J Aaos -2008

Perspectives on Modern Orthopaedics

Recent Developments in the Biology of Fracture Repair

Francois N. K. Kwong, MD Mitchel B. Harris, MD

Perspectives on Modern Orthopaedics articles provide an objective appraisal of new or controversial techniques or areas of investigation in orthopaedic surgery. Dr. Kwong is Research Fellow, Center for Molecular Orthopaedics, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA. Dr. Harris is Associate Professor of Orthopaedic Surgery, Harvard Medical School, and Chief, Orthopaedic Trauma Service, Brigham and Women’s Hospital, Partners Orthopaedic Trauma Service, Boston, MA. None of the following authors or a member of their immediate families has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Kwong and Dr. Harris. Reprint requests: Dr. Kwong, Center for Molecular Orthopaedics, Room BLI 044, 221 Longwood Avenue, Boston, MA 02115. J Am Acad Orthop Surg 2008;16:619625 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

Volume 16, Number 11, November 2008

Abstract Fracture repair is dependent on local and systemic molecular and cellular processes. During fracture repair, mesenchymal stem cells are systemically recruited to the fracture site, and cytokines are released from the fracture site into the vascular system. In a significant minority of fractures, healing delays result from adverse clinical factors that interfere with these processes. Extrinsic factors, such as aging and smoking, adversely affect the molecular and cellular processes occurring locally in the fracture site. Fracture fixation affects healing through local changes in the biologic signaling within the fracture callus. Current biologic treatment of fractures includes the local application of osteoinductive bone morphogenetic proteins (ie, BMP-2, BMP-7) and cell-based therapies. Although clinical results with bone morphogenetic proteins have been satisfactory, they have not been as impressive as those reported in animal studies. Further understanding of the biology of fracture repair may lead to improved treatment modalities.

F

racture healing is a highly efficient repair process resulting in newly formed bone, similar in quality to the original tissue. However, in a small but significant number of instances, adverse conditions impair this process, causing significant morbidity. Because fractures are common in the general population, delayed healing and nonunion are significant health care issues. Thus, there remains a need to develop treatment methods that enhance fracture healing and improve outcomes. Biologic methods of bone regeneration will continue to have an increasing role in the treatment of fractures. To further develop these methods, knowledge of the pathologic changes in the fracture repair process that lead to delayed union or nonunion is important.

Fracture healing may be seen as both a local and a systemic process (Figures 1 and 2). There are local molecular and cellular signaling pathways, and evidence is emerging of the systemic recruitment of mesenchymal stem cells (MSCs) to the fracture site. Extrinsic factors, such as drugs and aging, influence local processes to alter the outcome of fractures, while the biomechanics of fracture fixation affect the biology of fracture healing.

Pathophysiology of Delayed Fracture Healing and Nonunion Bone regeneration depends on three essential elements: progenitor cells, growth factors (osteoinduction), and the appropriate milieu (osteoconduction). Delayed fracture repair and 619

Recent Developments in the Biology of Fracture Repair

Figure 1

Illustration demonstrating molecular signaling. Fracture repair depends on molecular processes occurring both locally and systemically. BMPs = bone morphogenetic proteins, IGF-1 = insulin-like growth factor-1, NSAIDs = nonsteroidal anti-inflammatory drugs, TGF-β = transforming growth factor-β, - = inhibits

nonunion can result from a lack of osteoprogenitor cells, insufficient osteoinductive growth factors, or a defective milieu, or, more commonly, a combination of these factors. Disease or other adverse factors may delay fracture healing by affecting one or more of these elements. For example, a critical-sized bone defect (ie, one that does not heal spontaneously because of its size) would result in the absence of human MSCs (hMSCs) within the defect, a lack of osteoinductive signals, and a milieu that is nonconducive to healing. Excess motion at the fracture site impairs both the molecular and cellular processes within the defect. Hypoxia affects osteogenic differentiation of hMSCs by reducing the number of viable cells and altering the molecular signals produced.1 Blood supply is important to fracture repair as blood provides nutrients and oxygen for cell survival, and blood vessels are the route for inflammatory and osteoprogenitor cells that are recruited to the fracture site. Systemic factors may affect fracture repair by reducing the number of osteoprogenitor cells recruited

to the fracture site and/or by affecting the local osteoinductive signals. Nonunions are commonly classified on radiographs as hypertrophic or atrophic. Hypotrophic nonunion is generally thought to be the result of mechanical instability and is treated by restoring stability, usually by skeletal fixation. Atrophic nonunion is thought to result from biologic causes, principally poor vascularization, and is treated by restoration of the osteogenic potential, with resection of fibrous tissue and bone grafting or some other method of osteoinduction. Both groups of nonunion contain fibrous tissue, fibrocartilage, and adipose tissue, which are not normally present in healing fractures.2 The hypertrophic group also has hyaline cartilage and bone in varying proportions.

Local Molecular Signaling Osteoinductive Molecules Fracture repair is regulated by several growth factors with varying osteogenic potential, such as transforming growth factor-β, platelet-

Figure 2

Illustrations of cellular signaling and the role of mesenchymal stem cells (MSCs) in fracture healing. A, Source of MSCs. B, Action of MSCs within fracture callus. BMPs = bone morphogenetic proteins 620

Journal of the American Academy of Orthopaedic Surgeons

Francois N. K. Kwong, MD, and Mitchel B. Harris, MD

derived growth factor, insulin-like growth factor-1, and bone morphogenetic protein (BMP). Of these, BMP appears to be among the most consequential. BMP was discovered and named by Urist3 in 1965; he also first described the phenomenon of osteoinduction. Urist observed new bone formation occurring locally in rodents after they were given intramuscular implantation of bone cylinders decalcified with hydrochloric acid. This phenomenon was attributed to the presence of a protein, BMP, in bone matrix. Since that discovery, at least 16 different human BMPs have been identified. These proteins affect cells and tissues involved in the repair process in a number of ways, including the recruitment of MSCs from surrounding tissues to the fracture site, followed by their proliferation and differentiation into chondrocytes and osteoblasts, invasion of blood vessels, and, ultimately, bone formation. All of these effects are mediated by the binding of BMPs to specific transmembrane receptors on hMSCs, active osteoblasts, and mature chondrocytes as well as to the subsequent activation of various intracellular messenger systems.4 Therapeutic Application of BMPs Extensive animal data have demonstrated the potential of BMPs to induce healing of critical-sized (ie, large) bone defects.5-7 In animal models, BMPs alone (with their carrier matrix) have been shown to induce rapid bone bridging of a defect. The quality of the repair tissue was equivalent to or better than that obtained with autologous bone grafting, the standard treatment for bone defects and nonunions in clinical practice.6,7 At present, only BMP-2 (Infuse; Medtronic Sofamor Danek, Memphis, TN) and BMP-7 (OP-1 Implant; Stryker Biotech, Hopkinton, MA) have been approved by the US Food and Drug Administration for clinical use. Several clinical studies Volume 16, Number 11, November 2008

have already demonstrated the positive effect of the application of BMPs on the outcome of fractures and nonunions. Because a review of all available evidence is beyond the scope of this article, we will focus on the treatment of segmental bone defects in patients because this allows a direct comparison with the studies of BMPs in animals. In most clinical studies of the treatment of segmental bone defects, BMPs have been used in conjunction with allograft or autograft bone. Jones et al8 demonstrated that a combination of BMP-2 and allograft bone was equivalent to autologous bone for the treatment of segmental bone defects. In that study, patients with a tibial diaphyseal fracture and a residual cortical defect were randomly assigned to receive either autogenous bone graft or allograft with an onlay application of recombinant human BMP-2 (rhBMP-2). Radiographic and functional outcomes were similar in both groups. To date, the only published clinical study on the treatment of segmental defects with BMPs alone (with a nonosteoconductive carrier matrix only) in humans showed healing of criticalsized fibular defects in patients undergoing opening wedge high tibial osteotomy with fibulectomy.9 RhBMP-7 bound to collagen type 1 sponge induced bony union in five of six patients with a critical-sized fibular defect, whereas there was no healing in any of the six patients treated with the type 1 collagen carrier only. Despite these favorable results, no large studies have been done on the use of BMPs alone in humans. The pace of healing of segmental defects treated with BMPs differs significantly among species. Segmental defects in large animals treated with BMPs alone healed in <3 months,5,6 whereas in humans, critical tibial defects treated with allograft bone and BMP-2 required ≥6 months to achieve bony union.8 The

cause for this difference remains unclear. Clinically, poor fracture healing in humans may be associated with adverse factors not present in animal studies. For example, softtissue coverage of the fracture may not be adequate. The initial dose of BMPs given to human subjects (7 mg of BMP-7 and 2 g of collagen carrier, or 12 mg of rhBMP-2 and collagen sponge) was much higher than in the animal studies. Because the release of BMP inhibitors depends on the extracellular level of BMPs, it is postulated that this higher concentration of BMPs leads to the expression of several BMP antagonists, which further limits their efficacy and reduces the rate of bone healing. It is also speculated that BMP receptors in animals and humans are different in their degree of responsiveness to the BMP molecules. Role of BMPs and Their Inhibitors in Fracture Healing The activity of BMPs can be limited by several antagonists, which bind to them and interfere with their ability to induce receptor activation. One of the most characterized BMP inhibitors is noggin, a protein that binds to both BMP-2 and BMP-7 and antagonizes their actions by preventing binding with their membrane receptors.10 Its expression by osteoblasts is induced by BMP-2,10 implying that BMP-2 and noggin are involved in a negative feedback loop during bone formation. This may provide a physiologic mechanism that prevents overexposure of osteoblasts to BMP signaling. The balance between BMPs and their inhibitors is likely to be a critical determinant of fracture healing, with a decreased expression of BMPs and/or a relative increase of BMP antagonists adversely affecting healing. In a rat model of fracture nonunion, a downregulation of the gene expression of BMPs was demonstrated.11 In an animal model of atrophic nonunion, reversal of this decreased ex621

Recent Developments in the Biology of Fracture Repair

pression of osteoinductive factors, induced by an early local injection of rhBMP-7, prevented the development of nonunion.12 The expression of chordin, a BMP antagonist with a mode of action similar to that of noggin, was upregulated in an animal model of fracture nonunion,11 suggesting that downregulation of chordin in a fracture nonunion has the potential of improving bone healing. In normally healing fractures, the balance between BMPs and their inhibitors can also be manipulated to hasten repair. This would involve the addition of the osteoinductive factors (eg, BMP-2), inhibition of the activity of BMP inhibitors, or a combination of both methods. So far, biologic methods of enhancing bone regeneration have centered on the promotion of osteoinduction via the delivery of BMPs. However, it was recently demonstrated that noggin or chordin suppression can accelerate osteogenesis in vitro13,14 and that noggin knockdown increased the rate of intramembranous ossification in an animal model.14 We believe that these findings will be extended to fracture healing and that blockade of the activity of BMP inhibitors may provide a novel strategy for expediting fracture repair.

Local Cellular Signaling Complete fracture healing requires that a sufficient number of hMSCs differentiate into chondrocytes and osteoblasts, as well as other cells of the mesenchymal lineage, such as adipocytes, and stromal and endothelial cells. In addition to differentiation, the trophic, or nutritional, activity of MSCs in the repair of other tissues is now well established.15 This refers to the capacity of MSCs to secrete growth factors, which stimulate blood vessel formation and the proliferation of other local MSCs.15 It is postulated that MSCs exert a trophic activity in the early stages of fracture repair, although 622

this has not yet been specifically demonstrated in fractures. MSCs are thought to be recruited locally from the cortex, bone marrow, periosteum, and external soft tissues (Figure 2). The relative contribution of MSCs from each tissue is uncertain but is thought to depend on the local parameters present at the injured tissue, such as growth factors, oxygen gradient, and mechanical stability. The clinical relevance of muscle as a source of progenitor cells during fracture repair has been the subject of several recent studies.16,17 The presence in muscle of a population of adult stem cells that can differentiate into cells of different lineages has been suspected for some time based on two observations. First, muscle has the potential to turn into bone, as occurs during heterotopic ossification. Second, the original description of osteoinduction by Urist3 has been attributed to the effects of BMPs on progenitor cells within muscle tissue. However, the isolation of the relevant MSC population from this tissue is relatively recent.16 Clinically, the importance of muscle as a source of osteoprogenitor cells is underlined by the poor outcome of fractures in which muscle has been devitalized, although this poor outcome is often attributed to the coexisting damage to the periosteal blood supply. Muscle resection significantly reduces callus formation and the biomechanical properties of the healed bone, while a muscle crush does not significantly affect bone healing.18 Conversely, heterotopic ossification in acetabular fractures has been reduced as surgeons have become more aggressive in débriding injured and necrotic muscle from the surgical field.19

Systemic Recruitment of Cells and Molecular Signaling Traditionally, it was thought that the cells involved in fracture repair

were recruited only locally. However, a systemic mobilization and recruitment of osteoblastic precursors to the fracture site from the peripheral circulation have now been demonstrated in several recent studies. In a rabbit ulnar osteotomy model, it was demonstrated that some osteoblasts involved in fracture healing were systemically mobilized and recruited to the fracture from remote bone marrow sites.20 Shen et al21 demonstrated in a murine model that, following systemic injection of MSCs, osteoprogenitor cells localized to the fracture callus. These studies have implications for the development of future cellbased therapies for fracture healing. Cell-based therapies are needed when insufficient cells are present within a fracture callus (eg, segmental defect). In such a situation, even when all of the osteoprogenitor cells at the site of fracture are working to the maximum, there will be no bony union, nor will any osteoinductive agents be effective because maximal osteogenesis per cell is already occurring. In a level III study (casecontrol), Hernigou et al22 demonstrated the clinical effectiveness of local percutaneous injection of bone marrow aspirate in treating tibial nonunions. We believe that the studies mentioned here suggest that it might be possible to develop cellbased therapies in which cells are systemically administered and localized to the site of injury. Evidence is emerging that distant skeletal sites can be affected in response to a local bone injury.23 An increased osteogenic response has been detected in sites distant from the fracture in animal models.23 This may result from the release of growth factors (eg, transforming growth factor-β, insulin-like growth factor-1) from the fracture site into the systemic circulation, as shown in a clinical study.24 It is not known whether the level of these factors in serum reflects the repair activity of the fracture.

Journal of the American Academy of Orthopaedic Surgeons

Francois N. K. Kwong, MD, and Mitchel B. Harris, MD

Systemic Factors and Local Fracture Healing It is widely accepted that extrinsic factors have an influence on the outcome of fracture healing. However, it is often difficult to isolate the role of a particular systemic factor in clinical situations. For example, impaired fracture healing in the elderly may be related to age, osteoporosis, drugs, malnutrition, and/or anemia. Evidence gained from animal models as well as recently uncovered cellular and molecular processes have led to better understanding of the role of systemic factors. Nonsteroidal Anti-inflammatory Drugs During fracture repair, the enzyme cyclooxygenase-2 (COX-2) is activated to produce prostaglandins, which are needed during inflammation and are critical for starting the osteogenic response.25 Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit COX-2, dramatically reducing prostaglandin production, and therefore have the potential to negatively affect fracture repair. Although results in various animal studies have been conflicting, it is generally accepted that NSAIDs impair fracture healing in animal models in which a high dose has been administered.26 This inhibitory effect is most potent during the early phase of healing, thereby underlining the importance of the initial inflammatory reaction.26 Although it is not known in which clinical situations NSAIDs in high local concentrations will affect early-phase fracture healing, administration of NSAIDs has been associated with delayed union and pseudarthrosis.27 The inhibitory effect of COX-2 blockade in vitro has been shown to be reversed by the administration of BMP-2.28 Age Aging is an independent factor that negatively affects fracture reVolume 16, Number 11, November 2008

pair. Delayed fracture healing in the elderly may be caused by differences in molecular signaling locally within the fracture callus as well as to systemic factors. Meyer et al28 reported a decreased expression of BMP-2 and Indian hedgehog (a factor related to endochondral callus formation) in fracture calluses of older rats. Noggin expression was not changed with age. However, the decrease in expression of BMP-2 implies that the BMP inhibitor predominated over BMP-2 in older rats. Hormonal differences with aging may also be a factor. Sera obtained from aged donors are less potent inducers of osteoblast differentiation of hMSC than are sera obtained from young donors.29 These effects were specific for osteoblast differentiation because no donor age differences in the ability to support differentiation of other cell types were observed. Short-term bone marrow cultures established from young and old donors contain similar numbers of hMSCs and exhibit similar proliferation rates.30 In addition, the capacity of hMSC to differentiate into osteoblasts and adipocytes was maintained irrespective of donor age.31 These studies suggest that there are no intrinsic defects in hMSCs with aging and that extrinsic factors present in the aging environment of hMSCs may be responsible for the impaired osteoblast functions seen with aging. These observations need further investigation. If poor fracture repair in the elderly is related to impaired osteoinductive signals rather than to differences in the cellular component of the healing fractures, then the elderly patient with trauma is more likely to benefit from an osteoinductive agent, such as BMP-2, than from cell-based therapies. Smoking Smoking has an adverse effect on fracture healing. In one study, the time to union for tibial fractures among smokers was significantly

(P < 0.05) longer by 4 weeks than in nonsmokers.32 This effect may be mediated by either nicotine or some other, yet undefined components in cigarette smoke,33 or both. In animal models, nicotine has been shown to delay cellular differentiation into chondrocytes and to slow the physiologic transition from cartilaginous callus to bone.34 It is also highly likely that the compromise of microcirculation secondary to nicotine causes a delay in fracture repair. It remains to be seen whether the deleterious effects of smoking are reversible with smoking cessation and whether BMPs can improve healing in smokers. These questions should be investigated using animal models of fracture healing and smoking.

Influence of Fracture Fixation The local mechanical forces on a fracture resulting in movement at the fracture site are critical factors in the success of fracture repair. Excess motion can delay healing; casting and fracture fixation aim to provide a mechanical environment in which strains are decreased to avoid delayed union or nonunion. However, some movement, referred to as micromotion, is beneficial to fracture healing. Different fractures and different areas of the skeleton respond differently to mechanical forces and resultant strains. Yet precisely how these changes in local mechanical loading result in a cartilaginous callus or intramembranous ossification remains speculative. The influence of the mechanical environment on the fracture repair can be viewed at three levels: tissue, cellular, and molecular. Tissue differentiation requires mechanical stability. In an animal model, Claes et al35 demonstrated a strong association between fracture stability and the spatial distribution of newly formed blood vessels and specific tissue formation. It was also independently demonstrated in an 623

Recent Developments in the Biology of Fracture Repair

animal model that increased stability affected endochondral ossification by decreasing the overall amount of cartilage that formed at the fracture site.36 This was thought to be secondary to an increase in the rate of maturation of chondrocytes during the endochondral ossification stage of fracture healing. Conversely, orthopaedic surgeons often observe an increase in the size of fracture callus with increased movement around the fracture. Endochondral ossification is also affected by the type of intermittent forces applied to the fracture site. In a rat model of healing osteotomy, intermittent tensile strains stimulated endochondral ossification, as opposed to compressive strains, which favored direct intramembranous ossification.37 The method of fracture fixation also has an effect on the biology of the healing callus. In a murine model of femoral fracture healing, the fracture callus was significantly larger with intramedullary nail fixation than with plate fixation.38 The changes in gene expression following each fixation procedure were similar and occurred after the same postoperative time interval. However, the intramedullary group had significantly greater expression of genes related to cartilage, cell division, and inflammation (P < 0.05 for all), and there was greater expression of genes related to macrophage activity in the plate group than in the nail group (P < 0.001). Osteoprogenitor cells have the capacity to detect their mechanical environment and modify their rate of differentiation, a process mediated via effects on the BMP signaling pathway. Cyclic stretching of hMSCs or osteoblastic precursor cells in a collagen matrix increased their proliferation and osteogenic differentiation,39,40 a phenomenon associated with an increase in BMP-2 production. This increase in osteogenic differentiation may also be mediated by the downregulation of peroxisome proliferator–activated receptor 624

gamma in bone marrow stromal cells, a mediator that favors adipogenesis over osteogenesis.41 However, compression can also stimulate BMP production and decrease noggin production, thereby stimulating the in vitro differentiation of human osteoblastic cells.42 These studies indicate that the same changes in molecular signaling can be induced by different types of forces acting on the progenitor cells in various circumstances.

2.

3. 4.

5.

6.

Summary Significant advances have been made in the understanding of the biology of fracture healing. In particular, it is now understood that fracture repair is not only a local phenomenon but is itself under the influence of extrinsic factors. Adverse local and systemic clinical factors can affect the molecular and cellular processes involved and can lead to delayed fracture repair and nonunion. The management of these healing problems remains challenging, despite the introduction of therapeutic BMPs and other biologic methods of bone regeneration. Further understanding of the pathophysiology of fracture repair is needed to develop improved treatment strategies targeted to the molecular and cellular processes affected in specific clinical conditions.

7.

8.

9.

10.

References Evidence-based Medicine: References 9, 19, 22, 24, and 32 are level I/II prospective, randomized studies. The remaining references are casecontrol cohort studies, basic research studies, or expert opinion.

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Reed AA, Joyner CJ, Brownlow HC, Simpson AH: Human atrophic fracture non-unions are not avascular. J Orthop Res 2002;20:593-599. Urist MR: Bone: Formation by autoinduction. Science 1965;150:893-899. Kloen P, Di Paola M, Borens O, et al: BMP signaling components are expressed in human fracture callus. Bone 2003;33:362-371. Cook SD, Salkeld SL, Brinker MR, Wolfe MW, Rueger DC: Use of an osteoinductive biomaterial (rhOP-1) in healing large segmental bone defects. J Orthop Trauma 1998;12:407-412. Gerhart TN, Kirker-Head CA, Kriz MJ, et al: Healing segmental femoral defects in sheep using recombinant human bone morphogenetic protein. Clin Orthop Relat Res 1993;293: 317-326. Sciadini MF, Johnson KD: Evaluation of recombinant human bone morphogenetic protein-2 as a bone-graft substitute in a canine segmental defect model. J Orthop Res 2000;18:289302. Jones AL, Bucholz RW, Bosse MJ, et al: Recombinant human BMP-2 and allograft compared with autogenous bone graft for reconstruction of diaphyseal tibial fractures with cortical defects: A randomized, controlled trial. J Bone Joint Surg Am 2006;88: 1431-1441. Geesink RG, Hoefnagels NH, Bulstra SK: Osteogenic activity of OP-1 bone morphogenetic protein (BMP-7) in a human fibular defect. J Bone Joint Surg Br 1999;81:710-718. Abe E, Yamamoto M, Taguchi Y, et al: Essential requirement of BMPs-2/4 for both osteoblast and osteoclast formation in murine bone marrow cultures from adult mice: Antagonism by noggin. J Bone Miner Res 2000;15: 663-673. Niikura T, Hak DJ, Reddi AH: Global gene profiling reveals a downregulation of BMP gene expression in experimental atrophic nonunions compared to standard healing fractures. J Orthop Res 2006;24:1463-1471. Makino T, Hak DJ, Hazelwood SJ, Curtiss S, Reddi AH: Prevention of atrophic nonunion development by recombinant human bone morphogenetic protein-7. J Orthop Res 2005; 23:632-638. Kwong FN, Richardson SM, Evans CH: Chordin knockdown enhances the osteogenic differentiation of human mesenchymal stem cells. Arthritis Res Ther 2008;10:R65. Wan DC, Pomerantz JH, Brunet LJ,

Journal of the American Academy of Orthopaedic Surgeons

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et al: Noggin suppression enhances in vitro osteogenesis and accelerates in vivo bone formation. J Biol Chem 2007;282:26450-26459. Caplan AI: Adult mesenchymal stem cells for tissue engineering versus regenerative medicine. J Cell Physiol 2007;213:341-347. Jankowski RJ, Huard J: Myogenic cellular transplantation and regeneration: Sorting through progenitor heterogeneity. Panminerva Med 2004; 46:81-91. Gates CB, Karthikeyan T, Fu F, Huard J: Regenerative medicine for the musculoskeletal system based on musclederived stem cells. J Am Acad Orthop Surg 2008;16:68-76. Utvåg SE, Grundnes O, Rindal DB, Reikerås O: Influence of extensive muscle injury on fracture healing in rat tibia. J Orthop Trauma 2003;17: 430-435. Rath EM, Russell GV Jr, Washington WJ, Routt ML Jr: Gluteus minimus necrotic muscle debridement diminishes heterotopic ossification after acetabular fracture fixation. Injury 2002;33:751-756. Shirley D, Marsh D, Jordan G, McQuaid S, Li G: Systemic recruitment of osteoblastic cells in fracture healing. J Orthop Res 2005;23:1013-1021. Shen FH, Visger JM, Balian G, Hurwitz SR, Diduch DR: Systemically administered mesenchymal stromal cells transduced with insulin-like growth factor-I localize to a fracture site and potentiate healing. J Orthop Trauma 2002;16:651-659. Hernigou P, Poignard A, Beaujean F, Rouard H: Percutaneous autologous bone-marrow grafting for nonunions: Influence of the number and concentration of progenitor cells. J Bone Joint Surg Am 2005;87:1430-1437. Einhorn TA, Simon G, Devlin VJ, Warman J, Sidhu SP, Vigorita VJ: The osteogenic response to distant skeletal injury. J Bone Joint Surg Am 1990; 72:1374-1378. Kaspar D, Neidlinger-Wilke C, Holbein O, Claes L, Ignatius A: Mitogens

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are increased in the systemic circulation during bone callus healing. J Orthop Res 2003;21:320-325. Zhang X, Schwarz EM, Young DA, Puzas JE, Rosier RN, O’Keefe RJ: Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is critically involved in bone repair. J Clin Invest 2002;109:1405-1415. Simon AM, Manigrasso MB, O’Connor JP: Cyclo-oxygenase 2 function is essential for bone fracture healing. J Bone Miner Res 2002;17:963-976. Giannoudis PV, MacDonald DA, Matthews SJ, Smith RM, Furlong AJ, De Boer P: Nonunion of the femoral diaphysis: The influence of reaming and nonsteroidal anti-inflammatory drugs. J Bone Joint Surg Br 2000;82:655-658. Meyer RA Jr, Meyer MH, Tenholder M, Wondracek S, Wasserman R, Garges P: Gene expression in older rats with delayed union of femoral fractures. J Bone Joint Surg Am 2003;85: 1243-1254. Abdallah BM, Haack-Sørensen M, Fink T, Kassem M: Inhibition of osteoblast differentiation but not adipocyte differentiation of mesenchymal stem cells by sera obtained from aged females. Bone 2006;39:181-188. Stenderup K, Justesen J, Eriksen EF, Rattan SI, Kassem M: Number and proliferative capacity of osteogenic stem cells are maintained during aging and in patients with osteoporosis. J Bone Miner Res 2001;16:1120-1129. Justesen J, Stenderup K, Eriksen EF, Kassem M: Maintenance of osteoblastic and adipocytic differentiation potential with age and osteoporosis in human marrow stromal cell cultures. Calcif Tissue Int 2002;71:36-44. Adams CI, Keating JF, Court-Brown CM: Cigarette smoking and open tibial fractures. Injury 2001;32:61-65. Skott M, Andreassen TT, UlrichVinther M, et al: Tobacco extract but not nicotine impairs the mechanical strength of fracture healing in rats. J Orthop Res 2006;24:1472-1479. El-Zawawy HB, Gill CS, Wright RW,

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Sandell LJ: Smoking delays chondrogenesis in a mouse model of closed tibial fracture healing. J Orthop Res 2006;24:2150-2158. Claes L, Eckert-Hübner K, Augat P: The effect of mechanical stability on local vascularization and tissue differentiation in callus healing. J Orthop Res 2002;20:1099-1105. Le AX, Miclau T, Hu D, Helms JA: Molecular aspects of healing in stabilized and non-stabilized fractures. J Orthop Res 2001;19:78-84. Smith-Adaline EA, Volkman SK, Ignelzi MA Jr, Slade J, Platte S, Goldstein SA: Mechanical environment alters tissue formation patterns during fracture repair. J Orthop Res 2004;22: 1079-1085. Heiner DE, Meyer MH, Frick SL, Kellam JF, Fiechtl J, Meyer RA Jr: Gene expression during fracture healing in rats comparing intramedullary fixation to plate fixation by DNA microarray. J Orthop Trauma 2006;20:27-38. Ignatius A, Blessing H, Liedert A, et al: Tissue engineering of bone: Effects of mechanical strain on osteoblastic cells in type I collagen matrices. Biomaterials 2005;26:311-318. Sumanasinghe RD, Bernacki SH, Loboa EG: Osteogenic differentiation of human mesenchymal stem cells in collagen matrices: Effect of uniaxial cyclic tensile strain on bone morphogenetic protein (BMP-2) mRNA expression. Tissue Eng 2006;12:34593465. David V, Martin A, Lafage-Proust MH, et al: Mechanical loading downregulates peroxisome proliferatoractivated receptor gamma in bone marrow stromal cells and favors osteoblastogenesis at the expense of adipogenesis. Endocrinology 2007;148: 2553-2562. Mitsui N, Suzuki N, Maeno M, et al: Optimal compressive force induces bone formation via increasing bone morphogenetic proteins production and decreasing their antagonists production by Saos-2 cells. Life Sci 2006; 78:2697-2706.

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Symposium

Introduction Extremity War Injuries: Challenges in Definitive Reconstruction

T

J Am Acad Orthop Surg 2008;16:626627 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

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he January 2006 American Academy of Orthopaedic Surgeons/Orthopaedic Trauma Association (AAOS/OTA) Extremity War Injuries: State of the Art and Future Directions (EWI) symposium was the first combined effort of the AAOS, the OTA, and the United States military to discuss orthopaedic injuries sustained as a result of the Global War on Terror. This flagship symposium resulted in a special issue of the Journal of the American Academy of Orthopaedic Surgeons (JAAOS) discussing current care and describing future research directions on wound management, antibiotics and infection, management of segmental bone defects, stabilization of long bones, and amputee care.1 The AAOS/OTA/Society of Military Orthopaedic Surgeons (SOMOS) EWI II: Development of Clinical Treatment Principles symposium in January 2007 continued the AAOS collaboration with the military to review advances in treatment of extremity trauma, examine new challenges faced overseas, and define principles of delivery of forward care. An article summarizing EWI II presentations was published in JAAOS in October 2007.2 The third Extremity War Injuries symposium, AAOS/OTA/SOMOS EWI III: Challenges in Definitive Reconstruction, was held in January 2008 and provided a forum for review and discussion of research findings in the areas of soft-tissue defects, segmental bone defects, open tibial shaft fractures, and massive

periarticular reconstruction. In addition, EWI III symposium attendees were addressed by high-ranking administration officials and members of Congress, including Chairman of the Joint Chiefs of Staff ADM Michael Mullen, Assistant Secretary of Defense for Health Affairs S. Ward Casscells, MD, Senator Tom Harkin (D-IA), Representative Tom Latham (R-IA), Representative C. A. Dutch Ruppersberger (D-MD), and Representative Tim Walz (D-MN). In addition, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Director Stephen I. Katz, MD, PhD, Uniformed Services University of the Health Sciences President Charles L. Rice, MD, and Under Secretary of Defense for Personnel and Readiness David S. C. Chu, PhD, attended the event. In his comments, Senator Harkin stressed that the American people have a profound moral obligation to support those who have served. The EWI III symposium resulted in a Congressional call of support for additional federal funding for extremity war injury research through the US Department of Defense to offer our wounded soldiers better healing outcomes and daily living capabilities. In a letter circulated to every member of Congress, Senators Harkin and Kay Bailey Hutchison (RTX) and Representatives Latham and Ruppersberger urged their colleagues to sign a letter to the leadership of the Senate and House Defense Appropriations Subcommittees requesting support for an annual operating level of $50 million in fiscal

Journal of the American Academy of Orthopaedic Surgeons

year 2008, through supplemental appropriations, for the peer-reviewed Orthopaedic Extremity Trauma Research Program. Through programs like the EWI symposium series, the AAOS will continue to work with members of Congress to secure funding for research to ensure that our service men and women are receiving the best possible care. This paper represents a formal report of the outcomes of EWI III, including discussions related to research updates and funding challenges as well as treatment of segmental bone defects, soft-tissue defects, open tibial shaft fractures, and massive periarticular reconstructions. We would like to like to acknowledge the individuals, groups, and sponsors that helped make the symposium possible. We would like to thank the EWI III faculty for their guidance, dedication, and time: LTC Romney C. Andersen, MD; COL Mark R. Bagg, MD (Ret); Michael J. Bosse, MD (Ret); COL Paul J. Cutting, MD, FACS; COL William C. Doukas, MD; Robert Paul Dunbar, MD; COL Roman A. Hayda, MD; John E. Herzenberg, MD; MAJ Joseph R. Hsu, MD; LCDR John J. Keeling, MD; LTC James Keeney, MD (Ret); CPT MC L. Scott Levin, MD, FACS; Ronald W. Lindsey, MD;

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CDR Michael T. Mazurek, MD; Michael D. McKee, MD, FRCSC; Theodore Miclau, MD; Sean E. Nork, MD; Regis O’Keefe, MD, PhD; COL Elisha Powell IV, MD; LTC Craig Ruder, MD; Andrew H. Schmidt, MD; Marcus F. Sciadini, MD; LTC Scott B. Shawen, MD; Randy Sherman, MD, FACS; Douglas G. Smith, MD; Robert J. Spinner, MD; Marc F. Swiontkowski, MD; H. Thomas Temple, MD; J. Tracy Watson, MD; and Joshua Wenke, PhD. We would also like to thank James Beaty, MD; E. Anthony Rankin, MD; Joseph D. Zuckerman, MD; and the AAOS Board of Directors, as well as the AAOS Council on Research, Quality Assessment, and Technology, the AAOS Research Development Committee, and AAOS staff leadership, including Christy M. P. Gilmour, Erin L. Ransford, Kristy Glass, Robert S. Jasak, JD, David Lovett, JD, Lindsay F. Law, David C. Smith, and Karen Hackett, CAE, FACHE. The American Academy of Orthopaedic Surgeons, the Orthopaedic Trauma Association, and the Society of Military Orthopaedic Surgeons acknowledge the following industry contributors and their representatives for their financial support of the symposium and this article:

• Kinetic Concepts, Inc (Gold Level) • Medtronic (Silver Level) • Smith & Nephew Trauma (Silver Level) • Stryker (Silver Level) • Synthes (Silver Level) • DePuy (Additional Support) Andrew N. Pollak, MD EWI III Symposium Co-Chair Chief, Orthopaedic Trauma, RAC Shock Trauma Center University of Maryland School of Medicine Baltimore, Maryland [email protected] Col. James R. Ficke, MD EWI III Symposium Co-Chair Orthopaedic Consultant to the U.S. Army Surgeon General Chief, Orthopaedic Surgery Brooke Army Medical Center Fort Sam Houston, Texas [email protected]

References 1.

Pollak A, Calhoun J: Extremity war injuries: State of the art and future directions. J Am Acad Orthop Surg 2006;14:iii-S214. 2. Ficke JR, Pollak AN: Extremity war injuries: Development of clinical treatment principles. J Am Acad Orthop Surg 2007;15:590-595.

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Andrew N. Pollak, MD COL James R. Ficke, MD, MC USA Extremity War Injuries III Session Moderators*

Dr. Pollak is Chief, Orthopaedic Trauma, RAC Shock Trauma Center, University of Maryland School of Medicine, Baltimore, MD. Dr. Ficke is Orthopaedic Consultant to the US Army Surgeon General and Chief, Orthopaedic Surgery, Brooke Army Medical Center, Fort Sam Houston, TX. *COL Mark R. Bagg, MD (Ret); CPT L. Scott Levin, MD, FACS; CDR Michael T. Mazurek, MD; J. Tracy Watson, MD; LTC Romney C. Andersen, MD; Sean E. Nork, MD; COL Roman A. Hayda, MD; Theodore Miclau, MD; LCDR John Keeling, MD; Marc Swiontkowski, MD; and LTC James Keeney, MD (Ret). The opinions or assertions expressed herein are those of the authors and do not reflect those of the Army, Navy, Air Force, or the Department of Defense. Reprint requests: Dr. Pollak, University of Maryland School of Medicine, Room T3R54, 22 South Greene Street, Baltimore, MD 21201-1544. J Am Acad Orthop Surg 2008;16:628634 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

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Abstract The third annual Extremity War Injuries Symposium was held in January 2008 to review challenges related to definitive management of severe injuries sustained primarily as a result of blast injuries associated with military operations in the Global War on Terror. Specifically, the symposium focused on the management of soft-tissue defects, segmental bone defects, open tibial shaft fractures, and challenges associated with massive periarticular reconstructions. Advances in several components of soft-tissue injury management, such as improvement in the use of free-tissue transfer and enhanced approaches to tissue-engineering, may improve overall care for extremity injuries. Use of distraction osteogenesis for treatment of large bone defects has been simplified by the development of computer-aided distraction protocols. For closed tibial fractures, evidence and consensus support initial splinting for transport and aeromedical evacuation, followed by elective reamed, locked intramedullary nail fixation. Management of open tibial shaft fractures sustained as a result of high-energy combat injuries should include serial débridements every 48 hours until definitive wound closure and stabilization are recommended. A low threshold is recommended for early utilization of fasciotomies in the overall treatment of tibial shaft fractures associated with war injuries. For management of open tibial fractures secondary to blast or high-velocity gunshot injuries, good experiences have been reported with the use of ring fixation for definitive treatment. Treatment options in any given case of massive periarticular defects must consider the specific anatomic and physiologic challenges presented as well as the capabilities of the treating surgeon.

T

he third annual Extremity War Injuries Symposium (EWI III), jointly hosted by American Academy of Orthopaedic Surgeons (AAOS), the Orthopaedic Trauma Association (OTA), and the Society of Military Orthopaedic Surgeons,

was held in Washington, DC, on January 23 and 24, 2008. The goal of EWI III was to review progress on challenges related to management of severe injuries sustained primarily as a result of blast injuries associated with military operations in the

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Global War on Terror. Specifically, the symposium focused on the management of soft-tissue defects, segmental bone defects, and open tibial shaft fractures, as well as challenges associated with massive periarticular reconstructions. In addition, joint efforts of the AAOS and the OTA in developing and implementing a Visiting Scholars Program were reviewed. Clinical updates included reports on the operations at the Air Force Theater Hospital in Balad, Iraq, and the Combat Support Hospital in Baghdad, Iraq.

Distinguished Visiting Scholars Program The AAOS and OTA have jointly developed and implemented a Distinguished Visiting Scholars Program. Fifteen orthopaedic trauma specialists with widely recognized expertise in trauma clinical care and trauma education have spent a minimum of 2 weeks each at Landstuhl Regional Medical Center delivering clinical care and providing education for the clinical staff. Their experiences in treating wounded warriors and their interactions with military orthopaedic surgeons have also allowed them to receive a valuable education, with the intention of using this instruction to educate their colleagues in the civilian sector. This education relates particularly to understanding the nuances and severity of combat-related injury. Even more important, this education involves understanding the distinctions between the treatment of blast injury and the treatment of injuries more typically seen in a civilian environment, as well as the need for

additional research to better understand the best methods for clinical management of war injuries. Plans for the Distinguished Visiting Scholars Program started in July 2007. As of the time of EWI III, eight surgeons had served as distinguished visiting scholars. Twenty additional distinguished visiting scholars were scheduled to visit Landstuhl over the course of the next 18 months. Distinguished visiting scholars participate in all regular patient care activities, including intake assessment, ward rounds, and surgery. They also deliver lectures to orthopaedic surgical staff and other specialists. Applications for the program are available through [email protected]. Eligibility criteria for selection as a distinguished visiting scholar include 10 years or more of clinical trauma care experience, demonstrated excellence in trauma education, and recognized expertise in trauma clinical care. The program was modeled after a similar program for general trauma critical care surgeons developed by the American College of Surgeons and the American Association for the Surgery of Trauma.1 As reported at EWI III, the response to date from the distinguished visiting scholars, as well as that from participants in the general surgical program, has been uniformly positive. In addition, reaction from the military medical personnel stationed at Landstuhl suggests that the program has contributed to the education of military surgeons and to the care of wounded warriors. Current plans call for the program to continue for as long as casualties related to the conflicts in Afghanistan and Iraq warrant.

Research Update At the time of the first Extremity War Injuries Symposium in January 2006, the need for a comprehensive database of injuries and treatment outcomes after high-energy extremity trauma related to war injury was identified as a priority.2 The Military Orthopaedic Trauma Registry has now been established as an effective means of collecting comprehensive data about injuries sustained by military personnel in Iraq and Afghanistan. These data are currently being collected in conjunction with the Joint Theater Trauma Registry using abstractors located at the major medical centers where these patients are receiving care. Data collection will include information throughout the entire spectrum of casualty care, from initial resuscitation and surgery in the combat zone through definitive reconstruction. In addition, long-term data collection efforts are under way to help track outcomes following treatment of these severe injuries. Studies funded by the Department of Defense are included among these efforts to determine specific functional and patient-oriented outcomes following extremity trauma and limb salvage associated with blast injury. One such study, Military Extremity Trauma and Limb Salvage (METALS), is currently examining relative differences between amputation and limb salvage between 1 and 5 years after injury in warriors who have sustained high-energy extremity trauma. The Orthopaedic Extremity Trauma Research Program (OETRP) is a congressionally funded program focused specifically on improving care

Dr. Pollak or a member of his immediate family has received research or institutional support from Synthes, Stryker, Smith & Nephew, Zimmer, and Wyeth and is an employee or consultant of KCI. Dr. Hayda or a member of his immediate family has received research or institutional support from Howmedica, Synthes, and Smith & Nephew and has received miscellaneous nonincome support from Synthes. None of the following authors or a member of their immediate families has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Ficke, Dr. Andersen, Dr. Keeling, Dr. Keeney, Dr. Levin, Dr. Mazurek, Dr. Miclau, Dr. Nork, Dr. Bagg, Dr. Swiontkowski, and Dr. Watson.

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for extremity war injuries. The program is administered through the US Army Institute for Surgical Research at Fort Sam Houston, Texas; it uses a process similar to that utilized by the National Institutes of Health to evaluate and grade research proposals. A total of $19.3 million was appropriated by Congress for OETRP in 2006 and 2007, from which 26 studies have been funded. In total, 156 proposals were reviewed and given sufficiently high grades to warrant funding, suggesting that current congressional funding levels are sufficient to support only the top 17% of research grant applications. For 2008, $4.8 million was appropriated in the regular Department of Defense Appropriations Act. Additionally, as part of the Emergency Supplemental Appropriations Act for Defense, 2008, Congress recently approved $276.8 million for a series of specific research topics related to casualties sustained in Iraq and Afghanistan. Final determination is pending regarding how much of this money will be invested in the OETRP and other orthopaedicrelated research programs. The AAOS continues to work with the Department of Defense and Congress to achieve an annual operating level of at least $50 million for the OETRP specifically and for musculoskeletal research in general.

Management of Soft-tissue Defects Soft-issue injuries in the war zone represent perhaps the greatest challenge in limb reconstruction. Recent advances in several components of soft-tissue injury management may improve overall care for extremity injuries. One major ongoing concern regards the best method of managing open wounds during transportation from the military theater of operations to Landstuhl Regional Medical Center in Germany, as well as during transportation from Germany back 630

to the United States. Initial experiences suggested that utilization of traditional wet-to-dry dressings was safe and sufficiently effective. Disadvantages of this technique, however, include the inability to change dressings in flight, resulting in markedly prolonged intervals between dressing changes, with the resultant theoretic increase in infection risk. Additionally, although use of negativepressure wound therapy (NPWT) had been demonstrated to be safe and effective for wound management both within the theater of military operations and in the military hospitals in the United States, evidence supporting safety and efficacy of this technique during aeromedical transport was lacking.3 A retrospective review of the use of NPWT in aeromedical evacuation from Iraq and Afghanistan to Landstuhl Regional Medical Center indicates that the technique can be safely employed.4 A further prospective evaluation of safety is under way evaluating the use of NPWT during transport from Landstuhl Regional Medical Center to the United States. Improvement in the use of freetissue transfer for management of severe soft-tissue defects has resulted in apparent better utilization of this technique for limb salvage. Improvements include developing a better understanding of the scope of indications for utilization of free-tissue transfer techniques, increased understanding of the timing of appropriate free-tissue transfer in the combined context of patient and wound concerns, and appreciation of logistic considerations, including availability of an appropriately prepared and experienced microvascular surgeon.5,6 The soft tissues represent a composite of highly organized structures that include skin, muscle, tendon, ligament, nerve, and connective tissues. The proper organization of these tissues is required for locomotion and normal skeletal function. Current work is focused on under-

standing the properties of the individual components of the soft tissues and enhancing tissueengineering approaches to maximize the function of these components within the limb. One example is tendon reconstruction. Tendon function requires excellent tensile properties with near frictionless gliding. An animal model recently developed to study tendon defect reconstruction shows that coating a freezedried tendon allograft with a virus expressing growth differentiation factor 5 (GDF-5) markedly improves tendon gliding and accelerates wound healing.7,8 GDF-5 is a member of the transforming growth factor-beta/bone morphogenetic protein (TGF-β/BMP) signaling family that is involved in tendon formation. This and other work shows that approaches utilizing combinations of biocompatible materials, cells, and genes have the potential to meet some of the challenges of extremity reconstruction in the injured combatant that involve massive softtissue defects.

Segmental Bone Defects Segmental bone defects represent an ongoing challenge in the management of extremity trauma related to high-energy blast injuries. Although specific data regarding the prevalence of this problem are lacking, anecdotal reports from treating surgeons at all major military medical institutions suggest that defects lacking the capacity for spontaneous healing are common and that no single existing treatment option is appropriate for all defects. Furthermore, a subset of segmental defects cannot be predictably managed well with any existing treatment. Further development of treatment options therefore seems warranted from a clinical anecdotal standpoint. Several techniques have been used in civilian populations to treat bone defects, with varying degrees of

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success. Vascularized bone grafts have been successfully employed in civilian settings for the treatment of osteonecrosis of the femoral head and, anecdotally, in the reconstruction of segmental defects resulting from trauma, infection, and tumor resection.9,10 Limitations of this technique for treatment of traumatically acquired segmental defects concern structural adequacy of fibular grafts and donor site morbidity. Patients are understandably reluctant to consent to the harvest of tissue from an uninjured extremity in the context of limb-threatening, contralateral lower extremity trauma. Consensus opinion suggested that vascularized structural grafting was best suited for upper extremity defects.11 Early clinical experience with titanium mesh cages in conjunction with osteoinductive and osteoconductive grafting has been promising.12 Additional study is necessary to better understand the role for this technology in trauma and posttraumatic reconstruction. A major potential drawback to this technique is the incorporation of a foreign body into the endoskeleton of the bone in the context of an open injury with high propensity for both short- and long-term infectious complications. A substantial body of animal data, including studies with subhuman primates, suggests that use of recombinant BMPs (particularly BMP-2 and BMP-7) may be extremely effective in promoting healing of bone defects of critical size.13-15 Several human clinical comparative studies are available, and promising results already have been published. Prospective randomized analysis demonstrates efficacy in the use of recombinant BMP-2 for supplemental grafting of open tibial fractures at the time of surgical débridement and wound closure.16 Preliminary data in extremity war injuries also appear promising. More comparative studies would be helpful in better defining the role of recombinant proteins Volume 16, Number 11, November 2008

combined with structural and osteoconductive materials. An informal survey of military surgeons involved in the treatment of high-energy lower extremity war injuries suggests that distraction osteogenesis is the technique most frequently employed for treatment of bone defects that exceed approximately 8 cm in length, particularly in the tibia. Use of this modality has been simplified by the development of computer-aided distraction protocols that allow for correction of length and alignment without the need for major frame modification.17 As a result, utilization of these devices in the civilian sector has increased along with surgeon familiarity and comfort, a development that has likely led to a reciprocal increase in utilization and a progressive expansion of indications. However, two major drawbacks to the use of this treatment modality have been described. The first is the need for the patient to wear the frame for a prolonged period (typically 3 days for every millimeter of bone defect addressed).18 Second, the ring fixator that is typically employed limits access to the wound for flap coverage or dressing care. This often results in initiation of the distraction process being delayed until soft-tissue defects have been addressed, thereby further contributing to the substantial length of the treatment period. One technique described for employing distraction osteogenesis in the treatment of segmental bone defects uses internal rather than external fixation.19,20 Utilizing the intramedullary skeletal kinetic distractor involves creation of a corticotomy using an intramedullary saw, stabilization of the bone with an intramedullary nail, and transport over the nail using internal motors. There are no published series describing the use of this technique for trauma or posttraumatic defects, but the potential to address large defects without the need for prolonged

use of external fixation while maintaining access to the limb for wound care seems promising. A major potential drawback remains the need to rely on an internal fixation device for a prolonged period in the context of a high potential for infectious complications. Although high-quality comparison studies are lacking, the gold standard for treating small bony defects (<5 cm for segmental defects) remains autogenous cancellous graft.21 Potential sources include iliac crests and proximal tibia for large defects. For smaller defects, the distal radius and distal tibia are potentially valuable donor sites. Obvious drawbacks to the technique include limitations in the size of defect that can be adequately addressed and donor site morbidity, whose significance has varied widely in the available literature. For war-related injuries in particular, another major drawback concerns the potential need to address multiple bone defects associated with multiple limb trauma within the same patient. A simple option for addressing segmental defects is bony shortening. In the femur and tibia, subsequent lengthening can be done after initial shortening and healing. In the humerus, more substantial shortening can be considered as definitive treatment than in the lower extremity.

Management of Tibial Shaft Fractures More so than other topics covered at EWI III, the issue of management of tibial shaft fractures is one that can be guided by a substantial volume of medical literature associated with varying levels of scientific evidence. In the context of understanding the unique challenges posed by war injuries, discussions of the evidence, which is largely based on civilian injuries, yielded several recommendations for the treatment of tibial fractures sustained in a combat environment. 631

Extremity War Injuries: Challenges in Definitive Reconstruction

For closed tibial fractures, evidence and consensus support initial splinting for transport and aeromedical evacuation, followed by elective reamed, locked intramedullary nail fixation.22 Antibiotic prophylaxis using a first-generation cephalosporin preoperatively and for 24 hours postoperatively is recommended.23,24 Consensus opinion was that, unlike open tibial shaft fractures, closed fractures sustained in a combat environment are similar to those typically sustained and treated in a civilian environment, and they can therefore be treated similarly. Management of open tibial shaft fractures sustained as a result of high-energy combat injuries is more controversial. Recommendations were developed based on a combination of best-available medical evidence and consensus expert opinion based on experience in treating similar injuries in both Iraq and Afghanistan as well as at higher level treatment facilities in Germany and the United States. Evidence supporting early débridement of open tibial fractures in civilian settings is marginal. This early initial débridement of open tibial war injuries is recommended within 6 hours of injury when possible, based on logistic considerations, and when safe, based on physiologic considerations.25,26 Serial débridements every 48 hours until definitive wound closure and stabilization are recommended, despite the lack of supporting evidence other than expert opinion. Prophylaxis against infection using a first-generation cephalosporin is recommended on initial casualty presentation and for 24 hours after each surgical débridement. Although broader spectrum coverage often has been recommended for high-energy injuries sustained in civilian settings, studies are lacking comparing firstgeneration cephalosporins alone to broader coverage in war injuries.27 Open wounds can be managed efficaciously using NPWT dressings.3 Other options for wound manage632

ment also may be effective but, as with other components of injury management, specific comparison studies are lacking. Based purely on intuitive analysis, the combination of antibiotic beads with NPWT is unlikely to effectively deliver highconcentration local antibiotic therapy; however, the combination may represent an effective means of averting complication in the event of NPWT device failure. For multiple reasons, a low threshold is recommended for utilization of fasciotomies in the overall treatment of tibial shaft fractures associated with war injuries.28 First, many of these injuries result from high-energy blast mechanisms, thus increasing the risk for development of the complication. Second, logistic considerations put the injured warrior at risk for development of compartment syndrome during transit from one level of care to another when surgical decompression of the compartments involved may not be possible for a prolonged period. Third, anecdotal reports suggest that transportation of the injured warrior at altitude, such as occurs in a medevac helicopter or during fixed-wing transport, may further increase the risk of developing compartment syndrome. Finally, particularly for multiply injured patients, serial examination may be compromised, thus increasing the likelihood that early signs of developing compartment syndrome may be missed. The ongoing protocol for temporary stabilization of open tibial shaft fractures before definitive stabilization involves application of a monolateral external fixator in Iraq or Afghanistan before air evacuation to Germany and the United States.29,30 No studies have been published comparing the safety or efficacy of early definitive stabilization compared with staged treatment. Definitive treatment of open tibial fractures sustained in civilian environments with intramedullary nail stabilization is supported by prospec-

tive randomized studies.31,32 No similar studies are available comparing treatment options for battle-related injuries, but differences at least seem to be likely, based on differences in the injury mechanism. Opinions vary about the best method for management of open tibial fractures secondary to blast or high-velocity gunshot injuries, but concerns have been raised regarding anecdotally high infection rates in fractures treated with intramedullary nailing; good experiences have been reported with ring fixation for definitive treatment of these injuries.

Massive Periarticular Reconstructions Treatment of large defects of bone, cartilage, and soft-tissue associated with periarticular combat injuries represents a substantial, ongoing challenge for surgeons managing wounded warriors. Although some published reports have addressed treatment options, none includes control groups to allow for meaningful comparisons between treatment options. Furthermore, most series contain small numbers of patients and minimal outcome data.7,8,33-41 The consensus recommendation for management of massive periarticular defects was that treatment options used in any given case must consider the specific anatomic and physiologic challenges presented as well as the capabilities of the treating surgeon. Specific considerations should include soft-tissue envelope viability, presence or absence of evidence of infection, support of surrounding musculature, and available reconstruction options for relevant associated ligamentous or tendinous deficiencies. Age and activity demands of the patient, particularly with emphasis on the long-term effects on longevity of the reconstruction, also must be considered. Documentation of injury characteristics, treatments employed, and outcomes achieved will allow im-

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portant long-term future assessments of factors associated with successful management of these complex problems. This information can provide a good long-term basis for designing future prospective trials of treatment options for these injuries.42,43

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7.

8.

Conclusions The consensus at EWI III was that the opportunity to carefully review complicated management problems related specifically to war injuries was extremely valuable for the participants and, therefore, for injured warriors. In addition, substantial additional research directed at the treatment of high-energy extremity war injuries is critical and likely will lead to dramatic improvements in our military colleagues’ ability to achieve the best possible outcomes from these devastating injuries.

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Oper Orthop Traumatol 2005;17: 457-480. Garberina MJ, Fitch RD, Hoffmann ED, Hardaker WT, Vail TP, Scully SP: Knee arthrodesis with circular external fixation. Clin Orthop Relat Res 2001;382:168-178. Gross AE, Shasha N, Aubin P: Longterm follow-up of the use of fresh osteochondral allografts for posttraumatic knee defects. Clin Orthop Relat Res 2005;435:79-87. Kharrazi FD, Busfield BT, Khorshad DS, Hornicek FJ, Mankin HJ: Osteoarticular and total elbow allograft reconstruction with severe bone loss. Clin Orthop Relat Res 2008;466:205209. Lai D, Chen CM, Chiu FY, Chang MC, Chen TH: Reconstruction of juxtaarticular huge defects of distal femur with vascularized fibular bone graft

40.

41.

42.

43.

and Ilizarov’s distraction osteogenesis. J Trauma 2007;62:166-173. McAuliffe JA, Burkhalter WE, Ouellette EA, Carneiro RS: Compression plate arthrodesis of the elbow. J Bone Joint Surg Br 1992;74:300-304. Mears DC, Velyvis JH: Acute total hip arthroplasty for selected displaced acetabular fractures: Two to twelve-year results. J Bone Joint Surg Am 2002; 84:1-9. Bosse MJ, MacKenzie EJ, Kellam JF, et al: An analysis of outcomes of reconstruction or amputation after legthreatening injury. N Engl J Med 2002;347:1924-1931. Mackenzie EJ, Bosse MJ, Pollak AN, et al: Long-term persistence of disability following severe lower-limb trauma: Results of a seven-year follow up. J Bone Joint Surg Am 2005;87:18011809.

Journal of the American Academy of Orthopaedic Surgeons

Advancements in Ankle Arthroscopy

C. Niek van Dijk, MD, PhD Christiaan J. A. van Bergen, MD

Dr. van Dijk is Professor and Head, Department of Orthopaedic Surgery, Academic Medical Center, Amsterdam, The Netherlands. Dr. van Bergen is Research Fellow, Orthopaedic Research Center Amsterdam, Department of Orthopaedic Surgery, Academic Medical Center, Amsterdam. None of the following authors or a member of their immediate families has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. van Dijk and Dr. van Bergen. Reprint requests: Dr. van Bergen, Orthopaedic Research Center Amsterdam, Academic Medical Center, G4-262, Meibergdreef 9,1100 DD Amsterdam, The Netherlands. J Am Acad Orthop Surg 2008;16:635646 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

Volume 16, Number 11, November 2008

Abstract Important progress has been made during the past 30 years in arthroscopic ankle surgery. Ankle arthroscopy has gradually changed from a diagnostic to a therapeutic tool. Most arthroscopic procedures can be performed by using the anterior working area with the ankle in dorsiflexion or plantar flexion; there is no need for routine ankle distraction. Anterior ankle problems, such as anterior impingement syndrome, are approached by anteromedial and anterolateral portals and, if necessary, an accessory portal. Most osteochondral defects can be reached from anterior with the ankle in plantar flexion. For a far posterior location, the osteochondral defect can be approached from posterior. The twoportal hindfoot endoscopic technique (ie, both arthroscopic and endoscopic surgery), with the patient in the prone position, provides excellent access to the posterior ankle compartment and to posteriorly located extra-articular structures.

A

lthough Burman1 in 1931 found the ankle joint unsuitable for arthroscopy because of its typical anatomy, Tagaki2 and, later, Watanabe3 made considerable contributions to arthroscopic surgery. Watanabe3 in 1972 published the results of a series of 28 ankle arthroscopies. Numerous studies followed, and during the past 30 years, arthroscopy of the ankle joint has become an important procedure for the detection and treatment of chronic and posttraumatic problems. The main indications for anterior arthroscopy are for treatment of anterior impingement syndrome and talar osteochondral defects (OCDs).4,5 Endoscopic surgery (ie, both arthroscopic and endoscopic surgery), offers the possible advantages of direct visualization of structures, improved assessment of articular cartilage, less postoperative morbidity,

faster as well as functional rehabilitation, earlier resumption of sports, and outpatient treatment.6,7 The value of diagnostic arthroscopy is limited.4,8 Some authors advocate routine mechanical distraction combined with a 2.7-mm arthroscope.9 In most procedures, however, ankle arthroscopy can be performed more effectively without routine joint distraction.4,10 Posterior ankle problems pose a diagnostic and therapeutic challenge because of their nature and deep location. By means of a two-portal hindfoot approach with the patient in the prone position, posterior ankle joint problems (eg, loose bodies, ossicles, osteophytes, OCDs) can be treated.11 In the case of a posterior impingement syndrome, bony impediments (eg, os trigonum) can be detached and removed via the twoportal hindfoot approach.11 635

Advancements in Ankle Arthroscopy

Figure 1

Figure 2

Lateral (A) and anteromedial impingement (B) radiographs of the right ankle of a 32-year-old woman who reported progressive pain in the right ankle for 1 year. On palpation, a recognizable tenderness on the anteromedial distal tibia was noted. In the lateral view, no pathologic structures can be visualized. In the anteromedial impingement view, talar and tibial osteophytes are clearly visible (arrows).

Anterior Ankle Arthroscopy Indications and Contraindications Ankle problems that can be managed by means of routine anterior ankle arthroscopy include softtissue and bony impingement, synovitis, loose bodies, ossicles, and OCDs.5 Certain ankle fractures (eg, Weber type B distal fibular fracture, Tillaux fracture) also can be successfully treated by means of arthroscopy-assisted (open) reduction and internal fixation, which offers the advantage of direct visualization and treatment of concomitant intra-articular injuries.12-14 Other procedures include arthroscopic ankle stabilization by means of radiofrequency and arthroscopyassisted ankle arthrodesis. In case of multiple disorders (eg, a symptomatic OCD or ankle impingement with concomitant ankle instability), a combined treatment is often possible. Absolute contraindications are infection and severe degenerative changes. Relative contraindications 636

are degenerative changes with diminished range of motion, narrowing of the joint space, vascular disease, and edema.15 Diagnosis The value of diagnostic ankle arthroscopy without a preoperative diagnosis is limited; only 26% to 43% of patients benefit from the procedure.4,8 Hence, a diagnosis should be established preoperatively by physical examination and plain radiographs. If the diagnosis remains unclear, additional radiographs (eg, heel rise view, anteromedial impingement view) can be obtained16,17 (Figure 1). Furthermore, local infiltration can be performed. Temporary relief from pain after intra-articular infiltration suggests intra-articular pathology, such as soft-tissue impingement or an OCD. When an OCD, a loose body, or an ossicle is suspected, the lesion may be disclosed by magnetic resonance imaging (MRI) or spiral computed tomography (CT).17 If the CT scan is negative and the preoperative diagnosis remains unclear, it is unlikely

Positioning of the patient during anterior arthroscopy. The affected heel rests on the very end of the operating table, making it possible for the surgeon to fully dorsiflex the ankle joint by leaning against the sole of the foot.

that the patient will benefit from diagnostic arthroscopy.4,8 Routine Fixed Distraction Versus Dorsiflexion Previous investigators have reported the routine use of ankle joint distraction.9 The available noninvasive distraction devices are sterile and attach to the operating table. A strap connected to this distraction device is placed around the ankle. The surgeon using one of these devices stands beside the patient to perform the arthroscopic procedure. Ankle arthroscopy without distraction, however, allows the surgeon to stand at the bottom end of the operating table. In this position, the surgeon can lean against the patient’s foot, thereby bringing the ankle joint into the dorsiflexed position (Figure 2). Several important factors favor the use of dorsiflexion rather than distraction. First, distraction of the joint may result in tightening of the

Journal of the American Academy of Orthopaedic Surgeons

C. Niek van Dijk, MD, PhD, and Christiaan J. A. van Bergen, MD

Figure 3

Figure 4

A resterilizable distraction device, which permits the surgeon to move the ankle quickly from the dorsiflexed position to the distracted position and vice versa. Schematic lateral view of the ankle joint. A, In dorsiflexion, the anterior working area is enlarged. B, Distraction of the ankle joint (arrows) results in tightening of the anterior capsule, reducing the anterior working area.

anterior capsule, leading to a reduction of the anterior working area18 (Figure 3). Second, loose bodies and osteophytes are usually located in the anterior compartment of the ankle joint. Dorsiflexion creates an anterior working area, which makes removal easy. Introduction of saline solution opens the anterior working area. In the case of a loose body and distraction, the loose body may fall into the posterior aspect of the joint, which makes removal more difficult. Third, in the dorsiflexed position, the talus is concealed in the joint, thereby protecting the cartilage from potential iatrogenic damage.18 Mechanical distraction and use of a small-diameter arthroscope may be beneficial in some situations. These include treatment of ossicles, a softtissue impediment, a loose body caught in the joint space between the fibula and tibia (the intrinsic syndesmotic area), an OCD located in the posterior tibial plafond, and posterior ankle problems. An important alternative for the treatment of posterior ankle problems is a twoportal posterior arthroscopy.11 Should distraction be indicated, a resterilizable noninvasive distracVolume 16, Number 11, November 2008

tion device enables the surgeon to change quickly from the dorsiflexed position to the distracted position and vice versa19 (Figure 4). Surgical Technique The anterior dorsiflexion procedure4 is performed as outpatient surgery under general or epidural anesthesia. The patient is placed in the supine position with slight elevation of the ipsilateral buttock. A tourniquet is placed around the upper thigh. The heel of the affected foot rests on the very end of the operating table, thus making it possible for the surgeon to fully dorsiflex the ankle joint by leaning against the sole of the patient’s foot (Figure 2). The two primary anterior portals used for anterior ankle arthroscopy are the anteromedial and anterolateral, located at the level of the joint line. When their use is indicated, accessory anterior portals are located just in front of the tip of the medial or lateral malleolus. Some surgeons combine the anterior portals with a posterolateral portal.20 The anteromedial portal is made first. After a skin incision has been created just medial to the tibialis anterior tendon, the subcutaneous

layer is bluntly divided with a hemostat. The 4-mm, 30°-angle arthroscope, which we use routinely, is introduced in the fully dorsiflexed position. Saline solution is then introduced into the joint. Under arthroscopic control, the anterolateral portal is made by inserting a spinal needle lateral to the peroneus tertius tendon while respecting the superficial peroneal nerve (Figure 5). Depending on the procedure performed, the instruments can be exchanged between portals. After removal of the instruments, the arthroscopic incisions and accessory portals are closed with Ethilon sutures (Ethicon, Piscataway, NJ) to prevent sinus formation. Complications Several complications have been described, including injury to neurovascular structures, instrument breakage, articular surface damage, neuroma formation, infection, and reflex sympathetic dystrophy.20-23 The superficial peroneal nerve is at highest risk, and injury to this nerve is associated with the anterolateral portal.20 Reports of complications in ankle arthroscopy vary widely. With the use of either invasive or manual constant distraction, complication rates of 9% to 17% have been reported.20-23 637

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eventually result in osteoarthritis of the ankle.28

Figure 5

Anterior arthroscopy of a left ankle. A, External view. B, Arthroscopic view. Under arthroscopic control, the anterolateral portal is made by introducing a spinal needle lateral to the peroneus tertius tendon. AJ = anterior joint capsule, Lat = lateral, Med = medial, SN = spinal needle (guiding needle for a lateral portal), Tal = talus, Tib = tibia

Figure 6

Coronal (A) and sagittal (B) computed tomography reconstructions of a posteromedial osteochondral defect of the left talus in a 15-year-old girl. The patient presented with persistent deep pain on the anterior side of the left ankle and locking and giving way. One year before her visit, she had had a supination trauma, which had been treated nonsurgically.

In the largest series published to date, nearly 50% of complications were neurologic.20 The use of constant distraction might be indicative of higher complication rates. In a recent survey performed in our department in which 1,300 consecutive patients with ankle arthroscopy without routine joint distraction were included, the overall percentage of complications was 3.4%. This figure includes 1.4% for hindfoot endoscopy.24 638

Osteochondral Defects An OCD is a lesion involving articular cartilage and subchondral bone. The incidence of OCDs of the talar dome in patients with acute lateral ankle ligament ruptures is 4% to 7%.25,26 Talar OCDs are usually posteromedial (58%) or anterolateral (42%).27 Medial lesions are typically deep and cup-shaped; lateral lesions are shallow and wafer-shaped.28 Inappropriate treatment of OCDs may

Etiology Previous trauma to the ankle joint is reported in 93% of lateral lesions and 61% of medial lesions.27 In lateral lesions, the trauma mechanism is usually a combination of inversion and dorsiflexion; in medial lesions, the combination is inversion, plantar flexion, and rotation.29 In nontraumatic OCDs, possible causes are genetic, metabolic, vascular, endocrine, and degenerative factors as well as morphologic abnormalities.29,30 Clinical Presentation Patients with a chronic lesion typically experience persistent or intermittent deep ankle pain during or after activity, sometimes accompanied by swelling and limited range of motion. Often, on examination, few abnormalities are found. Affected ankles may have a normal range of motion with the absence of swelling and no recognizable tenderness on palpation. Diagnosis Routine radiographs consist of weight-bearing anteroposterior and lateral views of both ankles. The radiographs may show an area of detached bone surrounded by radiolucency. Initially, the damage may be too small to be visualized on a routine radiograph. A heel rise mortise view may reveal a posterior defect.17 For further diagnostic evaluation, CT and MRI have demonstrated similar accuracy.17 A multislice helical CT scan is preferred because it is more helpful for preoperative planning (Figure 6). Classification and Staging Several classifications based on radiography, CT, MRI, and arthroscopy have been proposed.29,31-33 The first and most frequently used classification was that of Berndt and Harty:29 stage I, a small compression fracture; stage II, incomplete avul-

Journal of the American Academy of Orthopaedic Surgeons

C. Niek van Dijk, MD, PhD, and Christiaan J. A. van Bergen, MD

sion of a fragment; stage III, complete avulsion of a fragment without displacement; and stage IV, displaced fragment. Scranton and McDermott34 later added stage V, representing cystic lesions. None of the current grading systems, however, is sufficient to direct the choice of treatment. Treatment Various surgical techniques for the treatment of symptomatic osteochondral lesions have been published. These are generally based on one of the following three principles:30 (1) débridement and bone marrow stimulation (microfracturing, drilling, abrasion arthroplasty); (2) securing a lesion to the talar dome (fragment fixation, retrograde drilling, bone grafting); and (3) development or replacement of hyaline cartilage (autologous chondrocyte implantation [ACI], osteochondral autograft transplantation [OAT; ie, mosaicplasty], allografts). The choice of treatment depends on the patient’s age, symptoms, duration of complaints, and location and size of the defect, as well as whether it concerns a primary or secondary OCD.30,35 Asymptomatic or low symptomatic lesions are treated nonsurgically for a trial period of 6 months, consisting of rest, ice, temporarily reduced weight bearing, and, in case of giving way, an orthosis.30,36 Symptomatic lesions are treated primarily by débridement and bone marrow stimulation.27 With this technique, all unstable cartilage is removed, including the underlying necrotic bone. Any cysts underlying the defect are opened and curetted. The sclerotic-calcified zone that is most commonly present is perforated by means of microfracturing into the vascularized subchondral bone. The underlying intraosseous blood vessels are disrupted and growth factors are released, leading to the formation of a fibrin clot in the created defect. The formation of local new blood vessels is stimulated, marrow Volume 16, Number 11, November 2008

cells are introduced into the OCD, and fibrocartilaginous tissue is formed.37 In case of a cystic defect ≥15 mm in size, a cancellous bone graft may be placed in the defect.35 Retrograde drilling, combined with cancellous bone grafting when necessary, may be performed for primary OCDs when there is intact cartilage with a large subchondral cyst.32 When primary treatment fails, OAT or ACI are options.38,39 Although both techniques are promising, results are not yet widely published, and the number of patients included in studies is small. OAT consists of harvesting one or more osteochondral plugs in a lesser–weight-bearing area of the knee and transplanting them into the talar defect.38 Although most reports show excellent results, the technique is associated with donor site morbidity, and a medial malleolar osteotomy is often required.40-42 ACI is the implantation of in vitro–cultured autologous chondrocytes, using a periosteal tissue cover after expansion of isolated chondrocytes. Despite excellent results reported by some investigators,39,43 disadvantages include the two-stage surgery, high cost, and reported donor site morbidity.40,43 Fragment fixation with one or two lag screws is preferred in acute or semiacute situations in which the fragment is ≥15 mm. In adolescents, fixation of an OCD always should be considered following failure of a 6-month period of conservative treatment. The size and location of the lesion determine whether to use a standard 4.0-mm arthroscope and treat the OCD in the anterior working area by full plantar flexion of the ankle, or to use a 2.7-mm arthroscope in combination with mechanical distraction.4,36 In patients with unlimited plantar flexion, all defects located in the anterior half of the talus or in the anterior part of the posterior half can be reached and treated by anterior arthroscopy.4,36 Other options are to

approach the defect from posterior by means of a two-portal hindfoot approach or to proceed by means of a medial malleolar osteotomy.11,44 Surgical Technique and Rehabilitation A 4.0-mm scope and a 4.5- or 5.5mm shaver are routinely used. In case of synovitis, a local synovectomy is performed with the ankle in the dorsiflexed position. The lesion is identified in the forced plantarflexed position by palpating the cartilage with a probe or hook (Figure 7). During this part of the procedure, a soft-tissue distractor can be applied (Figure 4). If possible, the full-radius resector is introduced into the defect. In doubtful cases, identifying the defect by introducing a spinal needle, probe, or curet can be useful before introduction of the resector. The key to success is identifying the anterior part of the defect and removing the unstable cartilage and subchondral necrotic bone. The instruments are subsequently brought into the defect to treat the posterior part. Every step in the débridement procedure is checked by regularly switching portals. After full débridement, the sclerotic zone is penetrated by means of a microfracture probe or a Kirschner wire (Figure 7). Postoperatively, a compression dressing is applied. Active plantar flexion and dorsiflexion are encouraged. Partial weight bearing (ie, egg shell pressure) is allowed as tolerated. We allow progress to full weight bearing within 2 to 4 weeks in patients with central or posterior lesions of up to 1 cm. Larger lesions and anterior lesions require partial weight bearing up to 6 weeks. Running on even ground is permitted after 12 weeks.30 Full return to normal and sporting activities is usually possible 4 to 6 months after surgery. Results In the treatment of osteochondral lesions, nonsurgical therapy yields a 639

Advancements in Ankle Arthroscopy

Figure 7

Arthroscopic images of débridement and drilling of a lateral osteochondral defect (OCD) of the right talus. A, The arthroscope is in the anteromedial portal. With the ankle in the neutral position, the OCD is out of the arthroscopic view. B, By bringing the ankle into the forced plantarflexed position, the OCD can be seen. C, The size of the lesion is identified by palpating the cartilage with a probe (arrows), which is inserted through the anterolateral portal. D, Next, a shaver is introduced for débridement of the defect. E, With the use of a Kirschner wire (K-wire), small holes are drilled in the subchondral bone. F, Arthroscopic view, after switching portals, of the microfractured lesion. G, During loosening of the tourniquet, sufficient hemorrhage in the defect is checked.

45% success rate.27 However, a trial period of nonsurgical treatment does not adversely affect the outcome of surgery.44 In a systematic review of the literature, treatment by débridement and bone marrow stimulation was superior to other methods, with a mean of 86% good or excellent results in 21 studies (total, 272 patients).27 However, OAT and ACI were not included because of the few number of studies using these methods, and sizes of the treated lesions were not described. A recent randomized controlled trial that compared chondroplasty, microfracture, and OAT showed similar results among these methods at 2-year follow-up.45 However, the chondroplasty and microfracture techniques are recommended because of less postoperative pain. Furthermore, costs are lower compared with those of other techniques.40 640

Anterior Ankle Impingement Chronic anterior ankle pain is commonly caused by formation of tibial or talar osteophytes at the anterior part of the ankle joint. Morris46 and later McMurray47 named this condition athlete’s ankle or footballer’s ankle; these terms later were replaced by anterior ankle impingement syndrome. The condition predominately affects soccer players, but it also occurs in runners, ballet dancers, high jumpers, and volleyball players.10 Etiology Various theories exist regarding the causes of anterior impingement: traction, trauma, recurrent microtrauma, and chronic ankle instability.7,47-49 The hypothesis of traction is not plausible because the anterior joint capsule is attached

more proximally to the site where the tibial spurs originate.50-52 In trauma secondary to or associated with supination stress, damage to the non–weight-bearing cartilage rim often occurs.26 A repair reaction is initiated, with cartilage proliferation, scar tissue formation, and calcification. Ankle sprains resulting from chronic instability as well as forced dorsiflexion enhance this process.49,53 The pain in anterior ankle impingement likely is caused by the inflamed soft tissue along the anterior tibiotalar joint line, which is compressed by the talar and tibial osteophytes during forced dorsiflexion.50,54 Clinical Presentation Anterior ankle impingement is characterized by anterior pain at the level of the ankle joint, swelling after activity, and, occasionally, limited dorsiflexion.7 Athletes with recurrent ankle sprains are prone to

Journal of the American Academy of Orthopaedic Surgeons

C. Niek van Dijk, MD, PhD, and Christiaan J. A. van Bergen, MD

this condition, and sporting activities are often reduced because of the pain. On palpation, recognizable tenderness is noted on the anterior bone at the joint level. Tenderness on palpation medial to the tibialis anterior tendon indicates anteromedial impingement; tenderness lateral to the peroneus tertius tendon indicates anterolateral impingement54 (Figure 8). Forced hyperdorsiflexion may provoke the pain, but this test is often false-negative. Diagnosis Standard anteroposterior and lateral radiographs may not detect the presence of osteophytes. When anteromedial osteophytes are suspected, an oblique radiograph should be added because some osteophytes may be undetected by standard radiographs.16 Anteromedial tibial or talar osteophytes may be overprojected by the anterolateral border of the distal tibia or by the lateral part of the talar neck and body, respectively. In the oblique anteromedial impingement view, the beam is tilted in a 45° craniocaudal direction, with the leg in 30° external rotation and the foot in plantar flexion in relation to the standard lateral radiograph position (Figure 9). The anteromedial impingement radiograph has a high sensitivity for detecting anteromedial osteophytes: 93% for tibial and 67% for talar osteophytes16 (Figure 1). Treatment and Rehabilitation Although nonsurgical treatment such as intra-articular injections and heel lifts is recommended in the early stage of anterior ankle impingement, outcome is frequently disappointing. The arthroscopic approach is performed as described above. With the ankle in the dorsiflexed position, the contour of the anterior tibia is identified by shaving away the tissue just superior to the osteophyte. A 4-mm chisel and/or motorVolume 16, Number 11, November 2008

ized shaver system is subsequently used to remove them. A compression bandage is applied, and partial weight bearing for 3 to 5 days is permitted as tolerated. Active dorsiflexion is encouraged. Results Open resection and arthroscopic resection of osteophytes were compared by Scranton and McDermott.6 The average length of hospitalization and time to recovery were shorter in the arthroscopic group. In prospective studies, success rates varied from 73% to 96%.51,55,56 A significant difference in outcomes was seen between patients with normal joint spaces (90% success) and those with joint space narrowing (50% success).51 This finding was later confirmed in two long-term follow-up studies.52,57 Because the alternative in these osteoarthritic patients is arthrodesis, a 50% success rate is acceptable. Both series52,57 also reported a high rate of recurrence of osteophytes. However, no statistical correlation was seen between recurrence of osteophytes and return of symptoms.

Figure 8

Localization of anterior impingement. When a patient recognizes the local tenderness on palpation lateral to the peroneus tertius tendon (A) or medial to the tibialis anterior tendon (B), the diagnosis of anterolateral or anteromedial impingement is made, respectively. AC = anterocentral region, AL = anterolateral region, AM = anteromedial region Figure 9

Hindfoot Endoscopy History The deep location of hindfoot structures makes direct access difficult. Historically, the hindfoot was approached by a three-portal technique (ie, anteromedial, anterolateral, posterolateral), with the patient in the supine position.20 The traditional posteromedial portal is associated with potential damage to the tibial nerve, the posterior tibial artery, and local tendons.15 A two-portal endoscopic approach with the patient in the prone position was introduced in 2000.11 This technique has been shown to provide excellent access to the posterior ankle compartment, the subtalar joint, and extra-articular structures.11

In the oblique anteromedial impingement view, the beam is tilted 45° in a craniocaudal direction, with the leg in 30° external rotation and the foot in plantar flexion in relation to the standard lateral radiograph position.

Indications The main indications for endoscopy in the posterior compartment of the talocrural joint are posterior641

Advancements in Ankle Arthroscopy

Figure 10

Figure 11

During hindfoot endoscopy the patient is placed in the prone position. A tourniquet (T) is applied around the upper leg, and a small support (S) is placed under the lower leg, which makes it possible to move the ankle freely. The forced hyperplantar flexion test. The patient is sitting with the knee flexed in 90°. The test is performed by repetitive, quick, passive hyperplantar flexion movements (arrow). This may be repeated in slight external or internal rotation of the foot. The investigator may apply this rotational movement on the point of maximal plantar flexion, thereby “grinding” the posterior talar process or os trigonum between the tibia and calcaneus.

ly located OCDs of the ankle joint, loose bodies, ossicles, posttraumatic calcifications or avulsion fragments, posterior tibial rim osteophytes, chondromatosis, and chronic synovitis.24 In the posterior compartment of the subtalar joint, the main indications are osteophytes, loose bodies, an intraosseous talar ganglion, and subtalar arthrodesis. Other extra-articular structures that can potentially be treated are the posterior tibial tendon, the flexor hallucis longus tendon, the peroneal tendons, the Achilles tendon, the deep portion of the deltoid ligament, and a symptomatic os trigonum or hypertrophic talar process.24 Posterior Ankle Impingement Posterior ankle impingement syndrome is a clinical diagnosis in 642

which the patient experiences pain in the hindfoot when the ankle is forced into a plantarflexed position (Figure 10). It is caused by overuse or trauma and mainly occurs in ballet dancers, downhill runners, and soccer players.54 After an injection of lidocaine, the forced hyperplantar flexion test should be negative. On plain radiographs and CT, an os trigonum or hypertrophic posterior talar process may be detected. Treatment consists of resection of a symptomatic os trigonum, reduction of a prominent posterior talar process, or removal of a soft-tissue impediment. Surgical Technique and Rehabilitation The procedure is performed as outpatient surgery under general or epidural anesthesia. The patient is placed in a prone position. A tourniquet is applied around the upper leg, and a small support is placed under the lower leg, making it possible to move the ankle freely (Figure 11). A soft-tissue distraction device can be used when indicated.19 For irrigation, normal saline with gravity flow is suitable. A 4.0-mm, 30° arthroscope is routinely used for posterior ankle arthroscopy. In addition to the standard excisional and motorized

instruments for treatment of osteophytes and ossicles, a 4-mm chisel and small periosteal elevator can be useful. With the ankle in the neutral position, a line is drawn from the tip of the lateral malleolus to the Achilles tendon, parallel to the foot sole. The posterolateral portal is situated just above this line, in front of the Achilles tendon (Figure 12, A). After a vertical stab incision is made, the subcutaneous layer is split by a mosquito clamp. The mosquito clamp is directed anteriorly, pointing in the direction of the interdigital web space between the first and second toe (Figure 13). When the tip of the clamp touches the bone, it is exchanged for a 4.0-mm arthroscope. The direction of view is 30° to the lateral side. The posteromedial portal is now made at the same level (Figure 12, B). After making a vertical stab incision in front of the medial aspect of the Achilles tendon, a mosquito clamp is introduced and directed toward the arthroscope shaft in a 90° angle. When it touches the shaft of the arthroscope, it is moved anteriorly in the direction of the ankle joint, all the way down, touching the arthroscope shaft until it reaches the bone (Figure 14). The arthroscope is now

Journal of the American Academy of Orthopaedic Surgeons

C. Niek van Dijk, MD, PhD, and Christiaan J. A. van Bergen, MD

Figure 12

Figure 13

Portal placement in a right ankle during hindfoot endoscopy. A, The posterolateral portal (PL) is made just above the line from the tip of the lateral malleolus (LM) to the Achilles tendon (AT), parallel to the foot sole, just in front of the Achilles tendon. B, The posteromedial portal (arrow) is made at the same level as the posterolateral portal, just above the line from the tip of the medial malleolus, in front of the medial aspect of the Achilles tendon. Figure 14

The posterolateral instrument (2) is directed anteriorly, pointing in the direction of the interdigital web space between the first and second toe (1).

Schematic transverse section of the right ankle joint at the level of the arthroscope. A = the posterolateral portal is made first. The arthroscope is directed toward the first web space. B = the posteromedial portal is made at the same level. The mosquito clamp is directed toward the arthroscope shaft at a 90° angle. C = when the mosquito clamp touches the shaft of the arthroscope, the clamp is moved anteriorly in the direction of the ankle joint, all the way down, touching the arthroscope shaft until it reaches the bone (curved arrow). All following instruments (eg, shaver) are introduced in the same manner. Volume 16, Number 11, November 2008

pulled slightly backward until the tip of the mosquito clamp comes into view. The clamp is used to spread the extra-articular soft tissue in front of the tip of the lens. In situations where scar tissue or adhesions are present, the mosquito clamp is exchanged for a 4.5-mm full-radius shaver. After removal of the very thin joint capsule of the subtalar joint by a few turns of the shaver, the posterior compartment of the subtalar joint can be visualized. At the level of the ankle joint, the posterior tibiofibular and talofibular ligaments are identified. The posterior talar process can be freed of scar tissue, and the flexor hallucis longus tendon is identified. The flexor hallucis longus tendon is an important landmark to prevent damage to the medial neurovascular bundle (Figure 15). One should always 643

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Figure 15

Figure 16

A and B, Hindfoot endoscopy of the right ankle. A combination of two separate procedures is shown. The flexor hallucis longus (FHL) is the important landmark in posterior ankle arthroscopy. Instruments should always stay lateral to this tendon. Viewing medial to the FHL (panel A) reveals the neurovascular bundle (tibial nerve [N], and the posterior tibial artery and veins [V]). This medial view is indicated only when a tarsal tunnel release is performed. Lat = lateral, M = mosquito clamp in lateral portal, Med = medial

stay lateral to this tendon and move medially only when release of the neurovascular bundle is indicated (eg, tarsal tunnel syndrome). After removal of the thin joint capsule of the ankle joint, the ankle joint can be entered and inspected. Removal of a symptomatic os trigonum or treatment of a nonunion of a posterior talar process fracture involves partial detachment of the posterior talofibular ligament, release of the flexor retinaculum, and release of the posterior talocalcaneal ligament (Figure 16). The os trigonum can be lifted from the subtalar joint by means of a small-sized bone elevator (Figure 17) and removed with a grasper. At the end of the procedure, hemorrhage is controlled by electrocautery, and the skin is closed with Ethilon sutures. A sterile compression dressing is applied. Postoperative treatment is functional and consists of weight bearing on crutches as tolerated for 3 days, after which the dressing is removed. The patient is advised to start rangeof-motion exercises as soon as possi644

Endoscopic view of a left ankle. Removal of a symptomatic os trigonum or treatment of a nonunion of a posterior talar process fracture involves partial detachment of the posterior talofibular ligament (PTFL), release of the flexor hallucis longus (FHL) retinaculum, and release of the posterior talocalcaneal ligament (TCL). Lat = lateral, Med = medial

Figure 17

ble after surgery. If necessary, physiotherapy is begun. Results We performed 146 endoscopic hindfoot procedures on 136 consecutive patients.24 The main indications were bony impingement, OCDs, and flexor hallucis longus tendinitis. Treatment was successful in most patients; two minor complications (1.4%) were seen (ie, an area of diminished sensation over the heel pad of the hindfoot in both cases).24 Similar results have been published by other surgeons.58 Furthermore, the technique described is considered to be a safe method, according to a recent anatomic study.59 It is recommended that the procedure be performed by an experienced arthroscopist who has practiced this type of surgery in a cadaveric setting at arthroscopy courses.60,61

Summary Over the last three decades, the field of arthroscopic foot and ankle sur-

Endoscopic view of a right ankle. The os trigonum can be lifted from the subtalar joint with a small bone elevator. Lat = lateral, Med = medial

gery has progressed significantly. Arthroscopy of the ankle joint has become the procedure of choice for the treatment of chronic and posttraumatic pathologies. The diagnosis should be established before surgery. When necessary, CT and additional radiographs (eg, heel rise view, anteromedial impingement view) can be obtained to confirm a clinical diagnosis and for preoperative planning. When the dorsiflexed position is used with anterior arthroscopy,

Journal of the American Academy of Orthopaedic Surgeons

C. Niek van Dijk, MD, PhD, and Christiaan J. A. van Bergen, MD

ankle distraction is necessary only in a minority of cases. Most OCDs can be treated by anterior arthroscopic débridement and microfracturing with the ankle in plantar flexion. The anterior impingement syndrome is treated by arthroscopic excision of osteophytes. Posterior ankle problems (eg, posterior impingement syndrome) can be effectively treated by means of a two-portal hindfoot approach with the patient in the prone position. This approach offers excellent access to the posterior ankle compartment, the subtalar joint, and extra-articular structures.

8.

9.

10.

11.

12.

Acknowledgment Peter A. J. de Leeuw, PhD fellow, is gratefully acknowledged for the kind preparation of Figures 1, 4 through 8, 10 through 13, and 15 through 17.

References Evidence-based Medicine: There are three level I/II studies (references 17, 27, and 45); the remainder are level III/IV and level V, including two online course descriptions. Citation numbers printed in bold type indicate references published within the past 5 years. 1.

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Burman MS: Arthroscopy or the direct visualization of joints: An experimental cadaver study. J Bone Joint Surg Am 1931;13:669-695. Tagaki K: The arthroscope. J JPN Orthop Assoc 1939;14:349-411. Watanabe M: Sefloc-Arthroscope (Watanabe no. 24 arthroscope): Monograph. Tokyo, Japan: Teishin Hospital, 1972. van Dijk CN, Scholte D: Arthoscopy of the ankle joint. Arthroscopy 1997; 13:90-96. Ferkel RD, Small HN, Gittins JE: Complications in foot and ankle arthroscopy. Clin Orthop Relat Res 2001;391:89-104. Scranton PE Jr, McDermott JE: Anterior tibiotalar spurs: A comparison of open versus arthroscopic debridement. Foot Ankle 1992;13:125-129. Cutsuries AM, Saltrick KR, Wagner J,

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Catanzariti AR: Arthroscopic arthroplasty of the ankle joint. Clin Podiatr Med Surg 1994;11:449-467. van Dijk CN, Verhagen RAW, Tol JL: Arthroscopy for problems after ankle fracture. J Bone Joint Surg Br 1997; 79:280-284. Boynton MD, Parisien JS, Guhl JF, Vetter CS: Setup, distraction, and instrumentation, in Guhl JF (ed): Foot and Ankle Arthroscopy, ed 3. New York, NY: Springer, 2004, pp 87-97. Tol JL, van Dijk CN: Anterior ankle impingement. Foot Ankle Clin 2006; 11:297-310. van Dijk CN, Scholten PE, Krips R: A 2-portal endoscopic approach for diagnosis and treatment of posterior ankle pathology. Arthroscopy 2000;16:871876. Takao M, Uchio Y, Naito K, Fukazawa I, Kakimaru T, Ochi M: Diagnosis and treatment of combined intra-articular disorders in acute distal fibular fractures. J Trauma 2004;57:1303-1307. Ono A, Nishikawa S, Nagao A, Irie T, Sasaki M, Kouno T: Arthroscopically assisted treatment of ankle fractures: Arthroscopic findings and surgical outcomes. Arthroscopy 2004;20:627631. Panagopoulos A, van Niekerk L: Arthroscopic assisted reduction and fixation of a juvenile Tillaux fracture. Knee Surg Sports Traumatol Arthrosc 2007;15:415-417. Ferkel RD, Fischer SP: Progress in ankle arthroscopy. Clin Orthop Relat Res 1989;240:210-220. Tol JL, Verhagen RAW, Krips R, et al: The anterior ankle impingement syndrome: Diagnostic value of oblique radiographs. Foot Ankle Int 2004;25: 63-68. Verhagen RAW, Maas M, Dijkgraaf MGW, Tol JL, Krips R, van Dijk CN: Prospective study on diagnostic strategies in osteochondral lesions of the talus: Is MRI superior to helical CT? J Bone Joint Surg Br 2005;87:41-46. Golano P, Vega J, Pérez-Carro L, Götzens V: Ankle anatomy for the arthroscopist: Part I. The portals. Foot Ankle Clin 2006;11:253-273. van Dijk CN, Verhagen RAW, Tol JL: Resterilizable noninvasive ankle distraction device. Arthroscopy 2001; 17:1-5. Ferkel RD, Heath DD, Guhl JF: Neurological complications of ankle arthroscopy. Arthroscopy 1996;12:200208. Guhl JF: New concepts (distraction) in ankle arthroscopy. Arthroscopy 1988;4:160-167.

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Barber FA, Click J, Britt BT: Complications of ankle arthroscopy. Foot Ankle 1990;10:263-266. Unger F, Lajtai G, Ramadani F, Aitzetmüller G, Orthner E: Arthroscopy of the upper ankle joint: A retrospective analysis of complications [German]. Unfallchirurg 2000;103:858-863. van Dijk CN: Hindfoot endoscopy. Foot Ankle Clin 2006;11:391-414. Bosien WR, Staples OS, Russell SW: Residual disability following acute ankle sprains. J Bone Joint Surg Am 1955;37:1237-1243. van Dijk CN, Bossuyt PMM, Marti RK: Medial ankle pain after lateral ligament rupture. J Bone Joint Surg Br 1996;78:562-567. Verhagen RAW, Struijs PAA, Bossuyt PMM, van Dijk CN: Systematic review of treatment strategies for osteochondral defects of the talar dome. Foot Ankle Clin 2003;8:233-242. Canale ST, Belding RH: Osteochondral lesions of the talus. J Bone Joint Surg Am 1980;62:97-102. Berndt AL, Harty M: Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 1959;41:988-1020. Zengerink M, Szerb I, Hangody L, Dopirak RM, Ferkel RD, van Dijk CN: Current concepts: Treatment of osteochondral ankle defects. Foot Ankle Clin 2006;11:331-359. Anderson IF, Crichton KJ, GrattanSmith T, Cooper RA, Brazier D: Osteochondral fractures of the dome of the talus. J Bone Joint Surg Am 1989; 71:1143-1152. Taranow WS, Bisignani GA, Towers JD, Conti SF: Retrograde drilling of osteochondral lesions of the medial talar dome. Foot Ankle Int 1999;20: 474-480. Hepple S, Winson IG, Glew D: Osteochondral lesions of the talus: A revised classification. Foot Ankle Int 1999;20:789-793. Scranton PE Jr, McDermott JE: Treatment of type V osteochondral lesions of the talus with ipsilateral knee osteochondral autografts. Foot Ankle Int 2001;22:380-384. Giannini S, Buda R, Faldini C, et al: Surgical treatment of osteochondral lesions of the talus in young active patients. J Bone Joint Surg Am 2005;87(suppl 2):28-41. Schuman L, Struijs PAA, van Dijk CN: Arthroscopic treatment for osteochondral defects of the talus: Results at follow-up at 2 to 11 years. J Bone Joint Surg Br 2002;84:364-368. O’Driscoll SW: Current concepts re-

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view: The healing and regeneration of articular cartilage. J Bone Joint Surg Am 1998;80:1795-1812. Hangody L, Fules P: Autologous osteochondral mosaicplasty for the treatment of full-thickness defects of weight-bearing joints. J Bone Joint Surg Am 2003;85(suppl 2):25-32. Baums MH, Heidrich G, Schultz W, Steckel H, Kahl E, Klinger HM: Autologous chondrocyte implantation for treating cartilage defects of the talus. J Bone Joint Surg Am 2006;88:303308. Giannini S, Vannini F: Operative treatment of osteochondral lesions of the talar dome: Current concepts review. Foot Ankle Int 2004;25:168175. Baltzer AWA, Arnold JP: Bonecartilage transplantation from the ipsilateral knee for chondral lesions of the talus. Arthroscopy 2005;21:159166. Reddy S, Pedowitz DI, Parekh SG, Sennett BJ, Okereke E: The morbidity associated with osteochondral harvest from asymptomatic knees for the treatment of osteochondral lesions of the talus. Am J Sports Med 2007;35: 80-85. Whittaker JP, Smith G, Makwana N, et al: Early results of autologous chondrocyte implantation in the talus. J Bone Joint Surg Br 2005;87:179-183. Alexander AH, Lichtman DM: Surgical treatment of transchondral talardome fractures (osteochondritis dissecans): Long-term follow-up. J Bone Joint Surg Am 1980;62:646-652. Gobbi A, Francisco RA, Lubowitz JH,

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Allegra F, Canata G: Osteochondral lesions of the talus: Randomized controlled trial comparing chondroplasty, microfracture, and osteochondral autograft transplantation. Arthroscopy 2006;22:1085-1092. Morris LH: Report of cases of athlete’s ankle. J Bone Joint Surg Am 1943;25: 220. McMurray TP: Footballer’s ankle. J Bone Joint Surg Br 1950;32:68-69. Tol JL, Slim E, van Soest AJ, van Dijk CN: The relationship of the kicking action in soccer and anterior ankle impingement syndrome: A biomechanical analysis. Am J Sports Med 2002;30:45-50. Biedert R: Anterior ankle pain in sports medicine: Aetiology and indications for arthroscopy. Arch Orthop Trauma Surg 1991;110:293-297. Tol JL, van Dijk CN: Etiology of the anterior ankle impingement syndrome: A descriptive anatomical study. Foot Ankle Int 2004;25:382386. van Dijk CN, Tol JL, Verheyen CCPM: A prospective study of prognostic factors concerning the outcome of arthroscopic surgery for anterior ankle impingement. Am J Sports Med 1997;25:737-747. Tol JL, Verheyen CP, van Dijk CN: Arthroscopic treatment of anterior impingement in the ankle: A prospective study with a five- to eight-year followup. J Bone Joint Surg Br 2001;83:9-13. Krips R, van Dijk CN, Halasi T, et al: Anatomical reconstruction versus tenodesis for the treatment of chronic anterolateral instability of the ankle

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joint: A 2- to 10-year follow-up, multicenter study. Knee Surg Sports Traumatol Arthrosc 2000;8:173-179. van Dijk CN: Anterior and posterior ankle impingement. Foot Ankle Clin 2006;11:663-683. Amendola A, Petrik J, WebsterBogaert S: Ankle arthroscopy: Outcome in 79 consecutive patients. Arthroscopy 1996;12:565-573. Baums MH, Kahl E, Schultz W, Klinger HM: Clinical outcome of the arthroscopic management of sportsrelated “anterior ankle pain”: A prospective study. Knee Surg Sports Traumatol Arthrosc 2006;14:482486. Coull R, Raffiq T, James LE, Stephens MM: Open treatment of anterior impingement of the ankle. J Bone Joint Surg Br 2003;85:550-553. Willits K, Sonneveld H, Amendola A, Giffin JR, Griffin S, Fowler PJ: Outcome of posterior ankle arthroscopy for hindfoot impingement. Arthroscopy 2008;24:196-202. Lijoi F, Lughi M, Baccarani G: Posterior arthroscopic approach to the ankle: An anatomic study. Arthroscopy 2003;19:62-67. Arthroscopy Association of North America. Master courses: Foot/ankle. Available at: http://www.aana.org/ cme/MastersCourses/descriptions.as px#Foot/Ankle. Accessed August 28, 2008. Amsterdam Foot & Ankle Platform. Available at: http://www.ankleplatf orm.com/page.php?id=854. Accessed August 28, 2008.

Journal of the American Academy of Orthopaedic Surgeons

Radiocarpal Fracture-dislocations

Asif M. Ilyas, MD Chaitanya S. Mudgal, MD

Dr. Ilyas is Director, Temple Hand Center, and Assistant Professor, Department of Orthopaedic Surgery and Sports Medicine, Temple University Hospital, Philadelphia, PA. Dr. Mudgal is Instructor in Orthopaedic Surgery, Harvard Medical School, Massachusetts General Hospital, Boston, MA. None of the following authors or a member of their immediate families has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Ilyas and Dr. Mudgal. Reprint requests: Dr. Mudgal, Yawkey Center, Suite 2100, 55 Fruit Street, Boston, MA 02114. J Am Acad Orthop Surg 2008;16:647655 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

Volume 16, Number 11, November 2008

Abstract Radiocarpal fracture-dislocations most often are caused by highenergy trauma. These difficult, uncommon injuries involve significant soft-tissue and osseous trauma, requiring meticulous reduction and fixation. The mechanism of injury is generally a severe shear or rotational insult. Anatomically, the dislocation results in disruption of the radiocarpal ligaments and, usually, both the radial and the ulnar styloid. Understanding the anatomy of the radiocarpal joint is central to understanding the osseous and softtissue constraints that are disrupted with a radiocarpal dislocation. Diagnosis can be reliably made on physical examination and radiographic evaluation. Radiocarpal fracture-dislocation injuries must be differentiated from Barton fractures. Associated injuries such as open fractures, neurovascular involvement, and distal radioulnar dislocations also must be taken into account. Closed reduction can be obtained relatively easily, but open reduction and internal fixation is typically necessary to ensure accurate anatomic restoration of injured bone and ligaments.

R

adiocarpal fracture-dislocations are complex injuries characterized by dislocation of the radiocarpal joint. The dislocation may be in either a dorsal or a volar direction and can be associated with fractures of the cortical rim of the distal radius, the radial styloid, and the ulnar styloid. Prior to the descriptions of Pouteau1 in 1783 and Colles2 in 1814, a deformed wrist after injury was often considered to be dislocated.3 However, these early authors, without the benefit of radiographic assessment of the injury, in most cases were making an educated guess. On occasion, a postmortem examination of the affected wrist was done. According to Malgaigne,4 fractures of the distal radius accounted for <10% of the fractures seen at l’Hotel Dieu in Paris between 1827 and 1830. However, Dupuytren,5

who worked at the same institution as did Malgaigne, believed that fractures of the distal radius were common. Both agreed that the previously held view of deformed wrists representing a dislocation rather than a fracture was incorrect.3 The radiocarpal dislocation injury was truly first recognized and described by Malle in 1838, when he identified a volar radiocarpal fracturedislocation.3 Shortly thereafter, Marjolin3 and Voillemier6 identified and reported dorsal radiocarpal fracturedislocations. All of these observations were made from examination of postmortem specimens. Radiocarpal fracture-dislocations are estimated to account for just 0.2% of all wrist injuries.7 Few large series exist, and most accounts in the literature consist of case reports.8-19 Destot8 reported the first 647

Radiocarpal Fracture-dislocations

Figure 1

Figure 2

Posteroanterior (A) and lateral (B) views of a dorsal radiocarpal fracture-dislocation.

Lateral view of a Barton fracture depicting the large articular fracture fragment (arrows) that, in contrast to a radiocarpal fracture-dislocation, remains in continuity with the carpus.

radiographically documented case of a radiocarpal fracture-dislocation in 1926. The patient had an open injury and eventually succumbed to sepsis. The few series that are available suggest that these injuries are the result of severe high-energy trauma and that they occur most commonly in young men.20-25 These injuries are associated with a spectrum of injury patterns. Dorsal dislocations are more common than volar dislocations20,22,24,25 (Figure 1). The soft-tissue disruption can lead to radiocarpal instability, resulting in ulnar translocation and multidirectional radiocarpal instability.19,26 Radiocarpal fracture-dislocation injuries must be differentiated from marginal or rim fractures of the distal radius. These latter injuries have been eponymously associated with John Rhea Barton,27 who in 1838 provided what is considered to be the earliest description of a marginal shearing fracture of the distal end of the radius. Radiocarpal fracturedislocations represent a high-energy shear and rotational injury to the 648

wrist with or without a fracture of the radius or ulna. In contrast, Barton fractures are compression injuries in which the articular surface of the fractured distal radius remains in contact with the proximal carpal row holding the intact radiocarpal ligaments (Figure 2). In addition, the displaced articular fragment in a Barton fracture forms a substantial part of the entire distal radial articular surface, which is in contrast to the smaller cortical rim or styloid fractures that typically occur with radiocarpal fracture-dislocations.

Anatomy and Pathophysiology The articular surface of the distal radius is biconcave and triangular, with the radial styloid process forming the apex of the triangle. The sigmoid notch forms the base and articulates with the head of the ulna. The extrinsic radiocarpal ligaments, capsule, and the scaphoid and lunate fossae of the distal radius provide stability to the radiocarpal joint.28

The volar surface of the distal radius is relatively flat. However, the very distal margin slopes volarly in the form of a ridge from which the strong volar radiocarpal ligaments originate. The short radiolunate ligament begins at the ulnar volar margin of the lunate facet and inserts on the volar surface of the lunate. The short radiolunate ligament is the primary soft-tissue restraint against volar translation of the carpus.29 More radially, the radioscapholunate ligament, the long radiolunate ligament, and the stout radioscaphocapitate ligaments take their origin along the volar rim of the distal radius.29 The stout radioscaphocapitate provides restraint against ulnar translation of the carpus.30 On the ulnar side of the wrist, the ulnolunate and ulnotriquetral ligaments originate on the volar side of the triangular fibrocartilage complex, which in turn inserts into the base of the ulnar styloid.31 The dorsal surface of the distal radius is convex and serves as the floor of the dorsal extensor compart-

Journal of the American Academy of Orthopaedic Surgeons

Asif M. Ilyas, MD, and Chaitanya S. Mudgal, MD

ments. When viewed from the lateral aspect, the most distal dorsal edge of the radius extends past the distal edge of the volar surface, providing the site of origin of the dorsal radiocarpal ligaments. Radiocarpal fracture-dislocations may be envisaged as an internal disarticulation of the wrist joint. This global injury of varying degrees is a product of several factors: position of the radiocarpal joint at impact, the strength of the radiocarpal ligaments, the strength of the bony structures, and the magnitude and rate of deforming forces. Bohler,32 who originally postulated the mechanism of injury for dorsal radiocarpal fracture-dislocations, stated that a compressive and rotational force occurs against a hyperextended and pronated wrist. Our understanding of injuries involving the carpus, its ligaments, and the distal radius changed considerably after the comprehensive description of injury mechanisms by Mayfield et al33 in 1980. These descriptions clarified the spectrum of injury that can occur with similar loading patterns. These authors were the first to suggest that the rotational force, which is an essential feature in the causation of radiocarpal fracture-dislocations, is in effect an “intercarpal supination.” They further demonstrated that wrist extension and ulnar deviation produced tension on the volar radiocarpal ligaments, which caused avulsions of the volar radial lip or radial styloid. Thus, it appears that in addition to a rotational component, radiocarpal fracture-dislocations involve a shear and angulatory component, with translation of the carpus resulting in peeling off of the carpus from the radius and ulna. Depending on the magnitude and direction of the force, the wrist deforms, with a variable amount of bony and soft-tissue injury. The most commonly avulsed fracture fragments include the radial styloid by the radioscaphocapitate ligament,30 the volar lunate facet by Volume 16, Number 11, November 2008

the short radiolunate ligament,29 and the ulnar styloid.

Figure 3

Clinical Features The patient typically presents with a painful, swollen, and deformed wrist. The most common mechanisms of injury are falls from a height, motor vehicle injuries, and industrial injuries.20-25 Consequently, open wounds and associated injuries are common (Figure 3). Recognition of this injury demands a complete trauma evaluation for injuries of all extremities and organ systems. In one series of open radiocarpal fracture-dislocations, an associated fracture or injury to other organ systems was found in every patient.22 Neurologic deficits of the injured extremity are common and are often associated with vascular insufficiency of the hand.20-24 Arterial occlusion secondary to the deformity may result in ischemia, which should be corrected by expeditious reduction of the joint with longitudinal traction.21 Neurologic injury is also common, particularly with open injuries.22,24 The median nerve is more often involved than is the ulnar nerve.24 Less commonly, a radiocarpal dislocation may be associated with an irreducible distal radioulnar joint dislocation when soft tissue (eg, tendon, nerves) or osteoarticular fragments become incarcerated within the joint.24,34,35

Radiographic Evaluation Plain radiographs consisting of posteroanterior and lateral views of the wrist are obtained initially to assist in making the diagnosis. Evaluation of fracture geometry is facilitated with radiographs obtained after provisional reduction with longitudinal traction. Examination of the radiographs should begin with identification of fractures of the distal radius, distal ulna, and carpal bones. An oblique view can aid in identifying fracture fragments. Fractures of the

Open wound associated with dorsal radiocarpal fracture-dislocation.

radial or ulnar styloid are examined carefully, with emphasis placed on their size and location. On the posteroanterior view, alignment of the carpus is evaluated by examining the position of the lunate relative to the radius. Normally, the lunate is in alignment with the ulnar column of the distal radius, with a minimum of two thirds of the lunate articulating with the distal radius.36 With complete radiocarpal ligament disruption, the carpus tends to translocate ulnarly down the radioulnar slope of the distal radius (Figure 4). The posteroanterior radiograph is also carefully examined for intercarpal ligament injury, such as scapholunate or lunotriquetral dissociation. The relationship of the radiocarpal and midcarpal joints is assessed by evaluating the alignment of the capitate, the lunate, and the articular surface of the lunate fossa of the distal radius. The three Gilula arcs—radiocarpal, proximal midcarpal, distal midcarpal—should be colinear.37 Disruption of the Gilula arcs or overlapping of normally equally spaced carpal bones is highly suggestive of injury to the supporting ligaments, the carpal bones, or both.37 Scapholunate ligament injuries in particular must be suspected when a radial styloid fracture exits at the interval between the scaphoid and the lunate fossae38 (Figure 5). 649

Radiocarpal Fracture-dislocations

Figure 4

Figure 5

Figure 6

Ulnar translation of the carpus after reduction of a radiocarpal dislocation. Note that the lunate is positioned over the distal ulna and not the lunate fossa of the distal radius.

Scapholunate ligament injury presenting with mild scapholunate diastasis. Note the radial styloid fracture exiting at the level of the scapholunate interval, indicating a high risk of a scapholunate ligament disruption. Such a disruption was confirmed intraoperatively.

Lateral view of dorsal dislocation illustrating loss of colinearity of the capitate, the lunate, and the articular surface of the radius.

mography can aid in the evaluation of cortical rim fractures, fracture depression of the articular surface, and the relationship of the carpus and distal radioulnar joint (Figure 7). Magnetic resonance imaging may be useful in studying soft-tissue injuries, particularly in evaluating the scapholunate and lunotriquetral ligaments. Occult injury to the intercarpal ligaments has been suggested to result in late intercarpal disruption.16,25

Figure 7

Classification A, Plain radiograph demonstrating radiocarpal fracture-dislocation. Anterior (B) and lateral (C) three-dimensional computed tomography scans illustrating ulnar and dorsal subluxation of the radiocarpal joint associated with a large radial styloid fracture fragment.

Loss of colinearity of the lunate with the articular surface of the radius on the lateral view indicates disruption of the radiocarpal joint (Figure 6). In general, the lateral view demonstrates the direction of the radiocarpal dislocation. Marginal rim fractures are best evaluated on the 650

lateral view. The so-called teardrop view or 10° proximal view is helpful in evaluating fractures of the volar rim and lunate facet.36 With technological advances, the routine use of computed tomography for wrist injuries is increasing. Although not mandatory, computed to-

Classification of radiocarpal fracture-dislocations ideally should encompass the identification of all bone and soft-tissue injuries, grading the risk of instability, and subsequently directing treatment. Two classification schemes have been discussed in the literature. Moneim et al21 classified radiocarpal fracture-dislocations into two types based on the presence or absence of concurrent injury to the intercarpal articulations (Table 1). In a type I injury, the normal carpal anat-

Journal of the American Academy of Orthopaedic Surgeons

Asif M. Ilyas, MD, and Chaitanya S. Mudgal, MD

omy is maintained, with dislocation of the radiocarpal joint. Type II injuries involve intercarpal injuries (specifically, scapholunate or lunotriquetral intercarpal ligament injuries) in addition to the radiocarpal dislocation. This second type represents a more complex pattern and could be considered a variation of a perilunate fracture-dislocation as described by Mayfield et al.33 Dumontier et al25 also classified radiocarpal fracture-dislocations into two groups, but their system is based on the extent of radial styloid involvement (Table 2). Group 1 injuries include pure ligamentous radiocarpal dislocations or dislocations with only a small cortical or radial styloid avulsion fracture. Group 2 injuries include dislocations with a large radial styloid fracture fragment involving at least one third of the scaphoid fossa of the distal radius. On the dorsal surface, the ligamentous injury represents more of a capsuloperiosteal avulsion than a true tear of the dorsal radiocarpal ligaments. Group 1 injuries consist of global ligamentous injuries, which have the potential for multidirectional instability; as such, they pose a greater treatment challenge than do group 2 injuries.25 In group 2 injuries, the radiocarpal ligaments remain attached to the fractured large radial styloid fragment.30 Stability can more reliably be restored with secure anatomic fixation of the fracture than can occur with the more pure ligamentous injuries seen in group 1.

Management Successful management of radiocarpal fracture-dislocations requires evaluation and treatment of the columns of the wrist, while taking into account the direction of dislocation and the presence of any intercarpal injuries. Three treatment principles are recommended: (1) concentric reduction of the radiocarpal joint, (2) identification and treatment of intercarVolume 16, Number 11, November 2008

Table 1 Moneim et al21 Classification of Radiocarpal Fracture-dislocation Type I Type II

Radiocarpal fracture-dislocation without associated intercarpal dissociation Radiocarpal fracture-dislocation with an associated intercarpal dissociation

Table 2 Dumontier et al25 Classification of Radiocarpal Fracture-dislocation Group 1

Group 2

Radiocarpal fracture-dislocation that is purely ligamentous or involves only a small cortical avulsion fracture off the radius Radiocarpal fracture-dislocation associated with a large radial styloid fracture fragment (involving at least one third of the scaphoid fossa)

pal injuries, and (3) stable repair of the osseous-ligamentous avulsions. To better direct surgical treatment and to address all aspects of the injury, we have adopted the columnar concept of the carpus as described by Navarro39 and modified by Taleisnik,40 as well as the columns of the distal radius and ulna as described by Rikli and Regazzoni.41 Each column of the distal radius and ulna, namely, the radial, the intermediate, and the ulnar, is approached separately in a stepwise fashion to achieve radiocarpal stability.41 Concomitantly, the columns of the carpus, which include the mobile lateral column (ie, scaphoid), the flexion-extension central column (ie, lunate, distal carpal row), and the rotatory medial column (ie, triquetrum), are evaluated for intercarpal ligamentous injury and resultant carpal instability.40 By addressing every column individually, radiocarpal and intercarpal stability can be achieved. Although closed reduction and cast immobilization have been reported to yield satisfactory results in the management of radiocarpal dislocations,10,11,14,21 we consider these injuries to be complex and unstable conditions that routinely warrant surgical reduction and fixation to attain a stable, concentric, and con-

gruent wrist. All irreducible dislocations, open injuries, and cases involving neurovascular embarrassment require surgical treatment.21,22,24,35 The steps in surgical treatment of radiocarpal fracture-dislocation are (1) provisional radiocarpal joint reduction, (2) decompression of neurovascular structures, (3) exposure and débridement of the joint, (4) treatment of intercarpal injuries, and (5) fracture fixation and/or softtissue repair (Figure 8). We recommend the use of general anesthesia. The wrist is provisionally reduced with longitudinal traction. An external fixator may be applied to hold the joint reduced. An extensile volar approach ulnar to the flexor tendons and median nerve is used so that both the carpal tunnel and Guyon canal can be decompressed as needed. The radiocarpal joint is examined through the volar capsular site of disruption. The joint is irrigated and débrided of any loose cartilage or bone fragments. Stay sutures or suture anchors are then placed in the area of capsular and ligament disruption but are not tied down. Fluoroscopy is used to identify any carpal fractures or interosseous ligament injuries, particularly of the scapholunate or lunotriquetral ligaments. Intercarpal ligament injuries are 651

Radiocarpal Fracture-dislocations

Figure 8

Treatment algorithm for radiocarpal fracture-dislocations. DRUJ = distal radioulnar joint, ExFix = external fixation, ORIF = open reduction and internal fixation Figure 9

Anteroposterior (A) and lateral (B) radiographs demonstrating open reduction and internal fixation of the radial and intermediate columns of a radiocarpal fracturedislocation. Note the screw fixation of the radial styloid and anchor fixation within the distal radius (ie, volar ligament repair). 652

confirmed and treated through a separate dorsal capsular incision. A subperiosteal approach through the floor of the third extensor compartment is used. The columns of the joint are approached sequentially. Beginning with the radial column, the fractured radial styloid is accurately reduced and internally fixed. Fixation options include a Kirschner wire, compression screw, or plate application (Figure 9). Either a Kirschner wire or screw fixation can provide stable fixation of the radial styloid. Screw fixation provides the added benefit of compression, assuming that the styloid fragment is large enough to accommodate a screw without requiring later removal and pin-tract complications. Volar, radial, or dorsal plating is selected based on the fracture personality and surgeon preference. Moving to the intermediate (ie, central) column, fractures of the lunate facet that are amenable to fixation should be repaired with internal fixation us-

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Asif M. Ilyas, MD, and Chaitanya S. Mudgal, MD

ing screws or a tension band wire loop.42 When fractures of the radial styloid and/or the lunate facet are not amenable to fixation, soft-tissue repair is undertaken by direct suture repair or with suture anchors (Figure 9). Stay sutures that previously were placed to repair the extrinsic volar ligaments are tied. The origins of the short radiolunate and radioscaphocapitate ligaments are repaired in particular to avoid late volar subluxation or ulnar translocation, respectively. Reduction and stability of the fixation is confirmed both visually and radiographically. The ulnar column is approached in the presence of injury to the distal radioulnar joint and ulnar support ligaments (ie, ulnolunate, ulnotriquetral) or when instability persists after fixation of the radial and intermediate (ie, central) columns. Large ulnar styloid fractures require internal fixation with screws or tension band wiring. This procedure usually restores a concentric distal radioulnar joint. In the presence of persistent instability, the distal radioulnar joint is examined and evacuated of any interposed tissue, followed by repair of the ulnocarpal ligaments. Persistent instability can be addressed by pinning the distal radioulnar joint in midsupination. Additional stability to the construct can be provided with the use of an external fixator or radiolunate pin. The external fixator is especially useful in situations in which daily care of an open wound is needed. Application of a radiolunate pin can be used intraoperatively to maintain stable reduction of the radiocarpal joint while fracture fixation and soft-tissue repair are undertaken. If necessary, the external fixator or radiolunate pin may be left in situ postoperatively for 4 to 6 weeks to reinforce reduction of the radiocarpal joint.

Outcome Despite being a complex wrist injury, radiocarpal fracture-dislocation Volume 16, Number 11, November 2008

can achieve a satisfactory outcome provided the surgeon follows these treatment principles: concentric reduction of the radiocarpal joint, treatment of intercarpal injuries, and sound repair of the osseousligamentous injury. There are few large series on this subject in the literature and, to our knowledge, only three with more than eight patients.22,24,25 Mudgal et al24 reported on a series of 12 patients who presented with radiocarpal fracture-dislocation. Four cases were open injuries, seven had neurologic compromise, two had an intercarpal ligamentous injury, and five had an associated injury. Excluding patients with concomitant intercarpal injury, mean wrist motion on follow-up assessment consisted of 53° of extension, 59° of flexion, 82° of pronation, and 74° of supination. These results are consistent with the other large series in the literature, which indicate that an overall 30% to 40% decrease in total arc of wrist flexion-extension can be expected following successful open treatment.22,25 Using the criteria of Knirk and Jupiter,43 Mudgal et al24 identified 3 of 12 patients as having evidence of radiocarpal arthritis. Dumontier et al23 reported that 3 of 27 patients developed radiocarpal arthritis, while Schoenecker et al44 reported that four of the six patients in their series developed arthritis. Factors predictive of an inferior outcome include open injury, complete radiocarpal ligamentous injury, associated nerve injury, and intercarpal ligamentous injury. Intercarpal injury, particularly of the scapholunate ligament, can significantly compromise outcome. Moneim et al21 used the presence of such an injury to classify and guide treatment. In their series, all three patients were treated surgically; unfortunately, all had an inferior outcome. Often, the negative impact of an intercarpal injury manifests late because the injury is initially missed and goes un-

treated, resulting in late midcarpal and radiocarpal instability.16,25 The presence of associated injuries is common and can portend an inferior outcome. Neurologic injuries are generally neurapraxic, and resolution can be expected with decompression.24 More severe nerve compression or stretch injuries result in an inconsistent neurologic recovery. Nyquist and Stern22 reported on 10 cases of open radiocarpal fracture-dislocations in which all 10 were complicated by an associated injury and 7 involved neurologic compromise. At follow-up, all patients had variable and inconsistent recovery of sensibility. This is consistent with a study by Soong and Ring,45 who reported on ulnar nerve palsies following distal radius fractures. These authors found that ulnar nerve injuries are typically neurapraxic and that patients usually experience normal or near-normal recovery of function following decompression. Ulnar translocation and multidirectional instability may result following complete radiocarpal ligamentous injury in which there is no fracture of the distal radius, as in the case of the group 1 injuries described by Dumontier et al.25 Early reports highlighted this instability pattern as a late finding encountered during closed treatment.14,17,26 In a cadaveric study of radiocarpal instability, Rayhack et al31 sequentially sectioned the radiocarpal ligaments and found that ulnar subluxation of the joint required transection of both the radioscaphocapitate and the radiolunate ligaments. Viegas et al46 confirmed this finding in their cadaveric study and further studied multidirectional instability. These authors found volar translation to be evident with less ligament disruption than that needed for ulnar translation. It was always evident in the presence of ulnar translation of the carpus. Such injury in conjunction with loss of the ulnolunate ligaments led to progression of the inju653

Radiocarpal Fracture-dislocations

ry from ulnar translocation to multidirectional instability. The authors suggested that the presence of ulnar translation represents a much more global ligament disruption.

Complications The most common complication following radiocarpal dislocation or fracture-dislocation is residual loss of motion and instability. On average, a patient can expect to lose 30% to 40% of total arc of wrist flexion/ extension.24,25 The other major complication is posttraumatic arthritis related to residual articular stepoff.22,24,25 Chronic radiocarpal and distal radioulnar instability or ulnar translation of the carpus are more common with group 1 injury patterns.14,15,17,25,26 Less commonly, septic arthritis, tendon rupture, and hardware irritation have been reported.24,25

References Evidence-based Medicine: No level I or II studies are cited. Level III/IV (case reports and case-control cohort studies) references include 7-26, 34, 35, 38, and 41-45. Level V (expert opinion) references include 1-6, 27, 36, 37, 39, and 40. Citation numbers printed in bold type indicate references published within the past 5 years. 1.

2.

3.

Summary Radiocarpal fracture-dislocations are the products of high-energy trauma and represent a shear and rotational injury to the wrist, with a variable amount of bone and soft-tissue injury. A high index of suspicion for associated injuries must be maintained, particularly for open wounds, neurologic compromise, and injuries to other organ systems. Radiographs are adequate for diagnosis but must be carefully scrutinized for injury to the normal carpal relationships. Although closed reduction has been described, we recommend open reduction and internal fixation for these complex and unstable injuries. A volar and dorsal surgical approach is used. Surgical principles include concentric reduction of the radiocarpal joint, identification and treatment of intercarpal injuries, and stable repair of the osseous-ligamentous avulsions. Despite the complexity of the original trauma, a satisfactory outcome is attainable. However, a residual loss of motion of 30% to 40% is expected. 654

4.

5.

6.

7.

8.

9.

10.

11.

12.

Pouteau C: Mémoire Contenant Quelques Réflexions sur Quelques Fractures de L’avant-Bras sur les Luxations Incomplètes du Poignet et sur Lateral Epicondylitis Diastasis. Paris, France: Ph. Pierres, 1783. Colles A: On the fracture of the carpal extremity of the radius. Edinburgh Med Surg J 1814;10:182-186. Fernandez DL, Jupiter JB: The fracture of the distal end of the radius: A historical perspective, in Fernandez DL, Jupiter JB (eds): Fractures of the Distal Radius: A Practical Approach to Management (Chapter 1), ed 2. New York, NY: Springer, 2002, pp 1-22. Malgaigne J: Treatise on Fractures. Philadelphia, PA: Translated by J. Packard Lippincott, 1859. Dupuytren G: On the Injuries and Diseases of Bone. London, UK: Translated by F. G. Clark Sydenham Society, 1847. Voillemier M: Histoire d’une luxation complète et récente du poignet en arrière suivit de réflexions sur le mécanisme de cette luxation. Arch Gen Med 1839;6:401-417. Dunn AW: Fractures and dislocations of the carpus. Surg Clin North Am 1972;52:1513-1538. Destot E: Injuries of the Wrist: A Radiological Study. New York, NY: Paul B. Hoeber, Inc, 1926. Weiss C, Laskin RS, Spinner M: Irreducible radiocarpal dislocation: A case report. J Bone Joint Surg Am 1970;52:562-564. Freund LG, Ovesen J: Isolated dorsal dislocation of the radiocarpal joint: A case report. J Bone Joint Surg Am 1977;59:277. Fehring TK, Milek MA: Isolated volar dislocation of the radiocarpal joint: A case report. J Bone Joint Surg Am 1984;66:464-466. Varodompun N, Limpivest P, Prinyaroj P: Isolated dorsal radiocarpal dislocation: Case report and literature

13.

14.

15.

16.

17.

18.

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20.

21.

22.

23.

24.

25.

26.

27.

review. J Hand Surg [Am] 1985;10: 708-710. Moore DP, McMahon BA: Anterior radio-carpal dislocation: An isolated injury. J Hand Surg [Br] 1988;13:215217. Penny WH III, Green TL: Volar radiocarpal dislocation with ulnar translocation. J Orthop Trauma 1988;2:322326. Thomsen S, Falstie-Jensen S: Palmar dislocation of the radiocarpal joint. J Hand Surg [Am] 1989;14:627-630. Naranja RJ Jr, Bozentka DJ, Partington MT, Bora FW Jr: Radiocarpal dislocation: A report of two cases and a review of the literature. Am J Orthop 1998;27:141-144. Howard RF, Slawski DP, Gilula LA: Isolated palmar radiocarpal dislocation and ulnar translocation: A case report and review of the literature. J Hand Surg [Am] 1997;22:78-82. Watanabe K, Nishikimi J: Transstyloid radiocarpal dislocation. Hand Surg 2001;6:113-120. Freeland AE, Ferguson CA, McCraney WO: Palmar radiocarpal dislocation resulting in ulnar radiocarpal translocation and multidirectional instability. Orthopedics 2006;29:604-608. Bilos ZJ, Pankovich AM, Yelda S: Fracture-dislocation of the radiocarpal joint. J Bone Joint Surg Am 1977; 59:198-203. Moneim MS, Bolger JT, Omer GE: Radiocarpal dislocation: Classification and rationale for management. Clin Orthop Relat Res 1985;192:199-209. Nyquist SR, Stern PJ: Open radiocarpal fracture-dislocations. J Hand Surg [Am] 1984;9:707-710. Dumontier C, Lenoble E, Saffar P: Radiocarpal dislocations and fracturedislocations, in Saffar P, Cooney WP III (eds): Fractures of the Distal Radius. London, UK: Martin Dunitz, 1995, pp 267-279. Mudgal CS, Psenica J, Jupiter JB: Radiocarpal fracture-dislocation. J Hand Surg [Br] 1999;24:92-98. Dumontier C, Meyer zu Reckendorf G, Sautet A, Lenoble E, Saffar P, Allieu Y: Radiocarpal dislocations: Classification and proposal for treatment. A review of twenty-seven cases. J Bone Joint Surg Am 2001;83:212-218. Fennell CW, McMurtry RY, Fairbanks CJ: Multidirectional radiocarpal dislocation without fracture: A case report. J Hand Surg [Am] 1992; 17:756-761. Barton JR: Views and treatment of an important injury of the wrist. Medical Examiner and Record of

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28.

29.

30.

31.

32.

33.

34.

Medical Science 1838;1:365-368. Ritt MJ, Stuart PR, Berglund LJ, Linscheid RL, Cooney WP III, An KN: Rotational stability of the carpus relative to the forearm. J Hand Surg [Am] 1995;20:305-311. Berger RA, Landsmeer JM: The palmar radiocarpal ligaments: A study of adult and fetal human wrist joints. J Hand Surg [Am] 1990;15:847-854. Siegel DB, Gelberman RH: Radial styloidectomy: An anatomical study with special reference to radiocarpal intracapsular ligamentous morphology. J Hand Surg [Am] 1991;16:40-44. Rayhack JM, Linscheid RL, Dobyns JH, Smith JH: Posttraumatic ulnar translation of the carpus. J Hand Surg [Am] 1987;12:180-189. Bohler L: Verrenkungen der handgelenke. Acta Chir Scand 1930;67:154177. Mayfield JK, Johnson RP, Kilcoyne RF: Carpal dislocations: Pathomechanics and progressive perilunar instability. J Hand Surg [Am] 1980;5: 226-241. Ayekoloye CI, Shah N, Kumar A, Kurdy N: Irreducible dorsal radiocar-

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35.

36.

37.

38.

39.

40.

pal fracture dislocation with dissociation of the distal radioulnar joint: A case report. Acta Orthop Belg 2002; 68:171-174. Fernandez DL: Irreducible radiocarpal fracture-dislocation and radioulnar dissociation with entrapment of the ulnar nerve, artery and flexor profundus II-V: Case report. J Hand Surg [Am] 1981;6:456-461. Medoff RJ: Essential radiographic evaluation for distal radius fractures. Hand Clin 2005;21:279-288. Gilula LA: Carpal injuries: Analytic approach and case exercises. AJR Am J Roentgenol 1979;133:503-517. Mudgal C, Hastings H: Scapho-lunate diastasis in fractures of the distal radius: Pathomechanics and treatment options. J Hand Surg [Br] 1993;18: 725-729. Navarro A: Cited by Scaramuzza RF: El moviomiento de rotacion en el carpo y su relacion con la fisiopatologica de sus lesiones traumaticas. Bol Trabajos Soc Argent Ortoped Traumatol 1976;34:337. Taleisnik J: The ligaments of the

41.

42.

43.

44.

45.

46.

wrist. J Hand Surg [Am] 1976;1:110118. Rikli DA, Regazzoni P: Fractures of the distal end of the radius treated by internal fixation and early function: A preliminary report of 20 cases. J Bone Joint Surg Br 1996;78:588-592. Chin KR, Jupiter JB: Wire-loop fixation of volar displaced osteochondral fractures of the distal radius. J Hand Surg [Am] 1999;24:525-533. Knirk JL, Jupiter JB: Intra-articular fractures of the distal end of the radius in young adults. J Bone Joint Surg Am 1986;68:647-659. Schoenecker PL, Gilula LA, Shively RA, Manske PR: Radiocarpal fracture–dislocation. Clin Orthop Relat Res 1985;197:237-244. Soong M, Ring D: Ulnar nerve palsy associated with fracture of the distal radius. J Orthop Trauma 2007;21: 113-116. Viegas SF, Patterson RM, Ward K: Extrinsic wrist ligaments in the pathomechanics of ulnar translation instability. J Hand Surg [Am] 1995;20: 312-318.

655

Venous Thromboembolism in Spine Surgery

Christopher A. Heck, MD Christopher R. Brown, MD William J. Richardson, MD

Abstract Venous thromboembolism is a life-threatening adverse event in spine patients and presents difficult decisions for the surgeon and patient. Prophylactic protocols have been established to prevent the occurrence of venous thromboembolism and its sequelae, including venous occlusion, edema, postthrombotic syndrome, and death. Despite the known benefits of prophylaxis, some surgeons choose not to use it because of concerns over increased bleeding complications and possible iatrogenic neurologic injury. Although mechanical prophylaxis remains an important element in venous thromboembolism prevention, low-molecular-weight heparin is better than other pharmacologic therapies in decreasing the incidence of major events.

V

Dr. Heck is Orthopaedic Spine Surgeon, Southern Orthopaedic Surgeons LLC, Montgomery, AL. Dr. Brown is Assistant Professor, Division of Orthopaedic Surgery, Duke University, Durham, NC. Dr. Richardson is Professor, Division of Orthopaedic Surgery, Duke University. None of the following authors or a member of their immediate families has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Heck, Dr. Brown, and Dr. Richardson. Reprint requests: Dr. Heck, Southern Orthopaedic Surgeons LLC, 2119 East South Boulevard, Montgomery, AL 36116. J Am Acad Orthop Surg 2008;16:656664 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

656

enous thromboembolism (VTE) causes significant morbidity and mortality and has a notable economic impact. Deep vein thrombosis (DVT) and pulmonary embolism (PE) occur in 48 and 69 per 100,000 patients per year, respectively. These events were identified as fatal in 2 and 17 per 100,000 patients per year, respectively.1 The cost per episode of DVT and PE averages $9,337 and $12,795, respectively. These costs are compounded by the increased risk of future VTE events and the occurrence of postthrombotic syndrome. Recurrent DVT and fatal PE have been reported to occur in 21.5% and 2.6% of patients, respectively, after a single previous DVT.2 Orthopaedic patients are at significant risk for thromboembolic disease. Considerable research has been conducted on the occurrence and treatment of VTE in connection with traumatic orthopaedic injuries, total joint arthroplasties, and spinal surgery. Increased age, intraoperative venous stasis, and postoperative immobilization and convalescence put

these patients at risk for developing VTE. Numerous studies demonstrate that the prophylactic use of pharmacologic anticoagulants, such as low-molecular-weight heparin (LMWH) and low-dose heparin, and mechanical devices, such as intermittent pneumatic compression sleeves, statistically reduces the incidence of VTE in the orthopaedic patient population.3-5 However, concerns about bleeding complications, wound hemorrhage, and compressive spinal epidural hematoma as well as the subsequent neurologic sequelae have resulted in diverse prophylactic and treatment protocols for VTE in the spine surgical patient population.6

Pathophysiology VTE, comprising DVT and PE, was described by Rudolph Virchow, a German physician and pathologist, in the 1850s. The Virchow triad of hypercoagulability, venous stasis, and venous intimal injury that leads to VTE was not described in the

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Christopher A. Heck, MD, et al

Figure 1

The coagulation cascade. Subendothelial collagen and tissue factor, both released during vessel intimal injury, initiate the intrinsic and extrinsic pathways, respectively, of the cascade. Ca++ = calcium, HMWK = high-molecular-weight kininogen, PK = prekallikrein

medical literature until approximately 100 years after his original work.7 Surgery patients with VTE often demonstrate many, if not all, of the characteristics of the Virchow triad. More recently, patient populations that are at increased risk for VTE from an inherited or acquired hypercoagulable state have been identified. Inheritable abnormalities include the factor V Leiden mutation; deficiencies of proteins C, S, and antithrombin III; mutations of Volume 16, Number 11, November 2008

the prothrombin promoter G20210A and methylenetetrahydrofolate reductase C677T genes; and polymorphism of the plasminogen activator inhibitor-1 4G/4G and platelet glycoprotein IIb/IIIa A1/A2 and A2/A2 proteins. Factor V Leiden mutation, which accounts for 25% of all inherited thrombophilic disorders, occurs as a result of a point mutation in the factor V gene, which makes the factor resistant to degradation by activated protein C and, thus, propels both the intrinsic and extrinsic coag-

ulation cascades forward8 (Figure 1). However, in a matched cohort of total hip arthroplasty (THA) patients with and without postoperative DVT, the incidence of factor V Leiden mutations (8% versus 4%, respectively) was not different.9 In fact, antithrombin III deficiency and prothrombin G20210A mutation were statistically correlated with postoperative PE in another matched cohort study of THA patients receiving postoperative DVT prophylaxis.10 Common acquired thrombo657

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philic states include malignancy, elevated hormone conditions, (eg, hormone replacement, oral contraceptive therapy, late pregnancy), and antiphospholipid antibodies (including lupus anticoagulant and anticardiolipin antibody). Malignancy has recently been associated with up to 20% of all new diagnoses of VTE.11 Venous stasis occurs during surgical positioning and retraction of venous structures. The condition is created by the absence of active muscle contraction, vessel occlusion from both external and internal (surgical retraction) sources, and postoperative bed rest and immobilization. Venous intimal injury during surgery can initiate both the intrinsic and extrinsic coagulation cascades. The intrinsic cascade begins when subendothelial collagen binds to plasma proteins, which, in turn, activate factor XII. The extrinsic cascade starts with activation of factor VII by calcium and tissue factor, a cellular membrane lipoprotein, which is exposed during intimal injury (Figure 1). With the exception of anterior lumbar interbody fusion procedures, during which the vena cava and common iliac veins are subject to injury, this mechanism of thrombosis initiation is not highly germane to the spine surgery population.

Elective Spinal Reconstruction and Decompression Incidence The natural history of VTE as a result of elective spinal surgery without prophylaxis is poorly reported. In 1966, Prothero et al12 reported on two series, each of 500 lumbar and lumbosacral fusion patients, compared one decade apart. They found that the initial incidence of VTE in spine patients was 4.2% and had decreased to 2.2% at the second evaluation. The method of surveillance and the use or nonuse of pro658

phylaxis were not noted. More recent studies have provided greater detail regarding prophylactic regimens and the subsequent incidence of VTE at the expense of providing an untreated control group. In a study employing only intermittent pneumatic compression prophylaxis and prospectively using duplex ultrasound screening, Epstein13 demonstrated a 2.8% incidence of VTE in patients undergoing multilevel laminectomy with instrumented fusion. In eastern Asia, extremely low rates of VTE have been described in patients undergoing THA without prophylaxis.14 Similarly, the only studies evaluating spine surgery cohorts without the use of mechanical or pharmacologic prophylaxis have come from that region. Using contrast venography, one study reported a 15.5% incidence of DVT, although only 0.9% of occurrences were proximal to or inclusive of the popliteal vein.15 No patients were clinically symptomatic. Pharmacologic prophylaxis to prevent VTE is not universally used in elective spine surgery. Many surgeons fear resulting complications, including wound hemorrhage and spinal epidural hematoma. In a prospective randomized double-blind investigation, a once-daily dose of LMWH and twice-daily low-dose heparin demonstrated similar DVT rates (1.1% and 2.2%, respectively). Venography confirmed this result. No bleeding complications or neurologic deficits were identified.16 More recently, in a retrospective study of 1,954 patients undergoing elective spine surgery in the cervical, thoracic, and lumbar spine, Gerlach et al17 reported a 0.05% risk of VTE and a 0% risk of PE when compression stockings were used in conjunction with pharmacologic prophylaxis consisting of LMWH (ie, nadroparin, 2,850 IU/day) initiated within 24 hours after surgery. Of concern, however, was a 0.4% incidence of spinal epidural hematoma.

A progressive postoperative neurologic deficit was present in 77% of patients with a spinal epidural hematoma. Only 60% of the patients who developed a progressive deficit were discharged with a normal neurologic examination, even after prompt surgical decompression. This rate of spinal epidural hematoma is slightly higher than other reports of 0.1% to 0.19%.18,19 Few data exist regarding warfarin utilization for VTE prophylaxis in spine surgery. In a prospective study group of 110 patients, 35 were randomized to receive warfarin and elastic stockings.20 No VTE was observed with prospective ultrasound screening. However, two patients experienced excessive postoperative blood loss. This did not occur in the other two randomized groups in which patients received mechanical prophylaxis alone. Risk Factors Identification of risk factors for VTE associated with elective spinal reconstruction is difficult because of a lack of specifics in the literature regarding surgical approaches in patients who sustain a VTE. In addition to the general surgical risk factors discussed above, a history of VTE, decreased postoperative mobility, and increased surgical time have been reported as risk factors.21 Although statistical support for spine-specific risk factors is lacking, several studies note common observations for patients who sustained a VTE. The most commonly cited association was an anterior or combined anterior/posterior approach to the thoracolumbar spine. Dearborn et al22 cited a 6.1% incidence of PE in 97 patients undergoing combined anterior/posterior approaches. However, in 201 patients undergoing a posterior-only approach, there was just one occurrence of PE (0.5%). Studying spine patients treated without pharmacologic or mechanical prophylaxis, Oda et al15 demonstrated a statistically significant risk

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Christopher A. Heck, MD, et al

of VTE associated with age and anatomic location of surgery. The average age of the 17 patients who sustained a VTE was 66 years, whereas those who did not had an average age of 58 years (P = 0.04). Also, there was a significantly higher rate (P = 0.003) of VTE among patients undergoing lumbar surgery (26.5%) versus those treated with cervical surgery (5.6%). No statistically significant difference was noted for thoracic spine surgery (incidence, 14.3%) compared with cervical or lumbar surgery. The investigators concluded that there was no statistically increased risk associated with sex, surgical time, surgical blood loss, duration of postoperative recumbency, or interval from surgery to venography. Other investigators have also noted the poor positive predictive value of DVT screening, with venography or ultrasound, for predicting the incidence of PE.22

Traumatic Fracture/Dislocation Incidence In a prospective study evaluating hypercoagulability in 101 trauma patients with a minimal and average Injury Severity Score of 15 and 27, respectively, the overall incidence of VTE was 30%.23 The authors did not find a statistically significant difference in the rate of VTE between those receiving prophylaxis and those not receiving it. They reported an increased rate of VTE in obese patients, in patients older than age 40 years, in patients treated with >3 days immobilization, and in patients with spine or lower extremity fractures. However, when a logistic regression model was used, only obesity (P = 0.004) and prolonged immobilization (P = 0.05) remained statistically significant risk factors. The authors concluded that trauma induces a hypercoagulable state, as evidenced by elevated coagulation markers that may remain ≤1 month after injury. One year later, however, Volume 16, Number 11, November 2008

in a retrospective databank analysis of more than 450,000 patients, different investigators noted only a 0.36% incidence of clinically evident VTE.24 Thus, the reported rates of VTE in the trauma population are largely dependent on the study methodology. In more clinically oriented retrospective investigations, symptomatic VTE in spine trauma patients with no or minimal neurologic injury (ie, Frankel scale E or D) is low. Tropiano et al25 reported an absence of VTE events in 45 patients with thoracolumbar or lumbar burst fractures treated with closed reduction and casting. A specific prophylactic protocol was not described. The patients were mobilized after only 12 hours postoperatively. In a retrospective review of 143 surviving trauma patients with thoracolumbar burst fractures, the rate of VTE was 2.1%, with no statistically significant difference between those treated surgically versus nonsurgically.26 Only one study prospectively compared alternative types of prophylaxis in patients with spinal trauma. Kurtoglu et al27 used duplex ultrasound to screen 120 patients with severe head and spinal trauma, including 11 patients with spinal fractures. Patients were randomized to receive either intermittent pneumatic compression or intermittent pneumatic compression and LMWH (enoxaparin, 40 mg/day). The LMWH was initiated approximately 24 hours after admission. Overall, there was a 5.8% incidence of DVT and a 5% incidence of PE. The latter occurred more frequently in patients with known DVT. There was no difference between treatment groups. More important, the investigators found no increased rate of cranial epidural hematoma exacerbation in the group treated with LMWH, as evidenced on follow-up computerized tomography scans of the head. Although the authors did not objectively evaluate for spinal epidural hematoma, none was found subjectively in either group.

Risk Factors Because of the aggressive monitoring and resuscitation of trauma patients, the reported rates of symptomatic VTE in such patients are very low. Thus, there are few identifiable risk factors for VTE in spine trauma patients. Risk factors for these patients, therefore, must be obtained from the general trauma literature. In a review of 1,602 trauma patients with VTE, Knudson et al24 identified the strongest factors to include ventilator dependency >3 days, age >40 years, lower extremity fracture, major head injury, venous injury, and major surgical procedure. Other studies suggest that independent risk factors also include obesity, blood transfusion, and spinal cord injury.23,28

Spinal Cord Injury Incidence When prophylaxis is not used, VTE in the patient with spinal cord injury is common, with a minimum incidence of 80%.28,29 However, when mechanical prophylaxis is initiated, the rates of VTE statistically decrease. In a small, prospective study, Green et al30 reported a 40% DVT rate in 15 patients who received intermittent pneumatic compression alone. Both low-dose heparin and LMWH have been shown to decrease the incidence of VTE in patients with spinal cord injury. In a multicenter randomized trial, the efficacy of low-dose heparin was compared with enoxaparin in 476 patients with spinal cord injury.31 Although all patients were evaluated for the safety arm of the study, only 107 were evaluated by prospective duplex ultrasound examination of the lower extremities and monitored for symptomatic PE, which was confirmed with imaging studies. VTE was found in 26 patients. No statistically significant difference was observed between treatment groups (12.4% for patients treated with 659

Venous Thromboembolism in Spine Surgery

Table 1 Venous Thromboembolism Prophylactic Guidelines Recommended by the Seventh American College of Chest Physicians Conference21 Type of Spine Surgery Elective reconstructive/ decompression

Traumatic fracture/dislocation Spinal cord injury

Risk Factors No risk factors One or more risk factors: age ≥60 years, BMI ≥30kg/m2, genetic thrombophilia, history of VTE, anterior or combined procedure, thoracic/lumbar/sacral procedure No spinal cord injury Evidence of systemic hemorrhage — —

Prophylactic Recommendations None Early (<24 hrs postoperatively) LMWH and IPC

Early LMWH and IPC Delayed LMWH and early IPC Early (24-72 hrs after injury) LMWH and IPC Conversion to warfarin (INR 2.5) until 4 months after injury

BMI = body mass index, INR = international normalized ratio, IPC = intermittent pneumatic compression, LMWH = low-molecular-weight heparin, VTE = venous thromboembolism

LMWH [enoxaparin] versus 16.3% for those treated with low-dose heparin). From this group of patients, 119 underwent 6 weeks of inpatient rehabilitation.32 The group treated with low-dose heparin had a 2.5 times greater risk of VTE during the rehabilitation phase than did the patients treated with LMWH (21.7% versus 8.5%, respectively; P = 0.052). Clinically symptomatic VTE events have been identified less frequently. In a retrospective review of medical records from 16,240 patients with spinal cord injury, Jones et al33 found a 5.4% incidence of VTE in the first 3 months after injury. This increased to 6.0% at 1 year. Risk Factors Spinal cord injury is a significant independent risk factor for VTE.28 Paradoxically, paraplegia has been associated with a higher incidence of thromboembolic disease than has quadriplegia. Jones et al33 found a statistically higher rate (P = 0.009) of 660

VTE at 3 months in complete paraplegics (11%) versus complete quadriplegics (7.8%). It is hypothesized that persons with lower-level injuries, such as at the thoracolumbar junction, develop flaccid paralysis, and consequently increased venous capacitance and stasis, which may increase the incidence of VTE compared with quadraplegic patients with spastic paralysis.34 Increased age in persons with spinal cord injury is a significant risk factor. Jones et al33 reported that patients older than age 30 years had a statistically higher rate of VTE; the rate then statistically diminished in patients older than age 80 years. Another commonly reported risk factor is the temporal relationship to injury. Several authors have documented that 79% to 95% of VTE diagnoses in patients with spinal cord injury occur within the first 3 months after injury.35,36 DeVivo et al37 further noted a higher risk for fatal PE for spinal cord injury—500 times that of uninjured matched

control patients—within 1 month after injury; this decreased to 20 times higher risk at 6 months. Despite the decreased risk with time, a bimodal distribution for VTE has been reported, peaking approximately at days 30 and 100 after injury.38 The first peak coincided with the previously reported early risk. The second peak, however, coincided with rehabilitation and was also associated with discontinuation of prophylaxis at approximately 55 days after injury. Aito et al39 recently evaluated the relationship between delayed prophylaxis and risk assessment. In patients admitted to their rehabilitation hospital, the authors identified a 2% rate of DVT in patients receiving prophylaxis <72 hours after injury versus a 26% rate in patients for whom prophylaxis was delayed longer than 7 days after injury. However, this study does not address what, if any, prophylaxis had been used at the primary hospital. Further, the severity of the injury may have increased the risk of DVT in patients who could not be transferred during the early (<72 hours) treatment period, thus potentially affecting the reported rate of DVT. Nevertheless, it is evident that patients are at an increased risk for VTE during the early stages after injury and that early prophylaxis is prudent.

Prophylaxis Guidelines issued by the Seventh American College of Chest Physicians (ACCP) Conference recommend no prophylaxis for patients without additional risk factors who receive elective spine surgery21 (Table 1). For the patient with a history of VTE or any previously listed risk factor, investigators recommend LMWH and intermittent pneumatic compression alone or in combination. For this patient population, data support the initiation of pharmacologic prophylaxis within 24

Journal of the American Academy of Orthopaedic Surgeons

Christopher A. Heck, MD, et al

hours after surgery.16,17 However, the treating surgeon should monitor for progressive neurologic deficits suggesting a spinal epidural hematoma. Data for warfarin use in this patient population are limited and discouraging; thus, warfarin is not recommended. For a patient who sustains a traumatic fracture or dislocation of the spine without spinal cord injury, the Seventh ACCP Conference recommends immediate mechanical compression devices and LMWH as soon as safety permits.21 Current data suggest that simultaneous utilization of intermittent pneumatic compression and LMWH may decrease both local occurrence and proximal propagation of DVT.31 Concern exists, however, that early pharmacologic prophylaxis may exacerbate local traumatic spinal epidural hematoma and iatrogenic neurologic deterioration. Recent prospective data indicate no increased incidence of spinal or cranial epidural hematoma when LMWH is initiated approximately 24 hours after injury in patients with no evidence of continuing hemorrhage.27 Recommendations by the Seventh ACCP Conference are the same for trauma patients with spinal cord injury.21 Although most reports describe the safety of LMWH when it is initiated within 72 hours of injury,31,39 there are data to mandate earlier initiation, within 24 hours after injury, in attempts to diminish the risk of VTE.40 However, the effect of pharmacologic anticoagulation on the injured spinal cord is unknown; thus, such therapy should be used with caution in patients with incomplete neurologic deficits. The Seventh ACCP Conference also recommends continuation of LMWH or conversion to warfarin with a target international normalized ratio of 2.5 during the rehabilitation phase.21 Because most VTE events do occur within 3 months after injury, current recommendations are to continue prophylaxis for 3 to 4 months, deVolume 16, Number 11, November 2008

Figure 2

T1-weighted axial (A) and T2-weighted sagittal (B) emergent magnetic resonance imaging scans demonstrating a dissecting, compressive epidural hematoma in a 79-year-old man who developed acute onset writhing low back pain after an L2/3 and L3/4 laminectomy, followed by lower extremity weakness over the next 24 hours. The patient underwent emergent decompression with eventual complete return of neurologic function.

pending on the activity level of the patient.33,35,36 Suggested rationales for this delayed decreased risk include acquired spasticity of the involved extremity muscle groups and intrinsic vascular changes in paralyzed limbs.34,41

Treatment Treatment of existing VTE in the postoperative spine surgery patient population remains controversial. Bleeding complications and subsequent neurologic deterioration have been associated with pharmacologic anticoagulation.42,43 Similar poor results and high mortality with observation alone are reported.42 For patients with a known VTE or who are considered to be at high risk for VTE but are not considered candidates for pharmacologic anticoagulation therapy, inferior vena cava filters have shown good results in the elective reconstruction and trauma patient population.44-47 Although a high rate of DVT occurs, the symptomatic PE rate is 0% to 1.3%, with no fatalities caused by filter insertion. This is in contrast with a 13% PE incidence in a retrospective, matched cohort of high-risk spine surgery patients. Aside from efficacy, these studies

also support the safety of the inferior vena cava filters. In appropriate patients, a retrievable inferior vena cava filter has a 95% success rate by the recommended 2-week retrieval date. Current multicenter investigations are evaluating whether this success rate can be achieved when retrieval is delayed to 4 weeks after insertion. No data exist regarding timing of pharmacologic therapy initiation for known VTE after elective surgery or traumatic injury. In the report by Cain et al43 on therapeutic anticoagulation for PE after spine surgery, five of six patients who sustained major bleeding complications did not receive therapeutic heparin until ≥6 days after surgery. Therefore, treatment is left to the discretion of the surgeon and should be based on clinical judgment.

Complications With Anticoagulation The most significant complication associated with perioperative pharmacologic prophylaxis in spine surgery is spinal epidural hematoma (Figure 2) and its neurologic sequelae. Incidence rates ranging from 0.1% to 0.7% have been reported.17-19 How661

Venous Thromboembolism in Spine Surgery

ever, this occurrence has also been studied in the absence of anticoagulation.48 Although pharmacologic prophylaxis and management of VTE may increase the risk of spinal epidural hematoma, because it is a rare outcome, minimal data exist regarding which patients are more susceptible to developing this complication. Using logistic regression to evaluate risk factors, Kou et al18 suggested that only patients having multilevel procedures and with coagulopathy were at a statistically higher risk of developing a spinal epidural hematoma. Typical signs and symptoms of spinal epidural hematoma include progressive neurologic deficit; however, they may be less specific, with back pain as the only symptom.17,49 In their report of 13 patients with postoperative spinal epidural hematoma, Gerlach et al17 found a new neurologic deficit in 77%. Once the diagnosis is made, early surgical decompression provides the best scenario for recovery of neurologic function. Vandermeulen et al50 described good or partial neurologic recovery in patients who had a surgical decompression within 8 hours after symptom onset. Gerlach et al17 reported a 60% complete neurologic recovery after early surgical decompression. Other sites of postoperative bleeding have been associated with pharmacologic prophylaxis in the spinal trauma population. In an evaluation of 476 patients with spinal cord injury, upper gastrointestinal and surgical site bleeding accounted for 16 of 19 major bleeding complications.31 No spinal epidural hematomas were reported.

Summary VTE in patients undergoing spine surgery remains difficult to prevent, diagnose, and treat. Aito et al39 documented symptoms in only 35% of patients with confirmed DVT despite prophylaxis. The variability of patients undergoing spine surgery 662

contributes to the complexity of its management. The utilization of mechanical and pharmacologic prophylaxis has led to decreased incidence of VTE in patients undergoing spine surgery. With current treatment protocols, including immediate mechanical and early (<24 hours) pharmacologic prophylaxis, symptomatic VTE rates are reported at approximately 0.05%, 2.1%, and 6.0% for patients who underwent elective spine surgery, sustained spinal fractures, and had spinal cord injury, respectively.17,26,33 Data exist to support prophylactic and treatment protocols for spine patients. After elective spine surgery, patients with no concurrent risk factors do not require prophylaxis. However, because most elective spine patients are elderly or have other risk factors, most of these patients should receive LMWH and intermittent pneumatic compression in the early postoperative period. Prophylaxis for the patient with spinal fracture often requires a multidisciplinary approach by the spine surgeon, trauma surgeon, and additional treating physicians. When no internal or external sources of bleeding are apparent, prophylaxis initiation should begin early with LMWH and intermittent pneumatic compression. Similar prophylaxis protocols should be followed for the patient with spinal cord injury. Data suggest that initiation of pharmacologic prophylaxis within 24 to 72 hours safely decreases the incidence of VTE. Conversion to warfarin should be continued for up to 4 months, with a target international normalized ratio of 2.0 to 3.0. When a VTE event occurs in the early postoperative or postinjury period, observation alone can result in poor outcomes. Inferior vena cava filter placement has been demonstrated to be safe, with the potential for removal in select patients. Once deemed safe by the treating surgeon, pharmacologic therapy should be initiated regardless whether the inferior vena cava filter is removed.

An increased risk of bleeding complications, including spinal epidural hematoma, exists with early initiation of pharmacologic prophylaxis. However, the risk/benefit ratio supports early prophylaxis rather than observation. Thus, the treating surgeon should be mindful of signs and symptoms of bleeding in these patients. Once a spinal epidural hematoma is diagnosed, prompt surgical decompression provides the best chance for neurologic recovery.

References Evidence-based Medicine: There are several level I/II randomized prospective studies (references 4, 5, 10, 16, 28, 32, and 38). The remaining references are level III/IV case control and cohort studies, case reports, or level V expert opinion. Citation numbers printed in bold type indicate references published within the past 5 years. 1.

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Silverstein MD, Heit JA, Mohr DN, Petterson TM, O’Fallon WM, Melton LJ III: Trends in the incidence of deep vein thrombosis and pulmonary embolism: A 25-year population-based study. Arch Intern Med 1998;158: 585-593. Hansson PO, Sörbo J, Eriksson H: Recurrent venous thromboembolism after deep vein thrombosis: Incidence and risk factors. Arch Intern Med 2000;160:769-774. Demers C, Ginsberg JS, Brill-Edwards P, Panju A, McGinnis J: Heparin and graduated compression stockings in patients undergoing fractured hip surgery. J Orthop Trauma 1991;5:387391. Planes A, Vochelle N, Darmon JY, Fagola M, Ballaud M, Huet Y: Risk of deep-venous thrombosis after hospital discharge in patients having undergone total hip replacement: Doubleblinded randomised comparison of enoxaparin versus placebo. Lancet 1996;348:224-228. Freedman KB, Brookenthal KR, Fitzgerald RH Jr, Williams S, Lonner JH: A meta-analysis of thromboembolic prophylaxis following elective total hip arthroplasty. J Bone Joint Surg Am 2000;82:929-938.

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Janku GV, Paiement GD, Green HD: Prevention of venous thromboembolism in orthopaedics in the United States. Clin Orthop Relat Res 1996; 325:313-321. Dickson B: Virchow’s triad? South Med J 2004;97:915-916. Handin RI: Disorders of coagulation and thrombosis, in Fauci AS (ed): Harrison’s Principles of Internal Medicine, ed 14. New York, NY: McGrawHill, 1998, pp 736-743. Woolson ST, Zehnder JL, Maloney WJ: Factor V Leiden and the risk of proximal venous thrombosis after total hip arthroplasty. J Arthroplasty 1998;13: 207-210. Westrich GH, Weksler BB, Glueck CJ, Blumenthal BF, Salvati EA: Correlation of thrombophilia and hypofibrinolysis with pulmonary embolism following total hip arthroplasty: An analysis of genetic factors. J Bone Joint Surg Am 2002;84:2161-2167. Lee AY, Levine MN: Venous thromboembolism and cancer: Risks and outcomes. Circulation 2003;107:I17I21. Prothero SR, Parkes JC, Stinchfield FE: Complications after low-back fusion in 1000 patients: A comparison of two series one decade apart.1966. Clin Orthop Relat Res 1994;306:511. Epstein NE: Efficacy of pneumatic compression stocking prophylaxis in the prevention of deep venous thrombosis and pulmonary embolism following 139 lumbar laminectomies with instrumented fusions. J Spinal Disord Tech 2006;19:28-31. Kim YH, Suh JS: Low incidence of deep vein thrombosis after cementless total hip replacement. J Bone Joint Surg Am 1988;70:878-882. Oda T, Fuji T, Kato Y, Fujita S, Kanemitsu N: Deep venous thrombosis after posterior spinal surgery. Spine 2000;25:2962-2967. Voth D, Schwarz M, Hahn K, DeiAnang K, al Butmeh S, Wolf H: Prevention of deep vein thrombosis in neurosurgical patients: A prospective double-blind comparison of two prophylactic regimen. Neurosurg Rev 1992;15:289-294. Gerlach R, Raabe A, Beck J, Woszczyk A, Seifert V: Postoperative nadroparin administration for prophylaxis of thromboembolic events is not associated with an increased risk of hemorrhage after spinal surgery. Eur Spine J 2004;13:9-13. Kou J, Fischgrund J, Biddinger A, Herkowitz H: Risk factors for spinal

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epidural hematoma after spinal surgery. Spine 2002;27:1670-1673. Yi S, Yoon do H, Kim KN, Kim SH, Shin HC: Postoperative spinal epidural hematoma: Risk factor and clinical outcome. Yonsei Med J 2006;47:326332. Rokito SE, Schwartz MC, Neuwirth MG: Deep vein thrombosis after major reconstructive spinal surgery. Spine 1996;21:853-858. Geerts WH, Pineo GF, Heit JA, et al: Prevention of venous thromboembolism: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S-400S. Dearborn JT, Hu SS, Tribus CB, Bradford DS: Thromboembolic complications after major thoracolumbar spine surgery. Spine 1999;24:1471-1476. Meissner MH, Chandler WL, Elliott JS: Venous thromboembolism in trauma: A local manifestation of systemic hypercoagulability? J Trauma 2003; 54:224-231. Knudson MM, Ikossi DG, Khaw L, Morabito D, Speetzen LS: Thromboembolism after trauma: An analysis of 1602 episodes from the American College of Surgeons National Trauma Data Bank. Ann Surg 2004; 240:490-498. Tropiano P, Huang RC, Louis CA, Poitout DG, Louis RP: Functional and radiographic outcome of thoracolumbar and lumbar burst fractures managed by closed orthopaedic reduction and casting. Spine 2003;28:24592465. Dai LY, Yao WF, Cui YM, Zhou Q: Thoracolumbar fractures in patients with multiple injuries: Diagnosis and treatment. A review of 147 cases. J Trauma 2004;56:348-355. Kurtoglu M, Yanar H, Bilsel Y, et al: Venous thromboembolism prophylaxis after head and spinal trauma: Intermittent pneumatic compression devices versus low molecular weight heparin. World J Surg 2004;28:807811. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP: A prospective study of venous thromboembolism after major trauma. N Engl J Med 1994;331: 1601-1606. Brach BB, Moser KM, Cedar L, Minteer M, Convery R: Venous thrombosis in acute spinal cord paralysis. J Trauma 1977;17:289-292. Green D, Rossi EC, Yao JS, Flinn WR, Spies SM: Deep vein thrombosis in spinal cord injury: Effect of prophylax-

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is with calf compression, aspirin, and dipyridamole. Paraplegia 1982;20: 227-234. Spinal Cord Injury Thromboprophylaxis Investigators: Prevention of venous thromboembolism in the acute treatment phase after spinal cord injury: A randomized, multicenter trial comparing low-dose heparin plus intermittent pneumatic compression with enoxaparin. J Trauma 2003;54:1116-1126. Spinal Cord Injury Thromboprophylaxis Investigators: Prevention of venous thromboembolism in the rehabilitation phase after spinal cord injury: Prophylaxis with low-dose heparin or enoxaparin. J Trauma 2003; 54:1111-1115. Jones T, Ugalde V, Franks P, Zhou H, White RH: Venous thromboembolism after spinal cord injury: Incidence, time course, and associated risk factors in 16,240 adults and children. Arch Phys Med Rehabil 2005; 86:2240-2247. Green D, Hartwig D, Chen D, Soltysik RC, Yarnold PR: Spinal cord injury risk assessment for thromboembolism (SPIRATE study). Am J Phys Med Rehabil 2003;82:950-956. Lamb GC, Tomski MA, Kaufman J, Maiman DJ: Is chronic spinal cord injury associated with increased risk of venous thromboembolism? J Am Paraplegia Soc 1993;16:153-156. El Masri WS, Silver JR: Prophylactic anticoagulant therapy in patients with spinal cord injury. Paraplegia 1981;19:334-342. DeVivo MJ, Kartus PL, Stover SL, Rutt RD, Fine PR: Cause of death for patients with spinal cord injuries. Arch Intern Med 1989;149:1761-1766. Thumbikat P, Poonnoose PM, Balasubrahmaniam P, Ravichandran G, McClelland MR: A comparison of heparin/warfarin and enoxaparin thromboprophylaxis in spinal cord injury: The Sheffield experience. Spinal Cord 2002;40:416-420. Aito S, Pieri A, D’Andrea M, Marcelli F, Cominelli E: Primary prevention of deep venous thrombosis and pulmonary embolism in acute spinal cord injured patients. Spinal Cord 2002;40: 300-303. Harris S, Chen D, Green D: Enoxaparin for thromboembolism prophylaxis in spinal injury: Preliminary report on experience with 105 patients. Am J Phys Med Rehabil 1996;75:326-327. Gaber TA: Significant reduction of the risk of venous thromboembolism in

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Venous Thromboembolism in Spine Surgery all long-term immobile patients a few months after the onset of immobility. Med Hypotheses 2005;64:1173-1176. 42. Swann KW, Black PM, Baker MF: Management of symptomatic deep venous thrombosis and pulmonary embolism on a neurosurgical service. J Neurosurg 1986;64:563-567. 43. Cain JE Jr, Major MR, Lauerman WC, West JL, Wood KB, Fueredi GA: The morbidity of heparin therapy after development of pulmonary embolus in patients undergoing thoracolumbar or lumbar spinal fusion. Spine 1995; 20:1600-1603. 44. Leon L, Rodriguez H, Tawk RG, Ondra SL, Labropoulos N, Morasch MD: The prophylactic use of inferior vena

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cava filters in patients undergoing high-risk spinal surgery. Ann Vasc Surg 2005;19:1-6. 45. Rosner MK, Kuklo TR, Tawk R, Moquin R, Ondra SL: Prophylactic placement of an inferior vena cava filter in high-risk patients undergoing spinal reconstruction. Neurosurg Focus 2004;17:E6. 46. Duperier T, Mosenthal A, Swan KG, Kaul S: Acute complications associated with greenfield filter insertion in high-risk trauma patients. J Trauma 2003;54:545-549. 47. Allen TL, Carter JL, Morris BJ, Harker CP, Stevens MH: Retrievable vena cava filters in trauma patients for high-risk prophylaxis and prevention

of pulmonary embolism. Am J Surg 2005;189:656-661. 48. Cuenca PJ, Tulley EB, Devita D, Stone A: Delayed traumatic spinal epidural hematoma with spontaneous resolution of symptoms. J Emerg Med 2004;27:37-41. 49. Han YM, Kwak HS, Jin GY, Chung GH, Song KJ: Spinal epidural hematoma after thrombolysis for deep vein thrombosis with subsequent pulmonary thromboembolism: A case report. Cardiovasc Intervent Radiol 2006;29:450-453. 50. Vandermeulen EP, Van Aken H, Vermylen J: Anticoagulants and spinalepidural anesthesia. Anesth Analg 1994;79:1165-1177.

Journal of the American Academy of Orthopaedic Surgeons

Surgical Management of Hip Fractures: An Evidence-based Review of the Literature. II: Intertrochanteric Fractures

Kevin Kaplan, MD Ryan Miyamoto, MD Brett R. Levine, MD Kenneth A. Egol, MD Joseph D. Zuckerman, MD

Dr. Kaplan is Sports Medicine Fellow, Kerlan Jobe Orthopaedic Clinic, Los Angeles, CA. Dr. Miyamoto is Sports Medicine Fellow, Steadman Hawkins Clinic, Vail, CO. Dr. Levine is Adult Reconstructive Surgeon, Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL. Dr. Egol is Chief of Fracture Service, Department of Orthopaedic Surgery, NYU–Hospital for Joint Diseases, New York, NY. Dr. Zuckerman is Professor and Chairman, Department of Orthopaedic Surgery, NYU–Hospital for Joint Diseases. Reprint requests: Dr. Zuckerman, Department of Orthopaedic Surgery, NYU–Hospital for Joint Diseases, 301 East 17th Street, New York, NY 10003. J Am Acad Orthop Surg 2008;16:665673 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

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Abstract Treatment of intertrochanteric hip fracture is based on patient medical condition, preexisting degenerative arthritis, bone quality, and the biomechanics of the fracture configuration. A critical review of the evidence-based literature demonstrates a preference for surgical fixation in patients who are medically stable. Stable fractures can be successfully treated with plate-and-screw implants and with intramedullary devices. Although unstable fractures may theoretically benefit from load-sharing intramedullary implants, this result has not been demonstrated in the current evidencebased literature.

I

ntertrochanteric hip fractures are extracapsular fractures of the proximal femur involving the area between the greater and lesser trochanter. Such fractures that extend into the area distal to the lesser trochanter are described as having a subtrochanteric component. The intertrochanteric region has an abundant blood supply, which makes fractures in this area much less susceptible to osteonecrosis and nonunion than are femoral neck fractures. Fractures just proximal to the intertrochanteric line, so-called basicervical fractures, are at greater risk for osteonecrosis (secondary to possibly being intracapsular) and malunion (as a result of head rotation during implant insertion). However, they may be treated with the same implants that are used for intertrochanteric fractures. Internal fixation of intertrochanteric fractures is the mainstay of

treatment, although prosthetic replacement is occasionally indicated. The major difficulty stems from the combination of the presence of often osteopenic bone and the adverse biomechanics of many intertrochanteric fracture patterns. Other factors affecting the choice of fixation include preexisting hip symptoms, the presence of osteoarthritis, bone quality, degree of comminution, and the patient’s medical condition. Most of the classification systems for intertrochanteric fractures have poor reliability and reproducibility. A simplified system to aid in evaluating treatment algorithms when assessing the literature is based on fracture stability, which is related to the condition of the posteromedial cortex. Fractures are considered stable in the absence of a comminuted posteromedial cortex, reverse obliquity, and subtrochanteric extension (Figure 1). 665

Surgical Management of Hip Fractures: An Evidence-based Review of the Literature. II: Intertrochanteric Fractures

Figure 1

Intertrochanteric hip fracture. A, Standard oblique fracture (type I). B, Reverse oblique fracture (type II).

The literature regarding intertrochanteric fractures points to the difficulty in applying evidence-based treatment algorithms. The current evidence is conflicting and does not always support the treatment modalities that are widely used in practice. Techniques and implants continue to be modified, making the older literature less relevant to current practice. Varying fracture patterns may not be distinguished in clinical studies. The ability to make absolute recommendations based on clear evidence is limited by these problems. The Centre for Evidence-Based Medicine created criteria for assigning levels of evidence (Table 1). We performed a thorough literature review to determine the most pertinent

and highest-level studies related to the treatment of intertrochanteric hip fracture. Although level IV case studies contribute general recommendations for the management of these fractures, we have focused on level I, II, and III studies.

Nonsurgical Versus Surgical Treatment Nonsurgical treatment of intertrochanteric hip fractures is usually reserved for patients with comorbidities that place these patients at unacceptable risk from anesthesia, the surgical procedure, or both. Mortality from surgical treatment typically results from cardiopulmonary complications, thromboembolism, and sepsis.1

There is a paucity of level I evidence concerning whether nonsurgical treatment can provide a comparable outcome to that of surgical fixation for intertrochanteric hip fractures (Table 2). In 1989, Hornby et al2 performed a randomized prospective study comparing nonsurgical treatment (ie, traction) with a sliding hip screw (SHS) in 106 patients with intertrochanteric hip fracture. Complications were low in both groups, with no significant difference in 6-month mortality, pain, leg swelling, or pressure sores. Anatomic reduction was achieved more commonly with surgical treatment, and these patients had shorter hospital stays. Patients treated with traction had greater loss of independence at 6-month follow-up. The authors recommended surgical treatment for medically stable patients. A 1981 prospective (level II) trial of 150 patients compared nonsurgical treatment (ie, skeletal traction with a tibial pin) with surgical treatment (eg, medial displacement osteotomy, valgus osteotomy).3 The authors concluded that excellent results were feasible with traction alone provided that a high standard of nursing care was maintained. Careful attention to bedside physical therapy, respiratory care, deep vein thrombosis prophylaxis, and prevention of ulcers were vital to satisfactory outcomes in nonsurgically treated patients. A 2003 retrospective level III study reviewed a population database to compare mortality rates in patients with severe comorbidities who were treated either nonsurgically or surgically for intertrochanteric hip fracture.4 The 30-day mortality rate was lower in patients treated surgically.

Dr. Egol or a member of his immediate family has participated in a speakers bureau or given paid presentations for Biomet; is an unpaid consultant for Biomet; has received research or institutional support from Biomet, Smith & Nephew, Stryker, and Synthes; and holds stock or stock options in Johnson & Johnson. Dr. Zuckerman or a member of his immediate family is affiliated with Neostem and Starmed as a board member, owner, officer, or committee member; has received royalties from Exactech; and has received research or institutional support from Exactech and Stryker. None of the following authors or a member of their immediate families has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Kaplan, Dr. Miyamoto, and Dr. Levine.

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Table 1 Levels of Evidence for Primary Research Question* Type of Study

Level

Therapeutic Studies— Investigating the results of treatment

Prognostic Studies— Investigating the effect of a patient characteristic on the outcome of disease

Diagnostic Studies— Investigating a diagnostic test

Economic and Decision Analyses—Developing an economic or decision model

I

High-quality RCT with statistically significant difference or no statistically significant difference but narrow confidence intervals Systematic review† of level I RCTs (and study results were homogeneous‡)

High-quality prospective Testing of previously developed diagnostic study§ (all patients were criteria on consecutive enrolled at the same patients (with universally point in their disease applied reference “gold with ≥80% follow-up of standard”) enrolled patients) Systematic review† of Systematic review† of level I studies level I studies

Sensible costs and alternatives; values obtained from many studies; with multiway sensitivity analyses Systematic review† of level I studies

II

Lesser quality RCT (eg, <80% follow-up, no blinding, or improper randomization) Prospective§ comparative study¶ Systematic review† of level II studies or level I studies with inconsistent results

Retrospective# study Development of diagnostic criteria on consecutive Untreated controls patients (with universally from an RCT applied reference “gold Lesser quality prospective standard”) study (eg, patients Systematic review† of enrolled at different points in their disease or level II studies <80% follow-up) Systematic review† of level II studies

Sensible costs and alternatives; values obtained from limited studies; with multiway sensitivity analyses Systematic review† of level II studies

III

Case-control study** Retrospective# comparative study¶ Systematic review† of level III studies

Case-control study**

Analyses based on Study of nonconsecutive limited alternatives patients (without and costs; and poor consistently applied reference “gold standard”) estimates Systematic review† of Systematic review† of level III studies level III studies

IV

Case series††

Case series

Case-control study Poor reference standard

Analyses with no sensitivity analyses

V

Expert opinion

Expert opinion

Expert opinion

Expert opinion

RCT = randomized clinical trial *A

complete assessment of quality of individual studies requires critical appraisal of all aspects of the study design

†A

combination of results from two or more prior studies

‡

Studies provided consistent results

§

The study was started before the first patient enrolled

¶Patients

treated one way (eg, cemented hip arthroplasty) compared with a group of patients treated in another way (eg, uncemented hip arthroplasty) at the same institution #

The study was started after the first patient enrolled

**Patients

identified for the study based on their outcome, called “cases” (eg, failed total arthroplasty), are compared to those who did not have that outcome, called “controls” (eg, successful total hip arthroplasty) ††Patients

treated one way with no comparison group of patients treated in another way

Data for this table are from http://www.ejbjs.org/misc/public/instrux.shtml and http://www.cebm.net/levels_of_evidence.asp Reproduced from Spindler KP, Kuhn JE, Dunn W, Matthew LE, Harrell FE Jr, Dittus RS: Reading and reviewing the orthopaedic literature: A systematic, evidence-based medicine approach. J Am Acad Orthop Surg 2005;13:220-229.

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Surgical Management of Hip Fractures: An Evidence-based Review of the Literature. II: Intertrochanteric Fractures

Table 2 Nonsurgical Versus Surgical Treatment of Intertrochanteric Hip Fracture Evidence

Treatment

Level I2

Results/Recommendations

Traction vs sliding hip screw

Level II3 and III4

Authors’ experience

No significant difference in 6-month mortality With surgical treatment, better anatomic reduction, decreased hospital stay, increased independence Traction with tibial Nonsurgical treatment can pin vs medial be as successful as surgical displacement treatment, provided a high osteotomy or valgus standard of nursing care is osteotomy maintained Surgical treatment results in Tibial traction with earlier mobilization and early mobilization lower perioperative vs surgical morbidity treatment Nonsurgical treatment is (dependent on preferred for the patient evaluation of the whose medical condition is fracture) not stable

Table 3 Intramedullary Versus Extramedullary Fixation for Intertrochanteric Hip Fracture Evidence Level I, II, and III6-23

Authors’ experience

Treatment

Results/Recommendations

Gamma nail (Stryker, No significant difference in Mahwah, NJ) vs DHS;6,17 IM wound complications, nail vs SHS;7,8,18 IM nail vs fracture union, mortality, DHS and side plate;9 Gamma or functional outcomes nail vs compression hip screw;10-12 DHS vs PFN;13,19 IM hip screw vs SHS;14 IM device vs fixed-angle screw-plate;15 SHS, Gamma nail, PFN;16 SHS vs short trochanteric nail23 DHS or IM implant (stable DHS or IM implant for fracture), IM device (unstable stable fractures (based on fracture) clinical experience and financial considerations) IM device (unstable fractures) aids in early mobilization and results in decreased blood loss and reduced surgical time

DHS = dynamic hip screw, IM = intramedullary, PFN = proximal femoral nail, SHS = sliding hip screw

However, when the authors compared surgical fixation with nonsurgical treatment with early mobilization (ie, out of bed to chair), they found no significant difference in mortality rate. Thus, when feasible, 668

the authors recommend early mobilization out of bed to chair in patients with nonsurgically managed hip fracture. The evidence-based literature supports surgical fixation2 while also

providing valuable information in regard to medically unstable patients who must be treated nonsurgically.3,4

Intramedullary Versus Extramedullary Fixation The mechanical environment and blood supply to the peritrochanteric region of the hip is more robust, making surgical treatment of intertrochanteric hip fractures different from that of femoral neck fractures. Because the risk of osteonecrosis is minimal, the need for prosthetic replacement is reduced. Experience with fixed-angle screw-plate constructs indicates that uncontrolled fracture impaction is a problem, with complications including implant joint penetration and implant failure.5 Two types of implant are used in the treatment of patients with intertrochanteric hip fracture: an SHS with a side plate, and an intramedullary (IM) nail with an SHS component. The latter may have several advantages over the SHS and side plate. The IM component helps to buttress against fracture collapse and medialization of the distal fracture fragment, particularly in unstable (ie, reverse obliquity) intertrochanteric fractures. Furthermore, the percutaneous insertion of the IM device may reduce the amount of surgical trauma. Numerous studies have compared these types of implant.5-14 The correct interpretation of these data to guide current practice is one of the major controversies in the treatment of intertrochanteric fractures (Table 3). In 1991, Bridle et al6 reported on 100 patients with 41 stable intertrochanteric fractures who were randomized to receive either a Gamma nail (Stryker, Mahwah, NJ) or a dynamic hip screw (DHS). In this level I study, no differences were demonstrated in surgical time, blood loss, wound complications, length of stay, or patient mobility at a minimum follow-up of 6 months. Loss of reduction (lag screw, nail cutout) was

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Kevin Kaplan, MD, et al

similar between the two groups; of the patients treated with the Gamma nail, four experienced femoral shaft fracture requiring revision surgery. For both groups, union occurred at an average of 6 months. Radford et al7 and Saudan et al8 found nearly identical results in their level I studies of 200 and 206 patients, respectively, who were randomized to receive either an IM nail or SHS fixation. In 2001, Adams et al9 published a prospective, randomized controlled trial assessing IM nailing versus a DHS and side plate in 400 patients. Revision rates, femoral shaft fractures, and lag screw cutout were slightly higher in patients treated with IM nailing but did not differ significantly from the cohort treated with a DHS. There was no difference in early or 1-year functional outcomes. Ahrengart et al10 randomized 426 intertrochanteric fractures to treatment with either the Gamma nail or a compression hip screw. The latter cohort required significantly less surgical time, and patients experienced less blood loss (P < 0.05). However, in unstable intertrochanteric fractures, surgical time was not significantly different between the two groups. In patients treated with the Gamma nail, difficulty was encountered with the distal locking technique. There was also a higher incidence of cephalic position of the compression screw within the femoral head, screw cutout, and intraoperative fracture in the Gamma nail group. Walking ability was the same in both groups. The authors recommended compression hip screws for less comminuted fractures, reserving Gamma nails for comminuted patterns. In 1995, O’Brien et al11 found no significant difference between Gamma nail and compression hip screw fixation in terms of blood loss, days in the hospital, time to union, and functional outcome. Utrilla et al12 found no difference in total surgical time in their level I Volume 16, Number 11, November 2008

study comparing the Gamma nail with a compression hip screw in 210 stable and unstable fractures. However, the Gamma nail group had a significantly lower postoperative transfusion requirement (P = 0.013). Mortality, fracture healing, and intra- and postoperative complication rates were not significantly different between the two groups. In patients with unstable fracture patterns, postoperative ambulation was significantly improved in the Gamma nail group (P = 0.017). Recovery of ambulation was a focus of the study by Pajarinen et al,13 who compared a DHS with a proximal femoral nail (PFN) (Synthes, Oberdorf, Switzerland) in 108 patients. Although the immediate postoperative outcomes did not differ between the two groups, patients treated with IM devices had a significantly faster return to preoperative ambulation levels (P = 0.04). Fracture healing was similar between the two groups at 4 months, with two patients in each group requiring revision. This study also suggested that the PFN provided faster restoration of walking ability than did the DHS in patients with unstable fracture patterns. Baumgaertner et al14 randomized 135 unstable intertrochanteric fractures to either an IM hip screw (Intramedullary Hip Screw [IMHS]; Smith & Nephew, Memphis, TN) or an SHS. Patients with unstable fractures treated with the IMHS required 23% less time in the operating room and experienced 44% less blood loss than did the SHS cohort. Functional outcome was not significantly different between the two groups. Sadowski et al15 reported the results of 39 unstable reverse obliquity intertrochanteric fractures managed with either an IM device or a fixed-angle screw-plate device (Dynamic Condylar Screw; Synthes). Clinical and radiographic follow-up demonstrated a shorter mean surgical time for patients treated with IM

nailing and a significantly higher rate of implant failure and nonunion in the group treated with the Dynamic Condylar Screw (P = 0.008 and P = 0.007, respectively). Excluding patients with nonunion or failure, there was no significant difference in postoperative walking ability or level of independence. In 2005, Papasimos et al16 performed a randomized, prospective study of 120 patients with unstable intertrochanteric fractures comparing an SHS, Gamma nail, and PFN. Mean blood loss, length of hospital stay, screw cutout, and fracture reduction were not statistically different between the three groups. Patients treated with PFN had a significantly longer surgical time (P < 0.05), which the investigators suggested was due to lack of surgeon experience with that device. Several level II studies have been published on this topic. In 1992, Leung et al17 reported the results of a prospective trial comparing Gamma nails with DHSs and found that patients treated with Gamma nails had smaller incisions, less intraoperative blood loss, and earlier full weight bearing. No significant difference was found in mortality and postoperative mobility (both groups lost one level of mobility). Of note, the investigators cited a higher incidence of fractures of the lateral cortex (three in the nail group and two in the DHS group) during insertion and noted two femoral shaft fractures within 3 months of surgery in the Gamma nail group. Guyer et al18 reviewed 100 patients treated with either an IM device or an SHS. There was no significant difference in intraoperative blood loss or perioperative complications between the two devices. The authors suggested that the Gamma nail was preferable to DHSs for unstable fracture patterns because three patients in the DHS group experienced proximal screw perforation during attempted mobilization. 669

Surgical Management of Hip Fractures: An Evidence-based Review of the Literature. II: Intertrochanteric Fractures

Nuber et al19 evaluated 129 patients with unstable intertrochanteric fractures treated with either a DHS or a PFN. Revision rates were similar between the two groups. However, there was a significantly shorter surgical time (44.3 versus 57.3 min) and hospital stay (18.6 versus 21.3 days) in the PFN cohort. Full weight bearing was possible immediately postoperatively in 97% of the proximal nail cohort, compared with 88% of the patients treated with a DHS. At 6-month follow-up, considerably lower pain intensity scores were found in the PFN cohort. In several level II trials comparing extramedullary and IM devices, the use of a nail was shown to have an increased risk of intraoperative and postoperative fracture, with an increased rate of revision.14,20-22 No significant differences were reported in regard to wound infection, medical complications, mortality, functional outcomes, postoperative complications, hip function, quality of life, and activities of daily living at 1 year postoperatively. Complications associated with the Gamma nail, particularly the intraoperative fracture rate, resulted in specific design and technique modifications. These changes, combined with increased surgeon experience, contributed to a lower rate of intraoperative complications in subsequent studies. One retrospective (level III) study reviewed 93 patients who were treated with either an SHS or a short trochanteric nail.23 Fracture healing was uneventful in 94% of the patients treated with SHS and in 89% of the patients treated with trochanteric nailing. Complications included one lag screw cutout in the SHS cohort compared with three in the trochanteric nail cohort. Other outcome measures were similar between the two groups, and the authors concluded that both methods resulted in successful treatment of intertrochanteric fractures. Analysis of level I studies provides insight regarding the two most 670

commonly used methods of intertrochanteric fracture fixation: IM nailing and DHS fixation. Most level I studies indicate that there are no significant differences in operating room time, blood loss, wound complications, length of stay, mobility, functional outcomes, loss of reduction, union rate, mortality, and complication rates when comparing IM devices with SHS constructs. However, several studies report a faster return to preoperative ambulation, reduced operating room time, and less blood loss when an IM device is used, especially in patients with unstable fracture patterns.6-16 Analysis of level II studies demonstrates a preference for IM devices. Surgical Outcomes Unfortunately, the 18 studies discussed herein provide inconsistent evidence for treatment recommendations. A well-defined outcome measure such as surgical time is a good example. Two level I studies indicated no significant difference in surgical time between IM and extramedullary implants.6,12 However, two level I studies and one level II study found a significantly higher surgical time when an SHS is used (P < 0.05), with longer times being associated with unstable patterns.14,15,19 Two level I studies demonstrated a longer surgical time with the use of an IM implant.10,16 Femoral Shaft Fracture Three level I studies and one level II study found an increased incidence of femoral shaft fracture at the tip of the implant when using IM nails.9,10,12,17 Most authors concluded that this increase was in part due to a lack of experience and to suboptimal hardware design. Newergeneration nails have a radius of curvature that better conforms to the anatomic shape of the femur. Although this statement is not supported by evidence-based literature, this feature may potentially reduce the rate of intraoperative frac-

ture.9,10,12,17 In contrast to earlier reports, recent studies show no significant difference in complications or revision rates between the two types of implants, which may be attributed to improved nail design and increasing surgeon experience.5,24 Blood Loss Six level I studies and one level II study found no significant difference in blood loss or transfusion rates between IM and extramedullary implants.6-8,11,16,18 However, two level I studies (P < 0.05,12 P < 0.01314) and one level II study (P < 0.05)17 found significantly less blood loss with IM implants, while one level I study states that there was significantly less blood loss with the use of a DHS (P < 0.05).10 Patient Ambulation and Complications Five level I studies suggested that patients regain equal ambulatory status regardless of fixation type.6-8,10,15 However, two level I and two level II studies concluded that IM devices expedite return to pretreatment ambulatory function.12,13,17,19 It is important to note that many current studies have not separated stable from unstable patterns when assessing ambulatory status. The literature is consistent, however, in regard to wound complications, fracture nonunion, mortality rates, and functional outcomes and overall incidence of complications, with no significant difference between IM and extramedullary implants.6-24 Authors’ Recommendation There is no consensus regarding the ideal implant for treating intertrochanteric fractures. However, based on the available evidence-based data, we recommend either a DHS or an IM device for stable intertrochanteric fractures. For unstable fractures, we recommend an IM device. Although this has not been proved in the current evidence-based literature, we believe that an IM device is a biome-

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Kevin Kaplan, MD, et al

chanically stronger construct and is better suited to preventing increased fracture collapse in unstable fractures. In addition, evidence suggests that IM devices aid in early mobilization, return of ambulatory function, decreased blood loss, and less surgical time.12,13,17,19 However, there seems to be a higher cost associated with the use of IM devices.5

Open Reduction and Internal Fixation Versus Arthroplasty Prosthetic hip replacement generally has not been considered a primary treatment option for intertrochanteric fractures. Unlike femoral neck fractures, which retain some of the femoral neck in addition to the abductor mechanism, intertrochanteric fractures involve more distal femoral bone, and often the greater trochanter and the abductor are not attached to the proximal femur. In this setting, prosthetic replacement for intertrochanteric fractures typically requires a more complex surgical procedure with potentially higher morbidity. In the patient with preexisting symptomatic degenerative arthritis, primary prosthetic replacement may be the best option. It can also be considered for intertrochanteric fractures with extreme comminution in severely osteoporotic bone in which internal fixation methods are unlikely to be successful.25 In 2005, Kim et al26 performed a prospective randomized (level I) study of unstable intertrochanteric fractures in elderly patients in which long-stem cementless calcar-replacement hemiarthroplasty was compared with a PFN. No significant differences were found between the two groups in terms of functional outcomes, hospital stay, time to weight bearing, and risk of complications. However, surgical time (P < 0.001), blood loss (P < 0.001), need for blood transfusions (P < 0.001), and mortality rates (P < 0.006) were all significantly lower in the PFN group. Volume 16, Number 11, November 2008

In another level I study, Stappaerts et al27 treated 47 patients with compression hip screws and 43 with hemiarthroplasty. No significant difference was found between surgical time, wound complications, or mortality rates. However, the hemiarthroplasty group was reported to have higher transfusion rates. Haentjens et al28 reported on a prospective (level II) study comparing the results of 79 consecutive patients aged 75 years and older who were treated with either bipolar hemiarthroplasty (37 patients) or internal fixation (42 patients). The bipolar group experienced easier and faster rehabilitation, with a lower incidence of decubiti and pulmonary complications. The decrease in complications was attributed to an earlier return to full weight bearing. The remainder of evidence regarding arthroplasty to treat intertrochanteric fractures comes from level III and IV studies. These studies suggest that a cemented hemiarthroplasty with standard implants is a reasonable alternative to open reduction and internal fixation. In addition, they indicate that arthroplasty has the advantage of early weight bearing and avoids the potential of fixation failure and the need for subsequent revision.29-33 There is no overwhelming evidence from randomized clinical trials to indicate that arthroplasty is more effective than IM and extramedullary fixation of intertrochanteric hip fractures (Table 4). No significant differences in complications have been reported between hemiarthroplasty or THA versus IM fixation.26,28 However, the incidence of decubiti and pulmonary complications may be higher with internal fixation.27 Two level I studies found a significantly lower transfusion rate when a PFN was used (P < 0.001,26 P < 0.0527). No significant difference in functional outcomes or rehabilitation was shown between unstable fractures treated with hemiarthroplasty or with a PFN.26 However,

one level II study concluded that patients treated with bipolar instrumentation had a faster rate of rehabilitation, although the time differences were not statistically significant.28 Based on the available evidence on, and our clinical experience with, intertrochanteric hip fractures, arthroplasty should be reserved for patients with preexisting symptomatic degenerative arthritis, those in whom internal fixation is not expected to be successful because of fracture comminution or bone quality, and in patients who require salvage for failed internal fixation.

Summary With ongoing improvements in endoprostheses and total hip replacements, increased surgeon experience, and the need to separate stable from unstable fractures, it is difficult to recommend one optimum treatment of intertrochanteric fractures from a purely evidence-based perspective. Even so, we believe that combining current evidence-based literature with clinical experience can guide clinical decision making. Surgical intervention is preferable to nonsurgical treatment of intertrochanteric fractures in the medically stable patient. This is the case despite evidence demonstrating that patients can have equivalent outcomes with nonsurgical treatment when nursing care is excellent. Patients treated nonsurgically may have a higher mortality rate if they are not mobilized early. Although there is no evidence-based literature to support these findings, nonsurgically treated patients appear to be at higher risk for complications such as decubiti, pneumonia, and deep vein thrombosis. When considering surgical intervention, it is important to consider the character of each fracture pattern, surgeon clinical experience, and the reported evidence regarding the various internal fixation implants. Pa671

Surgical Management of Hip Fractures: An Evidence-based Review of the Literature. II: Intertrochanteric Fractures

Table 4 ORIF Versus Hemiarthroplasty and THA for Intertrochanteric Hip Fracture Evidence Level I26,27 and

II28

Treatment

Results/Recommendations

Hemiarthroplasty vs PFN,26

compression hip screws vs hemiarthroplasty,27 hemiarthroplasty vs ORIF28

Level III and IV29-33

Hemiarthroplasty vs ORIF

Authors’ experience

Hemiarthroplasty vs ORIF

Shorter surgical time with PFN compared with hemiarthroplasty, shorter surgical time with THA versus IM and extramedullary implants No significant differences in complications Higher incidence of decubiti and pulmonary complications with bipolar hemiarthroplasty Significantly lower transfusion rate with PFN No significant differences in functional outcomes Faster rehabilitation in patients treated with bipolar instrumentation Cemented hemiarthroplasty a reasonable alternative to ORIF With arthroplasty, earlier weight bearing and lack of fixation failure, so no need for revision Arthroplasty reserved for patients with preexisting symptomatic degenerative arthritis and those in whom internal fixation is not expected to be successful because of comminution or bone quality, and as a salvage procedure for failed internal fixation

IM = intramedullary, ORIF = open reduction and internal fixation, PFN = proximal femoral nail, THA = total hip arthroplasty

tient outcome has not been shown to differ significantly between fixation of stable intertrochanteric fractures with plate-and-screw implants versus IM devices. Thus, factors in the decision-making process should include surgeon experience with the devices and cost-effectiveness of the procedure. Unstable intertrochanteric fractures are a distinct subset that biomechanically should benefit from an IM device; however, there is no overwhelming evidence to prove this recommendation. Studies on functional outcome have not yet been performed in sufficient detail to demonstrate significant differences between devices. Comparisons between specific types of IM implants have not been reported in sufficient numbers or detail 672

to determine whether nail design has an effect on outcome. Patients with severe degenerative disease or with comminuted fracture in osteoporotic bone can be successfully treated with an endoprosthetic replacement or a THA. This surgery is more complex than internal fixation and is associated with a higher rate of postoperative complications. The evidence-based literature does not show a significant difference in terms of time to ambulation and length of hospital stay between arthroplasty and internal fixation. However, given the variety of clinical presentations and fracture patterns, such treatment may be considered in select patients.

“Surgical Management of Hip Fractures: An Evidence-based Review of the Literature. I: Femoral Neck Fractures” appeared in the October 2008 issue of the Journal of the American Academy of Orthopaedic Surgeons.

References Evidence-based Medicine: References 1-3, 5-22, and 26-28 are level I/II prospective, randomized studies or systematic reviews of level I studies. The remainder are level III/IV case reports and case-control cohort studies. Citation numbers printed in bold type indicate references published within the past 5 years. 1.

2.

3.

4.

5.

6.

7.

8.

Parker MJ, Handoll HH: Conservative versus operative treatment for extracapsular hip fractures. Cochrane Database Syst Rev 2000;2: CD000337. Hornby R, Evans JG, Vardon V: Operative or conservative treatment for trochanteric fractures of the femur: A randomized epidemiological trial in elderly patients. J Bone Joint Surg Br 1989;71:619-623. Bong SC, Lau HK, Leong JC, Fang D, Lau MT: The treatment of unstable intertrochanteric fractures of the hip: A prospective trial of 150 cases. Injury 1981;13:139-146. Jain R, Basinski A, Kreder HJ: Nonoperative treatment of hip fractures. Int Orthop 2003;27:11-17. Parker MJ, Handoll HH: Gamma and other cephalocondylic intramedullary nails versus extramedullary implants for extracapsular hip fractures in adults. Cochrane Database Syst Rev 2005;4:CD000093. Bridle SH, Patel AD, Bircher M, Calvert PT: Fixation of intertrochanteric fractures of the femur: A randomised prospective comparison of the gamma nail and the dynamic hip screw. J Bone Joint Surg Br 1991;73:330-334. Radford PJ, Needoff M, Webb JK: A prospective randomised comparison of the dynamic hip screw and the gamma locking nail. J Bone Joint Surg Br 1993;75:789-793. Saudan M, Lübbeke A, Sadowski C, Riand N, Stern R, Hoffmeyer P: Per-

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9.

10.

11.

12.

13.

14.

15.

16.

trochanteric fractures: Is there an advantage to an intramedullary nail? A randomized, prospective study of 206 patients comparing the dynamic hip screw and proximal femoral nail. J Orthop Trauma 2002;16:386-393. Adams CI, Robinson CM, CourtBrown CM, McQueen MM: Prospective randomized controlled trial of an intramedullary nail versus dynamic screw and plate for intertrochanteric fractures of the femur. J Orthop Trauma 2001;15:394-400. Ahrengart L, Törnkvist H, Fornander P, et al: A randomized study of the compression hip screw and Gamma nail in 426 fractures. Clin Orthop Relat Res 2002;401:209-222. O’Brien PJ, Meek RN, Blachut PA, Broekhuyse HM, Sabharwal S: Fixation of intertrochanteric hip fractures: Gamma nail versus dynamic hip screw. A randomized, prospective study. Can J Surg 1995;38:516-520. Utrilla AL, Reig JS, Muñoz FM, Tufanisco CB: Trochanteric gamma nail and compression hip screw for trochanteric fractures: A randomized, prospective, comparative study in 210 elderly patients with a new design of the gamma nail. J Orthop Trauma 2005;19:229-233. Pajarinen J, Lindahl J, Michelsson O, Savolainen V, Hirvensalo E: Pertrochanteric femoral fractures treated with a dynamic hip screw or a proximal femoral nail: A randomised study comparing post-operative rehabilitation. J Bone Joint Surg Br 2005;87:7681. Baumgaertner MR, Curtin SL, Lindskog DM: Intramedullary versus extramedullary fixation for the treatment of intertrochanteric hip fractures. Clin Orthop Relat Res 1998;348:87-94. Sadowski C, Lübbeke A, Saudan M, Riand N, Stern R, Hoffmeyer P: Treatment of reverse oblique and transverse intertrochanteric fractures with use of an intramedullary nail or a 95 degrees screw-plate: A prospective, randomized study. J Bone Joint Surg Am 2002;84:372-381. Papasimos S, Koutsojannis CM, Pana-

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17.

18.

19.

20.

21.

22.

23.

24.

25.

gopoulos A, Megas P, Lambiris E: A randomised comparison of AMBI, TGN and PFN for treatment of unstable trochanteric fractures. Arch Orthop Trauma Surg 2005;125:462-468. Leung KS, So WS, Shen WY, Hui PW: Gamma nails and dynamic hip screws for peritrochanteric fractures: A randomised prospective study in elderly patients. J Bone Joint Surg Br 1992; 74:345-351. Guyer P, Landolt M, Eberle C, Keller H: The gamma-nail as a resilient alternative to the dynamic hip screw in unstable proximal femoral fractures in the elderly [German]. Helv Chir Acta 1992;58:697-703. Nuber S, Schönweiss T, Rüter A: Stabilisation of unstable trochanteric femoral fractures: Dynamic hip screw (DHS) with trochanteric stabilisation plate vs. proximal femur nail (PFN) [German]. Unfallchirurg 2003;106: 39-47. Hardy DC, Descamps PY, Krallis P, et al: Use of an intramedullary hip-screw compared with a compression hipscrew with a plate for intertrochanteric femoral fractures: A prospective, randomized study of one hundred patients. J Bone Joint Surg Am 1998;80: 618-630. Harrington P, Nihal A, Singhania AK, Howell FR: Intramedullary hip screw versus sliding hip screw for unstable intertrochanteric femoral fractures in the elderly. Injury 2002;33:23-28. Hoffmann R, Schmidmaier G, Schulz R, Schütz M, Südkamp NP: Classic nail versus DHS: A prospective randomised study of fixation of trochanteric femur fractures [German]. Unfallchirurg 1999;102:182-190. Crawford CH, Malkani AL, Cordray S, Roberts CS, Sligar W: The trochanteric nail versus the sliding hip screw for intertrochanteric hip fractures: A review of 93 cases. J Trauma 2006;60: 325-328. Egol KA, Chang EY, Cvitkovic J, Kummer FJ, Koval KJ: Mismatch of current intramedullary nails with the anterior bow of the femur. J Orthop Trauma 2004;18:410-415. Parker MJ, Handoll HH: Replacement

26.

27.

28.

29.

30.

31.

32.

33.

arthroplasty versus internal fixation for extracapsular hip fractures. Cochrane Database Syst Rev 2000;1: CD000086. Kim SY, Kim YG, Hwang JK: Cementless calcar-replacement hemiarthroplasty compared with intramedullary fixation of unstable intertrochanteric fractures: A prospective, randomized study. J Bone Joint Surg Am 2005;87: 2186-2192. Stappaerts KH, Deldycke J, Broos PL, Staes FF, Rommens PM, Claes P: Treatment of unstable peritrochanteric fractures in elderly patients with a compression hip screw or with the Vandeputte (VDP) endoprosthesis: A prospective randomized study. J Orthop Trauma 1995;9:292-297. Haentjens P, Casteleyn PP, De Boeck H, Handelberg F, Opdecam P: Treatment of unstable intertrochanteric and subtrochanteric fractures in elderly patients: Primary bipolar arthroplasty compared with internal fixation. J Bone Joint Surg Am 1989;71: 1214-1225. Chan KC, Gill GS: Cemented hemiarthroplasties for elderly patients with intertrochanteric fractures. Clin Orthop Relat Res 2000;371:206-215. Rodop O, Kiral A, Kaplan H, Akmaz I: Primary bipolar hemiprosthesis for unstable intertrochanteric fractures. Int Orthop 2002;26:233-237. Harwin SF, Stern RE, Kulick RG: Primary Bateman-Leinbach bipolar prosthetic replacement of the hip in the treatment of unstable intertrochanteric fractures in the elderly. Orthopedics 1990;13:1131-1136. Berend KR, Hanna J, Smith TM, Mallory TH, Lombardi AV: Acute hip arthroplasty for the treatment of intertrochanteric fractures in the elderly. J Surg Orthop Adv 2005;14:185-189. Haentjens P, Casteleyn PP, Opdecam P: Primary bipolar arthroplasty or total hip arthroplasty for the treatment of unstable intertrochanteric and subtrochanteric fractures in elderly patients. Acta Orthop Belg 1994;60 (suppl 1):124-128.

673

Surgical Techniques

Antibiotic Beads Thomas A. DeCoster, MD Shahram Bozorgnia, MD

The video that accompanies this article is “Preparation and Use of Antibiotic-Impregnated Beads for Orthopaedic Infections,” available on the Orthopaedic Knowledge Online Website, at http://www5. aaos.org/oko/jaaos/surgical.cfm

Dr. DeCoster is Professor and Vice Chair, Department of Orthopaedics and Rehabilitation, University of New Mexico School of Medicine, Albuquerque, NM. Dr. Bozorgnia is Trauma Fellow, Department of Orthopaedics and Rehabilitation, University of New Mexico School of Medicine. Dr. DeCoster or a member of his immediate family has received research or institutional support from Biomet, EBI, Orthofix, Smith & Nephew, Stryker, and Zimmer; has stock or stock options held in Merck and Wyeth; and has received royalties from Innomed. Neither Dr. Bozorgnia nor a member of his immediate family has received anything of value from or owns stock in a commercial company or institution related directly or indirectly to the subject of this article. Reprint requests: Dr. DeCoster, Department of Orthopaedics and Rehabilitation, University of New Mexico School of Medicine, 1127 University Boulevard NE, Albuquerque, NM 87131. J Am Acad Orthop Surg 2008;16:674678 Copyright 2008 by the American Academy of Orthopaedic Surgeons.

674

B

one infection, or osteomyelitis, can be one of the most difficult problems confronted by the orthopaedic surgeon. Common causes of osteomyelitis include open fractures, hematogenous spread of bacteria to bone, and orthopaedic surgical procedures complicated by infection. Assessment involves identification of the offending organism by tissue culture and sensitivity to antibiotics; radiographic assessment of the extent of the infection; clinical evaluation of the patient’s general health and ability to fight infection; and determination of the local anatomic condition of the bone and soft tissue. Treatment is individualized but generally involves prolonged use of systemic antibiotics, surgical débridement, and support of the patient’s overall health.1,2 Results are generally good but are not universally successful. Difficulties include recurrence or lack of control of infection, systemic toxicity to antibiotics, scar formation, and persistent nonunion of fractures.2 Other problems include expense and practical difficulties for the patient and the surgeon, including multiple surgical treatments, lengthy and frequent hospitalizations, and prolonged limb dysfunction. Control of infection eventually may be obtained, but patient function still may be limited by scar, stiffness, and weakness, as well as nonunion or malunion of the fracture. Late recurrence of infection is also a problem. To deliver therapeutic tissue levels of parenteral antibiotics to the target area, high serum levels of antibiotics must be achieved.3 These high serum levels, however, may result in an increased incidence of systemic side effects such as nephrotoxicity and ototoxicity.4 As an alter-

native, the use of antibioticimpregnated beads as an adjunct to other treatment offers advantages compared with systemic aminoglycosides. With the bead pouch technique, the systemic levels are low, and the systemic complications are virtually eliminated, while the local concentration, where it is needed, is extremely high.3 Antibiotic beads also offer the benefit of management of dead space. They are relatively inexpensive and are easy for the surgeon to insert and the patient to tolerate.5

Indications and Contraindications Antibiotic beads can be used in multiple different applications. Typical indications include prevention of infection (eg, open fracture antibiotic bead pouch prophylaxis), treatment of established bone infection (ie, acute and chronic osteomyelitis), treatment of infected joint arthroplasties, dead space management in patients with large soft-tissue injuries, and chronic infected nonunions. Contraindications to the use of antibiotic bead pouches in the treatment of open fractures include patient hypersensitivity to specific antibiotics, small wounds (for which beads are not necessary), and unsalvageable limbs (because beads do not overcome massive tissue injuries). Contraindication to the use of antibiotic beads in the treatment of osteomyelitis include patient hypersensitivity to a specific antibiotic and the presence of resistant and slime-forming organisms such as Enterococcus. The foreign-body surface of the methacrylate beads themselves is conductive to slimeproducing organisms, and the slime

Journal of the American Academy of Orthopaedic Surgeons

Thomas A. DeCoster, MD, and Shahram Bozorgnia, MD

barrier severely limits the efficacy of the antibiotics in controlling the infection.6,7

Figure 1

Figure 2

A string of antibiotic beads is placed into the wound for dead space management and to provide a high concentration of local antibiotic to the wound.

In open fractures with significant softtissue injuries, antibiotic beads can be placed in the open wound. The softtissue defect will be covered with an adhesive, porous, polyethylene wound film.

Specific Characteristics of Antibiotic Beads Antibiotic-impregnated polymethylmethacrylate (PMMA) cement beads are a popular modality used in conjunction with surgical débridement and intravenous antibiotic therapy for the treatment or prophylaxis of orthopaedic infections. The beads vary in size, type and amount of antibiotic used, and type of bone cement used. The beads can be prepared in advance by molding or by rolling by hand in the operating room. Nonbiodegradable PMMA cement is the most common carrier used. To incorporate antibiotics, antibiotic powder is mixed with the powdered cement polymer before adding the methylmethacrylate liquid monomer. The antibiotic must be water soluble, available as powder, able to remain stable despite the heat generated during the polymerization reaction, and hypoallergenic, as well as have a broad spectrum of activity. Antibiotic release is highest in the first 4 days following implantation; the remaining elution at therapeutic concentration persists for weeks to months.8 Wahlig et al3 showed that, if gentamicin-PMMA chains are implanted and the wound is closed, then the local concentrations of antibiotic achieved are 200 times the levels achieved with systemic antibiotic administration. However, the use of the beads in an open system or in combination with suction irrigation rapidly lowers local antibiotic concentrations, and the therapeutic advantage is diminished. Therefore, this technique is not recommended. Aminoglycosides are the most commonly used antibiotics in this context. They are effective against aerobic gram-negative bacilli and staphylococci as well as streptococVolume 16, Number 11, November 2008

ci, enterococci, and anaerobes.9 Among the aminoglycosides are tobramycin and gentamicin. Tobramycin has been substituted for gentamicin in the United States because it is available as a pharmaceuticalgrade powder, whereas gentamicin is not. There is extensive information on the elution patterns of aminoglycosides from beads in a variety of clinical scenarios.4,10 Vancomycin should be considered when there is a risk of resistant staphylococcal organisms, that is, methicillin-resistant Staphylococcus aureus. Vancomycin is available in powder form and is not neutralized by the heat of methacrylate polymerization. Effective elution of vancomycin has also been reported.11 Bead molds are available in a variety of sizes. A diameter of 8 mm is the largest and 2 mm, the smallest. Small-diameter beads are used in wounds of the hand and in other small wounds to maximize the surface area and antibiotic elution. Consistency in size and shape of the beads also facilitates their passage into tight spaces, including the medullary canal.

Surgical Technique The technique of application of antibiotic beads involves the production

of beads, followed by surgical placement within the débrided wound and in place of débrided bone (Figures 1 and 2). Following bead implantation, the soft tissue is closed. The beads allow for very high levels of antibiotic bathing of the wound and also assist in fighting infection. The beads occupy space, preventing the accumulation of hematoma that otherwise would be a potential site for infection. Antibiotic beads also provide management of dead space by preventing the formation of scar tissue in the bone-defect site. If infection persists, a repeat débridement, culture, and antibiotic bead exchange may be performed after several days or weeks. Once the infection is well controlled, the beads are surgically removed. For nonunion or a large bone void, bone graft may be placed in the area that the beads occupied. Although the antibiotic within the beads produces a high local concentration in the surrounding tissues, the systemic level of antibiotic resulting from beads is low, which minimizes complications, including renal toxicity and ototoxicity. The high local concentration of antibiotic reduces and often eliminates the need for intravenous antibiotics; therefore, intravenous access and compliance are not required. Osteomyelitis typically involves seques675

Antibiotic Beads

Figure 3

Figure 4

The liquid cement mixture is pressed forcefully with a tongue depressor into the bead mold.

The liquid cement mixture is pressed forcefully with a cement-filled syringe into the bead mold.

tration of dead infected bone with little to no blood supply. Many systemic antibiotics exhibit poor penetration of bone, even when the bone is vascularized. Hence, systemic antibiotics and blood-borne antimicrobial cells may not reach the area of greatest need. Antibiotic beads, however, provide high local concentrations of antibiotic not dependent on blood supply to the bone. Neither are the antibiotics dependent on bone penetration.5

Antibiotic Bead Preparation Technique Bead Preparation The bead preparation technique described here results in spherical, uniform tobramycin-impregnated video, “IngrediPMMA beads ( ents”). These beads can be made in advance, sterilely packaged, and stored in the operating room ready for use. Alternatively, beads can be prepared in the operating room at the time of implantation, with or without the use of bead molds. When this technique is used, sufficient time (at least 30 minutes) must be allowed for full curing of the cement to minimize toxic monomers. Materials The materials needed for the production of tobramycin-impregnated PMMA beads are the following: • One package (40 g) of PMMA 676

bone cement • 20 mL of liquid monomer • Two 1.2-g vials of tobramycin powder • Two twisted strands of 26-gauge wire • A cast-metal, Teflon-coated bead mold • One medium-size (approximately 200 mL) plastic bowl • Tongue depressors • Two 10-mL syringes • Tweezers from a suture-removal kit • Gloves Technique Twist together two strands of 26gauge wire (50 turns using a hand video, “Wire-Twisting Prodrill) ( cedure”). Carefully place the wire into the grooves of the bead mold video, and tighten the mold ( “Preparation Technique A [Spatula]”). A cool working environment and precooling of the mold and PMMA prolong the polymerization time. In a medium-size plastic bowl, mix most of one package of bone cement (ie, 35 of 40 g) with two 1.2-g vials of tobramycin powder. This allows a prolonged liquid phase, which facilitates better bead production. Stir thoroughly to ensure homogeneity of the mixture. Pour 20 mL of liquid monomer into the powder and stir vigorously for about 30 seconds until the mixture liquefies. Continue to stir the cement mixture, mov-

ing the cement away from the bottom and edges of the bowl to prevent hardening. With a tongue depressor, forcefully press the liquid cement mixture into the bead mold (Figure 3). Quickly and carefully fill all of the holes until the entire mold is filled with the cement mixture. It is imperative that this step is done in less than 8 minutes, before the mixture hardens. Smooth the surface of the mold by scraping off the remaining cement with a tongue depressor. Place the mold on its side and let it sit for 15 minutes as the cement hardens. An alternative technique for placing the cement into the mold holes is to pour 3 mL of the liquid cement mixture into a 10-mL syringe with the plunger removed and the tip capped, then replace the plunger and video, remove the syringe cap ( “Preparation Technique B [Syringe]”). While applying pressure, use the syringe to fill each hole in the mold with the cement mixture. Keep the syringe at a 90° angle as each hole is filled and apply pressure to maintain a tight seal between the mold and the syringe (Figure 4). Cement should bulge into the adjacent hole. Proceed rapidly because the syringe technique requires the cement to be in the liquid state. Four syringes typically are needed for two 20-bead chains. The tip of each syringe is cut off so that the lumen matches the diameter of the mold. Smooth the surface of the mold by scraping off the remaining cement with a tongue depressor. Place the mold on its side and let it sit for 15 minutes until the cement is completely hardened. After 15 minutes, take the mold apart and gently remove the beads by pulling the wire (Figure 5). Remove the excess cement (ie, flashing) between the beads using the tweezers from the suture kit. Excess cement in the mold also should be removed to facilitate the next use of the mold. A pair of scissors from a suture-removal set is the exact

Journal of the American Academy of Orthopaedic Surgeons

Thomas A. DeCoster, MD, and Shahram Bozorgnia, MD

Pearls • Remove all avascular, necrotic, and contaminated tissue before applying antibiotic beads. Infection resulting from inadequate débridement will not be overcome by the use of antibiotic beads. • Beads can be made in advance and stored in the operating room. • Thoroughly mix the bone cement with the antibiotic powder before adding the liquid monomer. • Fill all of the holes of the mold as quickly as possible before the mixture hardens. • An assistant is helpful. Pitfalls • Do not use the beads in an open system or in combination with suction irrigation because doing so prevents development of effective antibiotic levels in the wound. • Do not use the beads as an initial measure in inflamed and suppurating wounds. • Do not use the beads in the treatment of osteomyelitis in the presence of resistant organisms or slimeforming organisms (eg, Enterococcus) because effective elution of antibiotic is not achieved. • Do not substitute antibiotic beads for thorough wound débridement. • Do not insert handmade beads that are too large to fit into the medullary canal or too big to completely fill the wound. • Use care to produce bead chains in a timely fashion during the short available working time (8 minutes) as the methacrylate polymerizes. Failure to do so results in wasted material and surgeon frustration. These can be avoided by planning and relying on an assistant. • Do not leave beads in the patient so long (>3 weeks) that removal is difficult.

width of the slots in the mold and thus can be used to remove residual cement from the mold. Transfer the beads into gassterilization packages (Figure 6) and have them sterilized. Wash your hands and all work surfaces thoroughly after working with the cement. This same process can be performed in the operating room, using sterile technique, for immediate use.

Complications Complications caused by the use of antibiotic beads are uncommon; however, difficulty with bead removal can occur when the beads are left in place too long, especially in the medullary canal of long bones. Antibiotic beads reduce the rate of infection in open fractures, but they do not eliminate the risk. Beads help to control established infections, but not all infections will completely resolve. A major complication is persistent or recurrent infection. Also, spacers can fragment or dislodge when Volume 16, Number 11, November 2008

subjected to excessive or chronic loads. Infection resulting from inadequate débridement will not be overcome by the use of antibiotic beads. Knowledge of the effectiveness of antibiotic beads is limited. The optimal dose, duration of treatment, and relative efficacy of various antibiotic classes are not known. Differential elution of antibiotics from various forms of PMMA has been reported,12,13 but the ideal carrier medium is still a matter of debate. The role and efficacy of absorbable beads is not yet known. Local antibiotic delivery by pump or other mechanism is an alternative route of local antibiotic therapy. In addition, the efficacy of beads compared with the efficacy of other delivery methods is not yet known.

Figure 5

After 15 minutes, the mold is taken apart, and the beads are gently removed by pulling the wire. Figure 6

Summary Antibiotic beads are an attractive method of treatment in the management and prevention of osteomyelitis. Antibiotic beads provide high local concentrations of antibiotic at

The beads are transferred into gassterilization packages. 677

Antibiotic Beads

the site of infection without significant systemic toxicity. A variety of techniques to provide local antibiotics has been reported, including absorbable beads with various types of antibiotics, antibiotic sticks, coated nails, and coated joint spacers. Beads can be prepared in the operating room or in advance. Antibiotic beads assist in dead space management and help facilitate the filling of bone voids and healing of infected nonunions. Results demonstrate improved efficacy in the control of infection and enhanced outcomes, with financial and practical savings.14

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References Citation numbers printed in bold type indicate references published within the past 5 years. 1.

Gustilo RB, Anderson JT: Prevention of infection in the treatment of one thousand and twenty-five open fractures of long bones: Retrospective and prospective analyses. J Bone Joint Surg Am 1976;58:453-458.

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Patzakis MJ, Harvey JP Jr, Ivler D: The role of antibiotics in the management of open fractures. J Bone Joint Surg Am 1974;56:532-541. Wahlig H, Dingeldein E, Bergmann R, Reuss K: The release of gentamicin from polymethylmethacrylate beads. J Bone Joint Surg Br 1978;60:270-275. Schentag JJ, Lasezkay G, Plant ME, Jusko WJ, Cumbo TJ: Comparative tissue accumulation of gentamicin and tobramycin in patients. J Antimicrob Chemother 1978;4:2330. Cunningham A, Demarest G, Rosen P, DeCoster TA: Antibiotic bead production. Iowa Orthop J 2000;20:3135. van de Belt H, Neut D, Schenk W, van Horn JR, van Der Mei HC, Busscher HJ: Staphylococcus aureus biofilm formation on different gentamicinloaded polymethylmethacrylate bone cements. Biomaterials 2001;22:16071611. Ensing GT, van Horn JR, van der Mei HC, Busscher HJ, Neut D: Copal bone cement is more effective in preventing biofilm formation than Palacos R-G. Clin Orthop Relat Res 2008; 466:1492-1498. Anagnostakos K, Kelm J, Regitz T, Schmitt E, Jung W: In vitro evaluation of antibiotic release from and bacteria growth inhibition by antibiotic-

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loaded acrylic bone cement spacers. J Biomed Mater Res B Appl Biomater 2005;72:373-378. Popham GJ, Mangino P, Seligson D, Henry SL: Antibiotic-impregnated beads: Part II. Factors in antibiotic selection. Orthop Rev 1991;20:331337. Walenkamp GH, Vree TB, van Rens TJ: Gentamicin-PMMA beads: Pharmacokinetic and nephrotoxicological study. Clin Orthop Relat Res 1986; 205:171-183. Sasaki T, Ishibashi Y, Katano H, Nagumo A, Toh S: In vitro elution of vancomycin from calcium phosphate cement. J Arthroplasty 2005;20: 1055-1059. Greene N, Holtom PD, Warren CA, et al: In vitro elution of tobramycin and vancomycin polymethylmethacrylate beads and spacers from Simplex and Palacos. Am J Orthop 1998;27: 201-205. Nelson CL, Griffin FM, Harrison BH, Cooper RE: In vitro elution characteristics of commercially and noncommercially prepared antibiotic PMMA beads. Clin Orthop Relat Res 1992; 284:303-309. Henry SL, Seligson D, Mangino P, Popham GJ: Antibiotic-impregnated beads: Part I. Bead implantation versus systemic therapy. Orthop Rev 1991;20:242-247.

Journal of the American Academy of Orthopaedic Surgeons