF-β activation such as MMPs or integrins are altered [25],
which may lead to excessive or insufficient activation of TGF-β. Intra-articular
injury likely alters the mechanical stress distribution in articular cartilage directly or
indirectly through subchondral bone. Subchondral bone changes its structure con-
stantly in response to the mechanical environment. During the period of structural
fluctuation, the capacity of subchondral bone to dissipate the mechanical load is
altered or impaired. Because physiological mechanical stimulation is indispensable
for maintaining the function and structural integrity of articular cartilage, abnormal
mechanical stress (altered intensity or frequency) can promote catabolic events and
induce cartilage degeneration [26]. Although the soluble factors responsible for
propagating mechanical signals into biochemical signaling are still unclear, evi-
dence suggests an important role of TGF-β in mechanical transduction pathways in
chondrocytes [27]. In addition to TGF-β activation pathways, it has been reported
that shear forces can liberate active TGF-β from the sequestration of LAP in syno-
vial fluid [28]. TβR-I-specific inhibitor eliminated the anabolic effect of shear stress
in stimulating protein synthesis in the superficial zone of articular cartilage [29].
These findings indicate that abnormal biomechanical and biochemical environ-
ments alter the TGF-β activation process, and excessive or insufficient levels of
TGF-β, in turn, effect the chondrocytes’ survival and function.
The responsiveness of chondrocytes to TGF-β also depends on the expression
levels and activity of its receptors. The canonic TGF-β signaling pathway includes
the formation of the heteromeric complexes of type I and type II receptors. A
sequential phosphorylation and nuclear translocation of downstream Smads ulti-
mately triggers the expression of the target genes. Dysregulation of TGF-β signaling
pathways or differential expression of TGF-β receptors in the chondrocytes has
been reported in various in vivo studies, including a surgically induced PTOA ani-
mal model. TβR-II degradation and decreased TβR-I expression blunt the sensitivity
of articular chondrocytes to TGF-β, contributing to cartilage degeneration [30]. The
expression pattern of TβR-I in chondrocytes is markedly different in osteoarthritic
cartilage. The dominant TβR-I receptor shifts from ALK5 to ALK1 [31]. TGF-β
signals from these two pathways influence the metabolism of chondrocytes in an
opposing fashion [32]. TGF-β acts as an anabolic factor on chondrocytes, stimulat-
ing matrix protein production when signaling through ALK5, and as a catabolic
1 The Role of TGF-β in Post-traumatic Osteoarthritis 9
factor when ALK1 is mediating its downstream signaling [33]. In addition, there are
several other factors involved in the signaling transduction pathway of TGF-β by
modulating the sensitivity of receptors to the ligand or the internalization process of
the receptors. For example, endoglin can facilitate the binding of TGF-β to its recep-
tors with the preference to recruit ALK1 [34]. Therefore, elevated expression of
endoglin in chondrocytes may promote the catabolic effect by making ALK1/
pSmad1/5/8 the dominant signaling pathway of TGF-β. Betaglycan is a homolog of
endoglin but it has distinctive functions in regulating the TGF-β pathway. Betaglycan
can direct clathrin-mediated endocytosis of TβR-I and TβR-II [35] and increase the
sensitivity of TβR-II to its ligands [36]. CD109 is another identified TGF-β co-
receptor. It negatively regulates TGF-β signaling by promoting TGF-β receptor
internalization and degradation [37]. Thus, during osteoarthritis development, the
altered TGF-β signaling in articular cartilage may potentially be corrected by target-
ing these co-receptors or modulators.
As avascular tissue, articular cartilage is nourished mainly by the synovial fluid that
is secreted by the synovium. Therefore, articular cartilage is vulnerable to patho-
logical changes in the synovial system. Although osteoarthritis is defined as “non-
inflammatory arthritis,” synovial hyperplasia, macrophage infiltration, and
angiogenesis are common characteristics of osteoarthritic abnormality [38].
Histologically recognizable synovitis occurs in more than one-third of patients with
symptomatic osteoarthritis. Persistent or episodic synovitis has been found to be
related closely to osteoarthritic pain. The cytokines released by synovium have been
recognized as being of pathological and clinical importance in the development of
osteoarthritis. Notably, human and animal studies suggest that the concentration of
TGF-β1 might be used as a prognostic indicator for PTOA. In a rabbit meniscec-
tomy model, early postoperative concentrations of TGF-β1 in synovial lavage fluid
were correlated positively with the severity of PTOA [39]. In patients with acute or
chronic anterior cruciate ligament rupture, the levels of TGF-β in the synovial fluid
were consistent with the persistence of inflammatory reactions, and their synovial
fluid cytokine profiles were associated with the risk of developing PTOA [40].
TGF-β typically serves as an important immune suppressor during the process of
inflammation. Knocking out TGF-β1 in mice is usually lethal because it induces
severe inflammatory events. TGF-β receptors are expressed widely in immune cell
types and have broad activities in immune regulation. In most immune reactions,
TGF-β acts as a suppressor. Conversely, TGF-β sometimes plays a pro-inflammatory
role by promoting the differentiation of TH17 lineage cells [41]. TGF-β was found
to induce the differentiation from “attacking” type I macrophages toward “inflam-
matory molecule secreting” type II macrophages [42, 43]. This may underlie the
mechanism of TGF-β in augmenting the tumor necrosis factor-α- or interleukin
10 G. Zhen and X. Cao
orchestrate the signaling of local factors and thereby improve the microenvironment
in bone marrow [47]. TβR-II can form a complex with PTH type I receptor (PTH1R).
The binding of PTH with PTH1R downregulates TGF-β signaling by inducing
internalization of the TβR-II/PTH1R complex [47]. It is known that BMP and Wnt
signaling can promote the commitment of MSCs to osteoblastic lineage cells [48].
PTH upregulates BMP and Wnt signaling and, therefore, positively regulates osteo-
genesis. Additionally, angiogenesis is always coupled with osteogenesis during
bone formation. PTH has been shown to reduce the distance between newly formed
vessels and sites of bone formation [49]. Therefore, by coordinating the effects of
these osteogenic factors, PTH may alleviate abnormal bone formation while stimu-
lating normal bone turnover at the right location. Moreover, PTH is a well-recog-
nized anabolic factor during cartilage development and maintenance [50]. PTH may
be developed as a therapeutic agent because of its potential ability to rescue patho-
logical changes in both osteoarthritic cartilage and subchondral bone.
Summary
The diarthrodial joint works as a functional unit, and osteoarthritis affects almost all
of its structural components. TGF-β is a crucial factor that regulates the physiologi-
cal turnover of subchondral bone and articular cartilage. Dysregulation of TGF-β1
signaling leads to failure in maintenance of joint homeostasis during the develop-
ment and progression of osteoarthritis. Because the effects of TGF-β may differ
according to tissue type within the joint and may vary at different time points, dif-
ferential and tissue-specific treatments targeting TGF-β signaling may produce opti-
mal therapeutic effects.
References
1. Maffulli N, Longo UG, Gougoulias N, Caine D, Denaro V. Sport injuries: a review of out-
comes. Br Med Bull. 2011;97:47–80. [Link]
2. Riordan EA, Little C, Hunter D. Pathogenesis of post-traumatic OA with a view to intervention.
Best Pract Res Clin Rheumatol. 2014;28:17–30. [Link]
3. Hunter D. Osteoarthritis. Best Pract Res Clin Rheumatol. 2011;25:801–14. [Link]
org/10.1016/[Link].2011.11.008.
4. Dare D, Rodeo S. Mechanisms of post-traumatic osteoarthritis after ACL injury. Curr
Rheumatol Rep. 2014;16:448. [Link]
5. Lories RJ, Luyten FP. The bone-cartilage unit in osteoarthritis. Nat Rev Rheumatol.
2011;7:43–9. [Link]
6. Zhen G, et al. Inhibition of TGF-beta signaling in mesenchymal stem cells of subchondral
bone attenuates osteoarthritis. Nat Med. 2013;19:704–12. [Link]
7. Burr DB. The importance of subchondral bone in osteoarthrosis. Curr Opin Rheumatol.
1998;10:256–62.
12 G. Zhen and X. Cao
8. Goldring SR. Alterations in periarticular bone and cross talk between subchondral bone and
articular cartilage in osteoarthritis. Ther Adv Musculoskelet Dis. 2012;4:249–58. [Link]
org/10.1177/1759720X12437353.
9. Massague J. TGF-beta signaling in development and disease. FEBS Lett. 2012;586:1833.
[Link]
10. Cupp AS, Kim G, Skinner MK. Expression and action of transforming growth factor beta
(TGFbeta1, TGFbeta2, and TGFbeta3) during embryonic rat testis development. Biol Reprod.
1999;60:1304–13.
11. Annes JP, Munger JS, Rifkin DB. Making sense of latent TGFbeta activation. J Cell Sci.
2003;116:217–24.
12. Murphy-Ullrich JE, Poczatek M. Activation of latent TGF-beta by thrombospondin-1: mecha-
nisms and physiology. Cytokine Growth Factor Rev. 2000;11:59–69.
13. Heldin CH, Miyazono K, ten Dijke P. TGF-beta signalling from cell membrane to nucleus
through SMAD proteins. Nature. 1997;390:465–71. [Link]
14. Zhang YE. Non-Smad pathways in TGF-beta signaling. Cell Res. 2009;19:128–39. [Link]
org/10.1038/cr.2008.328.
15. Blobe GC, Schiemann WP, Lodish HF. Role of transforming growth factor beta in human
disease. N Engl J Med. 2000;342:1350–8. [Link]
16. Kalinina NI, Sysoeva VY, Rubina KA, Parfenova YV, Tkachuk VA. Mesenchymal stem cells
in tissue growth and repair. Acta Nat. 2011;3:30–7.
17. Tang Y, et al. TGF-beta1-induced migration of bone mesenchymal stem cells couples bone
resorption with formation. Nat Med. 2009;15:757–65. [Link]
18. Piera-Velazquez S, Li Z, Jimenez SA. Role of endothelial-mesenchymal transition (EndoMT)
in the pathogenesis of fibrotic disorders. Am J Pathol. 2011;179:1074–80. [Link]
org/10.1016/[Link].2011.06.001.
19. Stone RC, et al. Epithelial-mesenchymal transition in tissue repair and fibrosis. Cell Tissue
Res. 2016;365:495–506. [Link]
20. Loughlin J. Genetics of osteoarthritis. Curr Opin Rheumatol. 2011;23:479–83. [Link]
org/10.1097/BOR.0b013e3283493ff0.
21. Vinatier C, et al. Cartilage tissue engineering: towards a biomaterial-assisted mesenchymal
stem cell therapy. Curr Stem Cell Res Ther. 2009;4:318–29.
22. Shen J, et al. Deletion of the transforming growth factor beta receptor type II gene in articular
chondrocytes leads to a progressive osteoarthritis-like phenotype in mice. Arthritis Rheum.
2013;65:3107–19. [Link]
23. Yang X, et al. TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and
are required for maintaining articular cartilage. J Cell Biol. 2001;153:35–46.
24. Morales TI, Joyce ME, Sobel ME, Danielpour D, Roberts AB. Transforming growth factor-
beta in calf articular cartilage organ cultures: synthesis and distribution. Arch Biochem
Biophys. 1991;288:397–405.
25. Maeda S, Dean DD, Gomez R, Schwartz Z, Boyan BD. The first stage of transforming growth
factor beta1 activation is release of the large latent complex from the extracellular matrix
of growth plate chondrocytes by matrix vesicle stromelysin-1 (MMP-3). Calcif Tissue Int.
2002;70:54–65. [Link]
26. Farquhar T, et al. Swelling and fibronectin accumulation in articular cartilage explants after
cyclical impact. J Orthop Res. 1996;14:417–23. [Link]
27. Hinz B. The extracellular matrix and transforming growth factor-beta1: tale of a strained rela-
tionship. Matrix Biol. 2015;47:54–65. [Link]
28. Albro MB, et al. Shearing of synovial fluid activates latent TGF-beta. Osteoarthr Cartil.
2012;20:1374–82. [Link]
29. Neu CP, Khalafi A, Komvopoulos K, Schmid TM, Reddi AH. Mechanotransduction of bovine
articular cartilage superficial zone protein by transforming growth factor beta signaling.
Arthritis Rheum. 2007;56:3706–14. [Link]
30. Serra R, et al. Expression of a truncated, kinase-defective TGF-beta type II receptor in mouse
skeletal tissue promotes terminal chondrocyte differentiation and osteoarthritis. J Cell Biol.
1997;139:541–52.
1 The Role of TGF-β in Post-traumatic Osteoarthritis 13
31. van der Kraan PM, Blaney Davidson EN, van den Berg WB. A role for age-related changes
in TGFbeta signaling in aberrant chondrocyte differentiation and osteoarthritis. Arthritis Res
Ther. 2010;12:201. [Link]
32. Goumans MJ, et al. Activin receptor-like kinase (ALK)1 is an antagonistic mediator of lateral
TGFbeta/ALK5 signaling. Mol Cell. 2003;12:817–28.
33. van der Kraan PM, Goumans MJ, Blaney Davidson E, ten Dijke P. Age-dependent altera-
tion of TGF-beta signalling in osteoarthritis. Cell Tissue Res. 2012;347:257–65. [Link]
org/10.1007/s00441-011-1194-6.
34. Finnson KW, et al. Endoglin differentially regulates TGF-beta-induced Smad2/3 and Smad1/5
signalling and its expression correlates with extracellular matrix production and cellular dif-
ferentiation state in human chondrocytes. Osteoarthr Cartil. 2010;18:1518–27. [Link]
org/10.1016/[Link].2010.09.002.
35. Santander C, Brandan E. Betaglycan induces TGF-beta signaling in a ligand-independent
manner, through activation of the p38 pathway. Cell Signal. 2006;18:1482–91. [Link]
org/10.1016/[Link].2005.11.011.
36. Lopez-Casillas F, et al. Structure and expression of the membrane proteoglycan betaglycan, a
component of the TGF-beta receptor system. Cell. 1991;67:785–95.
37. Bizet AA, et al. The TGF-beta co-receptor, CD109, promotes internalization and degradation
of TGF-beta receptors. Biochim Biophys Acta. 2011;1813:742–53. [Link]
bbamcr.2011.01.028.
38. Mathiessen A, Conaghan PG. Synovitis in osteoarthritis: current understanding with therapeu-
tic implications. Arthritis Res Ther. 2017;19:18. [Link]
39. Fahlgren A, Andersson B, Messner K. TGF-beta1 as a prognostic factor in the process of early
osteoarthrosis in the rabbit knee. Osteoarthr Cartil. 2001;9:195–202. [Link]
joca.2000.0376.
40. Cameron ML, Fu FH, Paessler HH, Schneider M, Evans CH. Synovial fluid cytokine con-
centrations as possible prognostic indicators in the ACL-deficient knee. Knee Surg Sports
Traumatol Arthrosc. 1994;2:38–44.
41. Yoshimura A, Muto G. TGF-beta function in immune suppression. Curr Top Microbiol
Immunol. 2011;350:127–47. [Link]
42. Gong D, et al. TGFbeta signaling plays a critical role in promoting alternative macrophage
activation. BMC Immunol. 2012;13:31. [Link]
43. Gordon S. Alternative activation of macrophages. Nat Rev Immunol. 2003;3:23–35. https://
[Link]/10.1038/nri978.
44. Rosengren S, Corr M, Boyle DL. Platelet-derived growth factor and transforming growth fac-
tor beta synergistically potentiate inflammatory mediator synthesis by fibroblast-like synovio-
cytes. Arthritis Res Ther. 2010;12:R65. [Link]
45. Nishii T, Tamura S, Shiomi T, Yoshikawa H, Sugano N. Alendronate treatment for hip osteo-
arthritis: prospective randomized 2-year trial. Clin Rheumatol. 2013;32:1759–66. [Link]
org/10.1007/s10067-013-2338-8.
46. Iannone F, Lapadula G. The pathophysiology of osteoarthritis. Aging Clin Exp Res.
2003;15:364–72.
47. Qiu T, et al. TGF-beta type II receptor phosphorylates PTH receptor to integrate bone remodel-
ling signalling. Nat Cell Biol. 2010;12:224–34. [Link]
48. Lin GL, Hankenson KD. Integration of BMP, Wnt, and notch signaling pathways in osteoblast
differentiation. J Cell Biochem. 2011;112:3491–501. [Link]
49. Prisby R, et al. Intermittent PTH(1-84) is osteoanabolic but not osteoangiogenic and relocates
bone marrow blood vessels closer to bone-forming sites. J Bone Miner Res. 2011;26:2583–96.
[Link]
50. Orth P, et al. Parathyroid hormone [1-34] improves articular cartilage surface architecture and
integration and subchondral bone reconstitution in osteochondral defects in vivo. Osteoarthr
Cartil. 2013;21:614–24. [Link]
Chapter 2
Imaging Modalities for Post-traumatic
Arthritis
Key Points
• Magnetic field strength increases the signal to noise ratio (SNR) and can
influence cartilage detection and grading.
• T2 mapping, dGEMERIC, T1 rho, and Sodium imaging are advanced MRI
techniques that allow the biochemical evaluation of the cartilage.
• Bone marrow edema (also called bone marrow lesions) is commonly pres-
ent in patients with OA mainly in areas of mechanical loading.
Introduction
Conventional Radiography
Conventional radiography (CR) is the least expensive and most widely available
imaging modality to assess OA in the clinical practice. CR allows not only to detect
morphological changes of OA but also to follow the disease progression by measur-
ing the joint space narrowing (JSN) (Fig. 2.3) [4, 5]. Slowing of the JSN progression
is the official criterion approved by the Federal and Drug Administration (FDA) to
demonstrate efficacy of drugs in phase III trials of OA [4, 5].
JSN is a complex process that involves several anatomical structures depending
on the joint. For instance, in the knee joint, cartilage loss, meniscal degeneration,
and/or meniscal extrusion are involved in the joint space narrowing process [6].
In the clinical practice, radiologists don’t use scoring systems to report
OA. Kellgren and Lawrence (K-L) is the best-known semiquantitative grading sys-
tem to assess OA and was originally developed for anteroposterior knee radiogra-
phies [7]. The 5-point K-L scoring system stratifies OA according to four
conventional radiology findings: presence of bony osteophytes, joint space narrow-
ing, presence and degree of subchondral sclerosis, and bony deformity (Fig. 2.4) [7,
8]. K-L grade 0 indicates none OA, K-L grade 1 indicates doubtful OA, K-L grade
2 indicates minimal OA, K-L grade 3 indicates moderate OA, and K-L grade 4
indicates severe OA. Although the K-L scoring system could help to increase com-
munication between radiologists and clinicians, it shows some important limita-
tions that prevent its introduction in clinical practice and in research protocols. One
of the major limitations of K-L grading system is the grouping of the majorities of
patients in the grade of moderate OA (grade 3) [4]. Furthermore, K-L method shows
high interpretation variability with poor to moderate inter-observer agreement [9].
Experience and training seems to play an important role for reliability reporting.
Differences arise between readers on site and an expert centralized reader as well,
which highlight the importance to use a centralized reader in the research proj-
ects [10].
2 Imaging Modalities for Post-traumatic Arthritis 17
a b
c d
Fig. 2.1 (a) Anteroposterior and (b) lateral conventional radiographies and (c) coronal and (d)
sagittal CT MPR reconstruction of the elbow of a 60-year-old patient after internal fixation of a
radial head fracture. The patient developed post-traumatic OA of the elbow which is an atypical
location for primary OA. Radiographs and CT show humero-ulnar and humero-radial OA. The
osteophyte arising from the olecranon ulnae causes extension deficit
18 F. Del Grande et al.
a b
Fig. 2.2 (a) Anteroposterior shoulder view and (b) 3D reconstruction of the shoulder of a 25-year-
old patient. The 3D reconstruction (b) shows a displaced comminuted humerus fracture after
MVA. Two years later the patient developed a post-traumatic OA (a)
The major drawbacks of CR are lack of sensitivity [8, 11] and of reliability [9].
In clinical practice, standard anteroposterior and lateral views are generally suffi-
cient; additional views are rarely requested. The role of additional special projection
on knee MRI is debatable in the literature. In patients with arthroscopy-confirmed
grade II femorotibial chondromalacia, the 45°flexion PA and the standing AP view
are both insensitive to detect OA [11]. However, a more recent systematic review
concluded that the 45°flexion PA view was more sensitive than the standing AP
view for the detection of femorotibial OA, especially in patients suffering from
advanced OA [8]. The two studies showed contradictory results, probably because
of the relatively young population (average 38 years old) and the mild femorotibial
OA in the first study compared to the meta-analysis.
To the best of our knowledge, to date, only two studies focus on the reliability of
imaging of post-traumatic OA [12, 13]. K-L scoring system is reliable and corre-
lates with clinical symptoms in patients with ankle OA several years after open
reduction internal fixation of a malleolar fracture. Furthermore, adding the talar tilt
angle (modified K-L scale) will result in even better differentiation of clinical out-
comes [13].
In order to assess the reliability of grading systems for post-traumatic ankle OA,
Cleassen and colleagues analyzed three different methods: the Van Dick, the
Takakura, and the K-L methods. A total of 118 orthopedic surgeons and residents
graded 128 ankle radiographs after bi- or trimalleolar ankle fractures. The authors
2 Imaging Modalities for Post-traumatic Arthritis 19
Fig. 2.3 Anteroposterior
conventional radiography
of medial OA of the knee
with osteophytes,
subchondral sclerosis, and
joint space narrowing
found only fair inter-reader agreement for the Van Dick and low for the Takakura
and K-L classification systems. According to the results of the study, the authors
warned to use these classifications in the clinical practice [12].
MR Imaging
MRI has a high soft tissue contrast that allows to visualize the whole joint, i.e., the
bone, the synovia, the ligaments, the capsule, and mainly the cartilage [5, 14, 15].
Furthermore MRIs allow to assess the morphology and the composition of the
cartilage [16].
20 F. Del Grande et al.
a b
Fig. 2.4 (a) Coronal MPR CT reconstruction of the knee of a comminuted displaced fracture of
the proximal tibia of a 36-year-old male patient after MVA. (b) Anteroposterior conventional radi-
ography 6 years later shows severe medial knee OA (K-L 4)
beyond the scope of this chapter. It is only worthy to mention that these composi-
tional techniques are rarely used in clinical practice mainly because of long acqui-
sition time and the need to use special pulse sequences and/or dedicated
hardware [16].
Association between pain and imaging findings in OA is one of the greatest chal-
lenges for researchers, radiologists, and referring physicians. Hyaline cartilage is
avascular and aneural and as such cannot be the source of pain [21]. Pain transmis-
sion is probably the result of more complex and indirect mechanisms involving
other articular structures [21]. It is speculated that pain could be secondary to the
exposure of nociceptors of the subchondral bone, to the increased intraosseous pres-
sure secondary to vascular congestion, and/or to cartilage damage that can lead to
synovitis [21].
Prevalence studies on hip OA show only low correlation between imaging find-
ings and pain. In the Framingham OA study, a community-based prevalence study
in which symptomatic and asymptomatic subjects underwent hip radiographies,
nearly one out of five subjects shows CR features of hip OA, but less than 5% were
symptomatic [22].
Another population-based observational study emphasizes the low sensitivity of
CR for OA and the low correlation of MRI findings of OA with pain [23]. In the
study, a cohort of 710 patients without evidence of knee OA (K-L grade 0) under-
went MRI of the knee. The authors assessed the prevalence of MRI finding sugges-
tive for OA such as osteophytes, cartilage damage, bone marrow lesions, synovitis,
subchondral cysts, meniscal lesions, and bone attrition. Some interesting clinical
considerations came out from the study. First, 89% of subjects showed MRI features
compatible with OA. Second, a high prevalence of symptomatic (97%) and asymp-
tomatic (88%) subjects showed at least one MRI feature of OA. According to the
study, MRI features of OA are so common in asymptomatic subjects that should not
be used as a diagnostic tool for OA. The role of MRI will be rather to rule out other
pathologies that can mimic OA such as subchondral bone fractures, osteonecrosis,
and insufficiency fractures [23].
Although the correlation between pain and imaging finding is low, some imaging
findings such as bone marrow edema, synovitis/effusion, and bone attrition are pre-
dictive of pain in patients with OA.
Bone marrow edema (also called bone marrow lesions) is commonly present in
patients with OA mainly in areas of mechanical loading (Fig. 2.5) [24]. Bone mar-
row edema is considered a strong pain generator in patients with OA [25–27] and
predictive for OA progression [24]. Interestingly, the fluctuation of bone marrow
edema on MRI correlates with pain fluctuation [28]. Histologically, bone marrow
edema in patients with OA is a mixture of fibrosis, hemorrhage, trabecular fractures,
22 F. Del Grande et al.
a b
Fig. 2.5 (a) Coronal T1-weighted sequences and (b) T2-weighted sequences of a 71-year-old
female patient with painful OA. Note the osteophytes arising from the medial compartment of the
knee, the meniscus subluxation, and diffuse cartilage loss. T2-weighted sequences show the bone
marrow edema of medial condyle and the medial tibial plateau
and only a minor component of edema [29, 30]. Bone attrition is a common bony
feature in OA and plays an important role in association with bone marrow edema
to generate pain [27]. Lastly, several studies emphasize the association of synovitis/
joint effusion with knee pain [26, 27, 31, 32].
References
1. Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA, et al. Estimates of the
prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis
Rheum. 2008;58(1):26–35.
2. Suri P, Morgenroth DC, Hunter DJ. Epidemiology of osteoarthritis and associated comorbidi-
ties. PM R. 2012;4(5 Suppl):S10–9.
3. Brown TD, Johnston RC, Saltzman CL, Marsh JL, Buckwalter JA. Posttraumatic osteoar-
thritis: a first estimate of incidence, prevalence, and burden of disease. J Orthop Trauma.
2006;20(10):739–44.
4. Guermazi A, Hayashi D, Eckstein F, Hunter DJ, Duryea J, Roemer FW. Imaging of osteoarthri-
tis. Rheum Dis Clin N Am. 2013;39(1):67–105.
5. Roemer FW, Eckstein F, Hayashi D, Guermazi A. The role of imaging in osteoarthritis. Best
Pract Res Clin Rheumatol. 2014;28(1):31–60.
6. Hunter DJ, Zhang YQ, Tu X, Lavalley M, Niu JB, Amin S, et al. Change in joint space width:
hyaline articular cartilage loss or alteration in meniscus? Arthritis Rheum. 2006;54(8):2488–95.
7. Kellgren JH, Lawrence JS. Radiological assessment of osteo-arthrosis. Ann Rheum Dis.
1957;16(4):494–502.
2 Imaging Modalities for Post-traumatic Arthritis 23
8. Duncan ST, Khazzam MS, Burnham JM, Spindler KP, Dunn WR, Wright RW. Sensitivity
of standing radiographs to detect knee arthritis: a systematic review of Level I studies.
Arthroscopy. 2015;31(2):321–8.
9. Vilalta C, Nunez M, Segur JM, Domingo A, Carbonell JA, Macule F. Knee osteoarthritis:
interpretation variability of radiological signs. Clin Rheumatol. 2004;23(6):501–4.
10. Guermazi A, Hunter DJ, Li L, Benichou O, Eckstein F, Kwoh CK, et al. Different thresholds
for detecting osteophytes and joint space narrowing exist between the site investigators and
the centralized reader in a multicenter knee osteoarthritis study–data from the osteoarthritis
initiative. Skelet Radiol. 2012;41(2):179–86.
11. Wright RW, Boyce RH, Michener T, Shyr Y, McCarty EC, Spindler KP. Radiographs are not
useful in detecting arthroscopically confirmed mild chondral damage. Clin Orthop Relat Res.
2006;442:245–51.
12. Claessen FM, Meijer DT, van den Bekerom MP, Gevers Deynoot BD, Mallee WH, Doornberg
JN, et al. Reliability of classification for post-traumatic ankle osteoarthritis. Knee Surg Sports
Traumatol Arthrosc. 2016;24(4):1332–7.
13. Holzer N, Salvo D, Marijnissen AC, Vincken KL, Ahmad AC, Serra E, et al. Radiographic
evaluation of posttraumatic osteoarthritis of the ankle: the Kellgren-Lawrence scale is reliable
and correlates with clinical symptoms. Osteoarthr Cartil. 2015;23(3):363–9.
14. Hayashi D, Guermazi A, Crema MD, Roemer FW. Imaging in osteoarthritis: what have we
learned and where are we going? Minerva Med. 2011;102(1):15–32.
15. Wenham CY, Grainger AJ, Conaghan PG. The role of imaging modalities in the diagnosis, dif-
ferential diagnosis and clinical assessment of peripheral joint osteoarthritis. Osteoarthr Cartil.
2014;22(10):1692–702.
16. Crema MD, Roemer FW, Marra MD, Burstein D, Gold GE, Eckstein F, et al. Articular car-
tilage in the knee: current MR imaging techniques and applications in clinical practice and
research. Radiographics. 2011;31(1):37–61.
17. Quatman CE, Hettrich CM, Schmitt LC, Spindler KP. The clinical utility and diagnostic per-
formance of magnetic resonance imaging for identification of early and advanced knee osteo-
arthritis: a systematic review. Am J Sports Med. 2011;39(7):1557–68.
18. Masi JN, Sell CA, Phan C, Han E, Newitt D, Steinbach L, et al. Cartilage MR imaging at 3.0
versus that at 1.5 T: preliminary results in a porcine model. Radiology. 2005;236(1):140–50.
19. Kijowski R, Blankenbaker DG, Davis KW, Shinki K, Kaplan LD, De Smet AA. Comparison of
1.5- and 3.0-T MR imaging for evaluating the articular cartilage of the knee joint. Radiology.
2009;250(3):839–48.
20. Wong S, Steinbach L, Zhao J, Stehling C, Ma CB, Link TM. Comparative study of imaging at
3.0 T versus 1.5 T of the knee. Skelet Radiol. 2009;38(8):761–9.
21. Hunter DJ, Guermazi A, Roemer F, Zhang Y, Neogi T. Structural correlates of pain in joints
with osteoarthritis. Osteoarthr Cartil. 2013;21(9):1170–8.
22. Kim C, Linsenmeyer KD, Vlad SC, Guermazi A, Clancy MM, Niu J, et al. Prevalence of
radiographic and symptomatic hip osteoarthritis in an urban United States community: the
Framingham osteoarthritis study. Arthritis Rheum (Hoboken, NJ). 2014;66(11):3013–7.
23. Guermazi A, Niu J, Hayashi D, Roemer FW, Englund M, Neogi T, et al. Prevalence of
abnormalities in knees detected by MRI in adults without knee osteoarthritis: population
based observational study (Framingham Osteoarthritis Study). BMJ (Clinical Research ed).
2012;345:e5339.
24. Felson DT, McLaughlin S, Goggins J, LaValley MP, Gale ME, Totterman S, et al. Bone mar-
row edema and its relation to progression of knee osteoarthritis. Ann Intern Med. 2003;139(5
Pt 1):330–6.
25. Felson DT, Chaisson CE, Hill CL, Totterman SM, Gale ME, Skinner KM, et al. The association
of bone marrow lesions with pain in knee osteoarthritis. Ann Intern Med. 2001;134(7):541–9.
26. Lo GH, McAlindon TE, Niu J, Zhang Y, Beals C, Dabrowski C, et al. Bone marrow lesions
and joint effusion are strongly and independently associated with weight-bearing pain in knee
osteoarthritis: data from the osteoarthritis initiative. Osteoarthr Cartil. 2009;17(12):1562–9.
24 F. Del Grande et al.
27. Torres L, Dunlop DD, Peterfy C, Guermazi A, Prasad P, Hayes KW, et al. The relationship
between specific tissue lesions and pain severity in persons with knee osteoarthritis. Osteoarthr
Cartil. 2006;14(10):1033–40.
28. Zhang Y, Nevitt M, Niu J, Lewis C, Torner J, Guermazi A, et al. Fluctuation of knee pain and
changes in bone marrow lesions, effusions, and synovitis on magnetic resonance imaging.
Arthritis Rheum. 2011;63(3):691–9.
29. Bergman AG, Willen HK, Lindstrand AL, Pettersson HT. Osteoarthritis of the knee: correla-
tion of subchondral MR signal abnormalities with histopathologic and radiographic features.
Skelet Radiol. 1994;23(6):445–8.
30. Zanetti M, Bruder E, Romero J, Hodler J. Bone marrow edema pattern in osteoarthritic knees:
correlation between MR imaging and histologic findings. Radiology. 2000;215(3):835–40.
31. Baker K, Grainger A, Niu J, Clancy M, Guermazi A, Crema M, et al. Relation of synovitis to
knee pain using contrast-enhanced MRIs. Ann Rheum Dis. 2010;69(10):1779–83.
32. Hill CL, Gale DG, Chaisson CE, Skinner K, Kazis L, Gale ME, et al. Knee effusions, popli-
teal cysts, and synovial thickening: association with knee pain in osteoarthritis. J Rheumatol.
2001;28(6):1330–7.
Chapter 3
Economic Implications of Post-traumatic
Arthritis of the Hip and Knee
Key Points
• To understand how patient demographics, injury patterns, and the manage-
ment of hip and knee PTOA contribute to the disease burden
• To assess the direct and indirect economic burden associated with PTOA
of the hip and knee
Introduction
There are 27 million [1] people in the United States who have been diagnosed with
degenerative joint disease (DJD). Patients with osteoarthritis (OA) frequently pres-
ent with joint stiffness, pain, or instability due to degeneration of the articular sur-
face. In the event OA develops after an acute injury, this subcategory of OA is
referred to as post-traumatic osteoarthritis (PTOA). Posttraumatic osteoarthritis of
R. Iorio (*)
Brigham and Women’s Hospital, Member of the Faculty, Harvard Medical School,
Boston, MA, USA
e-mail: riorio@[Link]
K. Y. Kim
Department of Orthopaedic Surgery, UNLV School of Medicine, Las Vegas, NV, USA
A. A. Anoushiravani
Department of Orthopaedic Surgery, Albany Medical Center, Albany, NY, USA
W. J. Long
ISK Institute, Department of Orthopaedic Surgery, NYU Langone Medical Center,
Hospital for Joint Diseases, New York, NY, USA
the lower extremity comprises about 12% of OA overall, of which PTOA of the hip
and knee account for 0.5% and 6.3%, respectively [2].
Following the initial injury, there are two mechanisms by which OA may ulti-
mately develop. One pathway is through damage to the articular surface of the joint
at the time of injury followed by subsequent, chronic degeneration of the joint sec-
ondary to a continuous inflammatory response [3]. Another pathway is through
chronic inflammation to the articular surface caused by joint instability or incongru-
ity following an inadequately treated joint injury. The pathophysiologic mechanism
in PTOA and primary OA is similar; however, PTOA is initiated by an acute trau-
matic episode [4].
Given the association between PTOA and acute injury, the patient population
that typically develops PTOA is younger and more active than patients diagnosed
with primary OA [5]. Patients with a history of lower-extremity joint trauma will
on average develop OA 10 years sooner than those without a history of trauma
[6]. Despite extensive research aimed at better managing PTOA, over 40% of
patients with significant soft tissue injuries to the knee will develop symptom-
atic OA [3].
An abundant amount of resources have been dedicated to understanding the
management of OA. The Agency for Healthcare Research and Quality (AHRQ)
ranked OA as one of the top 5 most costly conditions in the United States [7]. Yet,
there is a paucity of literature evaluating the economic effects of secondary causes
of OA including PTOA. This is particularly concerning as recent studies have dem-
onstrated that the direct costs associated with managing PTOA are substantially
greater than those diagnosed with primary OA [8]. Additionally, as a growing num-
ber of individuals participate in high-risk activities, the incidence of PTOA is
expected to increase. Given this growing trend, PTOA poses a substantial financial
burden on the healthcare system. Thus, the aim of this review is to shed light on the
clinical and economic implications of PTOA. Emphasis will be placed on the direct,
indirect, and long-term costs associated with PTOA. Finally, we will present poten-
tial solutions which may improve the delivery of care and reduce the financial bur-
den on all stakeholders.
Post-traumatic osteoarthritis of the knee is responsible for 6.3% of the overall prev-
alence of OA [2]. Patients diagnosed with PTOA are on average 10 years younger,
and more active than those with primary OA [2], and have a five times greater likeli-
hood of developing PTOA with a past history significant for knee injury [9].
Specifically, the incidence of ligamentous and meniscal injury is associated with a
50% incidence of knee PTOA within 10–20 years [10]. Given the rapidly progres-
sive nature of PTOA and the young active population often affected by this disease
process, it is not uncommon to see debilitating manifestations of the disease within
the third and fourth decades of life.
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 27
Meniscus Injuries
Meniscal injuries are another common cause of degenerative knee changes and are
responsible for 23% of patients with PTOA [11]. Swenson et al. [15] observed that
following meniscal injury, the first signs of OA were identified 10 years after injury
Fig. 3.1 Patient with ACL reconstruction that went on to total knee arthroplasty
28 R. Iorio et al.
at an average age of 50 years. The investigators also reported that the age of the
patient at the time of the injury played a role in the timing of the onset of OA as
patients who had an isolated meniscal injury between the ages of 17 and 30 devel-
oped radiologic OA after 15 years, whereas patients over the age of 30 years devel-
oped degenerative changes within 5 years [15]. A study by Badlani et al. [16]
compared the characteristics of meniscal injury in those who did and did not develop
PTOA within 2 years of injury. The authors reported that complex tears, extrusion
of the meniscus, tears greater than one-third of the radial width of the meniscus, and
injuries longer than one-third of the longitudinal length of the meniscus occurred
more frequently in those who developed PTOA.
Intra-articular Fractures
Patients with fractures of the articular surface are at increased risk for developing
PTOA (Fig. 3.3). Studies have demonstrated that up to 31% of these patients will
develop PTOA of the knee depending on the location of the fracture [17]. In a study
by Honkone [18], 44% of patients with a previous history of tibial plateau fractures
developed arthritis within 7.6 years of surgery. Although Honkone and colleagues
demonstrated the high prevalence of arthritis within patients with history of tibial
plateau fractures, the mechanism and severity of injury is often the best prognostic
indicator of PTOA. Higher load injuries are more likely to be associated with imme-
diate damage to the surrounding cartilaginous structures, whereas joints may be
more forgiving to less severe injuries [19, 20].
Primary prevention strategies are implemented in order to prevent the initial injury
from occurring and are considered to be the most effective management tool for
prevention of PTOA. Specifically for ACL rupture prevention, neuromuscular train-
ing, aerobic conditioning, resistance training, and plyometrics have all been shown
to strengthen soft tissue around the knee, reducing the incidence of ligamentous
injury [21]. Recent literature has reported a 70% risk reduction in ACL ruptures
when proper exercise regimens are practiced [22]. The costs associated with pri-
mary prevention of PTOA are not unreasonable. Exercise programs using these pre-
ventative therapies have been estimated to cost between $50 and 400 USD per
session and may require a 3-hour commitment per week. Given the high costs asso-
ciated with ACL reconstruction ($38,121 to $88,538 USD) [23], primary prevention
is particularly worthwhile among high-risk patients.
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 29
Secondary Prevention
Secondary preventative measures are indicated in individuals who have already sus-
tained a joint injury. The goal of secondary prevention is to prevent worsening of a
joint injury. Although surgical techniques and knowledge surrounding the restora-
tion of joint stability and articular surface congruity have improved over the past
25 years, up to 50% of individuals sustaining a serious joint injury warranting surgi-
cal intervention will go on to develop OA [24]. While in the majority of patients,
arthroscopic repair of soft tissue, ACL reconstruction, and partial meniscectomy are
the current standard of care, the literature has not demonstrated a reduced incidence
of PTOA with these interventions (Fig. 3.1) [25].
Similarly, the benefits are unclear in patients undergoing autologous chondrocyte
implantation (ACI), microfracture, and chondroplasty. Knutsen et al. assessed 5-
[26] and 15-year [27] outcomes following ACI and microfracture repair in symp-
tomatic patients with cartilage defects and reported a failure rate as high as 43% and
33% for the respective procedures. In addition, the study also demonstrated that OA
develops in 33% of patients undergoing ACI and microfracture repair at 5 years and
greater than 50% of patients at 15 years. Given the similar long-term outlook, it is
important for providers and patients to be aware of the direct and indirect costs
associated with the various treatment modalities as there may be substantial differ-
ences between them.
Tertiary Prevention
When primary and secondary prevention measures have failed and PTOA has devel-
oped, alternative treatment modalities may be implemented to slow the progression
of OA. In younger, more active individuals, the clinician is left with the difficult task
of developing a treatment strategy aimed at minimizing pain, improving function,
and delaying TKA. Such an approach requires a host of patient-centered strategies
focusing on tiered interventions. The least invasive therapies should always be
implemented first regardless of the patient’s age. These interventions include weight
loss, orthotics, knee bracing, and physical therapy. Physical exercise has been shown
to provide pain relief, particularly when combined with strengthening and aerobic
activities. Various pharmacological treatments commonly used in combination with
first-line therapies include oral analgesic agents and intra-articular hyaluronic acid
or corticosteroid injections. Although nonsurgical interventions have been shown to
provide temporary relief, they do not have any impact on the reversal of the underly-
ing joint disease.
If nonsurgical management is unsuccessful, there are multiple surgical alterna-
tives available. Total knee arthroplasty (TKA) has been shown to alleviate knee pain
and improve knee function (Fig. 3.1). Although very effective, TKA in patients with
PTOA may be challenging due to anatomic malalignment, bony deficiency, joint
30 R. Iorio et al.
instability, contractures, compromised soft tissue, and retained hardware [28, 29].
These obstacles contribute to high complication rates, increased length of hospital
stay, readmissions, and worse functional outcomes than patients preoperatively
diagnosed with primary OA [8, 30].
Another method of surgical management particularly among younger patients
with significant deformities are osteotomies. These procedures are typically done in
younger (<50 years) more active patients with obvious bony malalignment.
Although an osteotomy has been shown to be associated with delaying the need for
TKA and improved pain and function scores [31], the benefits of surgery gradually
deteriorate as the disease progresses. Long-term studies have demonstrated 10-year
failure rates of 24.6% [32].
For patients with localized cartilaginous defects, osteochondral grafts may
be indicated. The procedure is almost exclusively conducted in younger patients
and has been associated with variable outcomes. A systematic review after a
mean follow-up of 58 months demonstrated an overall failure rate of 18%, while
65% of patients had little to no radiographic change in knee arthritis on
follow-up [33].
In order to deliver the highest quality of care, healthcare providers must empha-
size primary and secondary prevention. Tertiary prevention will frequently require
costly surgical procedures which may resolve the underlying joint pathology but
often with suboptimal outcomes. Thus, healthcare providers should continue to
investigate the pathophysiological association between mechanical injury and the
subsequent degenerative changes observed in the joint. Moreover, structured treat-
ment protocols are needed for the management of PTOA as these patients frequently
require multiple surgical interventions during their lifetime, each associated with an
independent list of complications and expenditures.
Although PTOA of the hip is substantially less common than PTOA of the knee [2],
its clinical and economic implications must also be considered. Unlike in the knee,
time between injury and the development of PTOA of the hip is slightly lengthier,
and the population that is affected is generally older. One population-based study
demonstrated that in patients who developed hip PTOA following a traumatic event
to the hip, the median age at which symptoms occurred was 66 years, approximately
13 years following the injury [34]. Furthermore, the study reported that injuries to
the hip have been associated with a 4.3-fold increase in the risk of hip osteoarthritis.
Although there are numerous mechanisms leading to PTOA of the hip, common
causes include articular incongruity and disruption of the articular surface most
frequently due to fractures or hip dislocations.
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 31
Hip/Acetabular Fractures
Hip fractures may predispose patients to secondary arthritis of the hip, mainly as a
result of failed subcapital hip fixation, and to a lesser extent intertrochanteric and
subtrochanteric fractures. The specific mechanisms that lead to PTOA include high-
energy fracture patterns, injury to the articular surface, and nonunions following
injury. In addition, avascular necrosis resulting from traumatic devascularization or
hardware placement following fracture fixation may subsequently cause PTOA of
the hip (Fig. 3.2) [35].
Although acetabular fractures of the hip are rare compared to other types of frac-
tures in the hip region, up to a quarter of these patients will go on to develop PTOA
[36]. Acetabular fractures have a bimodal distribution occurring in the elderly and
young males. The mechanism of injury in these two populations varies significantly.
Elderly patients are more likely to sustain acetabular fractures following low-energy
falls, whereas younger individuals typically sustain a high-energy injury [37].
Unfortunately, acetabular fractures predominantly occur in the elderly population,
and their incidence has increased substantially in the past quarter century as the
geriatric population continues to be the fastest growing subgroup in the United
States [38] (Fig. 3.3).
a c
Fig. 3.2 AP (a) and lateral (b) view of previous intertrochanteric hip fracture treated with a sliding
hip screw construct that went on to avascular necrosis. AP pelvis after removal of the sliding hip
screw and left total hip arthroplasty treated with a modular diaphyseal engaging stem (c)
32 R. Iorio et al.
Fig. 3.3 Tibial plateau fracture (a) that went on to total knee arthroplasty (b). Clinical picture of
the complex skin incision associated with reconstruction (c)
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 33
Fig. 3.3 (continued)
Posterior hip dislocations represent about 90% of all traumatic hip dislocations
[39], and almost all injuries are a result of motor vehicle collisions. Given the strong
association between these two events, young males (16–40 years) are most likely to
be affected [40]. Hip dislocations lead to PTOA due to joint incongruity and insta-
bility, resulting in chronic inflammation and damage to the articular surface of the
hip. In addition, hip dislocations may also result in acetabular fractures and osteo-
necrosis of the hip head. The overall occurrence rate of PTOA in the hip following
posterior hip dislocations ranges from 19% to 55%, with a direct correlation between
dislocation severity and the likelihood for future PTOA [41].
Primary Prevention
Given the nature of the injury mechanism responsible for the majority of hip PTOA,
preventing injury to the hip is somewhat more difficult than the knee. Broad mea-
sures have been shown to prevent acetabular fractures and hip dislocations which
include safe driving practices and stringent adherence to fall precautions in the
elderly. If fall precautions are in place, the cause should be investigated by a health-
care provider, medications should be reviewed, strength and balance exercises
implemented, and regular vision checkups obtained. Finally, various medical
34 R. Iorio et al.
Secondary Prevention
Once a hip injury has occurred, a number of secondary measures can be imple-
mented in an effort to prevent progression to PTOA. After an acetabular fracture,
sufficient anatomic reduction is essential to ensure the joint has the best chance of
survival. It should be emphasized that achieving anatomic reduction does not rule
out the occurrence of PTOA [42, 43]. When managing hip dislocations, prompt
reduction has been correlated with improved outcomes and reduced risk of compli-
cations such as the development of avascular necrosis of the femoral head. The
orthopedic literature supports hip reduction as soon as possible or within 12 hours
following the injury [41].
Tertiary Prevention
Once primary and secondary preventative measures have been exhausted, total hip
arthroplasty (THA) may ultimately be indicated. Initially, many of the same nonsur-
gical management strategies of PTOA of the knee are shared with management of
the hip. Once progression of PTOA of the hip can no longer be adequately managed
nonoperatively, more invasive interventions including THA may be required
(Fig. 3.2). Patients receiving these interventions are usually younger than those
receiving THA secondary to primary OA. Although the risk for revision surgery is
higher in younger patients, implant durability has improved substantially over the
last three decades making THA in younger patients feasible. Despite the improve-
ments, THA in the setting of PTOA has been linked with worse peri- and postopera-
tive outcomes [44]. Thus, the possibility for longer operative times, higher rates of
complications, early failures, and revision THA should be discussed with the
patient. In rare circumstances, when the arthritic disease in the hip joint is so severe
and previous attempts of THA have failed, rarely hip arthrodesis or resection arthro-
plasty may be indicated. Studies have demonstrated that although patients may be
functionally limited, these can be effective procedures for the management of pain.
However, arthrodesis has been associated with new onset ipsilateral knee and lower
back pain due to the straining forces being placed on the proximal and distal joints.
Other concerns associated with arthrodesis include highly variable union rates, like-
lihood of returning to work, and satisfaction rates, all of which should be discussed
at length prior to surgery [45].
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 35
There has been a robust effort to investigate the economic implications of primary
OA and methods of better managing it while minimizing costs. However, the lack
of large-scale epidemiologic studies evaluating the prevalence of PTOA has proven
to be a major barrier in the development of accurate economic models assessing the
financial fingerprint of PTOA on the US healthcare system. Although these two
diagnoses share many similarities, PTOA affects a younger more active population,
frequently requiring multiple surgical interventions. Thus, it should not be surpris-
ing that patients with PTOA have higher direct and indirect medical costs. Moreover,
many of these patients are uninsured further complicating management of this
debilitating disease. While it is well recognized that OA is one of the leading causes
of disability among all diseases, the costs associated with the management of OA
are difficult to approximate due to the debilitating nature of the disease and the
many modalities of treatment. A recent report by Kotlarz and colleagues [46] uti-
lized data from the Medical Expenditure Panel Survey (MEPS) and estimated that
OA costs the US healthcare system $185.5 billion USD annually, of which $149.4
billion USD was expensed to insurers [46]. The report also found that women
accounted for nearly two-thirds ($118 billion USD) of the dollars spent on manag-
ing OA, further demonstrating the gender discrepancies existing among those diag-
nosed with OA.
Although the literature surrounding the economic implications of PTOA is lim-
ited, a few recent studies have helped provide some perspective on the magnitude of
the associated direct costs. Brown and colleagues [2] were the first to utilize a state-
based model to estimate the prevalence and disease burden associated with PTOA at
a national level. The investigators demonstrated that 6.8% of all patients with OA
are due to PTOA of the hip and knee, 0.5% and 6.3%, respectively. Given these
reported prevalence rates, the total direct costs associated with PTOA of the hip and
knee can be measured at roughly $900 million and $11.7 billion annually (Fig. 3.4).
In a separate study by Chin et al. [47], cohorts of patients undergoing primary THA
were compared to conversion THA, a common salvage procedure of failed hip frac-
ture fixation secondary to PTOA. The conversion procedures were associated with
a significant increase of 26% in total hospital costs over primary OA treatment
which, notably, did not account for the commonly occurring postoperative compli-
cations and revision procedures following discharge. Despite the paucity of litera-
ture comparatively examining postoperative outcomes and resource expenditures
associated with PTOA, the available evidence clearly suggests an increased disease
burden in patients diagnosed with PTOA compared with primary OA.
The indirect disease burden associated with PTOA is somewhat more concern-
ing, as indirect costs associated with PTOA may be three times greater than direct
costs [48]. Given that this population is younger and more active and frequently
requires multiple surgical interventions (i.e., ACLR, arthroscopy, fracture fixation,
36 R. Iorio et al.
$185.5 billionADDIN
$12.6 billion
Fig. 3.4 Total direct cost of PTOA of the knee and hip
TJA) dispersed over their lifetime, the burden of PTOA economically and in terms
of the individual’s quality of life is substantially greater than primary
OA. Additionally, many individuals with PTOA are of prime working age with
higher rates of absenteeism, and overall work impairment compared with older age
groups, [49] and are frequently forced to apply for disability benefits at each treat-
ment juncture. Thus, although difficult to calculate the job-related loss of economic
activity due to injuries, indirect costs of PTOA of the hip and knee together may be
responsible for more than $35.3 billion annually, far exceeding the direct cost asso-
ciated with PTOA (Fig. 3.5).
Recommendations
Individuals diagnosed with posttraumatic and primary OA often present with simi-
lar symptoms; however, the mechanism of injury varies significantly. Patients with
PTOA have had an acute injury subsequently resulting in degenerative changes of
the joint, whereas individuals with primary OA have nonspecific wear and inflam-
mation leading to cartilage loss. Given the different mechanisms of injury and goals
of treatment, it is crucial that healthcare providers manage PTOA through a
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 37
$185.5 billionADDIN
$519.4 billion
$35.3 billion
Fig. 3.5 Total indirect cost of PTOA of the knee and hip
designated care pathway (ICP) with the aim of delivering high-quality care while
minimizing resource expenditures.
Our review demonstrates the paucity of literature examining postoperative out-
comes and resource expenditures associated with the management of PTOA. This is
at least in part due to the coding limitations associated with the International
Classification for Disease 9th Edition (ICD-9), which fails to differentiate between
primary and secondary OA. Fortunately, as of October 2015, the ICD-10 has been
successfully implemented enabling clinicians to diagnose indications for surgery
with greater specificity. If the ICD-10 codes are properly implemented, future
38 R. Iorio et al.
investigators may link clinical and billing information to better elucidate resource
utilization trends among individuals with OA. However, the utilization of ICD-10
codes alone is not sufficient as several issues still remain if these diagnostic codes
are to be used to estimate the prevalence and economic burdens associated with
complex disease processes such as PTOA.
First, the ICD-10 coding system utilizes nearly 70,000 unique diagnostic codes.
It is therefore essential that healthcare providers be familiar with the diagnostic
codes within the scope of their practice. Healthcare providers must also avoid “gam-
ing the system” by intentionally using a handful of nonspecific diagnostic codes. To
insure that healthcare providers are meaningfully using diagnostic codes, providers
should have the opportunity to participate in courses designed to better define the
strengths and limitations of the ICD-10 coding system. Additionally, as mandated
by the Affordable Care Act (ACA), healthcare organizations and their providers are
responsible for accurately documenting and reporting clinical metrics. Failure to
properly do so will likely result in penalties and withheld payments. Thus, we sug-
gest that healthcare organizations periodically audit the diagnostic codes being
assigned to episodes of care, improving institution-wide compliance, while also
strengthening the quality of the data collected.
Lastly, it is crucial that ICD-10 codes be aligned with CPT and Medicare Severity
Diagnosis-Related Groups (MS-DRGs) in order to differentiate arthroplasty proce-
dures by preoperative indication. Disease-specific procedure codes similar to those
used in conversion THA and revision arthroplasty may enable investigators to better
understand the clinical outcomes and disease burdens unique to PTOA. Without
proper coding methodology, it is nearly impossible to distinguish indications for
surgery at a macro level, thereby leaving many clinical questions unanswered.
Furthermore, proper coding practices would enable investigators to retrospectively
evaluate the value of care delivered, ensuring that care pathways are in line with
organizational standards. Such an approach will also ensure that healthcare organi-
zations are appropriately compensated for the services rendered.
Summary
Posttraumatic osteoarthritis of the hip and knee is a debilitating disease often affect-
ing younger, more active individuals. Currently an estimated 5.8 million individuals
are living with PTOA of the hip and knee at a direct and indirect cost of almost
$48.9 billion annually. As Americans continue to live active lifestyles, the number
of individuals living with PTOA is projected to steadily grow costing billions more
dollars in direct and indirect expenditures. It is therefore critical that healthcare
providers lobby for improved diagnostic and procedure codes so that PTOA can be
properly monitored and objectively evaluated. Through such an approach, providers
will have the resources needed to better address the complexities present in PTOA
patients. Once granular coding instruments have been developed and used for these
complex patients, the full economic impact of PTOA may be realized.
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 39
References
1. Lawrence RC, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in
the United States. Part II. Arthritis Rheum. 2008;58(1):26–35.
2. Brown TD, Johnston RC, Saltzman CL, Marsh JL, Buckwalter JA. Posttraumatic osteoar-
thritis: a first estimate of incidence, prevalence, and burden of disease. J Orthop Trauma.
2006;20(10):739–44.
3. Anderson DD, et al. Post-traumatic osteoarthritis: improved understanding and opportunities
for early intervention. J Orthop Res. 2011;29(6):802–9.
4. Buckwalter JA, Brown TD. Joint injury, repair, and remodeling: roles in post-traumatic osteo-
arthritis. Clin Orthop Relat Res. 2004;423:7–16.
5. Stiebel M, Miller LE, Block JE. Post-traumatic knee osteoarthritis in the young patient: thera-
peutic dilemmas and emerging technologies. Open Access J Sport Med. 2014;5:73–9.
6. Saltzman CL, et al. Epidemiology of ankle arthritis: report of a consecutive series of 639
patients from a tertiary orthopaedic center. Iowa Orthop J. 2005;25:44–6.
7. Soni A. Top 10 most costly conditions among men and women, 2008: estimates for the
U.S. civilian noninstitutionalized adult population, age 18 and older. 2011. 2011.
8. Kester BS, Minhas SV, Vigdorchik JM, Schwarzkopf R. Total knee arthroplasty for posttrau-
matic osteoarthritis: is it time for a new classification? J Arthroplasty. 2016;31(8):1649–1653.e1.
9. Gelber AC, Hochberg MC, Mead LA, Wang N-YY, Wigley FM, Klag MJ. Joint injury in young
adults and risk for subsequent knee and hip osteoarthritis. Ann Intern Med. 2000;133(5):321.
10. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cru-
ciate ligament and meniscus injuries: osteoarthritis. Am J Sports Med. 2007;35(10):1756–69.
11. Swenson DM, Collins CL, Best TM, Flanigan DC, Fields SK, Comstock RD. Epidemiology of
knee injuries among U.S. high school athletes, 2005/2006–2010/2011. Med Sci Sports Exerc.
2013;45(3):462–9.
12. Lebel B, Hulet C, Galaud B, Burdin G, Locker B, Vielpeau C. Arthroscopic reconstruction of
the anterior cruciate ligament using bone-patellar tendon-bone autograft: a minimum 10-year
follow-up. Am J Sports Med. 2008;36(7):1275–82.
13. Kraus VB, et al. Call for standardized definitions of osteoarthritis and risk stratification for
clinical trials and clinical use. Osteoarthr Cartil. 2015;23(8):1233–41.
14. Barenius B, Ponzer S, Shalabi A, Bujak R, Norlén L, Eriksson K. Increased risk of osteoarthri-
tis after anterior cruciate ligament reconstruction: a 14-year follow-up study of a randomized
controlled trial. Am J Sports Med. 2014;42(5):1049–57.
15. Roos H, Adalberth T, Dahlberg L, Lohmander LS. Osteoarthritis of the knee after injury to
the anterior cruciate ligament or meniscus: the influence of time and age. Osteoarthr Cartil.
1995;3(4):261–7.
16. Badlani JT, Borrero C, Golla S, Harner CD, Irrgang JJ. The effects of meniscus injury on the
development of knee osteoarthritis: data from the osteoarthritis initiative. Am J Sports Med.
2013;41(6):1238–44.
17. Rademakers MV, Kerkhoffs GMMJ, Sierevelt IN, Raaymakers ELFB, Marti RK. Operative
treatment of 109 Tibial plateau fractures: five- to 27-year follow-up results. J Orthop Trauma.
2007;21(1):5–10.
18. Honkonen SE. Degenerative arthritis after tibial plateau fractures. J Orthop Trauma.
1995;9(4):273–7.
19. Fithian DC, et al. Prospective trial of a treatment algorithm for the management of the anterior
cruciate ligament-injured knee. Am J Sports Med. 2005;33(3):335–46.
20. Racine J, Aaron RK. Post-traumatic osteoarthritis after ACL injury. R I Med J (2013).
2014;97(11):25–8.
21. Mandelbaum BR, et al. Effectiveness of a neuromuscular and proprioceptive training program
in preventing anterior cruciate ligament injuries in female athletes: 2-year follow-up. Am J
Sports Med. 2005;33(7):1003–10.
40 R. Iorio et al.
22. Grindstaff TL, Hammill RR, Tuzson AE, Hertel J. Neuromuscular control training programs
and noncontact anterior cruciate ligament injury rates in female athletes: a numbers-needed-
to-treat analysis. J Athl Train. 2006;41(4):450–6.
23. Mather RC, et al. Societal and economic impact of anterior cruciate ligament tears. J Bone
Joint Surg Am. 2013;95(19):1751–9.
24. Buckwalter JA, Felson DT. Post-traumatic arthritis: definitions and burden of disease. In:
Post-traumatic arthritis. Boston: Springer US; 2015. p. 7–15.
25. Riordan EA, Little C, Hunter D. Pathogenesis of post-traumatic OA with a view to interven-
tion. Best Pract Res Clin Rheumatol. 2014;28(1):17–30.
26. Knutsen G, et al. A randomized trial comparing autologous chondrocyte implantation with
microfracture. Findings at five years. J Bone Joint Surg Am. 2007;89(10):2105–12.
27. Knutsen G, et al. A randomized multicenter trial comparing autologous chondrocyte implanta-
tion with microfracture. J Bone Jt Surg. 2016;98(16):1332–9.
28. Shearer DW, Chow V, Bozic KJ, Liu J, Ries MD. The predictors of outcome in total knee
arthroplasty for post-traumatic arthritis. Knee. 2013;20(6):432–6.
29. Georgiadis GM, Skakun FWC. Total knee arthroplasty with retained tibial implants: the role
of minimally invasive hardware removal. Am J Orthop. 2016;45(7):E481.
30. Lunebourg A, Parratte S, Gay A, Ollivier M, Garcia-Parra K, Argenson J-N. Lower function,
quality of life, and survival rate after total knee arthroplasty for posttraumatic arthritis than for
primary arthritis. Acta Orthop. 2015;86(2):189–94.
31. Lustig S, et al. Post-traumatic knee osteoarthritis treated by osteotomy only. Orthop Traumatol
Surg Res. 2010;96(8):856–60.
32. Virolainen P, Aro HT. High tibial osteotomy for the treatment of osteoarthritis of the knee: a
review of the literature and a meta-analysis of follow-up studies. Arch Orthop Trauma Surg.
2004;124(4):258–61.
33. Chahal J, et al. Outcomes of osteochondral allograft transplantation in the knee. Arthroscopy.
2013;29(3):575–88.
34. Cooper C, et al. Individual risk factors for hip osteoarthritis: obesity, hip injury, and physical
activity. Am J Epidemiol. 1998;147(6):516–22.
35. Haidukewych GJ, Rothwell WS, Jacofsky DJ, Torchia ME, Berry DJ. Operative treatment of
femoral neck fractures in patients between the ages of fifteen and fifty years. J Bone Jt Surg.
2004;86(8):1711–6.
36. Giannoudis PV, Grotz MRW, Papakostidis C, Dinopoulos H. Operative treatment of displaced
fractures of the acetabulum. A meta-analysis. J Bone Joint Surg Br. 2005;87(1):2–9.
37. Mears DC. Surgical treatment of acetabular fractures in elderly patients with osteoporotic
bone. J Am Acad Orthop Surg. 1999;7(2):128–41.
38. Butterwick D, et al. Acetabular fractures in the elderly: evaluation and management. J Bone
Joint Surg Am. 2015;97(9):758–68.
39. Sowers M, Lachance L, Hochberg M, Jamadar D. Radiographically defined osteoarthritis
of the hand and knee in young and middle-aged African American and Caucasian women.
Osteoarthr Cartil. 2000;8(2):69–77.
40. Epstein HC. Traumatic dislocations of the hip. Clin Orthop Relat Res. 1973;92:116–42.
41. Kellam P, Ostrum RF. Systematic review and meta-analysis of avascular necrosis and post-
traumatic arthritis after traumatic hip dislocation. J Orthop Trauma. 2016;30(1):10–6.
42. Tannast M, Najibi S, Matta JM. Two to twenty-year survivorship of the hip in 810 patients with
operatively treated acetabular fractures. J Bone Joint Surg Am. 2012;94(17):1559–67.
43. Meena UK, Tripathy SK, Sen RK, Aggarwal S, Behera P. Predictors of postoperative outcome
for acetabular fractures. Orthop Traumatol Surg Res. 2013;99(8):929–35.
44. Srivastav S, Mittal V, Agarwal S. Total hip arthroplasty following failed fixation of proximal
hip fractures. Indian J Orthop. 2008;42(3):279–86.
45. Jain S, Giannoudis PV. Arthrodesis of the hip and conversion to total hip arthroplasty: a sys-
tematic review. J Arthroplast. 2013;28(9):1596–602.
3 Economic Implications of Post-traumatic Arthritis of the Hip and Knee 41
46. Kotlarz H, Gunnarsson CL, Fang H, Rizzo JA. Insurer and out-of-pocket costs of osteoarthritis
in the US: evidence from national survey data. Arthritis Rheum. 2009;60(12):3546–53.
47. Chin G, Wright DJ, Snir N, Schwarzkopf R. Primary vs conversion total hip arthroplasty: a
cost analysis. J Arthroplast. 2016;31(2):362–7.
48. Praemer A, Furner S, Rice DP. American Academy of Orthopaedic Surgeons. Musculoskeletal
conditions in the United States. American Academy of Orthopaedic Surgeons: Rosemont; 1999.
49. Dibonaventure MD, Gupta S, Mcdonald M, Sadosky A, Pettitt D, Silverman S. Impact of
self-rated osteoarthritis in an employed population: cross-sectional analysis of data from the
national health and wellness survey. Heal Qual Life Outcomes. 2012;10:30.
Part II
Post-traumatic Arthritis
of the Upper Extremity
Chapter 4
Post-traumatic Glenohumeral Arthritis
Uma Srikumaran and Eric Huish
Key Points
• Proximal humerus fractures, glenohumeral instability, and direct cartilagi-
nous trauma are all causes of post-traumatic glenohumeral arthritis.
• Various injury patterns and previous interventions may alter the anatomy
of the glenohumeral joint, which must be taken into account when surgical
treatment is planned.
• Total shoulder arthroplasty, reverse shoulder arthroplasty, and hemiarthro-
plasty are all utilized in the treatment of post-traumatic glenohumeral
arthritis, each with various benefits and shortcomings.
• Non-arthroplasty options for the treatment of glenohumeral post-traumatic
arthritis show transient benefit and may be beneficial in the appropriately
selected patient.
Introduction
U. Srikumaran (*)
The Johns Hopkins University, Division of Shoulder and Elbow Surgery,
Columbia, MD, USA
e-mail: us@[Link]
E. Huish
Stanislaus Orthopaedics & Sports Medicine Clinic, Modesto, CA, USA
Causes
Fractures
Instability
a b
Fig. 4.2 (a, b) AP and axillary radiographs of a shoulder with post-traumatic arthritis after dislo-
cation and subsequent repair
Other Causes
Treatment
There are many factors involved in determining the appropriate treatment of post-
traumatic glenohumeral arthritis. The surgeon should assess the severity of disease,
initial injury, previous treatments, patient age, and functional requirements.
Nonoperative Treatment
Preoperative Evaluation
Arthroplasty
a b
Fig. 4.3 (a, b) Preoperative and postoperative radiographs of a humerus with malunion and post-
traumatic arthritis treated with reverse shoulder arthroplasty utilizing a short humeral stem
Hemiarthroplasty
Humeral Resurfacing
If the rotator cuff is deficient, in presence of a functional deltoid and adequate bone
stock, a reverse shoulder arthroplasty may be considered. Although clinical out-
comes for the treatment of fracture sequelae show improvement, results are worse
than for acute fractures [10, 14]. To this end, patients who had previous fracture
surgery had worse outcomes than those treated initially nonoperatively [10].
52 U. Srikumaran and E. Huish
Reverse shoulder arthroplasty has also been used with good results as a revision
from a failed hemiarthroplasty due to development of glenoid arthritis or rotator
cuff failure [29]. However, these results are inferior to those obtained for primary
indications.
Reverse shoulder arthroplasty was originally reserved for elderly patients; how-
ever, in cases where no other option seems appropriate, reverse shoulder arthro-
plasty may be an option in a younger patient. Few studies evaluate patients under 60
undergoing reverse shoulder arthroplasty. The current literature shows good early
outcomes, but follow-up is limited, and the success rate and patient satisfaction are
less than in previous studies looking at an older population [35, 45]. This procedure
must be done with caution in a young patient, as long-term outcomes are not yet
widely reported with midterm outcomes showing a 15% failure rate, 25% reopera-
tion rate, and 38% complication rate after 5–15 years [16].
Alternative Options
Non-arthroplasty Surgery
Complications
Summary
The treatment options for post-traumatic arthritis of the glenohumeral joint are as
diverse as its causes. Patients are surgical candidates only after failure of nonopera-
tive treatments and thorough preoperative workup. While arthroplasty may be a
widely accepted treatment for older or lower-demand patients, there is controversy
surrounding the treatment of younger, active patients. In this group, surgical treat-
ment should be individualized after frank discussion of goals and expected out-
comes. While significant improvements are seen after surgical intervention, they
tend to fall short of expected results for primary procedures with high complication
rates. New and emerging implants and techniques may improve treatment in these
challenging cases.
54 U. Srikumaran and E. Huish
Annotated References
1. Anavian J, Gauger EM, Schroder LK, Wijdicks CA, Cole PA. Surgical and functional out-
comes after operative management of complex and displaced intra-articular glenoid fractures.
J Bone Joint Surg Am. 2012;94(7):645–53. This level IV study examined 33 displaced glenoid
fractures with >4mm step off treated surgically. The mean DASH score was 10.8 with 87%
of patients pain free and 90% of patients returning to pre-injury level of activity at 27 months
follow up.
2. Bartelt R, Sperling JW, Schleck CD, Cofield RH. Shoulder arthroplasty in patients aged fifty-
five years or younger with osteoarthritis. J Shoulder Elbow Surg. 2011;20(1):123–30. This
level IV study reviewed 46 TSA and 20 Hemiarthroplasties in patients age 55 and under. 10
year survival was 92% for TSA and 72% for hemi with less pain, greater forward elevation,
and higher satisfaction in the TSA group.
3. Beredjiklian PK, Iannotti JP, Norris TR, Williams GR. Operative treatment of malunion of a
fracture of the proximal aspect of the humerus. J Bone Joint Surg Am. 1998;80(10):1484–97.
4. Bohsali KI, Wirth MA, Rockwood CA Jr. Complications of total shoulder arthroplasty. J Bone
Joint Surg Am. 2006;88(10):2279–92.
5. Boileau P, Trojani C, Walch G, Krishnan SG, Romeo A, et al. Shoulder arthroplasty for
the treatment of the sequelae of fractures of the proximal humerus. J Shoulder Elb Surg.
2001;10(4):299–308.
6. Buscayret F, Edwards TB, Szabo I, Adeleine P, Coudane H, et al. Glenohumeral arthrosis in
anterior instability before and after surgical treatment: incidence and contributing factors. Am
J Sports Med. 2004;32(5):1165–72.
7. Cameron BD, Galatz LM, Ramsey ML, Williams GR, Iannotti JP. Non-prosthetic manage-
ment of grade IV osteochondral lesions of the glenohumeral joint. J Shoulder Elb Surg.
2002;11(1):25–32.
8. Carpenter SR, Urits I, Murthi AM. Porous metals and alternate bearing surfaces in shoulder
arthroplasty. Curr Rev Musculoskelet Med. 2016;9(1):59–66. This study discussed the use
of trabecular metal, highly cross-linked polyethylene and pyrocarbon as new materials being
used in shoulder arthroplasty.
9. Chong PY, Srikumaran U, Kuye IO, Warner JJ. Glenohumeral arthritis in the young patient.
J Shoulder Elbow Surg. 2011;20(2 Suppl):S30–40. This review article discusses glenohu-
meral osteoarthritis in young patients as well as management strategies both operative and
non-operative.
10. Cicak N, Klobucar H, Medancic N. Reverse shoulder arthroplasty in acute fractures provides
better results than in revision procedures for fracture sequelae. Int Orthop. 2015;39(2):343–8.
This study evaluated 37 patients undergoing reverse shoulder arthroplasty for acute fracture or
sequelae of fracture. Post-op range of motion was highest in the acute fracture group followed
by non-operatively treated fracture sequelae group and finally the previously operated group.
Constant score was higher in the group without prior surgery.
11. Cofield RH, Briggs BT. Glenohumeral arthrodesis operative and long-term functional results.
J Bone Joint Surg Am. 1979;61(5):668–77.
12. de Beer JF, Bhatia DN, van Rooyen KS, Du Toit DF. Arthroscopic debridement and biological
resurfacing of the glenoid in glenohumeral arthritis. Knee Surg Sports Traumatol Arthrosc.
2010;18(12):1767–73.
13. Debeer P, Brys P. Osteochondritis dissecans of the humeral head: clinical and radiological
findings. Acta Orthop Belg. 2005;71(4):484–8.
14. Dezfuli B, King JJ, Farmer KW, Struk AM, Wright TW. Outcomes of reverse total shoulder
arthroplasty as primary versus revision procedure for proximal humerus fractures. J Shoulder
Elbow Surg. 2016;25(7):1133–7. This level III study looked at 49 RSA performed for acute
fracture, fracture sequelae, failed hemiarthroplasty, and failed ORIF. At 32 months SPADI,
UCLA score, ASES score and Constant score were better in the primary surgery group than
the revision surgery group.
4 Post-traumatic Glenohumeral Arthritis 55
15. Eichinger JK, Miller LR, Hartshorn T, Li X, Warner JJ, et al. Evaluation of satisfaction and
durability after hemiarthroplasty and total shoulder arthroplasty in a cohort of patients aged
50 years or younger: an analysis of discordance of patient satisfaction and implant survival.
J Shoulder Elbow Surg. 2016;25(5):772–80. This level III study examined implant survival
and patient satisfaction for hemiarthroplasty and total shoulder arthroplasty in patients 50 and
younger. Implant survival was 95% for TSA and 89 for hemi with patient satisfaction 95% VS
71.6% respectively.
16. Ek ET, Neukom L, Catanzaro S, Gerber C. Reverse total shoulder arthroplasty for massive
irreparable rotator cuff tears in patients younger than 65 years old: results after five to fifteen
years. J Shoulder Elbow Surg. 2013;22(9):1199–208. This level IV study evaluated 40 RSA
in patients under 65 with 5–15 year follow up. SSV, forward elevation, pain, and strength all
improved but complication rate was 37.5% and failure was 15%.
17. Frangiamore SJ, Saleh A, Grosso MJ, Farias Kovac M, Zhang X, et al. Neer Award 2015:
Analysis of cytokine profiles in the diagnosis of periprosthetic joint infections of the shoul-
der. J Shoulder Elbow Surg. 2016;26(2):186–96. This level III study analyzed the levels of
9 cytokines in synovial fluid in patients with shoulder arthroplasty who were divided into
infected and non-infected groups. While many were elevated in the infection cases, a com-
bination of IL-6, TNF-α, and IL-2 showed a sensitivity of 0.80 and specificity of 0.93 for
infection.
18. Gadea F, Alami G, Pape G, Boileau P, Favard L. Shoulder hemiarthroplasty: outcomes and long-
term survival analysis according to etiology. Orthop Traumatol Surg Res. 2012;98(6):659–65.
This level IV study reviewed 272 hemiarthroplasties performed for fracture sequelae, primary
OA, cuff tear arthropathy, AVN, RA and other causes with a mean 10 years follow up. Survival
in the fracture sequelae group was the lowest of any group at 76.8%.
19. Gerber C, Werner CM, Vienne P. Internal fixation of complex fractures of the proximal
humerus. J Bone Joint Surg Br. 2004;86(6):848–55.
20. Gerber C, Hersche O, Berberat C. The clinical relevance of posttraumatic avascular necrosis of
the humeral head. J Shoulder Elb Surg. 1998;7(6):586–90.
21. Goss TP. Scapular fractures and dislocations: diagnosis and treatment. J Am Acad Orthop
Surg. 1995;3(1):22–33.
22. Green A, Norris TR. Shoulder arthroplasty for advanced glenohumeral arthritis after anterior
instability repair. J Shoulder Elb Surg. 2001;10(6):539–45.
23. Hovelius L, Olofsson A, Sandström B, Augustini BG, Krantz L, et al. Nonoperative treatment
of primary anterior shoulder dislocation in patients forty years of age and younger a prospec-
tive twenty-five-year follow-up. J Bone Joint Surg Am. 2008;90(5):945–52.
24. Itamura JM, Beckett M. Infection rates and frozen sections in revision shoulder and elbow
surgery holding cultures 21 days. J Shoulder Elbow Surg. 2013;22:e30–1. This abstract from
the ASES 2012 closed meeting examined 109 revision shoulder and elbow cases. 57 patients
had at least one positive culture, most commonly P. acnes. The average time to positive culture
for P. acnes was 12.5 days.
25. Iyengar JJ, Devcic Z, Sproul RC, Feeley BT. Nonoperative treatment of proximal humerus
fractures: a systematic review. J Orthop Trauma. 2011;25(10):612–7. This systematic review
looked at 12 studies totaling 650 patients with closed treated proximal humerus fractures at
45.7 months follow up. The overall union rate was 98% and the complication rate was 13%
with only 2% AVN.
26. Izquierdo R, Voloshin I, Edwards S, Freehill MQ, Stanwood W, et al. American academy of
orthopaedic surgeons clinical practice guideline on: the treatment of glenohumeral joint osteo-
arthritis. J Bone Joint Surg Am. 2011;93(2):203–5. These AAOS clinical practice guidelines
were based on a systematic review of the literature and recommendations are made based
on the strength of evidence. These recommendations for treating glenohumeral arthritis were
adopted by the AAOS board of directors in December 2009.
27. Johnson DL, Warner JJ. Osteochondritis dissecans of the humeral head: treatment with a
matched osteochondral allograft. J Shoulder Elb Surg. 1997;6(2):160–3.
56 U. Srikumaran and E. Huish
28. Lenart BA, Namdari S, Williams GR. Total shoulder arthroplasty with an augmented compo-
nent for anterior glenoid bone deficiency. J Shoulder Elbow Surg. 2016;25(3):398–405. This
level IV study reported on 5 patients undergoing TSA with an anterior glenoid augment for
anterior wear, malunited glenoid fracture, or post-traumatic arthritis. At 33.2 months there
were no dislocations or revision surgeries and good patient reported outcomes.
29. Levy J, Frankle M, Mighell M, Pupello D. The use of the reverse shoulder prosthesis for the
treatment of failed hemiarthroplasty for proximal humeral fracture. J Bone Joint Surg Am.
2007;89(2):292–300.
30. Levy O, Tsvieli O, Merchant J, Young L, Trimarchi A, et al. Surface replacement arthroplasty
for glenohumeral arthropathy in patients aged younger than fifty years: results after a mini-
mum ten-year follow-up. J Shoulder Elbow Surg. 2015;24(7):1049–60. This level IV study
reported on 54 humeral resurfacings in patients younger than 50 for various indications includ-
ing fracture sequelae and dislocation arthropathy. 81.6% survival was seen at 10 years but
18.5% were revised. Constant scores postoperatively were higher in patients undergoing con-
comitant microfracture of the glenoid.
31. Lo EY, Flanagin BA, Burkhead WZ. Biologic resurfacing arthroplasty with acellular human
dermal allograft and platelet-rich plasma (PRP) in young patients with glenohumeral arthritis-
average of 60 months of at mid-term follow-up. J Shoulder Elbow Surg. 2016;25(7):e199–207.
This level IV study reviewed 55 patients who underwent hemiarthroplasty with human dermal
matrix allograft glenoid resurfacing. A significant improvement was seen in the SANE score
and 81% of patients were satisfied or highly satisfied with the result. 9.1% were revised to TSA.
32. Matsen FA 3rd. The ream and run: not for every patient, every surgeon or every problem. Int
Orthop. 2015;39(2):255–61. This paper discusses the basics of the “ream and run” technique
and stresses the importance of patient selection and patient compliance with the postoperative
regimen.
33. Matsoukis J, Tabib W, Guiffault P, Mandelbaum A, Walch G, et al. Shoulder arthroplasty in
patients with a prior anterior shoulder dislocation results of a multicenter study. J Bone Joint
Surg Am. 2003;85-A(8):1417–24.
34. Millett PJ, Huffard BH, Horan MP, Hawkins RJ, Steadman JR. Outcomes of full-thickness
articular cartilage injuries of the shoulder treated with microfracture. Arthroscopy.
2009;25(8):856–63.
35. Muh SJ, Streit JJ, Wanner JP, Lenarz CJ, Shishani Y, et al. Early follow-up of reverse total
shoulder arthroplasty in patients sixty years of age or younger. J Bone Joint Surg Am.
2013;95(20):1877–83. This level IV study evaluated 67 RSA in patients 60 or younger at 36.5
months post op. Forward elevation, external rotation, ASES score and pain scores all improved
from preoperative values with 81% of patients satisfied or very satisfied. Forward elevation
greater than 100 degrees was the only predictor of satisfaction.
36. Owsley KC, Gorczyca JT. Fracture displacement and screw cutout after open reduction
and locked plate fixation of proximal humeral fractures [corrected]. J Bone Joint Surg Am.
2008;90(2):233–40.
37. Papadonikolakis A, Neradilek MB, Matsen FA 3rd. Failure of the glenoid component in
anatomic total shoulder arthroplasty: a systematic review of the English-language literature
between 2006 and 2012. J Bone Joint Surg Am. 2013;95(24):2205–12. This level IV sys-
tematic review showed rates of radiolucent lines, symptomatic loosening, and revision of the
glenoid component in 3853 TSA to be 7.3%, 1.2%, and 0.8% respectively.
38. Pape G, Zeifang F, Bruckner T, Raiss P, Rickert M, et al. Humeral surface replacement for the
sequelae of fractures of the proximal humerus. J Bone Joint Surg Br. 2010;92(10):1403–9.
39. Puskas GJ, Meyer DC, Lebschi JA, Gerber C. Unacceptable failure of hemiarthroplasty com-
bined with biological glenoid resurfacing in the treatment of glenohumeral arthritis in the
young. J Shoulder Elbow Surg. 2015;24(12):1900–7. This level IV study showed revision
to TSA after hemiarthroplasty and biologic glenoid resurfacing with Graftjacket, meniscal
allograft, and capsular interposition to be occur at rates of 83.3%, 60%, and 66.7% in a small
population of 17 patients with only 16 month follow up.
4 Post-traumatic Glenohumeral Arthritis 57
40. Romeo AA, Cole BJ, Mazzocca AD, Fox JA, Freeman KB, et al. Autologous chondrocyte
repair of an articular defect in the humeral head. Arthroscopy. 2002;18(8):925–9.
41. Ruckstuhl H, de Bruin ED, Stussi E, Vanwanseele B. Post-traumatic glenohumeral cartilage
lesions: a systematic review. BMC Musculoskelet Disord. 2008;9:107.
42. Schandelmaier P, Blauth M, Schneider C, Krettek C. Fractures of the glenoid treated by opera-
tion A 5- to 23-year follow-up of 22 cases. J Bone Joint Surg Br. 2002;84(2):173–7.
43. Scheibel M, Bartl C, Magosch P, Lichtenberg S, Habermeyer P. Osteochondral autologous
transplantation for the treatment of full-thickness articular cartilage defects of the shoulder. J
Bone Joint Surg Br. 2004;86(7):991–7.
44. Schoch BS, Barlow JD, Schleck C, Cofield RH, Sperling JW. Shoulder arthroplasty for post-
traumatic osteonecrosis of the humeral head. J Shoulder Elbow Surg. 2016;25(3):406–12. This
level III study examined 37 hemiarthroplasties and 46 TSA for post-traumatic osteonecrosis
at 8.9 years post op. The TSA group had less pain and higher satisfaction at last follow up. 15
year survival for hemi was 79.5% vs. 83% for TSA.
45. Sershon RA, Van Thiel GS, Lin EC, McGill KC, Cole BJ, et al. Clinical outcomes of reverse
total shoulder arthroplasty in patients aged younger than 60 years. J Shoulder Elbow Surg.
2014;23(3):395–400. This level IV study followed 36 RSA performed in patients younger than
60 for 2.8 years. Improvements were seen in ASES score, SST, SANE, and forward elevation.
25% were considered failures due to ASES score below 50.
46. Sperling JW, Kozak TK, Hanssen AD, Cofield RH. Infection after shoulder arthroplasty. Clin
Orthop Relat Res. 2001;382:206–16.
47. Strauss EJ, Verma NN, Salata MJ, McGill KC, Klifto C, et al. The high failure rate of biologic
resurfacing of the glenoid in young patients with glenohumeral arthritis. J Shoulder Elbow
Surg. 2014;23(3):409–19. This level IV study examined 41 patients who underwent biologic
glenoid resurfacing with meniscal allograft or human acellular dermal matrix at 2.8 year follow
up. Overall failure rate was 51.2%, 45.2% for meniscus and 70% for dermal matrix. Average
time to failure was 3.4 years and 2.2 years for meniscus and dermal matrix respectively.
48. Thanasas C, Kontakis G, Angoules A, Limb D, Giannoudis P. Treatment of proximal humerus
fractures with locking plates: a systematic review. J Shoulder Elb Surg. 2009;18(6):837–44.
49. Topolski MS, Chin PY, Sperling JW, Cofield RH. Revision shoulder arthroplasty with posi-
tive intraoperative cultures: the value of preoperative studies and intraoperative histology. J
Shoulder Elb Surg. 2006;15(4):402–6.
50. Zyto K, Kronberg M, Broström LA. Shoulder function after displaced fractures of the proxi-
mal humerus. J Shoulder Elb Surg. 1995;4(5):331–6.
Chapter 5
Post-traumatic Arthritis of the Elbow
Key Points
• The risk of post-traumatic arthritis of the elbow is very high after articular
injuries.
• CT arthrography is an excellent modality to assess intra-articular
abnormalities.
• Intra-articular glucocorticoid injections have no efficacy in this population.
• Several operative options are available in cases of failure of conservative
management.
Introduction
Post-traumatic elbow arthritis is relatively common with a reported risk of 44% fol-
lowing articular fractures [1]. Historically, this risk has been well recognized with
Dr. Bigelow [2] writing in 1868 “There is no class of injuries so frequently produc-
tive of discontent, and perhaps so often the cause of litigation, as traumatic lesions
of the elbow joint.” Elbow fracture management continues to progress from pre-
dominantly nonoperative management to operative treatment in line with principles
as shown by Jupiter in 1985 [3]. Treatment of these fractures is complex requiring
an understanding of the various nonoperative and operative treatment modalities as
well as understanding possible complications such as malunion, nonunion,
Operative planning for post-traumatic elbow arthritis begins with a thorough his-
tory and physical. The history should include the initial injury mechanism, initial
injuries sustained (fractures and instability), previous operative and nonoperative
treatment (especially ulnar nerve management), and any history of infection or
soft tissue procedures. Detailed information on symptomatic pain and stiffness
should be obtained. For example, pain throughout the range of motion suggests
diffuse arthritic changes, while terminal pain suggests impingement by an osteo-
phyte or soft tissue [20]. Pain at rest carries a wider differential diagnosis includ-
ing infection, cervical spine radiculopathy, soft tissue disease, and reflex
sympathetic dystrophy [21]. Patient expectations and lifestyle factors must also
be addressed as a manual laborer will have different functional demands and
expectations when compared with a sedentary desk worker.
The physical examination should include a thorough inspection of the entire
extremity to assess prior surgical incisions for both fracture treatment as well as
soft-tissue coverage procedures. Hand thenar musculature should also be assessed
(i.e., intrinsic hand wasting). Neurologic evaluation should assess upper extrem-
ity sensory and motor function as well as ulnar neuritis specifically. The patient’s
elbow range of motion should be tested and any painful points should be noted.
Collateral ligament stability of the elbow should also be evaluated.
Imaging evaluation should be aimed at obtaining a complete understanding of
the degree of arthritis, loose bodies, current hardware, and bone stock. Orthogonal
elbow radiographs are the standard initial imaging study. If the patient also com-
plains of wrist pain, full-length forearm and wrist views should be obtained to assess
for a potential Essex-Lopresti lesion. Computed tomography (CT) is typically
62 K. O’Malley et al.
required for further evaluation and is more effective than conventional radiography
in assessing osseous causes of elbow stiffness [22]. CT arthrography has been
shown to provide improved assessment of intra-articular abnormalities such as
osteocartilaginous bodies, hyperplastic synovium, and osteophytes [23]. While
three-dimensional (3D) CT has not been evaluated for preoperative planning in this
population, we find it extremely helpful for procedures such as arthroscopic or open
debridement in patients with large osteophytes and loose bodies. Other diagnostic
tests may include electromyographic evaluation in patients with a concerning exam
for neuropathy or an entrapment syndrome.
Treatment
Nonsurgical Treatment
Surgical Treatment
Several operative options are available once nonsurgical measures have been
exhausted. Surgical options include arthroscopic or open osteocapsular debride-
ment arthroplasty, interposition arthroplasty, partial joint arthroplasty (e.g., distal
humerus hemiarthroplasty or radiocapitellar arthroplasty), total elbow arthroplasty
(TEA), and elbow arthrodesis. Sears and colleagues [15] described an algorithmic
approach to selecting the appropriate surgical intervention for post-traumatic
elbow osteoarthritis. For patients who have pain at the terminal arc of motion, they
recommended arthroscopic or open debridement arthroplasty with possible ulnar
nerve transposition. For the patient who has pain throughout the entire arc of
motion, they describe the use of partial joint arthroplasty for arthritic changes iso-
lated to the radiocapitellar joint or distal humerus and interposition arthroplasty or
total elbow arthroplasty for the patient with diffuse osteoarthritic changes. For
younger patients who have exhausted most surgical options and do not wish to
have 10 pound weight restriction on their extremity from a total elbow arthro-
plasty, elbow arthrodesis is offered.
5 Post-traumatic Arthritis of the Elbow 63
b
5 Post-traumatic Arthritis of the Elbow 65
portal is then established under direct visualization utilizing a spinal needle. The
spot for the portal is typically 2–3 cm anterior the lateral epicondyle and at the supe-
rior most aspect of the capitellar cartilage (Fig. 5.2). The procedure proceeds then
in a stepwise manner beginning with a diagnostic arthroscopy followed by removal
of any loose bodies from the anterior compartment along with osteophytes and
synovitis. If the radiocapitellar joint is significantly involved, a radial head resection
may be performed through the soft spot portal. Prior to proceeding to the posterior
compartment, a fenestration hole is created through the olecranon fossa. Other
options include a combined arthroscopic and open procedure with arthroscopic
debridement being carried out anteriorly followed by a mini-open posterior elbow
debridement. This can be effective when the elbow has more severe arthrosis that
may require treatment both laterally and medially in the anterior elbow.
A posterior central portal is created 3 cm proximal to the tip of the olecranon and
this serves as the initial viewing portal. A posterolateral portal is made parallel to
the posterior central portal just outside the triceps tendon. Once these portals are
established, the posterior compartment is debrided, loose bodies removed, and syn-
ovectomy performed. The medial and lateral gutters are inspected for loose bodies
and plica that may be contributing to the pathology. Finally the tip of olecranon is
excised and if necessary the anterior capsule is released. If the patient had preopera-
tive symptoms of ulnar neuropathy, the ulnar nerve may be decompressed in situ.
Patients are allowed full range of motion immediately postoperatively without
weight-bearing restrictions.
66 K. O’Malley et al.
Recent literature has found overall good to excellent results with this procedure
in appropriately selected patients with mild to moderate arthritis [25–33, 36].
DeGreef et al. found good results in a cohort of patients with a mean age of 50 years
old who underwent arthroscopic osteocapsular debridement with an increase in
range of motion (ROM) from 94 to 123 degrees, a significant decrease in pain
scores, and an increase in the Mayo Elbow Performance Index (MEPI) by an aver-
age of 34 points [37]. These results are reflected in much of the recent literature
[25–33, 36]. Galle and colleagues reviewed a consecutive series of 46 patients who
underwent arthroscopic osteocapsular debridement. The mean age of the patients in
their study was 48 years. They found a significant increase in ROM (final ROM arc
12 degrees to 135 degrees), a decrease in pain, and an increase in the Mayo Elbow
Performance Score (MEPS) from 57 preoperatively to 88 postoperatively.
Furthermore they had no complications in their cohort of patients [28]. Finally, Lim
et al. investigated the preoperative factors associated with outcomes after
arthroscopic osteocapsular debridement. Through multivariate analysis they found
that preoperative range of motion was the main factor that affected postoperative
elbow function and range of motion, and through further analysis preoperative arc
of motion greater than 80 degrees was found to be the cutoff for improved postop-
erative function and arc of motion [30].
Interposition Arthroplasty
Given that the majority of patients with post-traumatic elbow arthritis tend to be
younger and of higher demand, interposition arthroplasty serves as a valuable surgi-
cal tool in treating this condition in patients who do not wish to have the weight-
bearing and activity restrictions associated with TEA. Options for interposition
arthroplasty include both autograft (e.g., anconeus, fascia lata) and allograft (e.g.,
Achilles tendon, fascia lata, dermis) [15, 25]. Contraindications to this procedure
include active infection, gross elbow instability or deformity, open physes, no flexor-
pronator power, and patients with deficient bone stock about the elbow [25, 38, 39].
As described by Morrey [40], this procedure is performed with the patient posi-
tioned in supine or lateral decubitus position. A posterior approach to the elbow is
typically utilized. Kocher’s interval is then developed between the extensor carpi
ulnaris and the anconeus. The lateral ulnar collateral ligament (LUCL) and elbow
extensors are released from the lateral epicondyle and tagged. A capsular release is
performed and osteophytes are removed. Next the ulnar and humeral articular sur-
faces are prepared so a congruent articulation is obtained and enough bone is
resected so that there is 2–3 mm of laxity to ensure that the joint is not overstuffed.
Following this, three to four drill holes are created in the humerus, and the graft is
prepared with three to four horizontal mattress sutures that are passed through the
drill holes to secure the graft to the distal humerus surface. The joint is then reduced
and range of motion assessed for areas of impingement. Finally, the stability of the
MUCL is assessed and the LUCL and the extensors are repaired back to the lateral
5 Post-traumatic Arthritis of the Elbow 67
Total elbow arthroplasty remains the final operative choice for the majority of
patients who have failed other operative interventions. It remains the definitive
functional treatment for elderly patients with severe end-stage post-traumatic osteo-
arthritis. It is not ideal for young active patients with post-traumatic arthritis espe-
cially in cases of instability due to increased rates of mechanical wear and the need
for early revision [15, 25].
The majority of TEA performed today utilizes a linked semi-constrained pros-
thesis. In addition to this design, there are unlinked TEA that rely on soft tissue
balancing and implant conformity to provide stability. By the nature of being
unlinked, these designs result in decreased bone-cement interface stresses and allow
load sharing between the implant and the soft tissues. However, an inability to bal-
ance the soft tissues is a contraindication to use of this design and as such is not
applicable to the majority of patients with post-traumatic osteoarthritis [25].
Procedure
range of motion. While these are positive results, they reported an 82% complica-
tion rate with six mechanical failures (54%) and as such recommended caution
when performing TEA in this young patient population [46]. These results correlate
to similar complications with mechanical failure and loosening as reported in sev-
eral earlier studies [47–52].
While there are high complication rates in the young adult population through-
out the literature, a successful TEA does improve function and decrease pain.
Park et al. reported the results of TEA performed in 23 patients under 40 years
old with post-traumatic arthritis with average follow-up of 10.8 years. The
authors found significant decreases in pain scores and increased MEPS with
improved range of motion with increasing arc of motion from 37.8° to 120.6°.
Furthermore, they reported 95% and 89% implants survival rates at 8 and 15
years, respectively [53]. Welsink et al. performed a systematic review of TEA
including all indications. Their review included 70 articles with 9379 TEA per-
formed with three different implants. There was an average follow-up time of
81 months of follow-up across all articles. They found for the newer Coonrad-
Morrey-style prosthesis that there was an 87.2% survival at 7 years for all indica-
tions with a mean range of motion of 30° to 129° with significant improvement
in outcomes. They reported an overall 11–38% complication rate with implant
loosening being the most common complication (7%) [54]. Furthermore aseptic
component loosening is the most common cause for revision TEA (38% of revi-
sions) as demonstrated by Prkic et al. in a systematic review on causes of TEA
failure [55].
Elbow Arthrodesis
Elbow arthrodesis remains a treatment option for a very specific patient: the rela-
tively young patient with severe unilateral post-traumatic elbow arthritis who can-
not tolerate weight-bearing limitations required for TEA and who is not a candidate
for interposition arthroplasty. Historically, elbow arthrodesis has not been tolerated
well because the adjacent joints do not compensate well for the motion loss seen
with arthrodesis [25].
Arthrodesis may be achieved with compression across the joint utilizing bent
plates, Ilizarov frames, compression screws, and cross strut grafts [25, 56, 57].
When performed, the elbow is typically fused at 90° of flexion although arthrodesis
at 30° to 45° may be considered for patients who require a specific position for
employment or for patients with lower extremity disorders that require the use of the
elbow and forearm for transfer. Patient input into the final elbow position can be
obtained by placing patients in a hinged elbow brace with varying degrees of flex-
ion. This allows a patient to “try out” the fusion position that will work best for
them [40].
70 K. O’Malley et al.
Conclusion
References
1. Schenker ML, Mauck RL, Ahn J, et al. Pathogenesis and prevention of posttraumatic osteoar-
thritis after intra-articular fracture. J Am Acad Orthop Surg. 2014;22(1):20–8.
2. Bigelow HJ. Insensibility during surgical operations produced by inhalation. Boston Med Surg
J. 1846;35(16):309–17.
3. Kozanek M, Bartonicek J, Chase SM, et al. Treatment of distal humerus fractures in adults: a
historical perspective. J Hand Surg Am. 2014;39(12):2481–5.
4. McKee MD. Trauma to the adult elbow and fractures of the distal humerus. Philadelphia:
Saunders/Elsevier; 2009.
5. O’Driscoll SW. Elbow arthritis: treatment options. J Am Acad Orthop Surg. 1993;1(2):106–16.
6. Guitton TG, Zurakowski D, van Dijk NC, et al. Incidence and risk factors for the development of
radiographic arthrosis after traumatic elbow injuries. J Hand Surg Am. 2010;35(12):1976–80.
7. Doornberg JN, van Duijn PJ, Linzel D, et al. Surgical treatment of intra-articular fractures of
the distal part of the humerus. Functional outcome after twelve to thirty years. J Bone Joint
Surg Am. 2007;89(7):1524–32.
8. Doornberg JN, Ring D, Fabian LM, et al. Pain dominates measurements of elbow function and
health status. J Bone Joint Surg Am. 2005;87(8):1725–31.
9. Herbertsson P, Josefsson PO, Hasserius R, et al. Uncomplicated Mason type-II and III frac-
tures of the radial head and neck in adults. A long-term follow-up study. The Journal of bone
and joint surgery American volume 2004;86-a(3):569–74.
10. Burkhart KJ, Mattyasovszky SG, Runkel M, et al. Mid- to long-term results after bipolar radial
head arthroplasty. J Shoulder Elb Surg. 2010;19(7):965–72.
11. Eriksson E, Sahlin O, Sandahl U. Late results of conservative and surgical treatment of fracture
of the olecranon. Acta Chir Scand. 1957;113(2):153–66.
12. Macko D, Szabo RM. Complications of tension-band wiring of olecranon fractures. J Bone
Joint Surg Am. 1985;67(9):1396–401.
13. Broberg MA, Morrey BF. Results of delayed excision of the radial head after fracture. J Bone
Joint Surg Am. 1986;68(5):669–74.
14. Amini MH, Sykes JB, Olson ST, et al. Reliability testing of two classification systems for
osteoarthritis and post-traumatic arthritis of the elbow. J Shoulder Elb Surg. 2015;24(3):353–7.
5 Post-traumatic Arthritis of the Elbow 71
15. Sears BW, et al. Posttraumatic elbow osteoarthritis. 5th ed. Philadelphia: Saunders/
Elsevier; 2017.
16. Germscheid NM, Hildebrand KA. Regional variation is present in elbow capsules after injury.
Clin Orthop Relat Res. 2006;450:219–24.
17. Morrey BF. The posttraumatic stiff elbow. Clin Orthop Relat Res. 2005;431:26–35.
18. Morrey BF, Askew LJ, Chao EY. A biomechanical study of normal functional elbow motion. J
Bone Joint Surg Am. 1981;63(6):872–7.
19. Giannicola G, Polimanti D, Bullitta G, et al. Critical time period for recovery of functional
range of motion after surgical treatment of complex elbow instability: prospective study on 76
patients. Injury. 2014;45(3):540–5.
20. Chammas M. Post-traumatic osteoarthritis of the elbow. Orthop Traumatol Surg Res.
2014;100(1 Suppl):S15–24.
21. Cheung EV, Adams R, Morrey BF. Primary osteoarthritis of the elbow: current treatment
options. J Am Acad Orthop Surg. 2008;16(2):77–87.
22. Zubler V, Saupe N, Jost B, et al. Elbow stiffness: effectiveness of conventional radiography and
CT to explain osseous causes. AJR Am J Roentgenol. 2010;194(6):W515–20.
23. Singson RD, Feldman F, Rosenberg ZS. Elbow joint: assessment with double-contrast CT
arthrography. Radiology. 1986;160(1):167–73.
24. van Brakel RW, Eygendaal D. Intra-articular injection of hyaluronic acid is not effective
for the treatment of post-traumatic osteoarthritis of the elbow. Arthroscopy. 2006;22(11):
1199–203.
25. Sears BW, Puskas GJ, Morrey ME, et al. Posttraumatic elbow arthritis in the young adult:
evaluation and management. J Am Acad Orthop Surg. 2012;20(11):704–14.
26. Kroonen LT, Piper SL, Ghatan AC. Arthroscopic management of elbow osteoarthritis. J Hand
Surg Am. 2017;42(8):640–50.
27. Kim SJ, Kim JW, Lee SH, et al. Retrospective comparative analysis of elbow arthroscopy used
to treat primary osteoarthritis with and without release of the posterior band of the medial col-
lateral ligament. Arthroscopy. 2017;33(8):1506–11.
28. Galle SE, Beck JD, Burchette RJ, et al. Outcomes of elbow arthroscopic Osteocapsular arthro-
plasty. J Hand Surg Am. 2016;41(2):184–91.
29. Merolla G, Buononato C, Chillemi C, et al. Arthroscopic joint debridement and capsular
release in primary and post-traumatic elbow osteoarthritis: a retrospective blinded cohort study
with minimum 24-month follow-up. Musculoskelet Surg. 2015;99(Suppl 1):S83–90.
30. Lim TK, Koh KH, Lee HI, et al. Arthroscopic debridement for primary osteoarthri-
tis of the elbow: analysis of preoperative factors affecting outcome. J Shoulder Elb Surg.
2014;23(9):1381–7.
31. Giannicola G, Bullitta G, Polimanti D, et al. Factors affecting choice of open surgical tech-
niques in elbow stiffness. Musculoskelet Surg. 2014;98(Suppl 1):77–85.
32. Adams JE, Wolff LH 3rd, Merten SM, et al. Osteoarthritis of the elbow: results of arthroscopic
osteophyte resection and capsulectomy. J Shoulder Elb Surg. 2008;17(1):126–31.
33. Krishnan SG, Harkins DC, Pennington SD, et al. Arthroscopic ulnohumeral arthroplasty for
degenerative arthritis of the elbow in patients under fifty years of age. J Shoulder Elb Surg.
2007;16(4):443–8.
34. Savoie FH 3rd, O’Brien MJ, Field LD. Arthroscopy for arthritis of the elbow. 5th ed.
Philadelphia: Saunders/Elsevier; 2017.
35. Mansat P, Morrey BF. The column procedure: a limited lateral approach for extrinsic contrac-
ture of the elbow. J Bone Joint Surg Am. 1998;80(11):1603–15.
36. MacLean SB, Oni T, Crawford LA, et al. Medium-term results of arthroscopic debridement and
capsulectomy for the treatment of elbow osteoarthritis. J Shoulder Elb Surg. 2013;22(5):653–7.
37. DeGreef I, Samorjai N, De Smet L. The Outerbridge-Kashiwagi procedure in elbow arthros-
copy. Acta Orthop Belg. 2010;76(4):468–71.
38. Laubscher M, Vochteloo AJ, Smit AA, et al. A retrospective review of a series of interposition
arthroplasties of the elbow. Shoulder Elbow. 2014;6(2):129–33.
72 K. O’Malley et al.
39. Baghdadi YM, Morrey BF, Sanchez-Sotelo J. Anconeus interposition arthroplasty: mid- to
long-term results. Clin Orthop Relat Res. 2014;472(7):2151–61.
40. Morrey BF. The Elbow and Its Disorders. 5th ed. Philadelphia: Saunders/Elsevier; 2017.
41. Cheng SL, Morrey BF. Treatment of the mobile, painful arthritic elbow by distraction interpo-
sition arthroplasty. J Bone Joint Surg. 2000;82(2):233–8.
42. Larson AN, Morrey BF. Interposition arthroplasty with an Achilles tendon allograft as a sal-
vage procedure for the elbow. J Bone Joint Surg Am. 2008;90(12):2714–23.
43. Adolfsson L, Nestorson J. The kudo humeral component as primary hemiarthroplasty in distal
humeral fractures. J Shoulder Elb Surg. 2012;21(4):451–5.
44. Steinmann SP. Hemiarthroplasty of the ulnohumeral and radiocapitellar joints. Hand Clin.
2011;27(2):229–32.. vi
45. Heijink A, Vanhees M, van den Ende K, et al. Biomechanical considerations in the pathogen-
esis of osteoarthritis of the elbow. Knee Surg Sports Traumatol Arthrosc. 2016;24(7):2313–8.
46. Schoch B, Wong J, Abboud J, et al. Results of total elbow arthroplasty in patients less than 50
years old. J Hand Surg Am. 2017;42(10):797–802.
47. Schoch BS, Werthel JD, Sanchez-Sotelo J, et al. Total elbow arthroplasty for primary osteoar-
thritis. J Shoulder Elb Surg. 2017;26(8):1355–9.
48. Lovy AJ, Keswani A, Dowdell J, et al. Outcomes, complications, utilization trends, and risk fac-
tors for primary and revision total elbow replacement. J Shoulder Elb Surg. 2016;25(6):1020–6.
49. Perretta D, van Leeuwen WF, Dyer G, et al. Risk factors for reoperation after total elbow
arthroplasty. J Shoulder Elb Surg. 2017;26(5):824–9.
50. Zhou H, Orvets ND, Merlin G, et al. Total elbow arthroplasty in the United States: evaluation
of cost, patient demographics, and complication rates. Orthop Rev. 2016;8(1):6113.
51. Giannicola G, Scacchi M, Polimanti D, et al. Discovery elbow system: 2- to 5-year results in
distal humerus fractures and posttraumatic conditions: a prospective study on 24 patients. J
Hand Surg Am. 2014;39(9):1746–56.
52. Giannicola G, Sacchetti FM, Antonietti G, et al. Radial head, radiocapitellar and total elbow
arthroplasties: a review of recent literature. Injury. 2014;45(2):428–36.
53. Park JG, Cho NS, Song JH, et al. Clinical outcomes of semiconstrained total elbow arthroplasty
in patients who were forty years of age or younger. J Bone Joint Surg Am. 2015;97(21):1781–91.
54. Welsink CL, Lambers KTA, van Deurzen DFP, et al. Total elbow arthroplasty: a systematic
review. JBJS Rev. 2017;5(7):e4.
55. Prkic A, Welsink C, The B, et al. Why does total elbow arthroplasty fail today? A systematic
review of recent literature. Arch Orthop Trauma Surg. 2017;137(6):761–9.
56. Kovack TJ, Jacob PB, Mighell MA. Elbow arthrodesis: a novel technique and review of the
literature. Orthopedics. 2014;37(5):313–9.
57. Sala F, Catagni M, Pili D, et al. Elbow arthrodesis for post-traumatic sequelae: surgical tactics
using the Ilizarov frame. J Shoulder Elb Surg. 2015;24(11):1757–63.
Chapter 6
Post-traumatic Arthritis of the Wrist
Sophia A. Strike and Philip E. Blazar
Key Points
• Radiocarpal and intercarpal arthritis, when caused by scapholunate liga-
ment injury or scaphoid nonunion, allow for treatment options based on
predictable patterns of degenerative change.
• Radiocarpal, ulnocarpal, and distal radioulnar joint arthritis may be caused
by intraarticular fractures of the distal radius or distal radius malunion.
• Isolated intercarpal arthritis can occur from less common injuries to the
carpus and associated ligaments.
Introduction
The wrist joint is a complex structure involving articulation of the eight carpal bones
and the forearm. Surrounding ligamentous structures maintain the normal static and
dynamic relationships of the osseous components. Alteration of the anatomic rela-
tionships through fracture, dislocation, or ligamentous injury can cause abnormal
carpal kinematics and, eventually, lead to articular degeneration. Pain, instability,
loss of motion, and deformity may negatively impact function. Functional wrist
motion has been reported at 5 degrees of flexion, 30 degrees of extension, 10 degrees
of radial deviation, and 15 degrees of ulnar deviation [1]. The motion required to
S. A. Strike (*)
Johns Hopkins University School of Medicine, Baltimore, MD, USA
e-mail: sstrike1@[Link]
P. E. Blazar
Brigham and Women’s Hospital, Boston, MA, USA
e-mail: pblazar@[Link]
perform daily activities will be unique to each patient based on functional demands
and compensatory mechanisms [2]. While traumatic injury remains a common
cause of arthritis of the wrist, atraumatic etiologies including inflammatory arthritis,
crystalline deposition, hemophilia, and primary osteoarthritis must be considered in
the evaluation of these patients [2].
Traumatic etiologies of wrist arthritis include injury to intercarpal, radiocarpal,
ulnocarpal, or radioulnar ligaments in isolation or as part of a perilunate injury,
nonunion (or malunion) after scaphoid fracture, as well as malunited distal radius
fractures [3, 4, 9]. All of these injuries can induce abnormal carpal mechanics and
over time cause pain and joint degeneration [3–6].
Posttraumatic arthritis may occur in predictable patterns throughout much of the
wrist as will be discussed in the chapter. This allows treatment to be tailored to the
stage of degeneration. The natural history of wrist injuries has been described in
cases such as scaphoid nonunion and distal radius fracture malunion but is less clear
for intercarpal injury such as scapholunate ligament injuries [13–15]. Surgical man-
agement of arthritis typically centers on removal or fusion of involved articulations,
and the complex structure of the wrist requires a thorough understanding of anat-
omy and kinematics to select an appropriate treatment for each patient.
Main Text
Wrist Anatomy
The intricate articulation of the osseous structures of the wrist with ligamentous
support allows for multiple directions of motion. The combination of intercarpal,
radiocarpal, and distal radioulnar joint motions provides multiple degrees of motion:
flexion/extension, radial/ulnar deviation, and pronation/supination. The surround-
ing ligaments of the wrist provide the stability necessary for this wide range of
motion [7]. Fractures or ligamentous injury can alter the normal mechanics of
motion of these articulations, resulting in abnormal joint loading and subsequent
osteoarthritis. This may occur in predictable patterns allowing treatment to be tai-
lored to each patient’s stage of arthritic change. Understanding the specific anatomy
of the wrist is paramount to understanding these patterns of degeneration.
The carpal bones are customarily described in two carpal rows: proximal and distal.
The proximal row consists of, from radial to ulnar, the scaphoid, lunate, triquetrum,
and pisiform (Fig. 6.1). This group of carpal bones is also termed the intercalary
segment as there are no extrinsic ligamentous connections directly to these struc-
tures. The movement of the proximal carpal row is based entirely on their
6 Post-traumatic Arthritis of the Wrist 75
Trapezium Hamate
Trapezoid Pisiform
Capitate
Triquetrum
Scaphoid
Lunate
Radius
Ulna
Fig. 6.1 Illustration: Carpus. Proximal row: Scaphoid, lunate, triquetrum, pisiform. Distal row:
trapezium, trapezoid, capitate and hamate
articulations with the distal carpal row and the radius and ulna as well as their liga-
mentous supports [6].
Ligaments of the wrist include palmar and dorsal radiocarpal, ulnocarpal, inter-
carpal, palmar midcarpal, proximal and distal interosseous, and distal radioulnar
ligaments [7]. The proximal interosseous ligaments, the scapholunate and lunotri-
quetral, provide interconnection between the bones of the proximal carpal row
allowing coordinated movement. These interosseous ligaments each contain proxi-
mal, volar, and dorsal components with the dorsal aspect of the scapholunate inter-
osseous ligament (SLIL) and the volar component of the lunotriquetral interosseous
ligament (LTIL) providing the strongest support for their respective joints [7, 9].
Injury to these ligaments results in atypical patterns of movement between the bones
within the carpal row, termed carpal instability dissociative (CID) [3, 6, 8, 9]. The
distal carpal row includes, from radial to ulnar, the trapezium, trapezoid, capitate,
and hamate (Fig. 6.1). Gelberman reviewed the ring concept of the carpal rows
highlighting the interconnected kinematics based on the scaphoid as a stabilizing
link between rows and the triquetrum as a pivot point for carpal motion [3]. With
radial deviation of the wrist, the distal row moves radially and forces the scaphoid
76 S. A. Strike and P. E. Blazar
and the entire proximal row into flexion to avoid direct impact. The scaphoid rests
in a position of slight flexion with a normal radiographic scapholunate angle of less
than 70 degrees [6] (Fig. 6.2). The lunate rests in a neutral position, hence the nor-
mal radiolunate angle of zero (Fig. 6.2).
The distal aspects of the radius and ulna form the distal radioulnar joint (DRUJ) that
allows the forearm to rotate in pronation and supination in coordination with the
proximal radioulnar joint at the elbow. The sigmoid notch of the radius provides a
concavity in which the ulna articulates. The surrounding soft tissue structures pro-
vide not only stability for the DRUJ but also prevent impingement at the ulnocarpal
6 Post-traumatic Arthritis of the Wrist 77
Ulnotriquetral
ligament
Volar radioulnar
ligament
Ecu sheath
Dorsal radioulnar
ligament
Radius Ulna
Wrist Arthritis
Evaluation
In contrast to normal kinematics, with carpal ring disruption the bones of the wrist
move in a discordant fashion [3]. Injuries causing disruption of the carpal ring may
be isolated intercarpal ligament injuries, SLIL injury associated with a distal radius
fracture, or multiple intercarpal ligament injuries associated with perilunate insta-
bility or dislocation [3, 9]. When associated with an extrinsic cause the resulting
deformity is termed carpal instability adaptive (CIA) [3, 6, 9]. When chronic in
nature, these injuries may lead to intercarpal and radiocarpal joint degeneration.
Chronic SLIL injuries causing carpal instability may lead to subsequent radiocarpal
and intercarpal arthritis although the natural history of SL ligament injuries is not
well documented [7, 13]. In the pathologic state where the SLIL is compromised,
the scaphoid will flex while the lunate will independently fall into extension leading
to dorsal angulation of the lunate relative to the radius on a lateral radiographic
view, termed dorsal intercalated segment instability (DISI) [3, 5, 6, 9, 13, 15]
(Fig. 6.4). As this process progresses the capitate may migrate proximally as well
[5]. There are no studies confirming that SL ligament tears, diagnosed with direct
visualization through arthroscopy, inevitably lead to arthritis [13]. When degenera-
tive changes do occur, radiographically, they will follow a predictable pattern
termed scapholunate advanced collapse, or SLAC, wrist [4, 10, 11]. First described
by Watson and Ballet based on their review of 4000 radiographs, of which 210
showed degenerative wrist arthritis, SLAC wrist was the most common pattern
affecting 57% of those patients [10]. Initially, changes are noted at the tip of the
radial styloid and the distal scaphoid (stage I), followed by involvement of the entire
radioscaphoid joint (stage II) (Fig. 6.5). These specific changes result from the
6 Post-traumatic Arthritis of the Wrist 79
incongruent geometry of the scaphoid with the radius when the scaphoid falls per-
sistently into flexion [5, 12]. The capitolunate joint is the first midcarpal joint
involved (stage III) (Fig. 6.6), and the final stages may include the rest of the carpus
although the radiolunate joint is characteristically uninvolved [2, 3, 5, 10–12]. This
is thought to be from the highly congruent nature of the lunate in the fossa of the
distal radius [10]. It is important to note that patients with a SLAC wrist pattern may
be asymptomatic. Further, atraumatic causes such as calcium pyrophosphate depo-
sition must be considered [2, 13]. Radiographs of the contralateral wrist in an
asymptomatic patient may also show SLAC changes [13].
Less commonly, nonunion of the scaphoid may lead to a scaphoid nonunion
advanced collapse (SNAC) wrist deformity [12, 13] (Fig. 6.7). The SNAC pattern
is similar to a SLAC wrist with the anatomic difference being the maintained
80 S. A. Strike and P. E. Blazar
attachment of the proximal pole of the scaphoid to the lunate via the SLIL and,
thus, an arthritis-free articulation between the proximal pole of the scaphoid and
the radius [3, 5, 11, 12, 15]. Two reports on the natural history of scaphoid non-
unions were published in the 1980s [14, 15]. Mack et al. evaluated 47 scaphoid
fractures with a range of five to 53 years of known nonunion and identified three
patterns of degeneration. At an average of 8.2 years, patients developed isolated
scaphoid sclerosis and cystic changes. By 17.0 years, radioscaphoid arthritis devel-
oped, and at an average of 31.6 years generalized arthritis of the wrist developed.
Overall they concluded that by 10 years all nonunions were displaced, unstable, or
arthritic, and by 20 years, generalized arthritis of the wrist was common. Ruby
et al. reviewed their series of 56 scaphoid nonunions and noted a 97% rate of osteo-
arthritis at 5 years or greater after injury [15]. These population studies suggest that
osteoarthritis is likely to develop in patients with an established scaphoid non-
union, particularly those that are displaced, and thus scaphoid fixation is often
recommended for nonunion even in asymptomatic patients, to prevent future
degenerative change.
6 Post-traumatic Arthritis of the Wrist 81
Management
Nonoperative options are the mainstay of initial treatment although there are no
long-term studies evaluating these methods specifically in SLAC/SNAC deformities
[4, 13]. As discussed previously, bracing, directed injections, and anti-inflammatory
medications may be used in appropriate patients for symptomatic management.
Symptoms refractory to conservative management or severe symptoms on presenta-
tion warrant consideration of surgical intervention.
Surgical management of SLAC and SNAC wrist is aimed at the stage of involve-
ment. Prior to the development of arthritic changes, direct repair or reconstruction
of the scapholunate ligament, with or without radial styloid excision, or treatment of
the scaphoid nonunion may be undertaken with the goal of preventing the
82 S. A. Strike and P. E. Blazar
A S4CF involves complete removal of the scaphoid with fusion of the remaining
capitate, lunate, hamate and the triquetrum [13]. Alternatively, a scaphoidectomy
and triquetrectomy can be performed with a three-corner fusion of the capitolunate,
capitohamate and hamatolunate joints. Both procedures require undamaged radiol-
unate articular cartilage, as this joint will remain intact [3, 12]. Correction of a DISI
deformity must be performed intra-operatively prior to stabilization or radiocapitate
impingement can result dorsally [2, 3, 12]. The radioscaphocapitate and long radio-
lunate ligament should be preserved to prevent ulnar translation of the carpus [2].
Meticulous surgical technique with preparation of fusion surfaces, removal of debris
and proper hardware sizing must be emphasized [13]. Benefits of a S4CF include
maintenance of carpal height, preservation of the radiolunate joint and no risk of
degeneration at the radiocapitate joint [3]. Risk of nonunion and hardware compli-
cations are disadvantages of this procedure [12]. Fusion fixation may be performed
with k wires, staples, headless screws or circular plates. K wire fixation is inexpen-
sive but risks pin tract infection, sensory nerve irritation and requires removal [3,
13]. Staples and headless screws provide compression at the expense of possible
dorsal impingement with staples, and technical difficulty in placing screws [3, 12].
Multiple studies have shown higher rates of nonunion and complications with circu-
lar plate fixation [3, 12, 13]. Saltzmann et al. reviewed seven studies and noted a
grouped nonunion rate of seven percent after S4CF [20]. Bain and Watts evaluated
clinical outcomes in 35 patients undergoing S4CF at 1, 2, and 10 years and reported
pain scores of 0/10 at 1 year, and 22% loss of wrist range of motion. Between 1 and
10 years, there was no significant change in pain, wrist function, patient satisfaction,
or arc of wrist motion, suggesting that results are sustainable [18]. Only two patients
went on to wrist arthrodesis [18]. Some authors have advocated capitolunate fusion
84 S. A. Strike and P. E. Blazar
Wrist Denervation
AIN, palmar cutaneous nerve, sensory branch of the radial nerve, dorsal branch of
the ulnar nerve, lateral and medial antebrachial cutaneous nerves and requires five
incisions around the wrist [23]. Simon et al. retrospectively reviewed 27 patients
undergoing complete wrist denervation by one surgeon. Forty-four percent of
patients had complete relief of pain that remained stable in 89%. Grip strength was
maintained at 85% of the contralateral arm. Six complications occurred including
one case of complex regional pain syndrome and five neuromas with two patients
requiring reoperation. Overall 67% of patients were very satisfied [24]. In a longer-
term review of 30 complete wrist denervations with average 10 year follow up, 28
patients had improved pain with 22 maintaining this effect through final follow up.
Grip strength was reported at 82% of the contralateral extremity [25]. In another
review of 71 complete wrist denervations, 22 wrists had complete pain relief and 40
wrists had considerable improvement. Nine patients required reoperation for insuf-
ficient pain relief [26]. A more recent study of 39 wrists undergoing total wrist
denervation with an average 56 months follow up resulted in pain improvement in
79.5% of cases with four revision procedures and four complications [49]. Complete
wrist denervation may provide and maintain sufficient pain relief without sacrific-
ing grip strength or future salvage procedures.
Severe arthritis of the radiocarpal joint or pancarpal arthritis requires total wrist
arthroplasty or arthrodesis [3] (Fig. 6.9). Total wrist arthroplasty removes painful
arthritic surfaces and replaces them with a prosthetic option. Early designs included
synovitis-inducing silicone implants and unstable prostheses [3]. Newer designs
have improved component fixation [3]. Arthroplasty preserves motion when com-
pared to arthrodesis but requires a lifelong lifting restriction, usually of ten pounds
or less, and is preferred in low demand patients only [2, 3].
Total wrist arthrodesis is preferred in young laborers and patients who want to
continue manual work [3]. Grip strength can be maintained particularly with the
wrist fused in slight extension [3]. Arthrodesis is typically performed with commer-
cially available pre-contoured dorsal plates and autogenous bone graft, with cited
fusion rates of 93–100% [3, 13]. In a retrospective review of 89 patients undergoing
wrist arthrodesis for posttraumatic arthritis, 98% of the 56 patients with plate fixa-
tion went on to union, while 82% of those receiving a different form of fixation
achieved union [27]. The complication rate after plate fixation was 51%, with 59%
of these requiring an additional procedure, while 79% of patients with a different
form of fixation had a complication but only 21% of these required an additional
procedure [27]. Arthrodesis is thought to be reliable for pain relief and allows
patients to perform most activities of daily living through compensation of other
joints [2]. Although many studies report patient satisfaction after total wrist arthrod-
esis, complete pain relief may be less often achieved than perceived based on these
series [28]. Jupiter and Adey reported persistent pain in 64% of their series of 22
patients who underwent arthrodesis for posttraumatic arthritis, suggesting that this
6 Post-traumatic Arthritis of the Wrist 87
pain relief procedure may be less predictable than previously thought [28]. De Smet
et al. compared PRC to wrist arthrodesis in a nonrandomized retrospective study of
61 patients with posttraumatic osteoarthritis of the radiocarpal joint. While there
was no difference in grip strength between groups, functional outcome scores,
maintenance of professional activity and complication rates were better in the PRC
88 S. A. Strike and P. E. Blazar
group [29]. Additional sources of pain must be considered when opting for wrist
arthrodesis and should be addressed.
Surgical Technique
Radiocarpal arthritis in the absence of intercarpal arthritis may result after an intra-
articular or malunited distal radius fracture [3, 6, 9]. Intra-articular step-off or loss
of normal volar tilt, radial height or inclination with malunion may alter points of
contact and load leading to degenerative changes.
Management
Radioscapholunate (RSL) arthrodesis may be performed for pain relief at the expense
of wrist motion, which is typically 33% of normal. Concomitant excision of the dis-
tal scaphoid may increase range of motion to 50–60% of normal [3]. Proponents of
scaphoidectomy have postulated that inclusion of the entire scaphoid in an RSL
arthrodesis leads to degeneration of the STT joint as the distal row is unable to flex
over the proximal row [30]. Garcia-Elias reviewed 15 cases of RSL arthrodesis with
distal scaphoidectomy for posttraumatic arthritis from distal radius fractures (13
patients) or perilunate fracture-dislocations (two patients). The midcarpal joints
were uninvolved in all patients. Complete pain relief was achieved in ten patients and
overall pain relief was noted to be greater than that reported in their previous series
of 27 patients who did not have a concomitant distal scaphoidectomy [30]. In com-
paring their outcomes to the literature on RSL arthrodesis alone, they note greater
motion in wrist flexion and radial deviation with distal scaphoidectomy [30].
6 Post-traumatic Arthritis of the Wrist 89
Scaphotrapeziotrapezoidal Arthritis
STT arthritis may cause radial-sided wrist pain. The posttraumatic nature of STT
arthritis is unclear. While it has been suggested that an isolated SL ligament rupture,
without instability or rotatory subluxation of the scaphoid, may cause degeneration
of the STT joint, this may be a reflection of the prevalence of STT arthritis as
opposed to confirmation that trauma is a common etiology of degeneration at this
joint [5].
Management
Management options for STT arthritis include joint debridement, distal scaphoidec-
tomy (open or arthroscopic), trapeziectomy, partial trapezoid resection, STT
arthrodesis or arthroplasty [5, 50, 51]. Excisional arthroplasty can be performed for
STT arthritis when not associated with dorsal midcarpal instability as distal scaph-
oid resection could cause collapse into DISI [31]. This technique is technically
simple with few complications and does not require prolonged immobilization [31].
Arthrodesis of the STT joint has been extensively although reports often include
patients with Kienbock’s disease in addition to traumatic etiologies [32]. Radial
styloidectomy should be performed at the time of fusion, with postoperative motion
expected to be approximately 65% of normal [4]. In a review of multiple studies
reporting on a total 238 patients, the average nonunion rate was 13%. The grouped
complication rate was 43% and included pin track infection, progressive arthrosis,
nerve irritation and osteomyelitis, amongst others [33]. Forty-nine percent of
patients reported persistent wrist pain [33]. Alternatively, Pequinot reported a small
series of patients undergoing pyrocarbon STT replacements citing a pain relief pro-
cedure that preserves carpal stability, has a low complication rate and does not pre-
clude salvage with fusion. Patients had a slight loss of pinch strength and wrist
motion with 10 degrees less radial deviation and 15 degrees less wrist extension
while grip strength was maintained at 4 year follow up [34].
Lunotriquetral Arthritis
Injury to the LTIL is significantly more rare than SLIL injury and typically occurs
from a fall onto an outstretched, supinated and extended wrist [2, 5]. Force transfers
from the pisiform into the triquetrum while the lunate remains tethered by the long
radiolunate ligament. The contradictory forces lead to rupture of the intervening
ligament [2]. These injuries may also occur as part of a perilunate dislocation (stage
III). An intact SLIL in the setting of an LTIL rupture will flex the lunate with the
scaphoid resulting in a volar intercalated segment instability (VISI) deformity [2, 5,
6, 9]. Ligament rupture with subsequent VISI deformity is not, however, clearly
90 S. A. Strike and P. E. Blazar
Management
Pisotriquetral Arthritis
Management
Arthritis of the DRUJ or ulnocarpal joint can have one of many traumatic causes. A
fracture of the distal radius with malunion may result in shortening that alters the
relative length of the ulna. Normally carrying approximately 20% of the load on the
forearm, the ulna is then overloaded inappropriately and ulnocarpal arthritis may
result [3, 4]. Furthermore, the relationship of the distal ulnar articulation with the
sigmoid notch of the radius may be changed predisposing to DRUJ arthritis [4, 38].
Alternatively, a soft tissue injury such as an injury to the TFCC, which includes the
stabilizing ligaments of the DRUJ, can also contribute to the development of post-
traumatic arthritis of the DRUJ and/or ulnocarpal joints [4].
Management
Treatment of ulnocarpal arthritis requires offloading the distal ulna. This can be
achieved through height restoration with a radial osteotomy, ulnar shortening, wafer
procedure or a distal ulnar resection, known as a Darrach procedure.
Arthritis of the DRUJ may be managed with partial or complete distal ulnar
resection, hemiresection interposition (HIT) arthroplasty, endoprosthetic replace-
ment or arthrodesis of the DRUJ with pseudarthrosis of the distal ulna, known as the
Sauve-Kapandji (SK) procedure [4, 38, 41, 52]. Procedures that maintain the TFCC
and ulnar styloid have the benefit of preventing ulnocarpal impingement [4].
Bowers performed a DRUJ HIT arthroplasty in 38 patients with the goal of pre-
serving the ulnocarpal ligament complex. At 2.5 year follow up, 100% of the
patients with a traumatic etiology of arthritis had painless range of motion with an
average 83 degrees of pronation to 83 degrees of supination and no instability [39].
Nawijn et al. reported higher satisfaction scores in patients undergoing HIT arthro-
plasty for inflammatory compared to posttraumatic DRUJ arthritis [53]. Santos
et al. reported on three patients undergoing DRUJ arthroplasty, two of who had
posttraumatic DRUJ arthritis. In the short term, both patients achieved pain relief
and had increased motion at the DRUJ [41]. Watson performed a matched ulnar
resection in 44 patients, in which a convex resection of the distal ulna is undertaken
92 S. A. Strike and P. E. Blazar
to match the concave shape of the distal radius with maintenance of the TFCC and
ulnocarpal ligaments [40]. Patients were followed for an average 6.5 years and
maintained 80.5 degrees of painless pronation and 88.5 degrees of supination [40].
Endoprosthetic replacement with a semiconstrained DRUJ arthroplasty has been
utilized in the management of DRUJ arthritis with early reports citing low compli-
cation rates and a more recent review reporting further surgery secondary to com-
plications in 29% of patients [54]. Commonly cited soft tissue complications may
be more frequent in patients with a history of rheumatoid arthritis or immunosup-
pression compared to those without [55].
The SK and Darrach procedures are often applicable in similar clinical situa-
tions, each with their benefits and complications. The Darrach procedure may be
complicated by ulnar translation of the carpus and/or distal ulnar stump instability
[4, 40, 41]. The SK procedure may be complicated by a persistently painful pseud-
arthrosis [40]. Studies on these procedures have been primarily in rheumatoid popu-
lations. George et al. published one of the only reports on the use of these procedures
in a posttraumatic setting [42]. They retrospectively reviewed the use of the SK or
Darrach procedures in patients under age 50 with DRUJ arthrosis after distal radius
fracture malunion. Twelve patients after an SK, and 21 patients after a Darrach were
included. At final clinical follow up there were no significant differences in subjec-
tive pain or functional scores, forearm or wrist rotation, or complication rates
between the two groups. One patient required conversion to a Darrach after initial
treatment with an SK [42]. The procedures are considered equivalent for treatment
of posttraumatic DRUJ arthritis in this group [42]. The SK procedure has been mod-
ified to include tenodesis of the ulnar shaft with a distally based portion of the FCU
tendon. In a review of 18 patients undergoing this modification, grip strength
increased from 36% to 73% of the contralateral upper extremity. Sixteen patients
had stable ulnar stumps and overall pain relief was satisfactory [38]. The procedure
is recommended in younger patients who place high demands on their wrist or as a
salvage procedure in patients with severely limited forearm rotation [38].
Summary
interventions in the wrist have proven to be successful pain relief operations at the
expense of wrist motion and grip strength although most patients are able to main-
tain adequate function.
References
1. Palmer AK, Werner FW, Murphy D, Glisson R. Functional wrist motion: a biomechanical
study. J Hand Surg Am. 1985;l0A(I):39–46.
2. Wolfe SW, Hotchkiss RN, Pederson WC, Kozin SH. Green’s operative hand surgery.
Philadelphia: Elsevier/Churchill Livingstone. 6th ed; 2011. p. 429–63.
3. Gelberman RH, Cooney WP, Szabo RM. Carpal instability. J Bone Joint Surg.
2000;82A(4):578–94.
4. Weiss KE, Rodner CM. Osteoarthritis of the wrist. J Hand Surg. 2007;32A(5):725–46.
5. Peterson B, Szabo RM. Carpal osteoarthrosis. Hand Clin. 2006;22(2006):517–28.
6. Linscheid RL, Dobyns JH, Beabout JW, Bryan RS. Traumatic instability of the wrist.
Diagnosis, classification, and pathomechanics. J Bone Joint Surg Am. 1972;54(8):1612–32.
7. Berger RA. The anatomy of the ligaments of the wrist and distal radioulnar joints. Clin Orthop
Relat Res. 2001;383:32–40.
8. Wolfe SW, Garcia-Elias M, Kitay A. Carpal instability nondissociative. J Am Acad Orthop
Surg. 2012;20(9):575–85. Annotation: this review article defines carpal instability nondisso-
ciative with a discussion of clinical presentation, pathophysiology and diagnosis. Subtypes of
carpal instability nondissociative are described as well as management principles, both nonop-
erative and surgical.
9. Lee DJ, Elfar JC. Carpal ligament injuries, pathomechanics, and classification. Hand Clin.
2015;31(3):389–98. Annotation: This articles reviews carpal instability, specifically volar and
dorsal intercalated segment instability. Normal wrist mechanics as well as pathological defor-
mities are discussed.
10. Watson HK, Ballet FL. The SLAC wrist: scapholunate advanced collapse pattern of degenera-
tive arthritis. J Hand Surg Am. 1984;9(3):358–65.
11. Strauch RJ. Scapholunate advanced collapse and scaphoid nonunion advanced collapse arthri-
tis—update on evaluation and treatment. J Hand Surg Am. 2011;36(4):729–35.
12. Kiefhaber TR. Management of scapholunate advanced collapse pattern of degenerative arthri-
tis of the wrist. J Hand Surg Am. 2009;34(8):1527–30.
13. Cohen MS, Kozin SH. Degenerative arthritis of the wrist: proximal row carpectomy versus
scaphoid excision and four-corner arthrodesis. J Hand Surg Am. 2001;26(1):94–104.
14. Mack GR, Bosset MJ, Gelberman R, Yu E. The natural history of scaphoid nonunion. J Bone
Joint Surg. 1984;66A(4):504–9.
15. Ruby LK, Stinson J, Belsky MR. The natural history of scaphoid non-union a review of
twenty-five cases. J Bone Joint Surg. 1985;67A(3):428–32.
16. Malerich MM, Clifford J, Eaton B, Eaton R, Littler JW. Distal scaphoid resection arthro-
plasty for the treatment of degenerative arthritis secondary to scaphoid nonunion. J Hand Surg.
1999;24(6):1196–205.
17. Ruch DS, Papadonikolakis A. Resection of the scaphoid distal pole for symptomatic scaphoid
nonunion after failed previous surgical treatment. J Hand Surg Am. 2006;31(4):588–93.
18. Bain GI, Watts AC. The outcome of scaphoid excision and four-corner arthrodesis for
advanced carpal collapse at a minimum of ten years. J Hand Surg Am. 2010;35(5):
719–25.
19. Hegazy G. Capitolunate arthrodesis for treatment of Scaphoid Nonunion Advanced Collapse
(SNAC) wrist arthritis. J Hand Microsurg. 2015;7(1):79–86. Annotation: a retrospective review
of twelve patients undergoing capitolunate arthrodesis with headless compression screws for
94 S. A. Strike and P. E. Blazar
scaphoid nonunion advanced collapse. This study found capitolunate arthrodesis to restore a
stable, functional wrist. No level of evidence provided.
20. Saltzman BM, Frank JM, Slikker W, Fernandez JJ, Cohen MS, Wysocki RW. Clinical out-
comes of proximal row carpectomy versus four-corner arthrodesis for post-traumatic wrist
arthropathy: a systematic review. J Hand Surg Eur Vol. 2015;40(5):450–7. Annotation: A sys-
tematic review of seven studies examining clinical outcomes after PRC or S4CF for SLAC/
SNAC wrist. Radial deviation and post-operative grip strength were found to be greater after
four-corner fusion while PRC had a lower overall complication rate. Level of Evidence III.
21. Mulford JS, Ceulemans LJ, Nam D, Axelrod TS. Proximal row carpectomy vs four corner
fusion for Scapholunate (Slac) or Scaphoid Nonunion advanced Collapse (Snac) wrists: a sys-
tematic review of outcomes. J Hand Surg Eur Vol. 2009;34(2):256–63.
22. Weinstein LP, Berger RA. Analgesic benefit, functional outcome and patient satisfaction after
partial wrist denervation. J Hand Surg Am. 2002;27(5):833–9.
23. Ferreres A, Foucher G, Santiago S. Extensive denervation of the wrist. Tech Hand Up Extrem
Surg. 2002;6(1):36–41.
24. Simon E, Zemirline A, Richou J, Hu W, Le Nen D. Complete wrist denervation: a ret-
rospective study of 27 cases with a mean follow-up period of 77 months. Chir Main.
2012;31(2102):306–10. Annotation: a retrospective review of 27 complete wrist denervations
performed by one surgeon. Stable pain relief was achieved in 89% of patients with a significant
improvement in range of motion of the wrist. Six complications were reported with overall
satisfaction in a majority of patients. No level of evidence provided.
25. Hohendorff B, Mühldorfer-Fodor M, Kalb K, Von Schoonhoven J, Prommersberger
KJ. Long-term results following denervation of the wrist. [Article in German]. Unfallchirurg.
2012;115(4):343–52. Annotation: A retrospective review of 61 total wrist denervations with an
average follow up of ten years. They conclude that total wrist denervation is an option for the
chronically painful wrist with long-term satisfaction. No level of evidence provided.
26. Schweizer A, von Känel O, Kammer E, Meuli-Simmen C. Long-term follow-up evaluation of
denervation of the wrist. J Hand Surg Am. 2006;31A(4):559–64.
27. Hastings H, Weiss AC, Quenzer D, Wiedeman GP, Hanington KR, Strickland JW. Arthrodesis
of the wrist for post-traumatic disorders. J Bone Joint Surg. 1996;78-A(6):897–902.
28. Adey L, Ring D, Jupiter JB. Health status after total wrist arthrodesis for posttraumatic arthri-
tis. J Hand Surg. 2005;30A(5):932–6.
29. De Smet L, Degreef I, Truyen J, Robijns F. Outcome of two salvage procedures for post-
traumatic osteoarthritis of the wrist: arthrodesis or proximal row carpectomy. Acta Chir Belg.
2005;105(6):626–30.
30. Garcia-Elias M, Lluch A, Ferreres A, Papini-Zorli I, Rahimtoola ZO. Treatment of radiocar-
pal degenerative osteoarthritis by radioscapholunate arthrodesis and distal scaphoidectomy. J
Hand Surg Am. 2005;30(1):8–15.
31. Garcia-Elias M. Excisional arthroplasty for Scaphotrapeziotrapezoidal osteoarthritis. J Hand
Surg Am. 2011;36(3):516–20.
32. Crook T, Warwick D. Avoiding fusion in wrist arthritis. J Bone Joint Surg. 2011:1–5.
33. Siegel JM, Ruby LK. Critical look at intercarpal arthrodesis: review of the literature. J Hand
Surg Am. 1996;21(4):717–23.
34. Pequignot JP, D'asnieres De Veigy L, Allieu Y. Arthroplasty for Scaphotrapeziotrapezoidal
arthrosis using a pyrolytic carbon implant. Preliminary results. [Article in French]. Chir Main.
2005;24(3–4):148–52.
35. Viegas SF, Patterson RM, Peterson PD, Pogue DJ, Jenkins DK, Sweo TD, et al. Ulnar sided peri-
lunate instability: an anatomic and biomechanical study. J Hand Surg Am. 1990;15(2):268–78.
36. Kirschenbaum D, Coyle MP, Leddy JP, New Brunswick NJ. Chronic lunotriquetral instability:
diagnosis and treatment. J Hand Surg Am. 1993;18(6):1107–12.
37. Shin AY, Weinstein LP, Berger RA, Bishop AT. Treatment of isolated injuries of the lunotri-
quetral ligament. A comparison of arthrodesis, ligament reconstruction and ligament repair. J
Bone Joint Surg Br. 2001;83(7):1023–8.
6 Post-traumatic Arthritis of the Wrist 95
38. Lamey DM, Fernandez DL. Results of the modified Sauve-Kapandji procedure in the treat-
ment of chronic posttraumatic derangement of the distal radioulnar joint. J Bone Joint Surg
Am. 1998;80(12):1758–69.
39. Bowers WH. Distal radioulnar joint arthroplasty: the hemiresection-interposition technique. J
Hand Surg Am. 1985;10(2):169–78.
40. Watson HK, Ryu J, Burgess RC. Matched distal ulnar resection. J Hand Surg Am.
1986;11(6):812–7.
41. Santos C, Pereira A, Sousa M, Trigeuiros M, Silva C. Indications for distal radioulnar arthro-
plasty: report on three clinical cases. Rev Bras Ortop. 2015;46(3):321–4. Annotation: A report
of three cases in which a metallic prosthesis was used to replace the DRUJ. At one year follow
up all three patients had improved pain and range of motion. No level of evidence provided.
42. George MS, Kiefhaber TR, Stern PJ. The Sauve–Kapandji procedure and the Darrach pro-
cedure for distal radio–ulnar joint dysfunction after Colles’ fracture. J Hand Surg Br.
2004;29(6):608–13.
43. Dargai F, Hoel G, Safieddine M, Payet E, Leonard R, Jaffarbanjee Z, et al. Tenyear radiologi-
cal and clinical outcomes of capitolunate arthrodesis with scaphoid and triquetrum excision
for advanced degenerative arthritis in the wrist: single-center, retrospective case series with
10patients. Hand Surg Rehabil. 2020;39(1):41–7. Epub 2019 Nov 1.
44. Aita MA, Nakano EK, Schaffhausser HL, Fukushima WY, Fujiki EN. Randomized clinical
trial between proximal row carpectomy and the four-corner fusion for patients with stage II
SNAC. Rev Bras Ortop. 2016;51(5):574–582. eCollection 2016 Sep-Oct.
45. Williams JB, Weiner H, Tyser AR. Long-term outcome and secondary operations after proximal
row carpectomy or four-corner arthrodesis. J Wrist Surg. 2018;7(1):51–6. Epub 2017 Jul 27.
46. Daar DA, Shah A, Mirrer JT, Thanik V, Hacquebord J. Proximal row carpectomy versus
four-corner arthrodesis for the treatment of SLAC/SNAC wrist: a cost-utility analysis. Plast
Reconstr Surg. 2019;143:1432.
47. Kazmers NH, Stephens AR, Presson AP, Xu Y, Feller RJ, Tyser AR. Comparison of direct
surgical costs for proximal row carpectomy and four-corner arthrodesis. J Wrist Surg.
2019;8(1):66–71. Epub 2018 Nov 16.
48. Abdelaziz AM, Aldahshan W, El-Sherief FAH, Wahd YESH, Soliman HAG. Posterior interos-
seous neurectomy alternative for treating chronic wrist pain. J Wrist Surg. 2019;8(3):198–201.
Epub 2019 Jan 29.
49. Picart B, Laborie C, Hulet C, Malherbe M. Total wrist denervation: retrospective study of 39
wrists with 56 months' follow-up. Orthop Traumatol Surg Res. 2019;105(8):1607–10. Epub
2019 Sep 5.
50. Catalano LW 3rd, Ryan DJ, Barron OA, Glickel SZ. Surgical management of
Scaphotrapeziotrapezoid arthritis. J Am Acad Orthop Surg. 2020;28(6):221–8.
51. Luchetti R, Atzei A, Cozzolino R. Arthroscopic distal scaphoid resection for Scapho-
Trapezium-trapezoid arthritis. Hand (N Y). 2019:1558944719864451.
52. Faucher GK, Zimmerman RM, Zimmerman NB. Instability and arthritis of the distal radioul-
nar joint: a critical analysis review. JBJS Rev. 2016;4(12):01874474-201612000-00001.
53. Nawijn F, Verhiel SHWL, Jupiter JB, Chen NC. Hemiresection interposition arthroplasty of the
distal radioulnar joint: a long-term outcome study. Hand (N Y). 2019;13:1558944719873430.
54. Bellevue KD, Thayer MK, Pouliot M, Huang JI, Hanel DP. Complications of semiconstrained
distal radioulnar joint arthroplasty. J Hand Surg Am. 2018;43(6):566.e1–9.
55. DeGeorge BR Jr, Berger RA, Shin AY. Constrained implant arthroplasty for distal radioulnar
joint arthrosis: evaluation and management of soft tissue complications. J Hand Surg Am.
2019;44(7):614.e1–614.e9. Epub 2018 Oct 18.
Chapter 7
Post-traumatic Arthritis of the Hand
Key Points
• The goal standard for interphalangeal joint arthritis is arthrodesis.
• Thumb MCP joint arthroplasty is a good option for low demand patients.
• The CMC arthritis treatment algorithm is similar to IP and MCP arthritis.
Introduction
Arthritis of the hand is a common ailment of the general population with a preva-
lence of approximately 20–30% [1]. Being the second most common location of
pain due to osteoarthritis, it is a common condition that hand surgeons must often
treat [1, 2]. The scale of the patient’s debilitation varies in severity, but the most
common complaints involve stiffness, limitations of daily activities, and aesthetic
deformity. Unlike large joints such as the knee or hip, where artificial joint replace-
ment has been successful for many years, the small joints of the hand have not
enjoyed such long-term success to a similar degree with replacement surgery. This
chapter will discuss current treatments and the available literature regarding out-
comes of posttraumatic osteoarthritis of the interphalangeal joints of the fingers and
thumb as well as of the metacarpophalangeal and carpometacarpal joints.
A. P. Harris
Warren Alpert Medical School of Brown University, Providence, RI, USA
e-mail: andrew_harris@[Link]
T. J. Kim (*) · C. Got
Brown University, Warren Alpert Medical School, Providence, RI, USA
Trauma can occur commonly at the distal interphalangeal (DIP) joint as it is located
at the most vulnerable distal aspect of the fingers. Fractures at the distal phalanx can
occur at the tuft (distal), shaft (middle), or at the articular surface (proximal).
Injuries involving the articular surface of the distal phalanx or at the head of the
middle phalanx can lead to arthritis at a later time. Bony mallet finger injuries and
flexor digitorum profundus avulsion injuries can also involve a significant portion of
the DIP joint and can similarly accelerate arthritis.
Treatment for arthritis at the finger joints is similar in algorithm to that of the
large joints. Conservative treatment is the first choice consisting of antiinflammatory
medications and occupational therapy. In contrast to larger joints, immobilization
may be implemented in finger and thumb osteoarthritis. This is often achieved in the
thumb with 1st CMC braces. Steroid injections are also an option but due to the
small volume of the joint, correctly injecting an intraarticular dose is challenging. A
steroid injection can often provide temporary relief for some patients. When these
conservative measures have failed, surgical treatment options can be considered,
including arthrodesis or arthroplasty. The gold standard for symptomatic end-stage
arthritis at this joint is an arthrodesis [3]. There are many different techniques but the
principle remains the same: removal of any remaining articular surface and sclerotic
bone on both sides of the joint, and creation of a stable fusion bed using hardware
such as a simple Kirschner wires (K-wire) or a compression screw (Fig. 7.1).
The compression screw is usually a cannulated screw which is usually placed in
retrograde fashion. After exposing the joint and preparing the joint surfaces, a
K-wire is advanced antegrade from the distal phalanx. As the wire tents the skin, a
stab incision is made over the wire, and the wire is advanced until it protrudes just
beneath the surface of the proximal aspect of the distal phalanx. The fusion surfaces
are then reduced, and the wire is advanced retrograde across the fusion surface
under direct visualization into the center of the middle phalanx. Then, while the
fusion surfaces are held in compression, the screw is advanced over the wire. There
are two main designs of compression screw that use the concept of variable thread
pitch to achieve compression when the screw is advanced. The Herbert-type com-
pression screw has a smooth center shaft with different thread pitches at the leading
and trailing ends. The other screw design is fully threaded where the pitch varies
along its entire length. Both types serve the same purpose in creating a compression
force across the fusion bed (Fig. 7.2). Rates of union, reported to be from 80% to
100%, are high regardless of technique (Fig. 7.3) [3, 4].
Complications from DIP arthrodesis can include nonunion, failure of hardware,
fracture of the distal phalanx, and infection. Stern et al. reported a nonunion rate of
11% for DIP joint arthrodesis [5]. In the event of a symptomatic nonunion, tech-
niques have been described to remove the screw, curette out the nonunion site, and
place a cortico-cancellous graft either from the distal radius or from the iliac crest
[6]. There are no large series reporting outcomes for revision arthrodesis; however,
the few cases reported have achieved successful revision arthrodesis with these
7 Post-traumatic Arthritis of the Hand 99
Fig. 7.1 Distal interphalangeal joint fusion with a compression screw and a proximal interphalan-
geal joint fusion with cerclage wire and Kirschner wires (AP and lateral views)
techniques [6]. Fractures of the distal phalanx can also occur as the average antero-
posterior diameter of the distal phalanx is 3.5 mm while the trailing thread diameter
of a Herbert standard screw is 3.9 mm, Acutrak Mini screw is 3.6 mm, and Stryker
TwinFix screw is 4.1 mm [7, 8]. This can lead to disruption of the dorsal cortex of
the distal phalanx and pressure on the germinal matrix, which can cause nail defor-
mities [9]. Thus, it is important to select a proper size screw that will fit both the
middle phalanx and the distal phalanx. Herbert compression screws usually range
from 2.5 mm to 3.0 mm with no smaller diameters available. Smaller screw sizes
have been developed, with Acutrak Micro (Regina, Canada) providing diameters
ranging from 2.0 mm to 2.4 mm.
100 A. P. Harris et al.
Fig. 7.2 Herbert
compression screw versus
fully threaded variable
pitch screw
Proximal interphalangeal (PIP) joint injuries are notorious for the subsequent stiff-
ness and arthritis that can occur. It is still a problem that has not yet been solved and
because of this, there are many different treatment options. The anatomy of the PIP
7 Post-traumatic Arthritis of the Hand 101
joint can be considered as a box with the volar plate forming the floor of the box, the
collateral ligaments forming the sides, and the extensor mechanism forming the
roof. At least two sides of the box must be disrupted for the box to become unstable.
The joint is in a vulnerable position away from the palm but has enough of a lever
arm so that when forces are applied from the fingertip, it can create significant injury.
Treatment options start with hand therapy, splinting, and antiinflammatories.
Because posttraumatic arthritis and stiffness in the PIP joint involves much more
than just the bony articular surface, therapy is essential. The soft tissue structures
that contract respond well to serial digital casting, ultrasound, heat, and stretching
[12–14]. Patient compliance is of utmost importance as it is a long and tedious pro-
cess. Surgical options include arthroplasty and arthrodesis. The gold standard for
symptomatic end-stage posttraumatic arthritis is arthrodesis. This is especially true
for the index finger where pinch strength is desired and for manual laborers with
increased demands on their hands. Other options for PIP joint arthrodesis are simi-
lar to the DIP joint with a tension band, compression screw, and plating commonly
utilized (Fig. 7.4).
102 A. P. Harris et al.
Fig. 7.4 Proximal interphalangeal joint arthrodesis with Kirschner wires and tension band (AP
and lateral view)
The two most widely used joint replacements are currently the titanium-
polyethylene and pyrocarbon implants. The titanium-polyethylene implants typi-
cally consist of proximal and distal titanium shafts, an alloyed proximal joint
surface, and an ultra-high-molecular-weight polyethylene distal joint surface. The
pyrocarbon implants consist of a radiopaque graphite core with a radiolucent pyro-
litic carbon coating. This implant material has a modulus of elasticity that is similar
to cortical bone. Both the titanium and pyrocarbon implants are unlinked, condylar
constrained, noncemented devices. The joint stability is maintained by the joint
surface geometry and the preserved collateral ligaments. A prospective randomized
trial studied the differences between silicone arthroplasty, titanium arthroplasty, and
pyrocarbon arthroplasty. Pain reduction and grip strength were similar in all groups.
Range of motion was superior only temporarily in the titanium and pyrocarbon
groups compared to the silicone group. The complications were more frequent and
severe in the surface replacement groups. The titanium devices group had 27%
removed and eventually replaced by silicone implants. The pyrocarbon group had
39% removed and replaced. Based on this and more recent studies that have demon-
strated poor outcomes with surface replacement arthroplasty, posttraumatic arthritis
is still an unsolved problem [21]. New techniques to gain stronger bone implant
fixation to avoid this all too common complication of loosening with joint surface
replacement are currently being investigated.
Arthrodesis is the gold standard for posttraumatic arthritis of the PIP joint. There
are multiple techniques to fuse the PIP joint, including screw fixation, K-wires, ten-
sion band, and plate fixation. All three techniques are commonly used and are often
dictated by surgeon preference; however, a study performed by Leibovic and
Strickland demonstrated screw fixation provided the lowest nonunion rate [22]. The
PIP is fused in the position of optimal function. The index and middle fingers are
usually more functional in 15–30 degrees of flexion as they are used in fine pinch.
The ulnar digits are more functional in 30–45 degrees of flexion as they are used in
grip. Obtaining these optimal fusion angles are key to retaining maximal hand
function.
Carpometacarpal Arthritis
Carpometacarpal (CMC) joints are susceptible to trauma much like the MCP, PIP,
and DIP articulations. The hand contains five CMC articulations, with the thumb
CMC articulation being the most complex and important in consideration of hand
function. Much like the MCP joints, the CMC joints of digits are more prone to
injury and dislocation during a clenched fist strike with direct transfer of force to
these articulations. The thumb CMC has two well-known intraarticular fracture pat-
tern eponyms known as the “Rolando” and “Bennett” with the most common mech-
anism of axially directed force to the thumb [32]. The Rolando fracture pattern is
characterized by intraarticular comminution of the 1st proximal metacarpal [33].
The Bennett fracture is characterized by a volar split of the proximal 1st metacarpal,
where the volar oblique ligament inserts on the fracture fragment [34]. Aside from
posttraumatic arthritis, idiopathic osteoarthritis of the thumb CMC is one of the
most commonly treated conditions for practicing hand surgeons.
Even after periarticular fracture fixation of the CMC joints, posttraumatic arthri-
tis may occur. The treatment algorithm employed is very similar to the MCP, PIP,
and DIP joints. Treatment begins with conservative management, consisting of non-
steroidal antiinflammatory drugs (NSAIDS), splinting, and hand therapy or occupa-
tional therapy. Splints specifically constructed for the thumb CMC have been shown
to provide significant improvement in hand function and pain relief and are often
employed early in treatment. Splinting of the CMC joints 2 through 5, however, is
difficult to accomplish while maintaining hand function. Corticosteroid injection is
often instituted in the setting of thumb CMC arthritis but is considered a temporary
solution as the duration of symptom relief has been shown to be dependent on sever-
ity of arthritis [35]. Meenagh et al., in a randomized controlled trial, showed no
clinical benefit of corticosteroid injection versus placebo for patients with moderate
to severe arthritis [36]. Injection of CMC joints 2 through 5 may also be attempted;
although, posttraumatic arthritis to these joints is much less common than to the
thumb [37].
After conservative modalities of treatment have been exhausted and pain and
function have not improved to the satisfaction of the patient, surgical intervention
may be warranted. Surgical options for the thumb include trapeziectomy (excisional
arthroplasty) with or without suspensionplasty or ligament reconstruction, CMC
fusion, and joint replacement [38, 39]. Excisional arthroplasty is considered the
gold standard treatment for relatively active patients [38]. Patients who are young,
healthy, or high demand and laborers may benefit from CMC fusion [39]. Low
demand patients may be considered for joint replacement. Silicone thumb CMC
joint replacements initially showed excellent results but were later found to be
fraught with complications including synovitis, silicone wear, subluxation, cold
creep, and bony erosion [38]. Early studies of pyrocarbon interpositional thumb
CMC implants have shown promising results for selected low-demand patients [40].
CMC articulations 2 through 5 have relatively small amounts of motion compared
to the thumb and generally respond well to fusion. However, Yong et al. have shown
106 A. P. Harris et al.
promising early results using the Dupert’s arthroplasty technique for the 5th CMC
joint, which involves resection of the base of the 5th metacarpal and fusion of the
proximal shaft to the 4th metacarpal [41].
Conclusion
References
1. Lawrence RC, Helmick CG, Arnett FC, et al. Estimates of the prevalence of arthritis and
selected musculoskeletal disorders in the United States. Arthritis Rheum. 1998;41(5):778–99.
[Link]
2. Oliveria SA, Felson DT, Reed JI, Cirillo PA, Walker AM. Incidence of symptomatic hand, hip,
and knee osteoarthritis among patients in a health maintenance organization. Arthritis Rheum.
1995;38(8):1134–41.
3. Leibovic SJ. Instructional Course Lecture. Arthrodesis of the interphalangeal joints with
headless compression screws. J Hand Surg. 2007;32(7):1113–9. [Link]
jhsa.2007.06.010.
4. Brutus J-P, Palmer AK, Mosher JF, Harley BJ, Loftus JB. Use of a headless compressive screw
for distal interphalangeal joint arthrodesis in digits: clinical outcome and review of complica-
tions. J Hand Surg. 2006;31(1):85–9. [Link]
5. Stern PJ, Fulton DB. Distal interphalangeal joint arthrodesis: an analysis of complications. J
Hand Surg. 1992;17(6):1139–45.
6. Owusu A, Isaacs J. Revision of failed distal interphalangeal arthrodesis complicated by retained
headless screw. J Hand Surg. 2013;38(7):1408–13. [Link]
7. Wyrsch B, Dawson J, Aufranc S, Weikert D, Milek M. Distal interphalangeal joint arthrodesis
comparing tension-band wire and Herbert screw: a biomechanical and dimensional analysis. J
Hand Surg. 1996;21(3):438–43. [Link]
8. Darowish M, Brenneman R, Bigger J. Dimensional analysis of the distal phalanx with consid-
eration of distal interphalangeal joint arthrodesis using a headless compression screw. Hand (N
Y). 2015;10(1):100–4. [Link]
9. Dickson DR, Mehta SS, Nuttall D, Ng CY. A systematic review of distal interphalangeal joint
arthrodesis. J Hand Microsurg. 2014;6(2):74–84. [Link]
10. Drake ML, Segalman KA. Complications of small joint arthroplasty. Hand Clin.
2010;26(2):205–12. [Link]
7 Post-traumatic Arthritis of the Hand 107
11. Sierakowski A, Zweifel C, Sirotakova M, Sauerland S, Elliot D. Joint replacement in 131
painful osteoarthritic and post-traumatic distal interphalangeal joints. J Hand Surg Eur Vol.
2012;37(4):304–9. [Link]
12. Hunter E, Laverty J, Pollock R, Birch R. Nonoperative treatment of fixed flexion deformity
of the proximal interphalangeal joint. J Hand Surg Edinb Scotl. 1999;24(3):281–3. [Link]
org/10.1054/jhsb.1999.0111.
13. Houshian S, Jing SS, Chikkamuniyappa C, Kazemian GH, Emami-Moghaddam-Tehrani
M. Management of posttraumatic proximal interphalangeal joint contracture. J Hand Surg.
2013;38(8):1651–8. [Link]
14. Nunley RM, Boyer MI, Goldfarb CA. Pyrolytic carbon arthroplasty for posttraumatic arthri-
tis of the proximal interphalangeal joint. J Hand Surg. 2006;31(9):1468–74. [Link]
org/10.1016/[Link].2006.07.017.
15. Dionysian E, Eaton RG. The long-term outcome of volar plate arthroplasty of the proximal
interphalangeal joint. J Hand Surg. 2000;25(3):429–37.
16. Lin S-Y, Chuo C-Y, Lin G-T, Ho M-L, Tien Y-C, Fu Y-C. Volar plate interposition arthro-
plasty for posttraumatic arthritis of the finger joints. J Hand Surg. 2008;33(1):35–9. [Link]
org/10.1016/[Link].2007.10.020.
17. Burton RI, Campolattaro RM, Ronchetti PJ. Volar plate arthroplasty for osteoarthritis of
the proximal interphalangeal joint: a preliminary report. J Hand Surg. 2002;27(6):1065–72.
[Link]
18. Swanson AB, de Groot Swanson G. Flexible implant resection arthroplasty of the proximal
interphalangeal joint. Hand Clin. 1994;10(2):261–6.
19. Bales JG, Wall LB, Stern PJ. Long-term results of Swanson silicone arthroplasty for proximal
interphalangeal joint osteoarthritis. J Hand Surg. 2014;39(3):455–61. [Link]
jhsa.2013.11.008.
20. Swanson AB, Maupin BK, Gajjar NV, Swanson GD. Flexible implant arthroplasty in the prox-
imal interphalangeal joint of the hand. J Hand Surg. 1985;10(6 Pt 1):796–805.
21. Daecke W, Kaszap B, Martini AK, Hagena FW, Rieck B, Jung M. A prospective, random-
ized comparison of 3 types of proximal interphalangeal joint arthroplasty. J Hand Surg.
2012;37(9):1770–1779.e1-e3. [Link]
22. Leibovic SJ, Strickland JW. Arthrodesis of the proximal interphalangeal joint of the fin-
ger: comparison of the use of the Herbert screw with other fixation methods. J Hand Surg.
1994;19(2):181–8. [Link]
23. Woon CY-L, Phoon E-S, Lee JY-L, Ng S-W, Teoh L-C. Hazards of steroid injection: sup-
purative extensor tendon rupture. Indian J Plast Surg. 2010;43(1):97–100. [Link]
org/10.4103/0970-0358.63971.
24. Lu H, Yang H, Shen H, Ye G, Lin X-J. The clinical effect of tendon repair for tendon spontane-
ous rupture after corticosteroid injection in hands. Medicine (Baltimore). 2016;95(41) https://
[Link]/10.1097/MD.0000000000005145.
25. Adkinson JM, Chung KC. Advances in small joint arthroplasty of the hand. Plast Reconstr
Surg. 2014;134(6):1260–8. [Link]
26. Chung KC, Kotsis SV, Kim HM. A prospective outcomes study of Swanson metacarpophalan-
geal joint arthroplasty for the rheumatoid hand. J Hand Surg. 2004;29(4):646–53. [Link]
org/10.1016/[Link].2004.03.004.
27. Cook SD, Beckenbaugh RD, Redondo J, Popich LS, Klawitter JJ, Linscheid RL. Long-
term follow-up of pyrolytic carbon metacarpophalangeal implants. J Bone Joint Surg Am.
1999;81(5):635–48.
28. Bicknell RT, MacDermid J, Roth JH. Assessment of thumb metacarpophalangeal joint
arthrodesis using a single longitudinal K-wire. J Hand Surg. 2007;32(5):677–84. [Link]
org/10.1016/[Link].2007.02.010.
29. Steiger R, Segmüller G. Arthrodesis of the metacarpophalangeal joint of the thumb.
Indications, technic, arthrodesis angle and functional effect. Handchir Mikrochir Plast
Chir Organ Deutschsprachigen Arbeitsgemeinschaft Handchir Organ Deutschsprachigen
108 A. P. Harris et al.
Savyasachi C. Thakkar, Erik A. Hasenboehler,
and Chandrashekhar J. Thakkar
Key Points
• Articular step-off greater than 2mm significantly increases the risk of post-
traumatic arthritis.
• The high failure rate of cemented acetabular components has made unce-
mented implants the mainstay for reconstruction in cases of posttraumatic
arthritis.
• The results of THA after acetabular fracture are humbling at 10 years when
compared to THA for cases unrelated to posttraumatic arthritis.
• The overall revision rates after THA following acetabular fractures are
substantially higher than those following a conventional primary THA and,
hence, a multispecialty treatment approach of these challenging injuries is
essential.
S. C. Thakkar (*)
Hip & Knee Reconstruction Surgery, Johns Hopkins Department of Orthopaedic Surgery,
Columbia, MD, USA
e-mail: savya@[Link]
E. A. Hasenboehler
Department of Orthopaedic Surgery, Adult Trauma Service,
The Johns Hopkins Medical Institution, Baltimore, MD, USA
e-mail: ehasenb1@[Link]
C. J. Thakkar
Joints Masters Institute, Mumbai, Maharashtra, India
Breach Candy Hospital, Mumbai, Maharashtra, India
Lilavati Hospital, Mumbai, Maharashtra, India
Hinduja Hospital, Mumbai, Maharashtra, India
Introduction
Acetabular fractures are challenging injuries that require careful planning and spe-
cific fixation for each fracture pattern. These injuries typically demonstrate a
bimodal distribution – young patients with high-energy trauma and old patients with
osteoporotic bone from low-energy falls [15]. Despite accurate open reduction and
internal fixation of challenging acetabular fractures, there is an undeniable risk of
developing posttraumatic arthritis that can compromise patient outcomes [19].
Certain select fracture types with significant comminution in poor bone quality
require activity modification and weight-bearing restrictions as open reduction and
anatomic fixation would not be successful. However, the majority of the fractures
require anatomic restoration of the articular surface, especially in young patients.
Elderly patients with poor bone quality may be treated conservatively allowing
imperfect articular surface congruency, followed by total hip arthroplasty
(THA) [20].
The incidence of posttraumatic arthritis is 13% in cases where the articular con-
gruity has been adequately restored (less than 2 mm). There is a marked increase in
posttraumatic arthritis to 44% when the step-off between acetabular articular frag-
ments is greater than 2 mm [6]. However, the reported incidence of posttraumatic
arthritis can be as high as 67% per some reports [17, 23]. Most cases of posttrau-
matic arthritis after acetabular fractures require THA as the mainstay of treatment.
Usually, such patients can fall into one of the following three categories [12]:
• Category I – Patients with hip degeneration due to the initial injury or because of
complications associated with prior treatments. Such patients may present with
osteonecrosis of the femoral head, fracture mal-union, or nonunion and remnant
fracture fragments.
• Category II – Comminuted fractures in elderly patients with osteoporosis that are
not amenable to primary open reduction internal fixation and must rely on heal-
ing by secondary congruence. In these cases, patients can either receive a THA
for an acute fracture or delayed arthroplasty for secondary congruence.
• Category III – The nature of the fracture precludes a good result with initial ana-
tomic fixation. Impacted and multifragmentary fractures through the weight-
bearing dome of the acetabulum are usually not amenable to good function even
after excellent open reduction and internal fixation leading to posttraumatic
arthritis.
THA remains the main treatment for posttraumatic arthritis after acetabular frac-
tures. However, it remains inferior when compared to THA for nonfracture-related
arthritis [7, 19, 21]. Increased failure in posttraumatic situations can be attributed to
cemented acetabular components, initial method of fracture fixation, preexisting
hardware, increased propensity for infection, younger age of the patient, abnormal
anatomy, sclerotic bone bed, and decreased acetabular bone stock [15]. Conversely,
cementless acetabular reconstruction has improved survivorship and has become
the preferred implant choice for posttraumatic arthritis of the acetabulum [1].
8 Post-traumatic Arthritis of the Acetabulum 113
In this chapter, we will outline our treatment algorithm for posttraumatic arthritis
of the acetabulum including surgical planning, implant selection, and surgical tech-
nique, and we will also present some representative cases highlighting key princi-
ples. In addition, we will review current outcomes associated with THA for
posttraumatic arthritis of the acetabulum.
Surgical Planning
Implant Selection
The high failure rate of cemented acetabular components has made uncemented
implants the mainstay for reconstruction in cases of posttraumatic arthritis [1, 5,
13]. Uncemented multihole porous metal cups allow the surgeon to plan screw tra-
jectories in the available host bone, while the porous metal surface can achieve ini-
tial scratch fit for primary stability. Based on the type of bone defect created due to
the initial injury and subsequent surgeries, it is also advisable, especially for com-
plex reconstructions, to have various porous metal augments and cages available.
Custom tri-flange components typically require 3D CT reconstructions and subse-
quent manufacturing from the implant company. In such cases implants should be
ordered several weeks in advance.
Surgical Technique
soft tissue dissection is required to visualize the acetabulum in its entirety. Release
of the insertion of the gluteus maximus tendon from the linea aspera should be per-
formed to allow the femur to be shifted anteriorly. Also, removal of the anterior
capsule and scar tissue allows for a pocket to be created for the femur to be trans-
lated anteriorly. A supra-acetabular Steinmann pin or a 90-degree bent Gelpi retrac-
tor, a right angle Hohmann retractor on the posterior column, a ball-spike pusher to
shift the femoral shaft anteriorly, and a blunt Hohmann retractor at the inferior bor-
der of acetabulum usually suffice for a clear 360-degree view of the socket.
Placing the cup in adequate anteversion and abduction is critical to the patient’s
function and implant longevity. With porous metal implants, it is essential to coat
the exposed surface of the implant to avoid excessive fibrosis. While closing the
incision, it is essential to not leave any dead space, and the use of drains with metic-
ulous soft tissue closure must be ascertained. Postoperative care resembles the pro-
tocol for THA such as posterior-hip precautions and physical therapy. However, the
weight-bearing status may vary depending on the stability of the reconstruction
construct and it may have to be modified on an individual basis. In the next section,
we will present several cases that reinforce the aforementioned principles.
Case Examples
We present case examples based on the three types of patients [20] described in the
surgical planning section of the chapter:
• Type I – Patients requiring a conventional total hip arthroplasty. Figures 8.1, 8.2,
and 8.3 are case examples of patients that had prior acetabular fractures which
had united with sufficient bone stock for primary total hip arthroplasty without
additional acetabular reconstruction.
• Type II – Patients requiring fracture stabilization along with THA. Figures 8.4,
8.5, and 8.6 are case examples of patients requiring acute fracture fixation and
concurrent THA to ensure adequate support for the implants.
• Type III – Patients requiring significant acetabular reconstruction to restore the
center of rotation. Figures 8.7, 8.8, and 8.9 are case examples of patients that rely
upon revision hip replacement principles to ensure optimal outcome.
Outcomes
We review several studies that report on the mid-term and long-term outcomes for
THA in cases of posttraumatic arthritis after acetabular fractures. A recent study
from the Mayo Clinic reported their mid-term results on 30 primary THAs that were
performed with a porous metal acetabular component after open reduction internal
fixation (ORIF) of acetabular fractures from 1999 through 2010 [22]. From these
116 S. C. Thakkar et al.
a b
c d
Fig. 8.1 (a) Pre-operative AP Pelvis radiograph of a 42 year-old male with an old acetabular frac-
ture leading to post-traumatic arthritis secondary to femoral head osteonecrosis. (b) Pre-operative
CT scan showing the incarcerated head fragment. (c) Intra-operative photograph of the incarcer-
ated femoral head. (d) Post-operative AP pelvis radiograph displaying press-fit acetabular and
femoral components
Fig. 8.2 (continued)
b
c
118 S. C. Thakkar et al.
Fig. 8.3 (a) Pre-operative AP pelvis radiograph of a patient with a chronic acetabular fracture and
medial protrusion of the femoral head. (b) 3D CT reconstructions of a patient with a chronic ace-
tabular fracture and medial protrusion of the femoral head. (c) Post-operative AP pelvis radiograph
displaying press-fit acetabular and femoral components with medial bone graft
8 Post-traumatic Arthritis of the Acetabulum 119
Fig. 8.3 (continued)
Fig. 8.4 (a) Pre-operative radiographs of a 67 year old patient with a both columns acetabular
fracture and antecedent hip pain associated with osteoarthritis. (b) 3D CT reconstruction of a 67
year old patient with a both columns acetabular fracture and antecedent hip pain associated with
osteoarthritis. (c) Post-operative AP pelvis radiograph displaying press-fit acetabular and femoral
components with medial bone graft and posterior column and wall fixation
120 S. C. Thakkar et al.
b c
Fig. 8.4 (continued)
a b
Fig. 8.5 (a) Pre-operative AP right hip radiograph of a 60 year-old gynecologist who sustained a
fracture-dislocation of her left hip after a fall. (b) 3D CT reconstructions of a 60 year-old patient
with the fracture dislocation. (c) Post-operative AP pelvis radiograph displaying press-fit acetabu-
lar and femoral components with posterior wall fixation
8 Post-traumatic Arthritis of the Acetabulum 121
b
122 S. C. Thakkar et al.
Fig. 8.6 (continued)
c
d
8 Post-traumatic Arthritis of the Acetabulum 123
Fig. 8.7 (continued)
cases, 28 (93%) THAs had a minimum follow-up of 2 years. The authors reported
that the fracture pattern was of the elementary type in 8 of 30 hips (27%, posterior
wall fracture in 6 hips, transverse fracture in 2 hips) and associated type in 13 of 30
hips (43%, T-type fracture in 5 hips, transverse-posterior wall fracture in 4 hips,
posterior column/posterior wall in 3 hips, and associated both column in 1 hip). The
fracture pattern was unknown in 9 of 30 hips. Nine of 30 hips (30%) had radio-
graphic evidence of osteonecrosis of the femoral head, and 6 of those had confirmed
traumatic dislocations at the time of their initial injury. A majority of patients under-
went the anterolateral approach, and only 9 of 30 hips were performed using the
posterolateral approach. No acetabular components were revised for aseptic loosen-
ing. Five-year survival with revision for any reason as the endpoint was 88% (95%
confidence interval, 0.70–0.96). Failures were related to infection. Three hips (11%)
underwent resection for infection, with all being treated with two-stage arthroplasty.
Harris hip scores improved from a median of 39 preoperatively (range, 3–87) to 82
at the most recent follow-up (range, 21–100; p < 0.01). Fifteen of 28 hips (54%) had
a good or excellent result, 3 (11%) had a fair result, and 10 (35%) had a poor result.
Two patients (7%) experienced at least one dislocation postoperatively. Both were
treated with a closed reduction and hip abduction brace treatment.
8 Post-traumatic Arthritis of the Acetabulum 125
c
126 S. C. Thakkar et al.
b
8 Post-traumatic Arthritis of the Acetabulum 127
Fig. 8.9 (continued)
128 S. C. Thakkar et al.
Another promising study from the Hospital for Special Surgery describes their
results with 32 THAs performed for posttraumatic arthritis after acetabular frac-
tures; 24 patients were treated with a prior ORIF, and 8 were managed conserva-
tively [18]. Average time from fracture to THA was 36 months (range, 6–227 months).
The average follow-up was 4.7 years (range, 2.0–9.7 years). With regard to fracture
classification, 16 patients (50%) had simple fracture patterns, and 16 patients (50%)
had associated patterns. One patient had a concomitant pelvic fracture. The most
common fracture patterns were isolated posterior wall fractures in 13 (41%) cases,
both-column fractures in 4 (13%) cases, and posterior column–posterior wall in 5
(16%) cases. Cementless acetabular components were used in all 32 cases. The
authors reported 79% 5-year end point survival for revision, loosening, dislocation,
or infection. Survival for aseptic acetabular loosening was 97%. Six (19%) revision
surgeries were necessary due to infection (two cases), aseptic acetabular loosening
(one case), aseptic femoral component loosening (two cases), and a liner exchange
for dislocation (one case). Revision surgery correlated with nonanatomic restora-
tion of the hip center and a history of infection (P < 0.05). Two other patients also
had at least one dislocation, but they both responded to conservative treatment with
closed reduction and bracing, which resulted in a dislocation rate of 9%. Harris hip
scores increased from 28 (0–56) to 82 points (20–100).
Studies from China have reviewed outcomes at 5 years and 6.3 years after THA
for acetabular fractures. Zhang et al. retrospectively analyzed 53 patients (55 hips)
who underwent THA because of failed treatment for acetabular fractures. The mean
duration of follow-up was 64 months (range, 32–123 months) in 49 patients [23].
Thirty-three hips (60%) had simple fracture patterns, and 22 (40%) had complex
patterns. The most common patterns were posterior wall fractures in 28 (51%) hips,
transverse-posterior wall fractures in 13 (23%) hips, and fractures of the posterior
column and posterior wall in 6 (11%) hips. Patients treated without ORIF under-
went a posterolateral approach to the hip. However, in patients with prior fixation, a
posterolateral approach was used in 28 hips, while a direct lateral approach and a
posterolateral plus anterolateral approach were used for removal of hardware in 2
hips, respectively. The authors used cement-less cups in 48 of 55 hips, and cemented
cups in 7 hips with 5 of them in combination with acetabular reinforcement rings
(ARRs). The authors report that with revision or definite radiographic loosening as
the end-point, the 5-year survival in their study was 100%. Three cement-less ace-
tabular components had a partial radiolucency (zones 2 and 3 [4]); in 2, the radiolu-
cency was less than 1 mm wide, and in 1, it was more than 2 mm wide. All of them
were associated with a good or excellent Harris hip score and were considered sta-
ble. A complete radiolucency, from zones 1 to 3, more than 2 mm wide, was seen in
1 cemented cup. None of the acetabular cups or ARRs showed any evidence of
migration. All bone grafts completely incorporated without any complications.
Complications included 1 dislocation and 3 sciatic nerve injuries. No instances of
deep wound infection were present. The dislocation was successfully treated with
closed reduction with no recurrence. The mean duration of follow-up was 64 months
(range, 32–123 months) in 49 patients (51 hips); 4 patients were lost to follow up.
The average Harris hip score increased from 49.5 (range, 22–78) before surgery to
8 Post-traumatic Arthritis of the Acetabulum 129
90.1 (range, 56–100) at the latest follow-up examination (P < 0.001). Results were
excellent for 36 hips, good for 11, fair for 2, and poor for another 2. In the ORIF
group, the average Harris hip score increased from 9.5 (range, 30–78) to 90.1 (range,
56–100) (P < 0.001), and in the non-ORIF group, it increased from 54.3 (range,
22–76) to 92.4 (range, 56–100) (P < 0.001). Moreover, the average postoperative
Harris score was significantly higher in the ORIF group than in the non-ORIF group
(P < 0.05). Similar significant improvements in average Harris hip scores were also
seen both in patients with cement-less acetabular reconstructions and in those with
cemented cups (P < 0.001). Another study from China evaluated outcomes of
cement-less acetabular components at 6.3 years (range, 3.1–8.4 years) after surgery
in 31 hips with posttraumatic arthritis after acetabular fractures [10]. Of the
31patients, 19 (65%) had undergone ORIF (open-reduction group), and 12 (35%)
had received conservative treatment for the acetabular fractures (conservative-treat-
ment group). 14 patients (45%) had elementary fracture patterns while 17 patients
(55%) had associated fracture types. The posterolateral approach to the hip was
used in all patients. At the follow-up of 6.1 years, the authors reported no infection
and no revision surgery. The rate of anatomical restoration of center of hip rotation
was 100% (19/19) in the open-reduction group, and 67% (8/12) in the conservative-
treatment group (P = 0.02), compared with 93% (13/14) in the simple group and
82% (14/17) in the complex group (P = 0.61). Anatomical restoration was positively
related to fracture treatment (r = 0.48; P = 0.006), but it had no relation to fracture
pattern (r = 0.16; P = 0.40). By the final follow-up evaluation, six acetabular com-
ponents had partial radiolucent lines at the bone implant interface, all 1 mm or less;
and they occurred in zone 1 in five hips and in zone 3 in one hip. Osteolysis was not
observed in any patient. Of the patients with structural bone graft, only one had
minor graft resorption. Four patients (13%) had complications after THA. One
patient whose complex fracture was treated conservatively fell 4 years after surgery,
causing posterior hip dislocation. Another patient whose complex fracture was
treated with ORIF had posterior hip dislocation 14 days after surgery because of
failure to adhere to posterior hip precautions. Both patients were successfully
treated with closed reduction; neither patient had a recurrent dislocation until the
latest follow-up evaluation. The sciatic nerve was injured during THA in one patient
in the open-reduction group who had a complex fracture. The patient had dorsal
pedal numbness and drop foot after surgery. The average Harris hip score increased
from 49 ± 15 before surgery to 89 ± 5 after surgery, and 29 patients (94%) had either
excellent or good results. The average Harris hip score for the open-reduction and
conservative-treatment groups increased to 87 ± 6 and 91 ± 3 (P = 0.07), respec-
tively, after surgery; for the complex and simple groups, it increased to 88 ± 6 and
90 ± 4 (P = 0.25), respectively. There was no significant difference between the
open-reduction and conservative-treatment groups or between the complex and
simple groups regarding the number of hips with excellent and good results.
The results of THA after acetabular fracture are humbling at 10 years when com-
pared to THA for cases unrelated to posttraumatic arthritis. Morrison et al. per-
formed a retrospective case-control study for patients at their institute between 1987
and 2011 [15]. During this period, the authors performed 95 THAs after acetabular
130 S. C. Thakkar et al.
fracture; of those, 74 (78%) met inclusion criteria and had documented follow-up
beyond 2 years in their institutional registry. They also selected 74 matched patients
based on an algorithm that matched patients based on preoperative diagnosis, date
of operation, age, gender, and type of prosthesis. All surgeries were performed
through the posterolateral approach. The primary outcomes were revision and inci-
dence of complications. Secondary outcomes were radiographic signs of hetero-
topic ossification or implant loosening. The majority of acetabular fractures were
treated by ORIF (58 of 74 [78%]), whereas 16 of 74 (22%) were treated nonopera-
tively. The most frequent type of fracture involved the posterior wall, accounting for
31% of all injuries. Fractures involving both columns were seen in 16%, whereas
other fracture types were less common and were observed in less than 10% of
patients. 49% of patients had elementary fracture types while 51% of patients had
associated patterns. The 10-year survivorship after THA was lower in patients with
a previous acetabular fracture than in the matched cohort (70%, 95% confidence
interval [CI] 64–78% versus 90%, 95% CI 86–95%; p < 0.001). Younger patients
(<60 years) had worse THA survivorship after acetabular fractures than did older
patients (60%, 95% CI 51–69% versus 83%, 95% CI 72–94%; p < 0.038), and both
had inferior survivorship to the matched cohort (92%, CI 87–97% and 96%CI
92–99%; p < 0.001). The 10-year survival for THA after a simple acetabular frac-
ture was 83% (95% CI 77–89%) as compared with 60% (95% CI, 52–68%;
p = 0.032) for associated fractures. Patients with previous acetabular fracture had a
higher likelihood of developing infection (7% [five of 74] versus 0% [zero of 74];
odds ratio [OR], 11.79; p = 0.028), dislocation (11% [eight of 74] versus 3% [two
of 74]; OR, 4.36; p = 0.048), or heterotopic ossification (43% [32 of 74] versus 16%
[12 of 74]; OR, 3.93; p < 0.001). In patients with previous acetabular fracture, 13
patients (20%) were revised for loose acetabular component, 6 patients for wear and
joint instability (8%), 2 for infection, and 1 each for femur fracture, loose femoral
component, and recurrent dislocation. Revisions for the matched cohort included 11
patients for cup loosening and one patient for recurrent dislocations.
Of the 51 patients in the acetabular fracture group, who did not have a revision,
6 had no radiographs available, 46 had well-fixed components, and none had cup
loosening. Of the 62 control patients without revision, 3 had no radiographs avail-
able, 59 had well-fixed components, and none had cup loosening.
To summarize the outcomes of THA in posttraumatic arthritis after acetabular
fractures, Makridis et al. performed a systematic review in 2014 [11]. In total 654
patients were reviewed (659 hips) with a median follow-up of 5.4 years (range
12 months – 20 years). Median follow-up was 3.9 years (range 12 months–12 years)
in the acute THA group and 6.3 years (range 12 months – 20 years) in the delayed
THA group. A large majority of fractures were posterior wall fractures (140 patients;
21.4%) followed by transverse/posterior wall fractures (63 patients; 9.6%), poste-
rior column-posterior wall fractures (51 patients; 7.8%), and both column fractures
(49 patients; 7.5%). Treatment of acetabular fractures was only described in 625
fractures of which 473 fractures (75.7%) were treated with ORIF and 152 fractures
(24.3%) nonoperatively. The majority of the studies reviewed by the authors
reported no failure of initial treatment of acetabular fractures. 237 patients (36%)
8 Post-traumatic Arthritis of the Acetabulum 131
were treated with acute total hip arthroplasty. Delayed total hip arthroplasty was
performed in the remainder of the reviewed patients following either operative or
nonoperative management of the initial acetabular fracture. In the early-THA cases,
the median interval between time of injury and total hip arthroplasty was 10 days
(1–29). In the delayed cases, the average time from injury to THA was 6.6 years
(2 months–45 years).
With regard to acetabular components, an uncemented acetabular component
was used in 484 patients (80.1%) and a cemented one in 120 patients (19.9%). For
femoral components, the data was available in 569 hips with 340 patients (59.8%)
receiving an uncemented and 229 patients (40.2%) a cemented femoral component.
An antiprotrusion acetabular cage was rarely used, and acetabular bone graft was
used in all cases. Anterolateral and posterolateral surgical approaches were used in
a majority of the cases. In the early THA group, Kaplan–Meier survivorship analy-
sis with any loosening, osteolysis, or revision as the end-point revealed that the
10-year cup survival was 81%. In the late THA group, this percentage was 76%. The
log-rank test showed that this difference was not significant (P = 0.287). In the late
THA group where the proportion of uncemented and cemented implants were avail-
able, Kaplan–Meier survivorship analysis with any loosening, osteolysis, or revi-
sion as the end-point revealed that the 10-year survival was 86.7% for the uncemented
cups and 81% for the cemented. The log-rank test showed that this difference was
not significant (P = 0.163). In the early THA group, 13 cups (7.5%) out of 173
implants were revised. Four cups were revised for aseptic loosening, one for trau-
matic loosening, six for dislocation, and two for infection. It was unclear how many
of these cups were cemented and how many were uncemented. In the late THA
group, 35 cups (9.6%) out of 365 implants were revised. Sixteen cups (45.7%) were
uncemented (13 were revised for aseptic loosening, 1 for traumatic loosening, and
2 for infection). Nineteen cups (54.3%) were cemented (17 were revised for aseptic
loosening, 1 for dislocation, and 1 for infection). The three most common complica-
tions were heterotopic ossification, infection, and dislocation which occurred in a
total of 292 out of 654 patients (44.6%). The Harris hip score was used to describe
the functional outcome with a median value of 88 points. Regardless of the type of
treatment, and according to the Harris hip score, younger patients achieved better
clinical outcomes than older patients (92.94 ± 4.48 versus 81.68 ± 4.58, respec-
tively) (P < 0.001). Almost all of the studies did not compare Harris hip scores for
acute versus delayed THA. Thirty-three patients died, and the overall mortality rate
was 5%. No patient died in the acute perioperative phase. The minimum time of
postoperative mortality was 4 months after surgery and maximum within 10 years
after surgery.
In conclusion, THA for posttraumatic arthritis associated with acetabular frac-
tures shows promising results and satisfactory functional and radiological outcomes.
However, there are no prospective studies to compare directly the outcomes follow-
ing acute or delayed total hip arthroplasty secondary to acetabular fractures. The
largely retrospective data available in the literature indicate that the clinical out-
comes, revision rates, and implant survivorship do not differ when either an early or
a late THA is performed. The overall revision rates after THA following acetabular
132 S. C. Thakkar et al.
fractures are substantially higher than those following a conventional primary THA,
and, hence, a multispecialty treatment approach of these challenging injuries is
essential.
References
1. Bellabarba C, et al. Cementless acetabular reconstruction after acetabular fracture. J Bone
Joint Surg Am. 2001;83:868–76.
2. Bone and Joint Trauma Study Group [GETRAUM]. Indications and technical challenges
of total hip arthroplasty in the elderly after acetabular fracture. Orthop Traumatol Surg Res.
2014;100:193–7.
3. Chokshi FH, Jose J, Clifford PD. Morel-Lavallee lesion. Am J Orthop. 2010;39:252–3.
4. DeLee JG, Charnley J. Radiological demarcation of cemented sockets in total hip replacement.
Clin Orthop. 1976;121:20–32.
5. Enocson A, Blomfeldt R. Acetabular fractures in the elderly treated with a primary Burch-
Schneider reinforcement ring, autologous bone graft and a total hip arthroplasty. A prospective
study with a 4-year follow-up. J Orthop Trauma. 2014;28:330–7.
6. Giannoudis PV, Grotz MR, Papakostidis C, Dinopoulos H. Operative treatment of displaced
fractures of the acetabulum. A meta-analysis. J Bone Joint Surg Br. 2005;87:2–9.
7. Huo MH, et al. Total hip replacements done without cement after acetabular fractures: a 4- to
8-year follow-up study. J Arthroplasty. 1999;14:827–31.
8. Judet R, Judet J, Letournel E. Fractures of the acetabulum: classification and surgical
approaches for open reduction. Preliminary report. J Bone Joint Surg Am. 1964;46:1615–46.
9. Kendoff D, et al. Value of 3D fluoroscopic imaging of acetabular fractures comparison to 2D
fluoroscopy and CT imaging. Arch Orthop Trauma Surg. 2008;128:599–605.
10. Lai O, et al. Midterm results of uncemented acetabular reconstruction for posttraumatic arthri-
tis secondary to acetabular fracture. J Arthroplast. 2011;26(7):1008–13.
11. Makridis KG, et al. Total hip arthroplasty after acetabular fracture: incidence of complications,
reoperation rates and functional outcomes: evidence today. J Arthroplast. 2014;29:1983–90.
12. Mears DC, Velyvis JH, Chang CP. Displaced acetabular fractures managed operatively: indica-
tors of outcome. Clin Orthop Relat Res. 2003;407:173–86.
13. Mears CD, Velyvis JH. Primary total hip arthroplasty after acetabular fracture. Instr Course
Lect. 2001;50:335–54.
14. Moed, et al. Computed tomographic assessment of fractures of the posterior wall of the acetab-
ulum after operative treatment. J Bone Joint Surg Am. 2003;85-A:512–22.
15. Morrison Z, et al. Total hip arthroplasty after acetabular fracture is associated with lower sur-
vivorship and more complications. Clin Orthop Relat Res. 2016;474:392–8.
16. Paprosky WG, Perona PG, Lawrence JM. Acetabular defect classification and surgical recon-
struction in revision arthroplasty: a 6-year follow-up evaluation. J Arthroplast. 1994;9:33–44.
17. Ragnarsson B, Mjöberg B. Arthrosis after surgically treated acetabular fractures. A retrospec-
tive study of 60 cases. Acta Orthop Scand. 1992;63:511.
18. Ranawat A, et al. Total hip arthroplasty for posttraumatic arthritis after acetabular fracture. J
Arthroplast. 2009;24(5):759–67.
19. Romness DW, Lewallen DG. Total hip arthroplasty after fracture of the acetabulum. Long-
term results. J Bone Joint Surg Br. 1990;72:761–4.
20. Thakkar Chandrashekhar J, Rajshekhar KT, Thakkar SC. Total hip arthroplasty after acetabu-
lar fractures. Arthropaedia. 2014;1:105–14.
21. Weber M, Berry DJ, Harmsen WS. Total hip arthroplasty after operative treatment of an ace-
tabular fracture. J Bone Joint Surg Am. 1998;80:1295–305.
8 Post-traumatic Arthritis of the Acetabulum 133
22. Yuan BJ, Lewallen DG, Hanssen AD. Porous metal acetabular components have a low rate of
mechanical failure in THA after operatively treated acetabular fracture. Clin Orthop Relat Res.
2015;473:536–42.
23. Zhang L, et al. Total hip arthroplasty for failed treatment of acetabular fractures. J Arthroplast.
2011;26(8):1189–93.
Chapter 9
Post-traumatic Arthritis of the Proximal
Femur
Key Points
• Optimal treatment for posttraumatic arthritis of the proximal femur is
patient specific.
• Hip arthroscopy is on the forefront of treatment modalities.
• Arthroplasty for proximal femur fractures is increasingly indicated during
the index fracture.
• Varus malunion is a common mode of failure following treatment of femo-
ral neck fractures.
Introduction
Epidemiology
PTOA figures will increase [4]. As such, an understanding of the disease and treat-
ment options currently available is a key component of the treating musculoskeletal
practitioners skill set.
Pathophysiology of Failure
a b
Fig. 9.1 (a) Radiograph demonstrating Pipkin IV fracture dislocation in a 48-year-old patient. (b)
3-D reconstruction CT image depicting substantial femoral head collapse. (c) Intraoperative image
of excised femoral head with split-depression fracture. (d) Treatment with index total hip arthro-
plasty (THA)
Fracture Specifics
Hip Dislocation
Though the articular surface in isolated femoral head fractures experiences substan-
tial shear forces, prompt reduction generally results in minimal long-term conse-
quences. In isolated dislocations without hip fracture, prompt reduction results in
excellent long-term clinical outcomes [8]. At 11-year follow-up, six of seven
patients with isolated dislocations had good to excellent Thompson and Epstein
objective outcome scores and only one patient had mild pain with cystic changes on
radiograph. Therefore, the poor functional outcome in 53% of posterior dislocations
and 25% of anterior dislocations seen in this study were attributed to other injuries
associated with the dislocation as rates of good to excellent subjective clinical out-
comes are 85–100% in isolated hip dislocations [8].
PTOA following femoral head fracture results primarily from direct chondral injury.
In the long term, failure following femoral head fractures results from avascular
necrosis, which is apparent in 10% of patients at 12 months postinjury [9].
Additionally at a mean of 12 months postoperatively, Scolaro et al. demonstrated
12% early fixation failure rate in a population primarily treated with open reduction
internal fixation (53%), fragment excision (25%), and hemiarthroplasty (2%) [9]. At
a mean of 5 years postinjury, PTOA is present in nearly 20% of patients [1]. Factors
predicting worse outcome include nonsurgical management and increasing Pipkin
type (Table 9.1) [1, 9, 10].
Fractures of the femoral head present a relatively difficult treatment challenge as
both exposure and fixation options are limited. Pipkin I fractures may be treated
nonoperatively with open fragment excision or internal fixation [11]. Recently,
internal fixation has been described using an arthroscopic approach though long-
term outcomes are pending [12]. In large Pipkin I fracture fragments, open reduc-
tion with internal fixation (ORIF) has demonstrated better clinical and radiographic
outcomes as compared to fragment excision [13, 14].
In Pipkin III fractures, Scolaro et al. recommend strong consideration of arthro-
plasty based on 100% failure of ORIF in their study [9]. However, AVN-related
failures have been markedly reduced with the vascular preserving surgical hip dis-
location popularized by Gans [15]. This is particularly true in Pipkin I and II frac-
tures treated with early (<6 hour) surgical hip dislocation – one study with a mean
of 36-month follow-up found 0% rate of osteonecrosis, and 100% union rate [11].
Another study demonstrated 85% excellent clinical outcomes (HHS score >80) uti-
lizing a surgical hip dislocation in all operatively managed Pipkin fractures and 8%
avascular necrosis rate [16].
9 Post-traumatic Arthritis of the Proximal Femur 139
Femoral Neck
a b
c d
Fig. 9.2 (a) Nondisplaced femoral neck fracture. (b) Immediate postoperative imaging.
(c) Femoral head collapse 6 months following index procedure. (d) Conversion to hemiarthroplasty
Intertrochanteric
a b
d
c
Fig. 9.3 (a) Minimally displaced intertrochanteric fracture. (b) Immediate postoperative radio-
graphs. (c) Varus failure 6 months after index procedure. (d) Valgus intertrochanteric osteotomy
with revision open reduction internal fixation
142 R. M. Amin et al.
10 degrees in the sagittal plane, and 15 degrees in the axial plane focuses load on the
superior femoral head, leading to arthrosis [33, 38].
Additionally, cut-out is of particular concern in trochanteric fractures (Fig. 9.4).
It is estimated to occur in approximately 2% of patients treated with intramedullary
nailing [39, 40]. Factors predicting cut-out including nonanatomic reduction, sub-
optimal bone quality, and tip-apex distance greater than 25 mm [39–41].
a b
c d
Fig. 9.4 (a, b) AP and lateral radiographs of left hip demonstrating cut out of cephalomedullary
device. (c, d) One year following removal of hardware and conversion to THA
9 Post-traumatic Arthritis of the Proximal Femur 143
Management
The most definitive management for PTOA of the femoral head is hemi-, or total
(THA), hip arthroplasty. These surgeries are supported by strong data demonstrat-
ing excellent outcomes, which have led some to opine that prevention of PTOA in
patients with prefracture arthrosis should be accomplished with arthroplasty in ame-
nable proximal femur fractures (7). However, arthroplasty in the setting of fracture
is still associated with inherent risk over internal fixation including higher rates of
wound infection, transfusion, and in-hospital morbidity. Additionally, due to limita-
tions in prosthetic longevity, physiologically younger patients may be better served
with osteosynthesis of native bone which may delay arthroplasty on average by
74 months [42]. Also, consideration of nonoperative and less invasive operative
options are necessary in femoral head PTOA.
Nonoperative
There is a limited role for nonoperative management at the index injury time. This
is usually reserved for critically ill patients. However, some Pipkin I fractures are
amenable to initial nonoperative management but this option is usually not recom-
mended as the rate of PTOA in nonoperatively managed Pipkin 1 fractures is 10%
higher compared to operatively treated patients [10].
In the long-term, given that posttraumatic arthritis is a subset of osteoarthritis, it
responds to the same conservative treatment that is well defined for the more com-
mon degenerative osteoarthritis. Antiinflammatory medications of varying potency
and physical therapy are first-line, and often permanent, solutions to arthritic pain.
Targeted intracapsular corticosteroid injections may also be of benefit from both a
diagnostic and therapeutic perspective.
Operative
Arthroscopy
In the trauma population hip arthroscopy has more sparse literature. A study
of 36 patients undergoing arthroscopy following closed reduction of hip disloca-
tion found a 92% rate of loose bodies, and 78% rate of loose bodies in patients
with imaging identifying concentric reduction and no loose bodies [48]. However,
no outcome measures were reported in this study [48]. In a recent 2015 study of
13 patients undergoing hip arthroscopy following femoral head dislocation or
acetabular fracture, 3.5-year follow-up demonstrated significant improvement in
VAS scores and Modified Harris Hip Scores [49]. However, only Tönnis grade 0
or 1 (Table 9.4) patients were included in the study, and only 7 of 13 patients
were femoral head dislocation patients. It is unknown how many of these patients
had a concomitant acetabular fracture, which limits application to the proximal
femur PTOA population. In another early study of hip arthroscopy in 38 patients,
the diagnosis of arthritis resulted in an average Harris Hip Score increase of 18
and 14 points in patients with chondral injury, and arthritis, respectively, over a
10-month period [50]. However, the Harris Hip Score in those patients with a
diagnosis of avascular necrosis decreased by 11 over the same time [50]. As
previously mentioned, the etiology of PTOA in proximal femur fractures is
strongly related to avascular necrosis. As such current data is inconclusive and
further study is necessary to determine whether arthroscopy has a role in the
treatment of young patients with severe PTOA following proximal femur
fractures.
Hip Preservation
Osteotomy
Core Decompression
Arthroplasty
Arthroplasty for proximal femur fractures is increasingly indicated during the index
fracture. Elderly patients with displaced femoral neck fractures treated with arthro-
plasty have significantly lower complications, reoperation rates, less postoperative
pain, and better overall function when compared to internal fixation [60]. Options
for arthroplasty include THA and hemiarthroplasty. Hemiarthroplasty is commonly
performed in those patients with relatively poorer health status, and risk factors for
recurrent dislocation as the risk of dislocation for THA following fractures is four
times higher than for THA performed due to arthritic indications [61–63] However
prosthetic-induced acetabular wear causes substantial pain, and at 14 months post-
operatively the clinical outcomes for THA are significantly better than hemiarthro-
plasty in properly selected patients [61, 62, 64]. Additionally, hemiarthroplasty
confers no mortality or infection benefit at 4 years postoperatively when compared
to THA, and uncemented prosthesis carries 720% higher chance of 5 year
146 R. M. Amin et al.
periprosthetic fracture when compared to cemented implants [61, 63, 65]. Therefore,
the decision to perform hemiarthroplasty as the index procedure should primarily
factor in poor projected patient longevity and household ambulation status as large
database outcomes trend toward no difference in short-term complications or mor-
tality in hemi- versus total hip arthroplasty [61, 63]. In younger patients aged 40–65,
recent data indicate these patients may have greater clinical benefit and overall more
cost-effective care with index THA (Fig. 9.1) [66].
With respect to painful PTOA, arthroplasty is the most definitive treatment
option. Nearly 50% of patients with femoral head injury or acetabular impaction
will require future arthroplasty [67]. The results of THA in patients with PTOA of
the hip following acetabular or proximal femur fractures are inferior compared to
primary degenerative OA. In one study of 1199 patients, 63 had THA for PTOA. They
fared worse with respect to perioperative complications and demonstrated 13%
revision rate due to persistent dislocation or infection at an average of 3.5 years
postoperatively [42]. When compared to primary THA, patients undergoing THA
conversion due to failed fixation of femoral neck fractures also have greater compli-
cations including deep infection, dislocation, and periprosthetic fracture [68].
However, 1 year functional outcomes were not substantially different [68].
As mentioned above, failure of fixation in intertrochanteric fractures increases
superior femoral head arthrosis via coxa vara. Arthroplasty is a salvage option for
the treatment of PTOA in this population as well. Compared to intertrochanteric
fractures undergoing primary arthroplasty due to fracture complexity or poor bone
quality, conversion arthroplasty resulted in significantly higher blood loss, operative
time, and risk of postoperative periprosthetic fracture. However, 1 year mortality
rates were not significantly different [69].
Hip Arthrodesis
Due to the above failure rate, and prospect of multiple revisions in young patients,
alternatives to arthroplasty including arthrodesis have been employed. Patients con-
sidered for this procedure include those with monoarticular disease, high functional
demand, and absence of lumbar or ipsilateral knee pathology [70]. Arthrodesis
allows for preservation of bone stock and gluteal musculature and affords the patient
satisfactory clinical outcomes while awaiting arthroplasty at a more age-appropriate
time [70]. While no studies are available specifically addressing postfracture
arthrodesis conversion to arthroplasty, one recent study evaluated 18 patients under-
going the aforementioned procedure. Eight of the 18 patients initially had arthrod-
esis for fracture. Patients undergoing conversion of previous arthrodesis to THA
have substantial clinical improvement but also have increased incidence of neuro-
logic injury and heterotopic ossification and tend to require use of ambulatory aids
over long distances [71].
9 Post-traumatic Arthritis of the Proximal Femur 147
Conclusion
PTOA is a common sequelae following proximal femur injury. Initial forces result
in chondral injury that is exacerbated by chronic changes in underlying bony sup-
port, which increases chondral contact pressures. Fortunately, advances in vascular-
preserving approaches and an emphasis on prompt treatment of proximal femur
fractures have improved long-term outcomes following these injuries. Given the
number of treatment options with strong outcomes in the literature, the optimal
treatment of symptomatic proximal femur PTOA is patient specific and ranges from
osteotomy to arthroplasty to arthrodesis. With data demonstrating increasingly
robust outcomes in PTOA hip arthroscopy, this surgical technique remains on the
forefront of new treatment options and will continue to have an expanding role in
the diagnosis and treatment of proximal femur PTOA.
References
12. Kekatpure A, Ahn T, Lee SJ, Jeong MY, Chang JS, Yoon PW. Arthroscopic reduction and
internal fixation for Pipkin Type I femoral head fracture: technical note. Arthrosc Tech.
2016;5(5):e997–e1000. [Link]
13. Kim K, Park S, Kim Y. Disc height and segmental motion as risk factors for recurrent lumbar
disc herniation. Spine (Phila Pa 1976). 2009;34(24):2674–8.
14. Park KS, Lee KB, Na BR, Yoon TR. Clinical and radiographic outcomes of femoral head frac-
tures: excision vs. fixation of fragment in Pipkin type I: what is the optimal choice for femoral
head fracture? J Orthop Sci. 2015;20(4):702–7. [Link]
15. Ganz R, Gill TJ, Gautier E, Ganz K, Krügel N, Berlemann U. Surgical dislocation of the adult hip.
J Bone Joint Surg [Br]. 2001;83(8):1119–24. [Link]
16. Masse A, Aprato A, Alluto C, Favuto M, Ganz R. Surgical hip dislocation is a reliable approach
for treatment of femoral head fractures. Clin Orthop Relat Res. 2015;473:3744–51. [Link]
org/10.1007/s11999-015-4352-4.
17. Yu Y-H, Hsu Y-H, Chou Y-C, Tseng I-C, Su C-Y, Wu C-C. Surgical treatment for Pipkin type
IV femoral head fracture: an alternative surgical approach via a modified Gibson approach in
nine patients. 2017;25(1):1–6. [Link]
18. Nikolopoulos K, Papadakis S, Kateros K, et al. Long-term outcome of patients with avascular
necrosis, after internal fixation of femoral neck fractures. Injury. 2003;34(7):525–8. https://
[Link]/10.1016/S0020-1383(02)00367-4.
19. Min B, Lee K, Bae K, Lee S, Lee S, Choi J. Result of internal fixation for stable femoral neck
fractures in elderly patients. Hip Pelvis. 2016;28(1):43–8.
20. Chen W-C, Yu S-W, Tseng I-C, Su J-Y, Tu Y-K, Chen W-J. Treatment of undisplaced femoral
neck fractures in the elderly. J Trauma. 2005;58(5):1035–1039; discussion 1039. [Link]
org/10.1097/[Link].0000169292.83048.17.
21. Kain MS, Marcantonio AJ, Iorio R. Revision surgery occurs frequently after percutane-
ous fixation of stable femoral neck fractures in elderly patients. Clin Orthop Relat Res.
2014;472(12):4010–4. [Link]
22. Clement ND, Green K, Murray N, Duckworth AD, McQueen MM, Court-Brown
CM. Undisplaced intracapsular hip fractures in the elderly: predicting fixation failure and
mortality. A prospective study of 162 patients. J Orthop Sci. 2013;18(4):578–85. [Link]
org/10.1007/s00776-013-0400-7.
23. Seo J, Shin S, Jun S, Cho C, Lim BH. The early result of cementless arthroplasty for femur
neck fracture in elderly patients with severe osteoporosis. Hip Pelvis. 2014;26(4):256–62.
24. Kim Y, Lee J, Song J, Oh S. The result of in situ pinning for valgus impacted femoral neck
fractures of patients over 70 years old. Hip Pelvis. 2014;26(4):263–8.
25. Slobogean GP, Sprague SA, Scott T, Bhandari M. Complications following young femoral
neck fractures. Injury. 2015;46(3):484–91. [Link]
26. Jo S, Lee SH, Lee HJ. The correlation between the fracture types and the complications after
internal fixation of the femoral neck fractures. Hip Pelvis. 2016;28(1):35–42. [Link]
org/10.5371/hp.2016.28.1.35.
27. Kang JS, Moon KH, Shin JS, Shin EH. Clinical results of internal fixation of subcapital femo-
ral neck fractures. Clin Orthop Surg. 2016;8:146–52.
28. Do LND, Marstein T, Foss OA, Basso T. Reoperations and mortality in 383 patients oper-
ated with parallel screws for Garden I-II femoral neck fractures with up to ten years. Injury.
2016;47(12):2739–42. [Link]
29. Liporace F, Gaines R, Collinge C, Gj H. Results of internal fixation of Pauwels type-3 ver-
tical femoral neck fractures. J Bone Joint Surg. 2008;90:1654–9. [Link]
JBJS.G.01353.
30. Stoffel K, Zderic I, Gras F, et al. Biomechanical evaluation of the femoral neck system in
unstable Pauwels III Femoral neck fractures: a comparison with the dynamic hip screw
and cannulated screws. J Orthop Trauma. 2017;31(3):131–7. [Link]
BOT.0000000000000739.
9 Post-traumatic Arthritis of the Proximal Femur 149
31. Slobogean GP, Stockton DJ, Zeng B, Wang D, Ma B, Pollak AN. Femoral neck shortening in
adult patients under the age of 55 years is associated with worse functional outcomes : analysis
of the prospective multi-center study of hip fracture outcomes in China. Injury. 2017; https://
[Link]/10.1016/[Link].2017.06.013.
32. Luo D, Zou W, He Y, et al. Modi fi ed dynamic hip screw loaded with autologous bone graft for
treating Pauwels type-3 vertical femoral neck fractures. Injury. 2017;48(7):1579–83. https://
[Link]/10.1016/[Link].2017.05.031.
33. MavrogenisAF, Panagopoulos GN, Megaloikonomos PD, et al. Complications after hip nailing for
fractures. Orthopedics. 2016;39(1):e108–16. [Link]
34. Dhammi I, Singh A, Mishra P, Jain A, Rehan-Ul-Haq, Jain S. Primary nonunion of intertro-
chanteric fractures of femur: analysis of results of valgization and bone grafting. Indian J
Orthop. 2011;45(6):514. [Link]
35. Lam SW, Teraa M, Leenen LPH, Van Der Heijden GJMG. Systematic review shows lowered
risk of nonunion after reamed nailing in patients with closed tibial shaft fractures. Injury.
2010;41(7):671–5. [Link]
36. Griffin XL, Costa ML, Parsons N, Smith N. Electromagnetic field stimulation for treating
delayed union or non-union of long bone fractures in adults. Cochrane Database Syst Rev.
2011;4:CD008471. [Link]
37. Bhandari M, Guyatt G, Tornetta P, et al. Study to prospectively evaluate reamed intramed-
ullary nails in patients with tibial fractures (S.P.R.I.N.T.): study rationale and design. BMC
Musculoskelet Disord. 2008;9:91. [Link]
38. McKellop HA, Sigholm G, Redfern FC, Doyle B, Sarmiento A, Luck JV Sr. The effect of
simulated fracture-angulations of the tibia on cartilage pressures in the knee joint. J Bone Joint
Surg Am. 1991;73(9):1382–91. [Link]
&db=PubMed&dopt=Citation&list_uids=1918121.
39. Bojan AJ, Beimel C, Taglang G, Collin D, Ekholm C, Jönsson A. Critical factors in cut-out
complication after gamma nail treatment of proximal femoral fractures. BMC Musculoskelet
Disord. 2013;14:1. [Link]
40. Bojan AJ, Beimel C, Speitling A, Taglang G, Ekholm C, Jönsson A. 3066 consecutive Gamma
Nails. 12 years experience at a single centre. BMC Musculoskelet Disord. 2010;11:133–43.
[Link]
41. Baumgaertner MR, Solberg BD. Awareness of tip-apex distance reduces failure of fixation
of trochanteric fractures of the hip. J Bone Joint Surg Br. 1997;79(6):969–71. [Link]
org/10.1302/0301-620x.79b6.7949.
42. Khurana S, Nobel TB, Merkow JS, Walsh M, Egol KA. Total hip arthroplasty for posttrau-
matic osteoarthritis of the hip fares worse than THA for primary osteoarthritis. Am J Orthop.
2015;44:321.
43. Viswanath A, Khanduja V. Can hip arthroscopy in the presence of arthritis delay the need for
hip arthroplasty? J Hip Preserv Surg. 2017;4(1):3–8. [Link]
44. Kemp JL, MacDonald D, Collins NJ, Hatton AL, Crossley KM. Hip arthroscopy in the setting
of hip osteoarthritis: systematic review of outcomes and progression to hip arthroplasty. Clin
Orthop Relat Res. 2014;473(3):1055–73. [Link]
45. Domb BG, Gui C, Lodhia P. How much arthritis is too much for hip arthroscopy: a systematic
review. Arthroscopy. 2015;31(3):520–9. [Link]
46. Haviv B, O’Donnell J. The incidence of total hip arthroplasty after hip arthroscopy in
osteoarthritic patients. Sport Med Arthrosc Rehabil Ther Technol. 2010;2:18. [Link]
org/10.1186/1758-2555-2-18.
47. Daivajna S, Bajwa A, Villar R. Outcome of arthroscopy in patients with advanced osteoarthri-
tis of the hip. PLoS One. 2015;10(1):1–6. [Link]
48. Mullis BH, Dahners LE. Hip arthroscopy to remove loose bodies after traumatic dislocation. J
Orthop Trauma. 2006;20(1):22–6. [Link]
150 R. M. Amin et al.
49. Hwang JT, Lee WY, Kang C, Hwang DS, Kim DY, Zheng L. Usefulness of arthroscopic
treatment of painful hip after acetabular fracture or hip dislocation. CiOS Clin Orthop Surg.
2015;7(4):443–8. [Link]
50. Byrd JWT, Jones KS. Prospective analysis of hip arthroscopy with 2-year follow-up.
Arthroscopy. 2000;16(6):578–87. [Link]
51. Ahmadpoor P, Reisi S, Makhdoomi K, Ghafari A, Sepehrvand N, Rahimi E. Osteoporosis
and related risk factors in renal transplant recipients. Tranplantation Proc. 2009;41(7):2820–2.
[Link]
52. Makhni EC, Stone AV, Ukwuani GC, Zuke W, Garabekyan T, Mei-dan O. A critical review man-
agement and surgical options for articular defects in the hip. Clin Sport Med. 2017;36:573–86.
[Link]
53. Trask DJ, Keene JS. Analysis of the current indications for microfracture of chon-
dral lesions in the hip joint. Am J Sports Med. 2016;44(12):3070–6. [Link]
org/10.1177/0363546516655141.
54. Domb BG, Gupta A, Dunne KF, Gui C, Chandrasekaran S. Microfracture in the hip results of a
matched-cohort controlled study with 2-year follow-up. Am J Sports Med. 2015;43(8):1865–74.
[Link]
55. Varghese VD, Livingston A, Boopalan PR, Jepegnanam TS. Valgus osteotomy for non-
union and neglected neck of femur fractures. World J Orthop. 2016;7(5):301–7. [Link]
org/10.5312/wjo.v7.i5.301.
56. Gupta S, Kukreja S, Singh V. Valgus osteotomy and repositioning and fixation with a dynamic
hip screw and a 135o single-angled barrel plate for un-united and neglected femoral neck frac-
tures. J Orthop Surg. 2014;22(1):20–4.
57. Rajagopa M, Samora JB, Ellis TJ. Efficacy of core decompression as treatment for osteone-
crosis of the hip: a systematic review. Hip Int. 2012;22(5):489–93. [Link]
HIP.2012.9748.
58. Fairbank AC, Bhatia D, Jinnah RH, Hungerford DS. Long-term results of core decompression
for ischaemic necrosis of the femoral head. J Bone Joint Surg Br. 1995;77(1):42–9. http://
[Link]/pubmed/7822394
59. Powell ET, Lanzer WL, Mankey MG. Core decompression for early osteonecrosis of the hip in
high risk patients. Clin Orthop Relat Res. 1997;335:181.
60. Ye CY, Liu A, Xu MY, Nonso NS, He RX. Arthroplasty versus internal fixation for dis-
placed intracapsular femoral neck fracture in the elderly: systematic review and meta -
analysis of short - and long - term effectiveness. Chin Med J. 2016;129(21) [Link]
org/10.4103/0366-6999.192788.
61. Evidence-based clinical practice guideline: management of hip fracture in the elderly; 2014.
62. Ullmark G. Femoral head fractures: Hemiarthroplasty or total hip arthroplasty? Hip Int.
2014;24(1):S12–4. [Link]
63. SooHoo NF, Farng E, Chambers L, Znigmond DS, Lieberman JR. Comparison of complica-
tion rates between hemiarthroplasty and total hip arthroplasty for intracapsular hip fractures.
Orthopedics. 2013;36(4):e384–9. [Link]
64. Roberts KC, Brox WT, Jevsevar DS, Sevarino K. Management of hip fractures in the elderly.
J Am Acad Orthop Surg. 2015;23(2):131–7. [Link]
65. Langslet E, Frihagen F, Opland V, Madsen JE, Nordsletten L, Figved W. Cemented ver-
sus uncemented hemiarthroplasty for displaced femoral neck fractures: 5-year followup of
a randomized trial. Clin Orthop Relat Res. 2014;472(4):1291–9. [Link]
s11999-013-3308-9.
66. Swart E, Roulette P, Leas D, Bozic KJ, Karunakar M. ORIF or arthroplasty for displaced
femoral neck fractures in patients younger than 65 years old: an economic decision analysis. J
Bone Joint Surg Am. 2017;99(1):65–75. [Link]
67. Clarke-Jenssen J, Roise O, Storeggen SAO, Madsen JE. Long-term survival and risk factors
for failure of the native hip joint after operatively treated displaced acetabular fractures. Bone
Joint J. 2017;99(B):834–40. [Link]
9 Post-traumatic Arthritis of the Proximal Femur 151
68. Mahmoud SSS, Pearse EO, Smith TO, Hing CB. Outcomes of total hip arthroplasty , as a
salvage procedure , following failed internal fixation of intracapsular fractures of the femoral
neck. Bone Joint J. 2016;98(B):452–60. [Link]
69. Lee Y, Kim JT, Alkitaini AA, Kim K, Ha Y, Koo K. Conversion hip arthroplasty in failed
fixation of intertrochanteric fracture : a propensity score matching study. J Arthroplast.
2017;32(5):1593–8. [Link]
70. Beaulé PE, Matta JM, Mast JW. Hip arthrodesis: current indications and techniques. J Am
Acad Orthop Surg. 2002;10(4):249–58.
71. Aderinto J, Lulu OB, Backstein DJ, Safir O, Gross AE. Functional results and complications
following conversion of hip fusion to total hip replacement. J Bone Joint Surg Br. 2012;94(11
Suppl A):36–41. [Link]
Chapter 10
Post-traumatic Arthritis of the Distal
Femur
Karthikeyan Ponnusamy and Ajit Deshmukh
Key Points
• Distal femoral fracture nonunions are associated with a high burden of
posttraumatic arthritis.
• Surgical options include osteoarticular autograft and allograft, realignment
osteotomies, and unicompartmental or total knee arthroplasty.
• It is critical to restore the joint line in the treatment of posttraumatic arthri-
tis of the knee.
• Higher levels of constraint may be necessary in TKA for posttraumatic
arthritis.
Epidemiology
Adults sustain distal femur fractures at a rate of 4.5/100,000. Most of these fractures
occur in female patients (67% vs. 33% in males) [1]. The two predominant age
groups presenting with this injury are young adults who are involved in high-energy
mechanisms and elderly who are involved in low-energy falls.
As with any periarticular fracture there are concerns that a combination of initial
trauma to the articular cartilage and residual articular step-off or malalignment can
accelerate the development of arthritic changes in the joint. One systematic review
examined the impact of articular step-off for various joints. When they looked at
studies for the distal femur, they only identified rabbit models that demonstrated
K. Ponnusamy
Pinnacle Orthopaedics, Canton, GA, USA
A. Deshmukh (*)
Department of Orthopaedic Surgery, New York University, New York, NY, USA
e-mail: [Link]@[Link]
that as long as the step-off was smaller than the thickness of the articular cartilage,
there was sufficient remodeling. However, in cases of step-off greater than the thick-
ness of the articular cartilage and knee instability there could be rapid articular
degeneration [2]. Another consideration is that residual malalignment from femoral
malunion can alter joint loading and lead to degenerative changes. Kettelkamp et al.
examined the significance of knee malalignment following fracture malunion and
reported that degenerative knee changes developed at a range of 10–60 years after
the fracture with an average of 31.7 years [3].
There are only a limited number of trials with sufficient follow-up to ascertain the
clinical impact of posttraumatic arthritis from distal femoral fractures. One study by
Rademakers et al. reported outcomes at a mean of 14 years (range 5–25 years) and
found radiological evidence of moderate to severe osteoarthritis in 36% of patients,
but 72% of these patients had good to excellent functional outcome scores [4].
Comparable results were reported by Thomson et al. at an average of 80 months
follow-up, where 54% of patients had significant degenerative changes in the knee
and 32% had no radiographic arthritic changes. None of these patients had under-
gone a total knee arthroplasty by the last follow-up [5]. To summarize, patients who
have sustained a distal femoral fracture are at risk of developing radiological find-
ings of arthritic changes, but clinical follow-up to 14 years afterward suggests almost
three quarters of patients are not impaired by these findings. However, there remain
a quarter of patients with radiological findings of posttraumatic arthritis that have
more severe symptoms. Further follow-up is needed to determine if and when the
previously asymptomatic patients with arthritic changes will become symptomatic.
Most cases of distal femur fractures are treated surgically with the following
implants as possible options: blade plates, locking plates, condylar screws, and ret-
rograde intramedullary nails [6]. Current first-line management usually focuses on
locking plates and retrograde intramedullary nails. In patients with significant medi-
cal comorbidities and limited ambulatory status, nonoperative options of functional
bracing or casting can be considered.
Surgical treatment of distal femur fractures is usually successful, but the non-
union rate is reported to be 10%. Nonunions have been most commonly associated
with open fractures, comminution, bone loss, and infection. Monroy et al. compared
the results of revision ORIF for distal femur nonunions vs. ORIF for acute distal
femur fractures and found that there was statistically no difference in time to union
(mean of 7 months for nonunions vs. 5 months for acute fractures) and no statistical
difference in range of motion and clinical outcome scores [7]. Ebraheim et al. in
their systematic review on the subject of nonunions in distal femur fractures also
found that open fractures and bone loss were the most common factors, followed by
hardware failure and infection. After revision fixation of nonunions, 97% healed at
an average of 9.86 months. They found that metaphyseal comminution was the
10 Post-traumatic Arthritis of the Distal Femur 155
fracture pattern most associated with nonunion. When the initial fixation utilized
dynamic condylar screws and blade plates, there was a higher likelihood of non-
union than with locking plates. The most common fixation used for revisions was
fixed angle platting with cancellous bone autograft, and this approach was success-
ful in achieving union for 97.4% of patients at an average time of 7.8 months [6].
Patient Evaluation
Despite the generally successful results of the management of distal femur frac-
tures, there will continue to be a subset of patients who will continue to have knee
pain due to nonunion, posttraumatic arthritis, knee instability, or other etiologies. As
with any patient, evaluation needs to begin with the history. Key aspects of the his-
tory that need to be determined is history regarding the treatment and outcomes
from initial distal femur fracture management and time course of symptoms since
then. Any aspects suggestive of infection must be highlighted, such as requiring
antibiotics in the postoperative period, prolonged wound drainage, and repeat sur-
geries. Prior operative reports should be obtained if possible to identify the implant
and facilitate the removal of the implant if warranted. The physical exam should
focus on locating the prior surgical incisions, knee range of motion and ligamentous
stability, and patellar tracking. Imaging should begin with standing AP radiograph,
PA flexed, lateral, and sunrise views. Advanced cross-sectional imaging can be con-
sidered in cases of nonunion with CTs or localized articular injuries or ligamentous
damage with MRIs. Prior hardware may affect the quality of the cross-sectional
imaging, and specific metal suppression techniques should be considered.
autograft or allografts can be considered. Gross et al. have published on the use of
osteochondral allografts for both the distal femur and proximal tibia [10]. Their
distal femur allograft survival rate was 95% at 5 years and 85% at 10 years. With
an average of 10-year follow-up, they had 9 of 60 undergo subsequent total knee
arthroplasty [10]. As reported by Kettelkamp et al., [3] malalignment after femo-
ral fractures can lead to degenerative arthritic changes in the knee at an average of
30 years after initial injury. Consequently, realignment osteotomies can be a use-
ful tool when managing a young patient with knee pain subsequent to malunited
distal femoral fracture. Lustig et al. reported their experience of treating posttrau-
matic knee arthritis with osteotomy alone (femur, tibia, or both). They found that
with an average of 3.8 years of follow-up, two of six patients with an intraarticu-
lar malunion went on to a total knee arthroplasty. Whereas, the 22 patients who
had an extraarticular malunion did not have an arthroplasty during the time of
follow-up. In addition, they found that, in general, patients had improvements in
pain scores, but those with extraarticular malunion had the greatest improve-
ment [2, 3].
For end stage posttraumatic arthritis, the treatment of choice would be
TKA. However, for patients who undergo TKA for posttraumatic arthritis, it has
been reported that they have higher complication rates than primary TKA for osteo-
arthritis. They have a higher risk for revision surgery with a hazard ratio of 2.23 (CI
95% 1.69–2.88) and postoperative infection of 2.85 (1.97–3.98) [11]. These cases
are technically more demanding, but patients can have good outcomes if appropri-
ate limb alignment and implant positioning are achieved [12].
In the elderly and frail patient population, the 1-year mortality rate has been reported
to be 22% after sustaining a supracondylar femur fracture. This older study went on
to further report that 9% of patients needed an above-knee amputation at a later time
point due to loss of fracture reduction and/or infection [13]. Due to this suboptimal
outcome, over the last couple decades several case series on the use of primary TKA
or distal femoral replacement for distal femur fractures have been published. The
goal was that an immediate arthroplasty would allow immediate weight bearing and
allow patients to regain mobility faster with the theory that they will have fewer
complications.
One case series did not demonstrate any improvement in mortality rate and
reported a 1-year mortality rate of 30%. They did find a revision rate of 9.5% which
is better than reports of complication rates up to 25% for primary TKA for post-
traumatic osteoarthritis [14].
10 Post-traumatic Arthritis of the Distal Femur 157
Malviya et al. examined the use of acute primary TKA for periarticular distal
femur and proximal tibia fractures. They reported that 10 of the 11 distal femur
fractures were treated with a rotating hinge, and one was treated with a varus/valgus
constrained implant and that they had good clinical outcomes in their case series
[15]. Bettin et al. reported on 18 patients who had sustained comminuted intraar-
ticular, osteoporotic, arthritic fractures and were treated with cemented distal femo-
ral replacements. They had two patients who had complications with their implants
(one periprosthetic fracture and one deep infection). They reported that the patients
in their series were extremely or very satisfied with their outcomes but did not have
a comparison arm [16]. Rosen and Strauss reported their use of distal femur replace-
ments in a case series of 24 patients for distal femur fractures and found 71%
returned to their preoperative ambulation level [17].
As of now only one retrospective comparative study of ORIF with distal femur
replacement has been reported by Hart et al. They found that at 1-year follow-up all
the distal femur replacement patients were ambulating while 25% of the ORIF
patients were wheelchair bound, but this was not statistically significant. They
found comparable reoperation rates of 10% in the distal femur replacement group
and 11% in the ORIF group. The ORIF group had fractures healed at an average of
24 weeks but had a nonunion incidence of 18% [18]. Due to the relative rarity of
converting a distal femur ORIF to TKA, Bohm et al. suggested that ORIF should be
used in most acute fracture cases. However, for specific patient populations with
prior arthritis, not compliant with weight-bearing restrictions, and very comminuted
fractures, a primary arthroplasty could be considered [19].
One of the surgical considerations for treating acute fractures is that higher levels
of constraint such as a rotating hinge prosthesis may be necessary since there is a
higher likelihood that the collateral ligaments are compromised by the fracture. In
order to determine the joint line in a highly comminuted fracture, one method that
can be used in acute fractures is obtaining a temporary reduction with the use of an
external fixator or other methods. Alternatively, the joint line can be determined
relative to anatomic landmarks such as 1 cm proximal to the fibular head or 2.5 cm
distal to the femoral epicondyles (based on their reduced position). Sizing the femur
in an acute fracture may be difficult, and estimates based on the trials may be
needed. In addition, depending on the level of bone loss/comminution, augments,
wedges, sleeves, or cones may be needed [20].
When acute fractures with severe comminution of the condyles are treated with
arthroplasty, then a distal femoral replacement may be needed. Some of the techni-
cal challenges are to determine the length and rotation of the femur. This can be
accomplished by obtaining provisional reduction with traction and from there the
rotation can be determined based on the transepicondylar axis. Another consider-
ation is whether to press-fit or cement the stem. Given the likely poor bone quality,
the stem will likely need to be cemented [19]. Arthroplasty can be more challenging
in these cases but focusing on proper alignment, positioning, and fixation can lead
to good patient outcomes.
158 K. Ponnusamy and A. Deshmukh
When comparing posttraumatic arthritis to osteoarthritis for the etiology for TKA,
it has been reported that TKA takes about 30 minutes longer in the posttraumatic
case [21]. Extensor mechanism issues are a common source of difficulty in per-
forming these procedures. Lateral release was needed in 47% of TKAs reported by
Weiss et al. [12] and 46% for Papadopoulos et al. [22]. Other techniques that
needed to be used were quadriceps V-Y turndown, vastus medialis advancement,
LCL transfer, extensor mechanism realignment, and collateral ligament recon-
struction [12, 22].
One of the first considerations for performing a total knee arthroplasty is deter-
mining the level of constraint needed. The next step is determining the joint line and
component rotation. If the fracture has healed in appropriate alignment and rotation,
then standard techniques can be used. However, in cases of deformity or retained
hardware that would prevent or severely complicate intramedullary alignment,
patient-specific instrumentation, imageless hand-held navigation devices, or com-
puter navigation can be very helpful to establish the alignment.
For larger bony defects, structural allograft or metal augments can be used. Prior
hardware and whether it will interfere with the procedure needs to be considered,
and the prior hardware can be appropriately removed or retained [12].
Limb alignment needs to be evaluated and malalignment needs to be corrected
with intraarticular resections for an arthroplasty or staged/simultaneous osteot-
omy. If intraarticular resections would compromise the collateral ligaments in
order to obtain the necessary alignment correction, a distal femoral osteotomy
can be secured with a long-stem femoral component or staged with a plate and
screw construct. Bone graft can be placed at osteotomy and nonunion sites [12].
Papadopoulos et al. reported a case series of 48 TKA after distal femoral frac-
tures and found malunions greater than 10 degrees in the coronal plane or 15
degrees in the sagittal plane in 21 knees (44%). Of these with malunions, they
were able to correct 15 through intraarticular bony resections and 6 needed oste-
otomies [22].
a b
Fig. 10.1 (a–c) Preoperative lower extremity alignment and AP/lateral distal femur
a b
Fig. 10.3 (a) Intraoperative fluoroscopy picture after the osteotomy was performed; (b) change in
alignment after insertion of the bone graft wedge with provisional fixation
10 Post-traumatic Arthritis of the Distal Femur 161
Fig. 10.4 Postoperative
picture of the patient’s
lower extremity
a b
Fig. 10.7 (a, b) AP and lateral of his knee demonstrating the extraarticular deformity with
advanced osteoarthritis and significant coronal plane malunion
164 K. Ponnusamy and A. Deshmukh
Fig. 10.8 Preoperative
templating for
intraarticular correction of
deformity
Femoral rotation was determined by flexing the knee to 90 degrees and aligning the
femoral cutting block with the tibial cut. Preoperative templating determined that a
100 mm sleeve-stem length could be used on the femoral side without reaching the
site of malunion. A varus-valgus constrained implant was used, and a stable knee
was achieved with good patellar tracking (Figs. 10.9 and 10.10).
10 Post-traumatic Arthritis of the Distal Femur 165
a b
References
Key Points
• Although tibial plateau fractures are not rare, symptomatic posttraumatic
osteoarthritis is rather infrequent.
• Stepwise treatment algorithms should be followed, starting with activity
modification, weight loss and physiotherapy, followed by analgesic
medication.
• Existing literature concerning operative treatment options for posttrau-
matic osteoarthritis is mainly limited to small case series with little
evidence.
• Corrective osteotomies should be evaluated; if degenerative lesions are too
advanced, unicondylar or total knee replacement can ameliorate function.
Introduction
Fig. 11.1 60-year-old patient who sustained a stairway fall with concomitant ACL/PCL/MCL
rupture and a nondisplaced fracture of the medial compartment (tibia and femur condyle). The
patient presented after 5 months at our office; standard X-rays show a secondary OA mostly
involving the medial compartment with joint space narrowing and bone loss, along with ACL and
PCL laxity. (a) Initial MRI sagittal image: anterior and posterior cruciate rupture visible. (b) Long
axes (b1) and knee anterior-posterior (b2) after 5 months showing subluxation and OA of the
medial compartment with beginning tibial bone loss. (c) Stress X-rays: (c1) anterior and posterior
drawer and (c2) varus and valgus stress. (d) Postop X-rays after a primary PS TKA anteroposterior
(d1) and lateral (d2). The MCL and LCL were intact
170 S. Hirsiger et al.
b1 b2
c1
Fig. 11.1 (continued)
11 Post-traumatic Arthritis of the Proximal Tibia 171
c2
d1 d2
Fig. 11.1 (continued)
172 S. Hirsiger et al.
Osteotomies
Osteochondral Allografts
a1 a2 b
Fig. 11.2 46-year-old patient with a status post three motor vehicle accidents. At age 17 he sus-
tained an open fracture (unknown open grade) of the right femoral diaphysis, treated with trans-
tibial traction. At 18 he had an open fracture of the right tibia and fibula (unknown open grade) also
treated nonoperatively. At the age of 43 he sustained a new open fracture Gustilo II of the right tibia
and fibula, treated with intramedullary nail fixation despite the preexisting malunion. The fracture
healed uneventfully, and the nail was removed after 2 years. The patient presented with worsening
right knee pain 1 year later, corresponding to a symptomatic lateral OA with gait disturbance due
to a complex valgus deformity of the lower right leg (shortening 5 cm, recurvatum 17°, valgus 11°,
tibial slope 15°, external rotation 38°). Decision was made to perform a dual femoral and tibio-
fibula distraction osteotomy with computer-guided correction using multiplanar external fixator
for the tibia and distraction nail for the femur. (a) Long leg axis showing the different deformities
of the right side ap (a1) and sagittal plane (a2). (b) Long leg axis after corrective femoral osteot-
omy for a preexisting recurvatum malunion of 17°. A tibial osteotomy was made thereafter without
complete correction of the deformity. (c) Status post removal of hardware, femur ap (c1) and lat-
eral views (c2), tibia ap (c3), and lateral (c4) (d) Long leg axis (EOS) at 4 weeks after femoral
osteotomy (deflexion, slight varisation, and lengthening) with retrograde expandable nail, and
tibia/fibula osteotomy (varisation and translation and slight lengthening) and fixation with hexa-
pod. (e) Long leg axis (EOS) after removal of the hexapod at 3.5 months, ap (e1) and lateral (e2)
views. The whole axis has a slight residual valgus, the tibia has healed, and the callotaxis after
femoral osteotomy is partially consolidated. (f) Long leg axis after healing of the femoral callo-
taxis before nail removal. The patient is still suffering from lateral OA but correction of the axis
did improve the situation and arthroplasty has been delayed
176 S. Hirsiger et al.
c1 c2
c3 c4 d
Fig. 11.2 (continued)
11 Post-traumatic Arthritis of the Proximal Tibia 177
e1 e2 f
Fig. 11.2 (continued)
presence of combined secondary tibial and femoral deformities or soft tissue com-
promise [70], resulting in technically more demanding surgeries with extended
operative time [71], increased length of stay, and 30-day readmission [72]. Abdel
et al. reported a high rate of complications in TKA for posttraumatic OA (34%)
compared to primary OA, 90% occurring within the first 2 years [73]. Houdek et al.,
in a larger retrospective cohort from the same institution, reported an overall
revision-free survival of 78% at 15 and 20 years of follow-up with a significant risk
for revision in patient aged 60 or less as well as patients with an infection, hema-
toma, deep vein thrombosis, or pulmonary embolism following arthroplasty [74].
Objective and subjective outcomes rely on sparse literature on (obviously) relatively
small series, showing comparable KSS [73], Patient-Reported Outcome
Measurements (PROMs), and satisfaction [69, 75]. In the existing studies, implants
with different degrees of constraint have been used, from cruciate-retaining to hinge
models with or without tibial augments and a long stem [20, 75–77]. Indeed, the
type of prosthesis should be adapted to ligamentous stability, bone stock, and bone
quality [78].
178 S. Hirsiger et al.
Primary TKA in the acute setting has been proposed in selected cases of complex
fractures in osteoporotic bones of elderly patients; experiences are limited to small
case series, but the results are promising [77, 79–82]. Of importance, autonomy in
the elderly population is reduced after tibial plateau fractures even when TKA is
done in first intention [83]. Additionally, age is an independent risk factor for mor-
tality within 30 days after TKA [84].
Summary
Conflict of Interest All authors declare that they have no conflict of interest to disclose and have
not received external funding.
Bibliography
1. Bala A, Penrose CT, Seyler TM, Mather RC 3rd, Wellman SS, Bolognesi MP. Outcomes after
total knee arthroplasty for post-traumatic arthritis. Knee. 2015;22(6):630–9.
2. Court-Brown CM, Caesar B. Epidemiology of adult fractures: a review. Injury.
2006;37(8):691–7.
3. Albuquerque RP, Hara R, Prado J, Schiavo L, Giordano V, do Amaral NP. Epidemiological
study on tibial plateau fractures at a level I trauma center. Acta Ortop Bras. 2013;21(2):109–15.
4. Schatzker J, McBroom R, Bruce D. The tibial plateau fracture. The Toronto experience
1968–1975. Clin Orthop Relat Res. 1979;(138):94–104.
5. Müller ME, Nazarian S, Koch P, Schatzker J. The comprehensive classification of fractures of
long bones. Berlin: Springer Science & Business Media; 2012.
6. Honkonen SE. Indications for surgical treatment of tibial condyle fractures. Clin Orthop Relat
Res. 1994;302:199–205.
7. Giannoudis PV, Tzioupis C, Papathanassopoulos A, Obakponovwe O, Roberts C. Articular
step-off and risk of post-traumatic osteoarthritis. Evidence today. Injury. 2010;41(10):986–95.
8. Yang G, Zhai Q, Zhu Y, Sun H, Putnis S, Luo C. The incidence of posterior tibial plateau frac-
ture: an investigation of 525 fractures by using a CT-based classification system. Arch Orthop
Trauma Surg. 2013;133(7):929–34.
9. Chen HW, Chen CQ, Yi XH. Posterior tibial plateau fracture: a new treatment-oriented clas-
sification and surgical management. Int J Clin Exp Med. 2015;8(1):472–9.
10. Luo CF, Sun H, Zhang B, Zeng BF. Three-column fixation for complex tibial plateau fractures.
J Orthop Trauma. 2010;24(11):683–92.
11. Wang Y, Luo C, Zhu Y, Zhai Q, Zhan Y, Qiu W, et al. Updated three-column concept in surgi-
cal treatment for tibial plateau fractures – a prospective cohort study of 287 patients. Injury.
2016;47(7):1488–96.
12. Gardner MJ, Yacoubian S, Geller D, Suk M, Mintz D, Potter H, et al. The incidence of soft
tissue injury in operative tibial plateau fractures: a magnetic resonance imaging analysis of 103
patients. J Orthop Trauma. 2005;19(2):79–84.
13. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cru-
ciate ligament and meniscus injuries: osteoarthritis. Am J Sports Med. 2007;35(10):1756–69.
180 S. Hirsiger et al.
14. Keene GC, Bickerstaff D, Rae PJ, Paterson RS. The natural history of meniscal tears in ante-
rior cruciate ligament insufficiency. Am J Sports Med. 1993;21(5):672–9.
15. Louboutin H, Debarge R, Richou J, Selmi TA, Donell ST, Neyret P, et al. Osteoarthritis in patients
with anterior cruciate ligament rupture: a review of risk factors. Knee. 2009;16(4):239–44.
16. Delamarter RB, Hohl M, Hopp E Jr. Ligament injuries associated with tibial plateau fractures.
Clin Orthop Relat Res. 1990;250:226–33.
17. Abdel-Hamid MZ, Chang CH, Chan YS, Lo YP, Huang JW, Hsu KY, et al. Arthroscopic
evaluation of soft tissue injuries in tibial plateau fractures: retrospective analysis of 98 cases.
Arthroscopy. 2006;22(6):669–75.
18. Borrelli J Jr. Management of soft tissue injuries associated with tibial plateau fractures. J Knee
Surg. 2014;27(1):5–9.
19. Pape D, Hoffmann A, Gerich T, Van der Kerkhofe M, Weber M, Pape HC. Fractures of the knee
joint in the elderly: osteosynthesis versus joint replacement. Orthopade. 2014;43(4):365–73.
20. Wilkes RA, Thomas WG, Ruddle A. Fracture and nonunion of the proximal tibia below
an osteoarthritic knee: treatment by long stemmed total knee replacement. J Trauma.
1994;36(3):356–7.
21. Lotz MK, Kraus VB. New developments in osteoarthritis. Posttraumatic osteoarthritis: patho-
genesis and pharmacological treatment options. Arthritis Res Ther. 2010;12(3):211.
22. Manidakis N, Dosani A, Dimitriou R, Stengel D, Matthews S, Giannoudis P. Tibial pla-
teau fractures: functional outcome and incidence of osteoarthritis in 125 cases. Int Orthop.
2010;34(4):565–70.
23. Parkkinen M, Madanat R, Mustonen A, Koskinen SK, Paavola M, Lindahl J. Factors pre-
dicting the development of early osteoarthritis following lateral tibial plateau fractures: mid-
term clinical and radiographic outcomes of 73 operatively treated patients. Scand J Surg.
2014;103(4):256–62.
24. Wasserstein D, Henry P, Paterson JM, Kreder HJ, Jenkinson R. Risk of total knee arthroplasty
after operatively treated tibial plateau fracture: a matched-population-based cohort study. J
Bone Joint Surg Am. 2014;96(2):144–50.
25. Oladeji LO, Dreger TK, Pratte EL, Baumann CA, Stannard JP, Volgas DA, et al. Total knee
arthroplasty versus osteochondral allograft: prevalence and risk factors following Tibial pla-
teau fractures. J Knee Surg. 2019;32(4):380–6.
26. Rademakers MV, Kerkhoffs GM, Sierevelt IN, Raaymakers EL, Marti RK. Operative treat-
ment of 109 tibial plateau fractures: five- to 27-year follow-up results. J Orthop Trauma.
2007;21(1):5–10.
27. Lizaur-Utrilla A, Collados-Maestre I, Miralles-Munoz FA, Lopez-Prats FA. Total knee arthro-
plasty for osteoarthritis secondary to fracture of the tibial plateau. A prospective matched
cohort study. J Arthroplast. 2015;30(8):1328–32.
28. Mehin R, O’Brien P, Broekhuyse H, Blachut P, Guy P. Endstage arthritis following tibia pla-
teau fractures: average 10-year follow-up. Can J Surg. 2012;55(2):87–94.
29. Eagle S, Potter HG, Koff MF. Morphologic and quantitative magnetic resonance imaging
of knee articular cartilage for the assessment of post-traumatic osteoarthritis. J Orthop Res.
2017;35(3):412–23.
30. Bruyere O, Cooper C, Pelletier JP, Maheu E, Rannou F, Branco J, et al. A consensus statement
on the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis
(ESCEO) algorithm for the management of knee osteoarthritis-from evidence-based medicine
to the real-life setting. Semin Arthritis Rheum. 2016;45(4 Suppl):S3–11.
31. Towheed TE, Maxwell L, Judd MG, Catton M, Hochberg MC, Wells G. Acetaminophen for
osteoarthritis. Cochrane Database Syst Rev. 2006;1:CD004257.
32. Cepeda MS, Camargo F, Zea C, Valencia L. Tramadol for osteoarthritis: a systematic review
and metaanalysis. J Rheumatol. 2007;34(3):543–55.
33. Singh JA, Noorbaloochi S, MacDonald R, Maxwell LJ. Chondroitin for osteoarthritis.
Cochrane Database Syst Rev. 2015;1:CD005614.
11 Post-traumatic Arthritis of the Proximal Tibia 181
34. Juni P, Hari R, Rutjes AW, Fischer R, Silletta MG, Reichenbach S, et al. Intra-articular corti-
costeroid for knee osteoarthritis. Cochrane Database Syst Rev. 2015;10:CD005328.
35. Hunter DJ. Viscosupplementation for osteoarthritis of the knee. N Engl J Med.
2015;372(26):2570.
36. Delanois RE, Etcheson JI, Sodhi N, Henn RF, Gwam CU, George NE, et al. Biologic therapies
for the treatment of knee osteoarthritis. J Arthroplast. 2019;34(4):801–13.
37. Bennell KL, Hinman RS, Metcalf BR, Buchbinder R, McConnell J, McColl G, et al. Efficacy
of physiotherapy management of knee joint osteoarthritis: a randomised, double blind, placebo
controlled trial. Ann Rheum Dis. 2005;64(6):906–12.
38. Fransen M, McConnell S, Harmer AR, Van der Esch M, Simic M, Bennell KL. Exercise for
osteoarthritis of the knee: a Cochrane systematic review. Br J Sports Med. 2015;49(24):1554–7.
39. Salamh P, Cook C, Reiman MP, Sheets C. Treatment effectiveness and fidelity of manual therapy
to the knee: a systematic review and meta-analysis. Musculoskeletal Care. 2016;15(3):238–48.
40. Bartels EM, Juhl CB, Christensen R, Hagen KB, Danneskiold-Samsoe B, Dagfinrud H, et al.
Aquatic exercise for the treatment of knee and hip osteoarthritis. Cochrane Database Syst Rev.
2016;3:CD005523.
41. White DK, Keysor JJ, Neogi T, Felson DT, LaValley M, Gross KD, et al. When it hurts, a
positive attitude may help: association of positive affect with daily walking in knee osteoar-
thritis. Results from a multicenter longitudinal cohort study. Arthritis Care Res (Hoboken).
2012;64(9):1312–9.
42. Messier SP, Mihalko SL, Legault C, Miller GD, Nicklas BJ, DeVita P, et al. Effects of
intensive diet and exercise on knee joint loads, inflammation, and clinical outcomes among
overweight and obese adults with knee osteoarthritis: the IDEA randomized clinical trial.
JAMA. 2013;310(12):1263–73.
43. Timmins KA, Leech RD, Batt ME, Edwards KL. Running and knee osteoarthritis: a systematic
review and meta-analysis. Am J Sports Med. 2016;45(6):1447–57.
44. Mobasheri A, Beatt M. An update on the pathophysiology of osteoarthritis. Ann Phys Rehabil
Med. 2016;59(5–6):333–9.
45. Chakravarty EF, Hubert HB, Lingala VB, Zatarain E, Fries JF. Long distance running and knee
osteoarthritis. A prospective study. Am J Prev Med. 2008;35(2):133–8.
46. Christensen R, Bartels EM, Astrup A, Bliddal H. Effect of weight reduction in obese patients
diagnosed with knee osteoarthritis: a systematic review and meta-analysis. Ann Rheum Dis.
2007;66(4):433–9.
47. Lubbeke A, Finckh A, Puskas GJ, Suva D, Ladermann A, Bas S, et al. Do synovial leptin levels
correlate with pain in end stage arthritis? Int Orthop. 2013;37(10):2071–9.
48. Thorlund JB, Juhl CB, Roos EM, Lohmander LS. Arthroscopic surgery for degenera-
tive knee: systematic review and meta-analysis of benefits and harms. Br J Sports Med.
2015;49(19):1229–35.
49. Mehl J, Paul J, Feucht MJ, Bode G, Imhoff AB, Sudkamp NP, et al. ACL deficiency and varus
osteoarthritis: high tibial osteotomy alone or combined with ACL reconstruction? Arch Orthop
Trauma Surg. 2017;137(2):233–40.
50. Woodacre T, Ricketts M, Evans JT, Pavlou G, Schranz P, Hockings M, et al. Complications
associated with opening wedge high tibial osteotomy--a review of the literature and of 15 years
of experience. Knee. 2016;23(2):276–82.
51. Marti RK, Kerkhoffs GM, Rademakers MV. Correction of lateral tibial plateau depression and
valgus malunion of the proximal tibia. Oper Orthop Traumatol. 2007;19(1):101–13.
52. Kerkhoffs GM, Rademakers MV, Altena M, Marti RK. Combined intra-articular and varus
opening wedge osteotomy for lateral depression and valgus malunion of the proximal part of
the tibia. J Bone Joint Surg Am. 2008;90(6):1252–7.
53. Frosch KH, Krause M, Frings J, Drenck T, Akoto R, Muller G, et al. Posttraumatic deformi-
ties of the knee joint : intra-articular osteotomy after malreduction of tibial head fractures.
Unfallchirurg. 2016;119(10):859–76.
182 S. Hirsiger et al.
54. Hughes A, Parry M, Heidari N, Jackson M, Atkins R, Monsell F. Computer hexapod-
assisted orthopaedic surgery for the correction of tibial deformities. J Orthop Trauma.
2016;30(7):e256–61.
55. Pitta M, Esposito CI, Li Z, Lee YY, Wright TM, Padgett DE. Failure after modern total knee
arthroplasty: a prospective study of 18,065 knees. J Arthroplast. 2018;33(2):407–14.
56. Nuelle CW, Nuelle JA, Cook JL, Stannard JP. Patient factors, donor age, and graft storage
duration affect osteochondral allograft outcomes in knees with or without comorbidities. J
Knee Surg. 2017;30(2):179–84.
57. Gudas R, Gudaite A, Pocius A, Gudiene A, Cekanauskas E, Monastyreckiene E, et al. Ten-year
follow-up of a prospective, randomized clinical study of mosaic osteochondral autologous
transplantation versus microfracture for the treatment of osteochondral defects in the knee
joint of athletes. Am J Sports Med. 2012;40(11):2499–508.
58. Shasha N, Krywulak S, Backstein D, Pressman A, Gross AE. Long-term follow-up of fresh
tibial osteochondral allografts for failed tibial plateau fractures. J Bone Joint Surg Am.
2003;85-A(Suppl 2):33–9.
59. Holschen M, Lobenhoffer P. Complications of corrective osteotomies around the knee.
Orthopade. 2016;45(1):13–23.
60. Niinimaki T, Eskelinen A, Makela K, Ohtonen P, Puhto AP, Remes V. Unicompartmental knee
arthroplasty survivorship is lower than TKA survivorship: a 27-year Finnish registry study.
Clin Orthop Relat Res. 2014;472(5):1496–501.
61. Brown NM, Sheth NP, Davis K, Berend ME, Lombardi AV, Berend KR, et al. Total knee
arthroplasty has higher postoperative morbidity than unicompartmental knee arthroplasty: a
multicenter analysis. J Arthroplast. 2012;27(8 Suppl):86–90.
62. Hopper GP, Leach WJ. Participation in sporting activities following knee replacement: total
versus unicompartmental. Knee Surg Sports Traumatol Arthroscopy. 2008;16(10):973–9.
63. Siman H, Kamath AF, Carrillo N, Harmsen WS, Pagnano MW, Sierra RJ. Unicompartmental
knee arthroplasty vs total knee arthroplasty for medial compartment arthritis in patients
older than 75 years: comparable reoperation, revision, and complication rates. J Arthroplast.
2017;32(6):1792–7.
64. Lustig S, Parratte S, Magnussen RA, Argenson JN, Neyret P. Lateral unicompartmental knee
arthroplasty relieves pain and improves function in posttraumatic osteoarthritis. Clin Orthop
Relat Res. 2012;470(1):69–76.
65. Svard UC, Price AJ. Oxford medial unicompartmental knee arthroplasty. A survival analysis of
an independent series. J Bone Joint Surg. 2001;83(2):191–4.
66. Berger RA, Meneghini RM, Jacobs JJ, Sheinkop MB, Della Valle CJ, Rosenberg AG, et al.
Results of unicompartmental knee arthroplasty at a minimum of ten years of follow-up. J Bone
Joint Surg Am. 2005;87(5):999–1006.
67. Argenson JN, Parratte S, Bertani A, Flecher X, Aubaniac JM. Long-term results with a lateral
unicondylar replacement. Clin Orthop Relat Res. 2008;466(11):2686–93.
68. Sah AP, Scott RD. Lateral unicompartmental knee arthroplasty through a medial approach.
Study with an average five-year follow-up. J Bone Joint Surg Am. 2007;89(9):1948–54.
69. Weiss NG, Parvizi J, Hanssen AD, Trousdale RT, Lewallen DG. Total knee arthroplasty in
post-traumatic arthrosis of the knee. J Arthroplast. 2003;18(3 Suppl 1):23–6.
70. Shearer DW, Chow V, Bozic KJ, Liu J, Ries MD. The predictors of outcome in total knee
arthroplasty for post-traumatic arthritis. Knee. 2013;20(6):432–6.
71. Dexel J, Beyer F, Lutzner C, Kleber C, Lutzner J. TKA for posttraumatic osteoarthritis is more
complex and needs more surgical resources. Orthopedics. 2016;39(3 Suppl):S36–40.
72. Kester BS, Minhas SV, Vigdorchik JM, Schwarzkopf R. Total knee arthroplasty for posttrau-
matic osteoarthritis: is it time for a new classification? J Arthroplast. 2016;31(8):1649–53.. e1
73. Abdel MP, von Roth P, Cross WW, Berry DJ, Trousdale RT, Lewallen DG. Total knee
arthroplasty in patients with a prior tibial plateau fracture: a long-term report at 15 years. J
Arthroplast. 2015;30(12):2170–2.
11 Post-traumatic Arthritis of the Proximal Tibia 183
74. Houdek MT, Watts CD, Shannon SF, Wagner ER, Sems SA, Sierra RJ. Posttraumatic total
knee arthroplasty continues to have worse outcome than total knee arthroplasty for osteoarthri-
tis. J Arthroplast. 2016;31(1):118–23.
75. Scott CE, Davidson E, MacDonald DJ, White TO, Keating JF. Total knee arthroplasty follow-
ing tibial plateau fracture: a matched cohort study. Bone Joint J. 2015;97-B(4):532–8.
76. Lonner JH, Pedlow FX, Siliski JM. Total knee arthroplasty for post-traumatic arthrosis. J
Arthroplast. 1999;14(8):969–75.
77. Nau T, Pflegerl E, Erhart J, Vecsei V. Primary total knee arthroplasty for periarticular fractures.
J Arthroplast. 2003;18(8):968–71.
78. Bedi A, Haidukewych GJ. Management of the posttraumatic arthritic knee. J Am Acad Orthop
Surg. 2009;17(2):88–101.
79. Nourissat G, Hoffman E, Hemon C, Rillardon L, Guigui P, Sautet A. Total knee arthroplasty
for recent severe fracture of the proximal tibial epiphysis in the elderly subject. Rev Chir
Orthop Reparatrice Appar Mot. 2006;92(3):242–7.
80. Parratte S, Bonnevialle P, Pietu G, Saragaglia D, Cherrier B, Lafosse JM. Primary total knee
arthroplasty in the management of epiphyseal fracture around the knee. Orthop Traumatol
Surg Res. 2011;97(6 Suppl):S87–94.
81. Malviya A, Reed MR, Partington PF. Acute primary total knee arthroplasty for peri-articular
knee fractures in patients over 65 years of age. Injury. 2011;42(11):1368–71.
82. Vermeire J, Scheerlinck T. Early primary total knee replacement for complex proximal tibia
fractures in elderly and osteoarthritic patients. Acta Orthop Belg. 2010;76(6):785–93.
83. Boureau F, Benad K, Putman S, Dereudre G, Kern G, Chantelot C. Does primary total knee
arthroplasty for acute knee joint fracture maintain autonomy in the elderly? A retrospective
study of 21 cases. Orthop Traumatol Surg Res. 2015;101(8):947–51.
84. Belmont PJ Jr, Goodman GP, Waterman BR, Bader JO, Schoenfeld AJ. Thirty-day postopera-
tive complications and mortality following total knee arthroplasty: incidence and risk factors
among a national sample of 15,321 patients. J Bone Joint Surg Am. 2014;96(1):20–6.
85. Wu J, Ma L, Wu L, Jin Q. Wnt-beta-catenin signaling pathway inhibition by sclerostin
may protect against degradation in healthy but not osteoarthritic cartilage. Mol Med Rep.
2017;15(5):2423–32.
86. Bouaziz W, Funck-Brentano T, Lin H, Marty C, Ea HK, Hay E, et al. Loss of sclerostin pro-
motes osteoarthritis in mice via beta-catenin-dependent and -independent Wnt pathways.
Arthritis Res Ther. 2015;17:24.
Chapter 12
Post-traumatic Arthritis of the Ankle
Nigel N. Hsu and Lew Schon
Key Points
• The ankle joint is more susceptible to posttraumatic arthritis than the hip or
the knee joint.
• Ankle biomechanics play a major role in posttraumatic arthritis.
• Weight-bearing CT scans are new imaging modalities to help with the
diagnosis and management of posttraumatic ankle arthritis.
• The mainstay of surgical treatment is total ankle arthroplasty and ankle
arthrodesis.
Introduction
Posttraumatic osteoarthritis accounts for 12% of arthritis across all joints, which
represents 5.6 million people, and cost the US health care 3.06 billion dollars annu-
ally [1]. For the ankle joint, posttraumatic arthritis is the primary cause of arthritis
accounting for 70–79.5% of ankle arthritis [1, 2] compared to 1.6% in the hip and
9.8% in the knee. This variation is due to the mechanical, biochemical, and anatomi-
cal factors of the ankle. Although the prevalence of ankle osteoarthritis is about 9
times lower than that of the knee and hip [3], in 2010, approximately 4400 total ankle
replacements and 25,000 ankle fusions were performed in the United States [4].
Fifty percent of elderly patients have some form of arthrosis of the foot or ankle [5].
N. N. Hsu (*)
Department of Orthopaedic Surgery, Johns Hopkins University, Baltimore, MD, USA
e-mail: Nhsu4@[Link]
L. Schon
Department of Orthopaedic Surgery, Mercy Medical Center, Baltimore, MD, USA
Anatomy
Primary osteoarthritis of the ankle is less common compared to the knee and hip due
to its anatomy and biochemical factors. The bony anatomy of the ankle joint confers
a high degree of stability and congruence when the joint is loaded [6]. The bony
anatomy, ligaments, and joint capsule guide and restrain movement between the
talus and the mortise. There is minimal translation of the talus relative to the mortise
during normal motion due to the soft tissue around the ankle.
Although the ankle has a smaller area of contact between articular surfaces com-
pared to the hip and knee (350 mm2 at 500 N of load compared to 1100 mm2 for the
hip and 1120 mm2 for the knee) [7–9], the tensile fracture stress and tensile stiffness
of ankle articular cartilage deteriorate less rapidly with age than those of the hip
[10]. The articular cartilage of the ankle is 1–2 mm compared to the articular carti-
lage in the hip and knee, which is 3–6 mm [11, 12]. The metabolism of cartilage
degradation is also different between the ankle and that of the knee. The catabolic
cytokine interleukin-1 (IL-1) inhibits proteoglycan synthesis of chondrocytes more
in the knee than the ankle, and this is in part due to fewer IL-1 receptors in the ankle
articular chondrocyte [3].
The high peak contact stress from smaller contact area, the congruency of the
joint, and thinness of ankle articular cartilage make the ankle joint more susceptible
to posttraumatic osteoarthritis than the hip and knee. Injuries that damage the joint
congruency and articular cartilage lead to joint degeneration within 2 years of injury
[6]. Newer studies have found that posttraumatic osteoarthritis can occur after ankle
fracture despite anatomic reduction [13], and early inflammatory response could
lead to irreversible damage to the cartilage [14]. The synovial fluid analysis showed
that after intraarticular ankle fracture, there is a proinflammatory and extracellular
matrix degrading environment similar to that described in idiopathic osteoarthritis.
Specifically IL-6, IL-8, MMP-1, MMP-2, MMP-3, MMP-9, and MMP-10 were sig-
nificantly elevated compared to normal synovial fluid [15].
Epidemiology
Trauma and abnormal ankle biomechanics are the most common causes of degen-
erative changes [16]. Traumatic injuries of the ankle include malleolar fractures,
pilon fracture, talus fracture, fracture dislocations, osteochondritis dessicans, ankle
sprains, and instability. The most common causes of posttraumatic ankle arthritis
are rotational ankle fractures (37%), recurrent ankle instability (14.6%), and single
12 Post-traumatic Arthritis of the Ankle 187
sprain with continued pain (13.7%) [2]. The severity of ankle fractures is correlated
to the development of posttraumatic ankle arthritis. Lindsjo reported that the preva-
lence of ankle arthritis is 14% after ankle fractures and ranges from 4% in Weber A
to 33% in Weber C fractures [17]. Pilon fracture of the tibial plafond is a high-
energy injury that causes significant morbidity. Posttraumatic osteoarthritis after
pilon fracture is 26.6% [18]. Talus fracture is associated with both subtalar and tib-
iotalar posttraumatic osteoarthritis. The rate of arthritis after talar fracture is
47–97% [19].
Patient Evaluation
Conservative Treatment
Operative Treatment
a1 a2 a3
b1 b2 b3
Fig. 12.1 (a) Shows the preoperative AP, oblique, and lateral radiographs of a patient with bimal-
leolar ankle fracture who developed posttraumatic ankle arthritis with collapse of the talus and
valgus deformity. (b) Shows the postoperative AP, oblique, and lateral radiographs after treatment
with removal of hardware and ankle arthrodesis
metaanalysis of the available outcome studies in 2007 that included 852 patients
who underwent total ankle arthroplasty with second-generation implants and found
68% of excellent and good results [34]. The 5-year and 10-year implant survival
rates were 78% and 77% with 7% revision rate [34]. A multicenter prospective non-
randomized trial comparing Scandinavian Total Ankle Replacement (STAR) to
ankle fusion in 593 patients showed that by 24 months, TAA had better function and
equivalent pain relief as the fusion group [35]. Another multicenter prospective trail
in Canada comparing 281 TAA and 107 AA in 5.5 year follow-up reported similar
improvement in pain and function, but there was a higher major complication rate
(19% vs. 7%) and higher revision rate (17% vs. 7%) in ankles treated with TAA vs.
190 N. N. Hsu and L. Schon
a1 a2 a3
b1 b2 b3
Fig. 12.2 (a) Shows the preoperative AP, oblique, and lateral radiographs of a patient with a lat-
eral malleolar ankle fracture with syndesmosis injury status post ORIF and tightrope fixation who
developed posttraumatic ankle arthritis. (b) Shows the postoperative AP, oblique, and lateral radio-
graphs after treatment with transfibular total ankle arthroplasty
AA [36]. A new total ankle coinvented by the senior author was introduced in the
USA 4.5 years ago. The design allows for conservation of bone stock, coronal plane
orientation of the rails, porous tantalum surfaces, and highly crosslinked polyethyl-
ene. A fibular osteotomy is performed for full joint exposure with preservation of
the deep deltoid. This osteotomy allows for correction of sagittal and coronal plane
deformities. Of the 105 performed by the senior author, 80% had deformity correc-
tion of the tibia, talus, and fibula. Early results are promising with no fibular non-
union, malunion, or implant failure after 12 -months follow-up [37].
In patients with posttraumatic impingement syndrome, ankle arthroscopic
debridement can be considered [38]. Arnold reported 81% good or excellent
12 Post-traumatic Arthritis of the Ankle 191
b1 b2
Fig. 12.3 (a) Shows an intraoperative photograph of the fresh allograft of the talar dome and tibial
plafond prior to implantation. (b) Show AP and lateral postoperative radiographs of a patient with
posttraumatic ankle osteoarthritis treated with bipolar fresh total osteochondral allograft. Note the
small screw fixation in the tibia and talus
12 Post-traumatic Arthritis of the Ankle 193
a1 a2 a3
c1 c2 c3
Fig. 12.4 (a) Show the preoperative AP, oblique, and lateral radiographs of a patient with varus
deformity ankle arthritis treated with medial opening wedge osteotomy. (b) Shows the intraopera-
tive image of the medial ankle with an allograft wedge. (c) Show the postoperative AP, oblique, and
lateral radiographs demonstrating restored alignment
194 N. N. Hsu and L. Schon
a1 a2
b1 b2 b3
Fig. 12.5 (a) Shows the preoperative oblique and lateral radiographs of a young patient with post-
traumatic ankle arthritis. (b) Shows the postoperative AP, oblique, and lateral radiographs after
distraction arthroplasty with an external fixator that allows for ankle range of motion
Summary
References
1. Brown TD, Johnston RC, Saltzman CL, Marsh JL, Buckwalter JA. Posttraumatic osteoar-
thritis: a first estimate of incidence, prevalence, and burden of disease. J Orthop Trauma.
2006;20(10):739–44.
2. Saltzman CL, Salamon ML, Blanchard GM, et al. Epidemiology of ankle arthritis: report
of a consecutive series of 639 patients from a tertiary orthopaedic center. Iowa Orthop
J. 2005;25:44–6.
3. Huch K, Kuettner KE, Dieppe P. Osteoarthritis in ankle and knee joints. Semin Arthritis
Rheum. 1997;26(4):667–74.
4. Terrell RD, Montgomery SR, Pannell WC, et al. Comparison of practice patterns in total ankle
replacement and ankle fusion in the United States. Foot Ankle Int. 2013;34(11):1486–92.
LOE: This level IV cross-sectional study examined CPT codes for total ankle replacement and
ankle arthrodesis were searched through the PearlDiver Patient Record Database from 2004 to
2009 and found a 57% increase in total ankle replacement from 2004 to 2009.
5. Lawrence RC, Helmick CG, Arnett FC, et al. Estimates of the prevalence of arthritis and
selected musculoskeletal disorders in the United States. Arth Rheum. 1998;41(5):778–99.
6. Coughlin MJ, Saltzman CL, Mann RA. Mann’s surgery of the foot and ankle: expert consult-
online. Philadelphia: Elsevier Health Sciences; 2013.
7. Beaudoin AJ, Fiore SM, Krause WR, Adelaar RS. Effect of isolated talocalcaneal fusion on
contact in the ankle and talonavicular joints. Foot Ankle. 1991;12(1):19–25.
8. Brown TD, Shaw DT. In vitro contact stress distributions in the natural human hip. J Biomech.
1983;16:373–84.
9. Ihn JC, Kim SJ, Park IH. In vitro study of contact area and pressure distribution in the human
knee after partial and total meniscectomy. Int Orthop. 1993;17(4):214–8.
10. Kempson GE. Age-related changes in the tensile properties of human articular cartilage: a
comparative study between the femoral head of the hip joint and the talus of the ankle joint.
Biochim Biophys Acta. 1991;1075(3):223–30.
11. Ateshian GA, Soslowsky LJ, Mow VC. Quantitation of articular surface topography and carti-
lage thickness in knee joints using stereophotogrammetry. J Biomech. 1991;24(8):761–76.
12. Athanasiou KA, Niederauer GG, Schenck RC Jr. Biomechanical topography of human ankle
cartilage. Ann Biomed Eng. 1995;23(5):697–704.
13. Dirschl DR, Marsh JL, Buckwalter JA, et al. Articular fractures. J Am Acad Orthop Surg.
2004;12(6):416–23.
14. Catterall JB, Stabler TV, Flannery CR, Kraus VB. Changes in serum and synovial fluid bio-
markers after acute injury (NCT00332254). Arthritis Res Ther. 2010;12(6):R229.
15. Adams SB, Setton LA, Bell RD, et al. Inflammatory cytokines and matrix metalloproteinases
in the synovial fluid after intra-articular ankle fracture. Foot Ankle Int. 2015;36(11):1264–71.
LOE: This level V study examined inflammatory cytokines in synovial fluid of 21 patients
with an intra-articular ankle fracture. The contralateral ankle was used as matched control. The
synovial fluid exhibits a largely pro-inflammatory and extra-cellular matrix degrading environ-
ment similar to that described in idiopathic osteoarthritis.
16. Stauffer RN, Chao EYS, Brewster RC. Force and motion analysis of the normal, diseased, and
prosthetic ankle joint. Clin Orthop Relat Res. 1977;127:189–96.
17. Lindsjo U. Operative treatment of ankle fracture-dislocations. A follow-up study of 306/321
consecutive cases. Clin Orthop Relat Res. 1985;199:28–38.
18. Lomax A, Singh A, et al. Complications and early results after operative fixation of 68 pilon
fractures of the distal tibia. Scott Med J. 2015;60(2):79–84. This level IV study reviewed 68
closed pilon fractures retrospectively with mean follow up of 7.7 months and found 1.6% deep
infection rate, 6.3% wound breakdown, 7.8% nonunion and malunion, and 26.6% posttrau-
matic arthritis.
19. Daniels TR, Smith JW. Talar neck fractures. Foot Ankle. 1993;14(4):225–34.
196 N. N. Hsu and L. Schon
20. Mei-Dan O, Kish B, Shabat S, et al. Treatment of osteoarthritis of the ankle by intra-
articular injections of hyaluronic acid: a prospective study. J Am Podiatr Med Assoc.
2010;100(2):93–100.
21. Witteveen AG, Hofstad CJ, Kerkhoffs GM. Hyaluronic acid and other conservative treatment
options for osteoarthritis of the ankle. Cochrane Database Syst Rev. 2015;(10):Cd010643. This
level IV study reviewed six randomized controlled trials including 240 patients with ankle
osteoarthritis comparing hyaluronic acid to placebo and found insufficient data to conclude
whether there is benefit or harm for HA as treatment for ankle OA compared to placebo.
22. Angthong C, Khadsongkram A, Angthong W. Outcomes and quality of life after platelet-rich
plasma therapy in patients with recalcitrant hindfoot and ankle diseases: a preliminary report
of 12 patients. J Foot Ankle Surg. 2013;52(4):475–80. This study reviewed 12 patients with
hindfoot and ankle osteoarthritis treated with platelet-rich plasma and 16 month follow up.
Mean visual analog score was significantly greater than the pretreatment score and 33% of the
patients had unsatisfactory results.
23. Mei-Dan O, Carmont MR, Laver L, Mann G, Maffulli N, Nyska M. Platelet-rich plasma
or hyaluronate in the management of osteochondral lesions of the talus. Am J Sports Med.
2012;40(3):534–41. This level II randomized controlled trial had 32 patients aged 18 to 60
years were allocated to intra-articular injections of HA or PRP for OCLs of the talus and
followed for 28 weeks. The pain scores and functional scores for both groups improved for 6
months and PRP had significantly better outcome than HA.
24. Chahla J, Cinque ME, Shon JM, et al. Bone marrow aspirate concentrate for the treat-
ment of osteochondral lesions of the talus: a systematic review of outcomes. J Exp Orthop.
2016;3(1):33. This systematic review identified 47 studies on the outcomes of BMAC for the
treatment of chondral defect and osteoarthritis of the talus. There is paucity of long-term data
and high-level evidence supporting BMAC.
25. Mann RA, Rongstad KM. Arthrodesis of the ankle: a critical analysis. Foot Ankle Int.
1998;19(1):3–9.
26. Mann RA. Arthrodesis of the foot and ankle. In: Mann RA, Coughlin MJ, editors. Surgery of
the foot and ankle. St. Louis: CV Mosby; 1999. p. 651–69.
27. Buchner M, Sabo D. Ankle fusion attributable to posttraumatic arthrosis: a long-term followup
of 48 patients. Clin Orthop. 2003;406:155–64.
28. Coester LM, Saltzman CL, Leupold J, Pontarelli W. Long-term results following ankle
arthrodesis for post-traumatic arthritis. J Bone Joint Surg Am. 2001;83(2):219–28.
29. O’Brien TS, Hart TS, Shereff MJ, Stone J, Johnson J. Open versus arthroscopic ankle arthrod-
esis: a comparative study. Foot Ankle Int. 1999;20(6):368–74.
30. Winson IG, Robinson DE, Allen PE. Arthroscopic ankle arthrodesis. J Bone Joint Surg.
2005;87(3):343–7.
31. Kitaoka HB, Patzer GL. Clinical results of the Mayo total ankle arthroplasty. J Bone Joint Surg
Am. 1996;78(11):1658–64.
32. Easley ME, Vertullo CJ, Urban WC, Nunley JA. Total ankle arthroplasty. J Am Acad Orthop
Surg. 2002;10(3):157–67.
33. Pyevich MT, Saltzman CL, Callaghan JJ, Alvine FG. Total ankle arthroplasty: a unique design.
Two to twelve-year follow-up. J Bone Joint Surg Am. 1998;80(10):1410–20.
34. Haddad SL, Coetzee JC, Estok R, Fahrbach K, Banel D, Nalysnyk L. Intermediate and long-
term outcomes of total ankle arthroplasty and ankle arthrodesis. A systematic review of the
literature. J Bone Joint Surg. 2007;89(9):1899–905. LOE: 4.
35. Saltzman CL, Mann RA, Ahrens JE, et al. Prospective controlled trial of STAR total ankle
replacement versus ankle fusion: initial results. Foot Ankle Int. 2009;30(7):579–96.
36. Daniels TR, ASE Y, Penner M, et al. Intermediate-term results of total ankle replacement and
ankle arthrodesis: a COFAS multicenter study. J Bone Joint Surg Am. 2014;96(2):135–42.
This level IV study reviewed 321 patients in the Canadian Orthopaedic Foot and Ankle Society
Prospective Ankle Reconstruction Database treated with total ankle replacement or ankle
arthrodesis at a mean follow-up of 5.5 years. The major complication rate was 7% for arthrod-
12 Post-traumatic Arthritis of the Ankle 197
esis and 19% for ankle replacement. There were minimal differences in AOS and SF-36 scores
between the two groups at follow up.
37. Tan EW, Maccario C, Talusan PG, Schon LC. Early complications and secondary procedures
in transfibular total ankle replacement. Foot Ankle Int. 2016;37(8):835–41. This level IV study
reviewed 20 total ankle replacements aged 41 to 80 years with a mean follow-up of 18 months.
There was no fibular nonunion, delayed union, or implant failure.
38. Arnold H. Posttraumatic impingement syndrome of the ankle–indication and results of
arthroscopic therapy. Foot Ankle Surg. 2011;17(2):85–8. This level IV study reviewed 32
patients aged 16 to 65 years who underwent arthroscopic debridement for posttraumatic ankle
impingement. 26 patients had good or excellent results according to the West Point Ankle
Score, 5 patients rated fair result and 1 bad.
39. Rasmussen S, Hjorth JC. Arthroscopic treatment of impingement of the ankle reduces pain and
enhances function. Scand J Med Sci Sports. 2002;12(2):69–72.
40. Hahn DB, Aanstoos ME, Wilkins RM. Osteochondral lesions of the talus treated with fresh
talar allografts. Foot Ankle Int. 2010;31(4):277–82.
41. Giannini S, Buda R, Pagliazzi G, et al. Survivorship of bipolar fresh total osteochondral ankle
allograft. Foot Ankle Int. 2014;35(3):243–51. This level IV case series reviewed 26 patients
who underwent BFTOA with a mean follow-up of 40.9 months. AOFAS score improved sig-
nificantly from 26.6 to 77.8 and 6 failures occurred.
42. Bugbee WD, Khanna G, Cavallo M, McCauley JC, Gortz S, Brage ME. Bipolar fresh osteo-
chondral allografting of the tibiotalar joint. J Bone Joint Surg. 2013;95(5):426–32. This level
IV study reviewed 86 ankles that underwent BFTOA with a mean follow-up of 5.3 years in
young, active patients with tibiotalar arthritis. 29% of the ankle underwent graft-related reop-
erations. Graft surgical was 76% at 5 years and 44% at 10 years.
43. Hintermann B, Knupp M, Barg A. Supramalleolar osteotomies for the treatment of ankle
arthritis. J Am Acad Orthop Surg. 2016;24(7):424–32. This review article discussed supramal-
leolar osteotomy in patients with asymmetric valgus or varus ankle arthritis.
44. Takakura Y, Takaoka T, Tanaka Y, Yajima H, Tamai S. Results of opening-wedge osteotomy
for the treatment of a post-traumatic varus deformity of the ankle. J Bone Joint Surg Am.
1998;80(2):213–8.
45. Pagenstert G, Knupp M, Valderrabano V, Hintermann B. Realignment surgery for valgus ankle
osteoarthritis. Oper Orthop Traumatol. 2009;21(1):77–87.
46. Knupp M, Stufkens SA, Bolliger L, Barg A, Hintermann B. Classification and treatment
of supramalleolar deformities. Foot Ankle Int. 2011;32(11):1023–31. This level IV study
reviewed 92 patients who underwent supramalleolar osteotomy for asymmetric arthritis of the
ankle joint with a mean follow-up of 43 months and found significant improvement of clinical
scores with 10.6% converted to total ankle replacement or arthrodesis.
47. Paley D, Lamm BM, Purohit RM, Specht SC. Distraction arthroplasty of the ankle–how far
can you stretch the indications? Foot Ankle Clin. 2008;13(3):471–84, ix.
48. Tellisi N, Fragomen AT, Kleinman D, O’Malley MJ, Rozbruch SR. Joint preservation of the
osteoarthritic ankle using distraction arthroplasty. Foot Ankle Int. 2009;30(4):318–25.
49. Nguyen MP, Pedersen DR, Gao Y, Saltzman CL, Amendola A. Intermediate-term follow-
up after ankle distraction for treatment of end-stage osteoarthritis. J Bone Joint Surg Am.
2015;97(7):590–6. This level IV study reviewed 36 patients who underwent ankle distraction
surgery with a mean follow-up of 8.3 years. 45% had undergone either ankle arthrodesis or
total ankle arthroplasty. Positive predictors of ankle survival included a better AOS score at 2
years, older age at surgery and fixed distraction.
Chapter 13
Post-traumatic Arthritis of the Foot
Ram K. Alluri and Eric W. Tan
Key Points
• The most common traumatic orthopaedic injuries of the hindfoot and mid-
foot are calcaneus fractures and tarsometatarsal (TMT) fracture-
dislocations (Lisfranc injury), respectively.
• The hindfoot is structurally composed of the talus and calcaneus, and its
functionality is primarily dependent on motion through the talonavicular
and subtalar (talocalcaneal) joints.
• The Lisfranc complex is a major stabilizer of the midfoot and is composed
of the five metatarsal base articulations with the cuboid and cuneiforms.
• The mainstay for surgical treatment involves selective arthrodesis with the
goal of a creating a stable, functional, and painless plantigrade foot.
Introduction
Traumatic injuries of the foot are common after high-energy trauma, and second
only to hip, thigh, and knee injuries [1]. Although these injuries of the foot are typi-
cally not life threatening, they can result in significant long-term functional disabil-
ity, and in patients with multiple injuries, those with foot injuries have significantly
worse outcomes than matched patients without foot injuries [2]. Much of the dis-
ability sustained after traumatic injuries to the foot is due to acute and chronic post-
traumatic degenerative changes of the articular surfaces.
The most common traumatic orthopaedic injuries of the hindfoot and midfoot
are calcaneus fractures and tarsometatarsal (TMT) fracture-dislocations (Lisfranc
injury), respectively. Calcaneus fractures account for approximately 2% of all frac-
tures, and it is the most frequently fractured bone of the foot [3]. Fracture-dislocations
of the TMT joint are relatively uncommon, only accounting for 0.2% of all frac-
tures; [4] however, up to 20% of these TMT injuries are initially missed or misdiag-
nosed [5]. In both injuries, patients can develop symptomatic posttraumatic
osteoarthritis due to intraarticular fracture fragments, altered biomechanics result-
ing in pathologic force distribution, and direct articular surface damage. Previous
studies have demonstrated that chondrocyte injury and death can immediately occur
due to forceful impaction during the traumatic event [6].
In this chapter, we will discuss the relevant anatomy, evaluation, and manage-
ment of patients who sustain a calcaneus fracture or TMT fracture-dislocation and,
subsequently, develop posttraumatic osteoarthritis of the hindfoot or midfoot.
Anatomy and Biomechanics
Anatomy
The hindfoot is structurally composed of the talus and calcaneus, and its functional-
ity is primarily dependent on motion through the talonavicular and subtalar (talocal-
caneal) joints. The majority of hindfoot motion occurs through the talonavicular
joint with fusion of this joint resulting in 90% loss of subtalar motion. Conversely,
subtalar fusion only results in 26% loss of talonavicular motion [7]. The subtalar
joint is composed of two articulations. Anteriorly, the lip and sustentaculum of the
calcaneus rotate about the talar head; posteriorly, the posterior facet of the calcaneus
provides a surface for which the talus can glide upon. The spring ligament and the
proximal articular surface of the navicular bone augment the calcaneus to form a
complete socket stabilizing the talar head. Overall, the axis of the subtalar joint is
oblique due to the more medial anterior talocalcaneal articulation relative to the
posterior articulation.
The midfoot is composed of navicular, cuboid, and three cuneiform bones and
articulates proximally with the hindfoot and distally with the forefoot. Functionally,
the midfoot is often described in terms of medial, middle, and lateral columns. The
rigid medial and middle columns are composed of articulations between the first
metatarsal base and medial cuneiform, second metatarsal base and intermediate
cuneiform, and third metatarsal base and lateral cuneiform. The mobile lateral col-
umn consists of the cuboid and fourth and fifth metatarsal bases. There are 5–10
degrees of motion at the first TMT joint and minimal motion occurs at the second
and third TMT joints. The fourth and fifth TMT joints are most mobile, with 10–20
degrees of movement. The osseous stability of the midfoot is partly because of the
wedge shape of the metatarsal bases and cuneiforms resulting in a transverse arch,
13 Post-traumatic Arthritis of the Foot 201
or “Roman arch,” of the foot in the coronal plane. A second osseous stabilizer is
provided by recession of the second metatarsal base relative to the first and third
tarsometatarsal joints.
The Lisfranc complex is a major stabilizer of the midfoot and is composed of the
five metatarsal base articulations with the cuboid and cuneiforms. This complex is
stabilized by a combination of ligamentous attachments and a unique bony configu-
ration at the second metatarsal base. The dorsal ligaments are the weakest while the
interosseous and plantar ligaments are the strongest [8]. The specific Lisfranc liga-
ment stabilizes 1–2 intermetatarsal bases, attaching the second metatarsal base to
the medial cuneiform. While intermetatarsal ligaments are present between the sec-
ond, third, fourth, and fifth metatarsal bases, there is no intermetatarsal ligament
stabilizing the 1–2 metatarsal bases directly. Therefore, the integrity of the Lisfranc
ligament is critical for stability.
Altered Biomechanics
Fractures of the calcaneus can result in significant articular damage and progressive
hindfoot deformity resulting in a heel that is wide, flattened, and in varus (Figs. 13.1
and 13.2). Widening of the hindfoot may cause significant difficulty with shoe wear.
The varus deformity can cause lateral deviation of the peroneal tendons and sural
nerve compression [9]; severe varus deformity can cause symptomatic subfibular
impingement between the lateral wall of the calcaneus and distal fibula [9]. When
Fig. 13.1 Axial heel view and lateral radiographs of a simple, intraarticular calcaneal fracture
202 R. K. Alluri and E. W. Tan
Fig. 13.2 Axial heel view and lateral radiographs of a complex, intraarticular calceanal fracture
with significant intraarticular comminution and joint depression
the hindfoot assumes a pathological varus alignment, the transverse tarsal joint
remains locked, resulting in subsequent degeneration of the adjacent midfoot joints
due to persistently increased loads during gait [9]. Hindfoot varus deformity can
also cause lateral column overloading of the midfoot. In addition to varus deformity,
loss of hindfoot height from depression of the posterior calcaneal facet can also
occur after calcaneal fractures [9]. This causes the talus to adopt a more dorsiflexed
position, which may result in anterior impingement of the talus on the anterior tibial
plafond [9]. Additionally, the lever arm of the Achilles tendon is reduced, which can
significantly alter normal gait patterns [9].
Traumatic injuries to the Lisfranc complex occur during torsion of the forefoot
and axial load transmission to the midfoot (Figs. 13.3 and 13.4). These injuries
result in direct articular damage and altered midfoot biomechanics due to instability
and resultant collapse of the longitudinal arch. The normal intact midfoot arch func-
tions as a lever, efficiently transmitting force from the forefoot to hindfoot, and loss
of this arch results in decreased mechanical efficiency [10]. This leads to abnormal
loading of the midfoot and adjacent joints, resulting in arthritic degeneration.
Commonly, patients develop a valgus deformity of the hindfoot, midfoot flattening
from the loss of the longitudinal arch, and forefoot abduction and dorsiflexion
because of pathologic changes in the peroneus brevis and posterior tibialis tendons,
respectively.
13 Post-traumatic Arthritis of the Foot 203
Fig. 13.3 Anteroposterior (AP), oblique, and lateral radiographs of a subtle Lisfranc injury with
mild diastasis between the medial cuneiform and the base of the second metatarsal that could be
missed during initial presentation
Fig. 13.4 Anteroposterior (AP), oblique, and lateral radiographs of a severe Lisfranc injury with
homolateral shift of the first through fifth tarsometatarsal joints
204 R. K. Alluri and E. W. Tan
During the acute injury, a calcaneus fracture can be treated operatively or nonopera-
tively; however, no definite consensus exists with regard to ideal treatment. Current
relative indications for operative management include large extraarticular fractures,
fractures with greater than 2 mm of intraarticular displacement, flattening of
Bohler’s angle and the angle of Gissane, varus malalignment of the tuberosity,
impending skin necrosis from displaced tongue-type fractures, and open fractures.
Relative nonoperative indications include anterior process fractures involving <25%
of the calcaneocuboid joint, fractures with preserved calcaneal height, nondisplaced
fractures, fractures with less than 2 mm of intraarticular displacement, or patients
with comorbidities (smoking, diabetes, vascular disease) placing them at increased
risk for postoperative complications [11].
Prior studies have stressed the importance of achieving an anatomic reduction to
prevent accelerated wear of the subtalar joint. Minimal displacement of 1–2 mm has
been shown to alter contact pressures of the subtalar joint and posterior facet, result-
ing in significant gait disturbance [12, 13]. Whether achieved through open or closed
reduction, anatomic reduction of calcaneal fractures attempts to recreate a congru-
ent subtalar joint, reduce the lateral wall, and take the hindfoot out of varus while
restoring calcaneal height. Therefore, most surgeons advocate initial operative man-
agement to achieve an anatomic reduction of the joint surface to potentially decrease
the incidence of subtalar osteoarthritis requiring secondary arthrodesis [14, 15].
Several prior studies have attempted to delineate the ideal management of dis-
placed intraarticular calcaneal fractures. In a study by Agren et al., surgical treat-
ment was associated with higher complications and similar functional outcomes at
1 year compared to nonoperative management [16]. Buckley et al. also found little
difference in SF-36 or VAS outcome scores between operatively and nonoperatively
treated calcaneus fractures [15]. However, the authors did note higher rates of even-
tual arthrodesis in patients who received initial nonoperative management [15].
Csizy et al. noted similar findings with a six times higher subtalar arthrodesis rate in
patients receiving initial nonoperative management [14].
Regardless of initial operative or nonoperative management, a high number of
patients who sustain calcaneal fractures with significant intraarticular involvement
will develop posttraumatic osteoarthritis [17]. The initial injury results in the dis-
placement of intraarticular fracture fragments and irreversible cartilage damage. In
a study by Radnay et al., 69 patients who sustained a calcaneal fracture requiring
eventual arthrodesis were reviewed [18]. Thirty-four (49%) underwent initial opera-
tive management, and 35 (51%) were treated initially nonoperatively [18]. Worse
functional outcomes after subtalar arthrodesis were noted in patients who were ini-
tially treated with nonoperative management [18]. Patients with initial nonoperative
management also had greater postoperative wound complications, potentially due to
greater restoration of calcaneal height resulting in postoperative tension along the
surgical wound [18].
13 Post-traumatic Arthritis of the Foot 205
Patient Evaluation
History
Physical Exam
The physical exam should consist of a gait assessment, range of motion measure-
ment, and careful inspection of ankle and foot alignment. Alignment should be
assessed with the patient standing as this best allows for examination of hindfoot
varus or valgus, medial arch height, and forefoot abduction. Patients should also be
asked to walk to assess for dynamic flatfoot deformity or subfibular impingement.
Abnormal alignment should be assessed for passive correctability, and in a patient
with unilateral injury, the contralateral, uninjured side can serve as a reliable con-
trol. In cases of severe deformity, the quality of the soft tissue and presence of ulcers
or impending skin breakdown should be assessed. Previous surgical scars should be
examined as they can dictate choice of surgical exposure. The dorsalis pedis and
posterior tibial pulses should be assessed; nonpalpable pulses may require a preop-
erative vascular consult. Lastly, the strength and sensation of the foot should also be
formally assessed and documented.
In patients with posttraumatic hindfoot deformity and osteoarthritis, the hindfoot
is often in varus and collapsed, and therefore evaluation for contractures of the
gastrocnemius-soleus complex and anterior ankle impingement is important.
Additionally, patients with posttraumatic hindfoot osteoarthritis may have a wid-
ened calcaneus that can cause skin breakdown over the lateral malleolus from con-
tact friction.
In patients with posttraumatic midfoot deformity and osteoarthritis, excessive
pronation and midfoot collapse may be noted secondary to loss of the longitudinal
arch and acquired forefoot abduction. These patients may have pain with palpa-
tion over the midfoot; however, the degree of arthrosis visualized on radiographs
may not correlate with symptoms found on physical examination. In most cases,
patients endorse greatest pain at the second TMT joint as this is the least mobile
joint of the midfoot and undergoes the greatest posttraumatic arthritic change. To
a lesser extent, they may endorse pain at the first and third TMT joints. Patients
with arthrosis of the lateral column may not endorse significant pain because of
the inherent mobility of this column. Stress testing of individual metatarsocunei-
form joints (the “piano key” test) may also help elicit pain across the affected
midfoot TMT joints as it places compression along the medial and lateral midfoot
[26]. A positive test will produce localized pain at the involved tarsometatarsal
joint. Additionally, the examiner may be able to aggravate posttraumatic midfoot
osteoarthritis symptoms by having the patient perform a single heel rise or stair
ascent as these activities require significant load transmission across the midfoot.
Lastly, dorsal osteophytes may cause difficulty with shoe wear, neuritis, or
tendonitis.
13 Post-traumatic Arthritis of the Foot 207
Imaging
a b
c d
Fig. 13.5 (a) Normal lateral radiograph of the foot. (b) Bohler’s angle. (c) Angle of Gissane. (d)
Meary’s angle. Normal values for the respective angles are listed within the image. The curved red
line demonstrates where the angle should be measured
208 R. K. Alluri and E. W. Tan
Nonoperative Management
Operative Management
Hindfoot
Fig. 13.6 Lateral
radiograph of an
intraarticular calcaneus
fracture that was initially
treated with open reduction
and internal fixation (upper
image). The patient
eventually developed
significant subtalar
posttraumatic
osteoarthritis.
Postoperative lateral
radiograph after removal of
hardware and in situ
subtalar arthrodesis (lower
image). (Images courtesy
of Dr. David E. Oji, MD)
210 R. K. Alluri and E. W. Tan
preserve the normal bone contour and subchondral bone. The exposed subchondral
bone is then meticulously prepared and perforated to improve blood flow. The sub-
talar joint is then aligned in approximately 0–5 degrees of valgus and fixed using
partially threaded 6.5 mm screws. It is important to obtain correct hindfoot position-
ing prior to arthrodesis to maximize functional outcomes. Residual bony deficits
can be filled with autologous bone graft, bone allograft, synthetic bone, or cancel-
lous chips.
Previous studies have demonstrated union rates ranging from 84% to 98% after
in situ arthrodesis on average 12 weeks after surgery [29, 30] and improvement in
functional outcomes after arthrodesis: [18, 31] the AOFAS hindfoot score can be as
high as 89 at final follow-up [32], and 93% of patients have good to fair outcomes
using the Angus and Cowell rating system [31]. Overall patient satisfaction can
range from 70% to 90% [33, 34]. The most common complication after this proce-
dure is wound infection, which has recently been shown to be as high as 18%,
especially in patients with an original open fracture or infection after the index
operation [30]. Other complications include neuromas and chronic regional pain
syndrome. Patients at higher risk for poorer functional outcomes include those ini-
tially treated nonoperatively, smokers, diabetics, and patients of advanced age [18,
35, 36].
In patients with loss of hindfoot height and symptomatic anterior tibial impinge-
ment, distraction bone-block subtalar arthrodesis is indicated (Fig. 13.7). An in situ
arthrodesis in these patients, even with lateral wall decompression, will not opti-
mize posttraumatic hindfoot function. The added distraction with a structural bone
graft and arthrodesis will reestablish the calcaneal height as well as the inclination
of the talus and normalize the gastrocnemius-soleus lever arm. Most commonly, the
subtalar joint is approached with a posterior or posterolateral incision for this pro-
cedure. Alternatively, a sinus tarsi incision may also be utilized. However, an exten-
sile lateral approach, commonly used for initial operative fixation of calcaneal
fractures, should be avoided due to concerns about wound healing after distraction,
particularly along the horizontal limb. After initial dissection through the soft tis-
sues, a lateral wall exostectomy may be performed; the bone can be used as bone
graft. The subtalar joint is then distracted using a large distractor or laminar spreader
to correct the calcaneal height and varus malalignment. The joint surfaces are then
prepared in a similar fashion to in situ subtalar arthrodesis. Next, the structural bone
graft is inserted into the distraction gap and the hindfoot is placed into 0–5 degrees
of valgus. Once aligned, the fusion may be secured using partially threaded 6.5 mm
screws placed from the posteroinferior aspect of the calcaneus into the talar dome.
Tricortical iliac crest bone autograft is the main choice for structural grafting.
However, structural allografts such as the femoral neck allograft and tricortical iliac
crest allograft are alternative options. Initial reports comparing structural allograft
to autograft demonstrated significantly lower union rates with allograft [37]; how-
ever, more recent studies report 92% union rates with allograft and favorable out-
comes [38]. Augmentation of structural graft with synthetic bone graft substitutes or
cancellous chips can be utilized at the surgeon’s discretion.
13 Post-traumatic Arthritis of the Foot 211
a b
c d
Fig. 13.7 (a, b) Axial heel view and lateral radiographs of an intraarticular calcaneus fracture
initially treated nonoperatively. The patient developed significant subtalar posttraumatic osteoar-
thritis with varus hindfoot alignment and anterior talar impingement due to loss of calcaneal
height. (c). Intraoperative fluoroscopic image demonstrating distraction of the subtalar joint using
a laminar spreader (d). Intraoperative fluoroscopic image after distraction bone-block arthrodesis
of the subtalar joint
Midfoot
a c
b d
Fig. 13.8 (a, b) Anteroposterior (AP) and lateral radiographs of a patient with a prior Lisfranc
injury who developed significant midfoot posttraumatic osteoarthritis. (c, d) Postoperative radio-
graphs after arthrodesis of the first, second, and third tarsometatarsal joints of the midfoot. (Images
courtesy of Dr. David E. Oji, MD)
lamina spreader can aid in restoring alignment and, occasionally, in more severe
deformities, a wedge resection across the midfoot may be necessary [28].
In addition, soft tissue procedures may be needed to fully correct the deformity.
In the presence of severe abduction deformity, lengthening or complete release of
the peroneus brevis tendon may be needed. The tendon can also be transferred to the
peroneus longus to help stabilize the medial column of the midfoot. Furthermore, in
the presence of equinus deformity, percutaneous lengthening of the Achilles tendon
or a Strayer gastrocnemius recession may be necessary.
After reestablishing alignment of the midfoot, residual bony deficits should be
filled with autologous bone graft, bone allograft, synthetic bone graft substitutes, or
cancellous chips. To stabilize the arthrodesis, multiple techniques are available
including use of Kirschner wires, staples, compression screws as well as dorsal,
medial, and plantar plates. There is no clear evidence indicating which construct
leads to the best clinical outcomes [10]. However, Marks et al. demonstrated that
midfoot fusions fixed with a plantarly applied plate result in superior biomechanical
stability compared to midfoot fusion constructs with screw fixation [43]. In most
cases, adequate stability can be achieved with partially threaded cancellous screws
214 R. K. Alluri and E. W. Tan
or cortical lag screws placed across each joint of the arthrodesis construct. In cases
of severe deformity, the addition of compression plates or plantar plate fixation will
add additional stability and should be considered.
The results of midfoot fusion for posttraumatic osteoarthritis after a TMT joint
fracture-dislocation are generally favorable. Union is achieved in greater than 90%
of patients with some studies demonstrating 98% union rates [44, 45]. Sangeorzan
et al. reported good to excellent results in 11 of 16 patients (69%), and 15 of 16
(94%) were satisfied with the procedure [46]. Mann et al. reported 93% patient
satisfaction following selective arthrodesis [44], and Johnson and Johnson reported
84% patient satisfaction [47]. AOFAS-midfoot scores can improve by up to 34
points with final scores ranging from 71 to 78 [48, 49]. Several studies have shown
that the quality of the initial reduction during the acute TMT fracture-dislocation
correlates with better outcomes after secondary midfoot arthrodesis [20, 46] while
workplace injuries and delay to treatment can negatively affect outcomes [46]. The
most common complications after midfoot fusion include superficial infections,
neuritis, and neuromas [44, 47, 48]. Nerve injuries are common in midfoot fusion
due to the anatomic location of the cutaneous nerves, particularly the deep peroneal
nerve, and the soft tissue retraction needed for adequate exposure and preparation
of the joint surfaces.
Similar to subtalar fusion of the hindfoot, concerns exist for adjacent joint degen-
erative changes after select midfoot fusion; however, no clinical studies exist that
have objectively evaluated this potential complication.
Conclusions
References
17. Flemister AS Jr, Infante AF, Sanders RW, Walling AK. Subtalar arthrodesis for complications
of intra-articular calcaneal fractures. Foot Ankle Int. 2000;21(5):392–9.
18. Radnay CS, Clare MP, Sanders RW. Subtalar fusion after displaced intra-articular calcaneal
fractures: does initial operative treatment matter? J Bone Joint Surg Am. 2009;91(3):541–6.
19. Watson TS, Shurnas PS, Denker J. Treatment of Lisfranc joint injury: current concepts. J Am
Acad Orthop Surg. 2010;18(12):718–28.
20. Myerson MS, Fisher RT, Burgess AR, Kenzora JE. Fracture dislocations of the tarsometatarsal
joints: end results correlated with pathology and treatment. Foot Ankle. 1986;6(5):225–42.
21. Dubois-Ferrière V, Lübbeke A, Chowdhary A, Stern R, Dominguez D, Assal M. Clinical out-
comes and development of symptomatic osteoarthritis 2 to 24 years after surgical treatment
of tarsometatarsal joint complex injuries. J Bone Joint Surg Am. 2016;98(9):713–20. A retro-
spective study of 61 patients who underwent operative management for TMT joint complex
injuries. 72.1% of patients had radiographic evidence of arthrosis but only 54.1% were symp-
tomatic. Risk factors for osteoarthritis included nonanatomic reduction and a history of smok-
ing. Level of Evidence: IV.
22. Kuo RS, Tejwani NC, Digiovanni CW, Holt SK, Benirschke SK, Hansen ST Jr, et al. Outcome
after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am.
2000;82(11):1609–18.
23. Philbin T, Rosenberg G, Sferra JJ. Complications of missed or untreated Lisfranc injuries. Foot
Ankle Clin. 2003;8(1):61–71.
24. Jeffreys TE. Lisfranc’s fracture-dislocation: a clinical and experimental study of tarso-
metatarsal dislocations and fracture-dislocations. J Bone Joint Surg Br. 1963;45:546–51.
25. Coetzee JC. Making sense of Lisfranc injuries. Foot Ankle Clin. 2008;13(4):695–704.
26. Keiserman LS, Cassandra J, Amis JA. The piano key test: a clinical sign for the identification
of subtle tarsometatarsal pathology. Foot Ankle Int. 2003;24(5):437–8.
27. Ågren PH, Tullberg T, Mukka S, Wretenberg P, Sayed-Noor AS. Post-traumatic in situ fusion
after calcaneal fractures: a retrospective study with 7-28 years follow-up. Foot Ankle Surg.
2015;21(1):56–9. A retrospective review of 29 patients who underwent in situ arthrodesis for
calcaneal malunion and subtalar arthritis. Patients with significant deformity who underwent
in situ arthrodesis without restoring hindfoot alignment generally had poor outcomes. Level of
Evidence: IV.
28. Thordarson DB. Fusion in posttraumatic foot and ankle reconstruction. J Am Acad Orthop
Surg. 2004;12(5):322–33.
29. Haskell A, Pfeiff C, Mann R. Subtalar joint arthrodesis using a single lag screw. Foot Ankle
Int. 2004;25(11):774–7.
30. Dingemans SA, Backes M, Goslings JC, de Jong VM, Luitse JS, Schepers T. Predictors of
nonunion and infectious complications in patients with posttraumatic subtalar arthrodesis. J
Orthop Trauma. 2016;30(10):e331–5. A retrospective study of 93 patients who underwent
subtalar arthrodesis. Patients at risk for complications included those who had an initial open
fracture or infection. Alcohol, nicotine, and drug abuse were not associated with a higher risk
for complications. Level of Evidence: IV.
31. Davies MB, Rosenfeld PF, Stavrou P, Saxby TS. A comprehensive review of subtalar arthrod-
esis. Foot Ankle Int. 2007;28(3):295–7.
32. Mann R, Beaman D, Horton GA. Isolated subtalar arthrodesis. Foot Ankle Int.
1998;19(8):511–9.
33. Dahm D, Kitaoka HB. Subtalar arthrodesis with internal compression for posttraumatic arthri-
tis. J Bone Joint Surg Br. 1998;80(1):134–8.
34. Sammarco GJ, Tablante EB. Subtalar arthrodesis. Clin Orthop Relat Res. 1998;349:73–80.
35. Chahal J, Stephen DJ, Bulmer B, Daniels T, Kreder HJ. Factors associated with outcome after
subtalar arthrodesis. J Orthop Trauma. 2006;20(8):555–61.
36. Easley ME, Trnka HJ, Schon LC, Myerson MS. Isolated subtalar arthrodesis. J Bone Joint
Surg Am. 2000;82(5):613–24.
13 Post-traumatic Arthritis of the Foot 217
37. Trnka HJ, Easley ME, Lam PW, Anderson CD, Schon LC, Myerson MS. Subtalar distraction
bone block arthrodesis. J Bone Joint Surg Br. 2001;83(6):849–54.
38. Myerson MS, Neufeld SK, Uribe J. Fresh-frozen structural allografts in the foot and ankle. J
Bone Joint Surg Am. 2005;87(1):113–20.
39. Rammelt S, Grass R, Zawadski T, Biewener A, Zwipp H. Foot function after subtalar distrac-
tion bone-block arthrodesis. A prospective study. J Bone Joint Surg Br. 2004;86(5):659–68.
40. Garras DN, Santangelo JR, Wang DW, Easley ME. Subtalar distraction arthrodesis using inter-
positional frozen structural allograft. Foot Ankle Int. 2008;29(6):561–7.
41. Bednarz PA, Beals TC, Manoli A 2nd. Subtalar distraction bone block fusion: an assessment
of outcome. Foot Ankle Int. 1997;18(12):785–91.
42. Burton DC, Olney BW, Horton GA. Late results of subtalar distraction fusion. Foot Ankle Int.
1998;19(4):197–202.
43. Marks RM, Parks BG, Schon LC. Midfoot fusion technique for neuroarthropathic feet: biome-
chanical analysis and rationale. Foot Ankle Int. 1998;19(8):507–10.
44. Mann RA, Prieskorn D, Sobel M. Midtarsal and tarsometatarsal arthrodesis for primary degener-
ative osteoarthrosis or osteoarthrosis after trauma. J Bone Joint Surg Am. 1996;78(9):1376–85.
45. Suh JS, Amendola A, Lee KB, Wasserman L, Saltzman CL. Dorsal modified calcaneal plate
for extensive midfoot arthrodesis. Foot Ankle Int. 2005;26(7):503–9.
46. Sangeorzan BJ, Veith RG, Hansen ST Jr. Salvage of Lisfranc’s tarsometatarsal joint by arthrod-
esis. Foot Ankle Int. 1990;10(4):193–200.
47. Johnson JE, Johnson KA. Dowel arthrodesis for degenerative arthritis of the tarsometatarsal
(Lisfranc) joints. Foot Ankle. 1986;6(5):243–53.
48. Komenda GA, Myerson MS, Biddinger KR. Results of arthrodesis of the tarsometatarsal joints
after traumatic injury. J Bone Joint Surg Am. 1996;78(11):1665–76.
49. Richter M, Wippermann B, Krettek C, Schratt HE, Hufner T, Therman H. Fractures and frac-
ture dislocations of the midfoot: occurrence, causes and longterm results. Foot Ankle Int.
2001;22(5):392–8.
Index
post-traumatic osteoarthritis M
acetabular fractures, 31 Malleolar fracture, 18
hip dislocations, 33 Mayo Elbow Performance Index
osteonecrosis, 33 (MEPI), 66
total direct cost, 35, 36 Medial opening wedge
total indirect cost, 36, 37 osteotomy, 191
Humeral resurfacing, 51 Medicare Severity Diagnosis-Related Groups
Hyaline cartilage, 21 (MS-DRGs), 38
Meniscal injuries, 27, 28
Mesenchymal stem cells (MSCs), 7
I Metacarpophalangeal (MCP) joint arthritis,
ICD-10 coding system, 37, 38 103, 104
Intercarpal and radiocarpal arthritis
management, 81–83
S4CF vs. PRC, 83, 85 N
scaphoid nonunion advanced collapse, 79 Non-inflammatory arthritis, 9
scapholunate advanced collapse, 78, 79
surgical technique, 88
total wrist arthrodesis, 86, 87 O
total wrist arthroplasty, 86 Osteoarthritic synovial system, 9
wrist denervation, 85, 86 Osteoarthritis (OA)
International osteoarthritis research society atypical locations, 16, 17
(IOARS), 172 pain and imaging findings, 21, 22
Interpositional arthroplasty, 66, 67 posttraumatic vs. idiopathic, 16
Intra-articular distal humerus fractures, 60 Osteocapsular debridement
Intra-articular fractures, 28, 32 arthroplasty, 63–66
Isolated intercarpal arthritis Osteochondral allografts (OCA), 173
lunotriquetral arthritis, 89, 90 Osteonecrosis, 33
pisotriquetral arthritis, 90, 91
scaphotrapeziotrapezoidal arthritis, 89
P
Parathyroid hormone (PTH), 10
J Patient-specific finite element stress
Joint space narrowing (JSN), 16, 19 analysis, 4
Pauwel III fractures, 139
Pipkin I fractures, 138
K Pipkin III fractures, 138
Knee Pipkin IV fractures, 136, 139
management Pisotriquetral arthritis, 90, 91
primary prevention, 28 Posttraumatic arthritis (PTOA)
secondary prevention, 29 arthroplasty, 143, 145, 146
tertiary prevention, 29, 30 core decompression, 145
post-traumatic osteoarthritis epidemiology, 135, 136
anterior cruciate ligament injury, 27 femoral head fracture, 138, 139
intra-articular fractures, 28, 32 femoral neck fracture, 139
meniscal injuries, 27, 28 hip arthrodesis, 146
total direct cost, 35, 36 hip arthroscopy, 143, 144
total indirect cost, 36, 37 hip dislocation, 138
hip preservation, 144
intertrochanteric fractures, 141, 142
L non-operative management, 143
Latency-associated peptide (LAP), 6 pathophysiology, 136, 137
Lunotriquetral arthritis, 89, 90 trochanteric fractures, 142
Lunotriquetral interosseous ligament (LTIL), 75 varus malunion, 145
222 Index
TGF-beta signaling plays a critical role in osteoblast differentiation by phosphorylating the PTH receptor, which integrates signals necessary for bone remodeling. This activation facilitates the osteoanabolic actions that contribute to bone formation as TGF-beta is integral to promoting alternative macrophage activation, creating a conducive environment for skeletal development .
Imaging modalities such as radiographs may be inadequate for diagnosing wrist arthritis post-trauma as they might not capture early subclinical cartilage lesions or small osteophyte formations. To improve diagnostic accuracy, clinicians should incorporate dynamic tests like the scaphoid shift test and consider advanced imaging, such as MRI, for detailed evaluation of soft tissue and cartilage status when radiographs are inconclusive .
Hip arthroscopy for joint preservation can offer temporary symptomatic relief and is minimally invasive compared to other interventions like arthroplasty. Long-term outcomes are limited, as significant chondral pathology often leads to arthroplasty within a few years. Thus, for lasting results in advanced cases, arthroscopy might be less effective than more definitive procedures like arthroplasty .
Synovial fluid cytokine profiles provide valuable insights into the inflammatory state of a joint with post-traumatic osteoarthritis, indicating active degradation and inflammation levels. Elevated pro-inflammatory cytokines suggest a more aggressive disease course, prompting early intervention strategies such as biologics to modulate inflammatory pathways and potentially slow disease progression .
PRP therapy for osteochondral lesions of the talus offers potential benefits such as improved pain scores and function over short-term periods, as evidenced by better outcomes compared to hyaluronic acid treatments. However, drawbacks include variability in patient response and a lack of long-term efficacy data, which suggests the need for cautious consideration of PRP as a treatment option .
Posterior tibial ligamentous instability after tibial plateau fractures can exacerbate joint misalignment and stress, promoting degenerative changes that lead to symptomatic osteoarthritis. Such instability increases joint motion irregularity, elevating risks of cartilage wear and joint surface incongruity, thereby hastening osteoarthritic progression .
CD109 acts as a TGF-beta co-receptor that promotes the internalization and degradation of TGF-beta receptors. By facilitating this process, CD109 modulates the intensity and duration of TGF-beta signaling, potentially attenuating prolonged inflammatory responses and facilitating tissue remodeling and homeostasis .
Arthroplasty offers the benefit of pain alleviation and function improvement in knee joints affected by post-traumatic osteoarthritis. However, it carries risks such as infection, complications from prior malalignment, and reduced prosthetic longevity, especially in younger patients. Factors influencing outcomes include patient age, comorbidities, and the degree of joint damage, which may lead to longer recovery times and higher revision rates .
Total ankle replacement and ankle arthrodesis offer distinct outcomes: ankle replacement generally allows for better functional preservation and range of motion, whereas arthrodesis provides stable pain relief at the expense of joint flexibility. Long-term, arthrodesis may result in adjacent joint degeneration due to altered mechanics, whereas replacement involves higher complication rates but preserves more natural biomechanical function albeit with prosthetic longevity concerns .
In ACL-deficient knees, synovial fluid cytokine concentrations can serve as prognostic indicators of joint inflammation and potential degeneration. Elevated cytokines may reflect ongoing inflammatory processes within the joint that could exacerbate cartilage degradation and accelerate osteoarthritic changes, complicating rehabilitation and the prognosis of knee joint health .