Historically, surgeons have utilized circular and monolateral external fixation for the management of complicated high-energy orthopedic trauma and reconstruction of congenital or posttraumatic deformities through the Ilizarov and deBastiani principles of callotasis and distraction osteogenesis.1-3 Demonstrating success in bone healing and deformity correction in limbs that would have otherwise left patients with permanent disabilities or necessitated limb amputation, external fixation has found its way into the treatment of Charcot foot, arguably one of the most challenging problems for patients with diabetes. As our understanding of the Charcot disease process has evolved in regard to the disease’s pathophysiology, the optimal intervention period and identifying limitations with traditional internal fixation methods, external fixation seems to be the next step in Charcot treatment. However, as with anything new that takes center stage, there will always be undefined uses that invite controversy and debate. While the incidence rate for Charcot neuroarthropathy is low (occurring in less than 0.3 to 0.9 percent of patients with diabetes per year), Charcot neuroarthropathy is considered one of the more devastating manifestations of profound neuropathy and longstanding diabetes mellitus.4,5 While the condition is commonly associated with joint destruction, subluxation/dislocation and instability, four- and 10-year retrospective longitudinal studies from diabetes specialty clinics evaluating the natural history of this neuropathic arthropathy revealed that Charcot rarely led to limb loss when patients were diagnosed and managed early in the disease process.4,6 Additionally, researchers found that surgical intervention was only necessary in 25 percent of all patients surgeons followed for acute Charcot neuroarthropathy. Out of this group, surgeons treated 64 percent of patients successfully with exostectomies and only 36 percent necessitated arthrodesis. In their 10-year retrospective series of 115 patients with Charcot, Fabrin et al., reported that 5 percent required surgical intervention with 2 percent undergoing below-knee amputation and 3 percent requiring arthrodesis.4 Achieving stable internal fixation may be difficult in the Charcot foot with localized osteoporotic bone, large spatial defects from either joint destruction or resection of osteomyelitis. Usually, these cases of significant bone loss require bone grafting for structural support and long screws and large plates to span the defect. In cases of longstanding deformities, single-stage corrections may be limited by chronic soft tissue contractures and peripheral scarring of the neurovacsular bundle, leading to complications of inadequate deformity correction, wound dehiscence and local ischemic tissue loss. Complications with wound healing, poor screw purchase, hardware failure, nonunion and recurrence of deformity are potential sequelae of open arthrodesis with internal fixation in Charcot reconstruction. External circular fixation can provide mechanical stability to structurally deficient bone and maintain skeletal alignment where internal fixation options for direct stabilization are limited. A Closer Look At The Ex-Fix Controversy There has been evidence to suggest that external fixation methods can provide advantages in Charcot reconstruction when internal fixation is unsuccessful. However, much of the controversy surrounding external fixation stems from the lack of consensus regarding treatment goals and indications for use. The utilization of circular fixation for Charcot is broad and has been reported for: • the management of skeletal defects associated with surgical resection of osteomyelitis; • acute fracture dislocations; • gradual deformity correction; • static neutralization frames to protect high risk fusion sites in patients not capable of non-weightbearing; • elective rearfoot/ankle fusions; • protecting fasciocutaneous flaps; and • offloading ulcers. As logical as this may seem to some surgeons, this widespread use has not been accompanied with meaningful statistical evidence to justify the role of ex-fix in Charcot foot reconstruction yet there is continued nationwide promotion of its use. Additionally, few studies examine the same outcomes for success. The lack of uniform outcome measures makes it difficult to interpret the existing literature and generate meaningful comparisons as to whether surgical reconstruction is superior to total contact casting, and whether external fixation is superior to internal fixation. External fixation comes with a considerable economic price and patient risk. The cost of external fixation may range from $6,000 to $30,000 per patient for initial application. Additionally, experts have quoted a 100 percent complication rate with external fixation in Charcot reconstruction. Therefore, with a device which requires frequent postoperative follow-up, has high complication rates and is cost prohibitive, the indications of external fixation need to be clear. For external fixation in Charcot reconstruction, the risk to benefit ratio for unconventional applications may be disproportionately high in comparison to that of internal fixation. By using this device on the diabetic foot, you must ask: Are you saving the limb or putting it at risk? Should You Consider External Fixation Over Internal Fixation? In general, most of the literature agrees that one should consider surgical reconstruction when Charcot deformity is: acutely or chronically unstable, nonplantigrade, unshoeable/unbraceable or when it is associated with longstanding ulceration unresponsive to traditional offloading methods. The question is not who is a candidate for external fixation but who is not a candidate for internal fixation. Osteopenic bone. Bone demineralization in the Charcot foot may be the result of disuse of the limb from nonweightbearing or offloading treatments, or may be due to local pathology one may see in the acute Charcot process.7,8 Researchers have considered decreased bone mineral density as a risk factor for complications such as hardware failure and loss of deformity correction due to insufficient stability or purchase of internal fixation.9,10Osteomyelitis and large skeletal defects. In the presence of infected bone, the introduction of internal fixation may serve as a source for infection involving unaffected areas of adjacent bone. With staged procedures involving wound debridement, one must often excise infected bone and provide long-term parental antibiotic therapy prior to introducing internal fixation for final reconstruction. In addition, structural defects may require a large bone graft with long reconstruction or locking plates and screws to achieve direct stabilization. This method often requires wide surgical exposure, stripping the periosseous blood supply to the bone and increasing the probability for nonunion. External fixation may provide indirect stabilization of the skeletal defect spanning the area of bone resection or to protect bone graft through percutaneous methods that limit soft tissues exposure. Inability to offload the affected limb. Overweight and obese patients are significantly associated with diabetes, cardiovascular disease, arthritis and general poor health status.11 The energy consumption required for five minutes of three-point crutch ambulation is markedly elevated as it reportedly increases the heart rate by 53 percent and oxygen uptake by 32 percent.12 Combined with limited cardiac reserve and obesity, most Charcot patients demonstrate difficulty or an inability to offload the affected limb safely despite physical therapy training. With unintentional weightbearing, the patients’ excessive weight may exceed the mechanical limits of internal fixation devices, compromising the purchase of these devices to bone or causing implant failure. External fixation may provide stable reduction of the realignment arthrodesis, simultaneously allowing a shared loading of the fusion site without exceeding the mechanical limits of the fixator maintaining the correction. Unstable or non-braceable limb deformities. Both acute and chronic Charcot neuroarthropathy may result in severe and unstable limb deformities that are not structurally stable for weightbearing. Additionally, one cannot reasonably offload these deformities with casting or bracing without exposing the limb to areas of focal high pressures, leading to ulceration. With joint fragmentation, bone resorption and severe deformity that one sees with acute Charcot, internal fixation may not adequately achieve direct stabilization to maintain alignment of open arthrodesis. External fixation may span areas of demineralized bone and maintain the alignment in arthrodesis. In cases of correction of severe chronic Charcot, osseous correction may be limited by adapted soft tissue and neurovascular structures that may not tolerate acute, single stage correction without complications of soft tissue contracture, wound dehiscence or soft tissue necrosis. One may gradually correct deformities with circular spatial frame or hinge axis methods that allow concomitant soft tissue lengthening and relaxation to occur. Conservative Management: Can It Have An Impact? Plantigrade stable foot. Various authors consider a clinically stable, plantigrade, shoeable/braceable foot a successful and desirable outcome of treatment for Charcot neuroarthropathy.4,6,9,10,13-24 Despite significant radiographic patterns of breakdown that are common to see during the quiescent phase, there is little evidence to support elective prophylactic realignment procedures in these patients with clinically stable plantigrade feet that can be safely fit into extra-depth shoes or braces. Furthermore, complications associated with Charcot reconstruction with internal fixation, including limb loss, may not be considered reasonable risks in this lower risk patient group. Stage 0 and 1. In regard to clinical manifestations of acute Charcot neuroarthropathy in the absence of radiographic signs of joint destruction or deformity, which surgeons refer to as Stage 0 or pre-Charcot, various authors suggest it is best to use compression therapy and subsequent nonweightbearing cast immobilization.22,23,26 This conservative method, including total contact casting, is also widely advocated as the gold standard for Eichenholtz stage I Charcot. In this stage, one may see radiographic signs of early joint fragmentation, destruction and debris formation without significant fracture displacement, joint dislocation or mechanical axis malalignments. However, surgical intervention during these early stages of Charcot is controversial. There is only one level IV retrospective report in the medical literature supporting surgical intervention with internal fixation during the acute Eichenholtz stage I Charcot neuroarthropathy.24 Another report recommended surgical intervention during Eichenholtz stage I only if one encounters severe unstable reducible joint dislocations before seeing radiographic evidence of joint destruction and bone fragmentation.9 There have been anecdotal reports of utilizing external fixation for realignment stabilization for acute Charcot dislocations. However, further investigation is necessary to validate the efficacy of indirect stabilization in cases of Stage 0 and 1 without deformity. What You Should Know About Other Surgical Procedures For Charcot Exostectomy. Charcot rocker bottom foot deformity often leaves plantar osseous prominences, increasing the risk for tissue breakdown. Simple plantar exostectomies are generally successful with a reported average 84 percent healing rate and 20 percent recurrence of skin breakdown.6,9,14,15,21 With the procedure’s satisfactory success rates, less technical difficulty and lower complication rates, one may consider exostectomies for stable uncomplicated Charcot deformities with plantar prominences. Surgeons may consider realignment arthrodesis if plantar ulceration recurs. Proponents for arthrodesis may argue that recurrence of ulceration and progression of Charcot may be high with exostectomies as opposed to realignment arthrodesis. However, there is little uniform, long-term data to provide meaningful comparisons between the two treatment groups. Normal bone density. When patients have normal bone mineralization, one may consider internal fixation the method of choice that can provide stable compression to fusion sites and avoid the risk of external fixation complications.19,27 Even in cases of severe dislocations during acute Charcot with the absence of profound joint fragmentation and bone resorption, internal fixation may provide stable fixation and reduction of deformity.9 Early Weightbearing: Is It Worth The Cost And Potential Risks Of Ex-Fix? Patient can maintain non-weightbearing or a partial weightbearing regimen. Facilitating early protected weightbearing while maintaining alignment of the arthrodesis site can be an advantage of external fixation. Ilizarov supported early weightbearing in lower extremity external fixation cases, observing that controlled weightbearing stimulus via “shared loading” promotes bone regeneration. Allowing early weightbearing to stimulate healing of the fusion site has been a common indication for external fixation. However, a patient capable of non-weightbearing with crutches is likely capable of performing touch toe weightbearing for shared loading of the arthrodesis with internal fixation and in a contact cast. If a patient’s postoperative regimen for arthrodesis involves non-weightbearing and the patient is able to safely maintain non-weightbearing, external fixation may be unconventional in this circumstance and one may not be able to justify the disproportionate cost of external fixation over the lower cost of internal fixation. Understanding The Importance Of Appropriate Patient Selection Poor rehabilitation and health status. The rationale of limb salvage for some surgeons is the association between increased energy expenditure with loss of limb length and a 66 percent increased incidence of contralateral limb loss within five years.28-30 Though one may attribute the relationship of contralateral limb loss after the index amputation to increased mechanical stress on the remaining limb leading to ulceration and infection, surgeons must also consider the event of limb loss as a marker of the disease state of diabetes. The development of Charcot is not a result of a local phenomenon but is a reflection of the overall disease state of diabetes. Charcot develops as a result of profound neuropathy including autonomic nerve dysfunction, all of which are functions of longstanding diabetes and neuropathy.31,32 Researchers have associated the presence of autonomic neuropathy and renal disease with increased cardiovascular risk and mortality in patients with diabetes.33-35 One retrospective analysis involving diabetic patients with Charcot neuroarthropathy reported a 45 percent mortality rate with a mean interval of 3.7 years.36 This is not considerably different from prospective data on three-year mortality rates (reported near 38 percent) of diabetic patients with major limb amputations.37 With poor rehabilitative outcomes in patients with diabetes and cardiovascular disease, and mortality rates similar in Charcot disease and amputation, limb salvage in cases of severe deformity, ulcer and frank infection may not be an economic nor appropriate option when amputation is likely the ultimate result. One should not consider amputation as a failure but as a reasonable treatment option for Charcot limb deformities in patients who have accumulated risk factors for poor outcomes for limb salvage. Your tolerance of risk. Although one can generally reduce complications with experience, bear in mind that even experts have quoted a 100 percent complication rate when it comes to external fixation with Charcot reconstruction. Common complications of pin tract infections include cellulitis, osteomyelitis, external fixation component failure, unscheduled trips to the operating room for half pin or fine wire exchange, frame loosening requiring adjustments and stress fractures of the tibia. It is not a question of if one will encounter a complication but when. External fixation product training seminars can demonstrate the basic methods of frame application but these seminars cannot prepare surgeons to deal with the more difficult aspect of external fixation — outpatient management. Ensuring successful outcomes of external fixation require weekly pin tract care and surgeon availability. If occurrence of a tibial pin tract infection is sufficient to influence a surgeon to abandon the frame, then one should reconsider the utilization of the external fixator for Charcot reconstruction. Patient acceptance. Reports of depression, destructive behavior, social isolation and sleeping disorders have been associated with external fixation use. Social support systems or groups can provide a practical exchange of information that helps patients cope with common issues regarding external fixation treatment. Without patient acceptance of external fixation, compliance issues and early abandonment of external fixation may compromise the outcomes for success. In Conclusion What is the strongest evidence we have? For the most part, a majority of the current peer-reviewed literature indicates that internal fixation methods for salvaging acute and chronic Charcot deformities have been successful with an average reported fusion rate of 87 percent.9,10,13,16,20,24 The majority of the published information regarding external fixation for Charcot is primarily limited to non peer-reviewed articles, technique descriptions, observational studies and few level IV retrospective analyses.17,19,27,41-47 Only one level II prospective analysis of neutral circular frames for reconstruction of non-plantigrade Charcot midfoot deformities has demonstrated good clinical restoration with plantigrade feet ulcer and infection free at a one-year follow-up.48 Without case controlled, randomized clinical trials, advocates of this method have not produced the level of evidence to demonstrate that external fixation methods improve limb salvage rates beyond traditional offloading practices and internal fixation. In other words, one can successfully manage a majority of Charcot with conservative therapy and external fixation is not a substitute for cases in which internal fixation works well. Is there a place for circular frames in diabetic Charcot neuroarthropathy? The answer is yes. There are promising retrospective analyses, early prospective studies and anecdotal evidence, which deserve further attention. However, we must continue to critically investigate the best indications of external fixation use, moving from an “in my hands” approach to prospective comparative trials. At this point, the indications for Charcot reconstruction with external fixation seem to be few and far between. Dr. Liu is a Clinical Associate Professor in the Department of Orthopaedics at the University of Texas Health Science Center at San Antonio, Tx. He received his fellowship training in trauma and reconstruction at the University Hospitals of Dresden, Germany and Catania, Italy. Dr. Liu currently practices at the Austin Diagnostic Clinic multispecialty group in Austin, Tx. Dr. Steinberg is an Assistant Professor in the Department of Plastic Surgery at the Georgetown University School of Medicine in Washington, D.C.
1. De Bastiani G, Aldegheri R and Renzi Brivio L. The treatment of fractures with a dynamic axial fixator. J Bone Joint Surg Br, 66(4): 538-45, 1984.
2. Ilizarov GA, Lediaev VI and Shitin VP. [The course of compact bone reparative regeneration in distraction osteosynthesis under different conditions of bone fragment fixation (experimental study)]. Eksp Khir Anesteziol, 14(6): 3-12, 1969.
3. Ilizarov GA and Ledyaev VI. The replacement of long tubular bone defects by lengthening distraction osteotomy of one of the fragments. 1969. Clin Orthop Relat Res, (280): 7-10, 1992.
4. Fabrin J, Larsen K and Holstein PE. Long-term follow-up in diabetic Charcot feet with spontaneous onset. Diabetes Care, 23(6): 796-800, 2000.
5. Lavery LA, Armstrong DG, Wunderlich RP, Tredwell J and Boulton AJ. Diabetic foot syndrome: evaluating the prevalence and incidence of foot pathology in Mexican Americans and non-Hispanic whites from a diabetes disease management cohort. Diabetes Care, 26(5): 1435-8, 2003.
6. Armstrong DG, Todd WF, Lavery LA, Harkless LB and Bushman TR. The natural history of acute Charcot's arthropathy in a diabetic foot specialty clinic. Diabet Med, 14(5): 357-63, 1997.
7. MK, Sinacore DR, Fielder FA, and Johnson JE. Bone mineral density during total contact cast immobilization for a patient with neuropathic (Charcot) arthropathy. Phys Ther, 85(3): 249-56, 2005.
8. Petrova NL, Foster AV and Edmonds ME. Calcaneal bone mineral density in patients with Charcot neuropathic osteoarthropathy: differences between Type 1 and Type 2 diabetes. Diabet Med, 22(6): 756-61, 2005.
9. Myerson MS, Henderson MR, Saxby T and Short KW. Management of midfoot diabetic neuroarthropathy. Foot Ankle Int, 15(5): 233-41, 1994.
10. Papa J, Myerson M and Girard P. Salvage, with arthrodesis, in intractable diabetic neuropathic arthropathy of the foot and ankle. J Bone Joint Surg Am, 75(7): 1056-66, 1993.
11. Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS and Marks JS. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA, 289(1): 76-9, 2003.
12. Waters RL Campbell J and Perry J. Energy cost of three-point crutch ambulation in fracture patients. J Orthop Trauma, 1(2): 170-3, 1987.
13. Alvarez RG, Barbour TM and Perkins TD. Tibiocalcaneal arthrodesis for nonbraceable neuropathic ankle deformity. Foot Ankle Int, 15(7): 354-9, 1994.
14. Brodsky JW and Rouse AM. Exostectomy for symptomatic bony prominences in diabetic charcot feet. Clin Orthop Relat Res, (296): 21-6, 1993.
15. Catanzariti AR, Mendicino R and Haverstock B. Ostectomy for diabetic neuroarthropathy involving the midfoot. J Foot Ankle Surg, 39(5): 291-300, 2000.
16. Early JS and Hansen ST. Surgical reconstruction of the diabetic foot: a salvage approach for midfoot collapse. Foot Ankle Int, 17(6): 325-30, 1996.
17. Fabrin J, Larsen K and Holstein PE. Arthrodesis with external fixation in the unstable or misaligned Charcot ankle in patients with diabetes mellitus. Int J Low Extrem Wounds, 6(2): 102-7, 2007.
18. Helm PA, Walker SC and Pullium G. Total contact casting in diabetic patients with neuropathic foot ulcerations. Arch Phys Med Rehabil, 65(11): 691-3, 1984.
19. Pinzur MS. The role of ring external fixation in Charcot foot arthropathy. Foot Ankle Clin, 11(4): 837-47, 2006.
20. Pinzur MS and Kelikian A. Charcot ankle fusion with a retrograde locked intramedullary nail. Foot Ankle Int, 18(11): 699-704, 1997.
21. Rosenblum BI, Giurini JM, Miller LB, Chrzan JS and Habershaw GM. Neuropathic ulcerations plantar to the lateral column in patients with Charcot foot deformity: a flexible approach to limb salvage. J Foot Ankle Surg, 36(5): 360-3, 1997.
22. Schon LC, Easley ME and Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res, (349): 116-31, 1998.
23. Sella EJ and Barrette C. Staging of Charcot neuroarthropathy along the medial column of the foot in the diabetic patient. J Foot Ankle Surg, 38(1): 34-40, 1999.
24. Simon SR, Tejwani SG, Wilson DL, Santner TJ and Denniston NL. Arthrodesis as an early alternative to nonoperative management of charcot arthropathy of the diabetic foot. J Bone Joint Surg Am, 82-A(7): 939-50, 2000.
25. Walker SC, Helm PA and Pullium G. Total contact casting and chronic diabetic neuropathic foot ulcerations: healing rates by wound location. Arch Phys Med Rehabil, 68(4): 217-21, 1987.
26. Yu GV and Hudson JR. Evaluation and treatment of stage 0 Charcot's neuroarthropathy of the foot and ankle. J Am Podiatr Med Assoc, 92(4): 210-20, 2002.
27. Pinzur MS. Neutral ring fixation for high-risk nonplantigrade Charcot midfoot deformity. Foot Ankle Int, 28(9): 961-6, 2007.
28. Goldner MG. The fate of the second leg in the diabetic amputee. Diabetes, 9: 100-3, 1960.
29. Huang CT, Jackson JR, Moore NB, Fine PR, Kuhlemeier KV, Traugh GH and Saunders PT. Amputation: energy cost of ambulation. Arch Phys Med Rehabil, 60(1): 18-24, 1979.
30. Waters RL, Perry J Antonelli D and Hislop H. Energy cost of walking of amputees: the influence of level of amputation. J Bone Joint Surg Am, 58(1): 42-6, 1976.
31. Rajbhandari SM, Jenkins RC, Davies C and Tesfaye S. Charcot neuroarthropathy in diabetes mellitus. Diabetologia, 45(8): 1085-96, 2002.
32. Young MJ, Marshall A, Adams JE, Selby PL and Boulton AJ. Osteopenia, neurological dysfunction, and the development of Charcot neuroarthropathy. Diabetes Care, 18(1): 34-8, 1995.
33. Maser RE, Pfeifer MA, Dorman JS, Kuller LH, Becker DJ and Orchard TJ. Diabetic autonomic neuropathy and cardiovascular risk. Pittsburgh Epidemiology of Diabetes Complications Study III. Arch Intern Med, 150(6): 1218-22, 1990.
34. Rossi E. Cardiovascular disease in diabetes and operative risk. Rays, 22(4): 595-602, 1997.
35. Sibal L, Law HN, Gebbie J and Home P. Cardiovascular risk factors predicting the development of distal symmetrical polyneuropathy in people with type 1 diabetes: A 9-year follow-up study. Ann NY Acad Sci, 1084: 304-18, 2006.
36. Gazis A, Pound N, Macfarlane R, TreeceK, Game F and Jeffcoate W. Mortality in patients with diabetic neuropathic osteoarthropathy (Charcot foot). Diabet Med, 21(11): 1243-6, 2004.
37. Larsson J, Agardh CD, Apelqvist J and Stenstrom A. Long-term prognosis after healed amputation in patients with diabetes. Clin Orthop Relat Res, (350): 149-58, 1998.
38. Martin L, Farrell M, Lambrenos K and Nayagam D. Living with the Ilizarov frame: adolescent perceptions. J Adv Nurs, 43(5): 478-87, 2003.
39. Patterson M. Impact of external fixation on adolescents: an integrative research review. Orthop Nurs, 25(5): 300-8; quiz 309-10, 2006.
40. Roukis TS, Stapleton JJ and Zgonis T. Addressing psychosocial aspects of care for patients with diabetes undergoing limb salvage surgery. Clin Podiatr Med Surg, 24(3): 601-10, 2007.
41. Herbst SA. External fixation of Charcot arthropathy. Foot Ankle Clin, 9(3): 595-609, x, 2004.
42. Jolly GP, Zgonis T and Polyzois V. External fixation in the management of Charcot neuroarthropathy. Clin Podiatr Med Surg, 20(4): 741-56, 2003.
43. Roukis TS and Zgonis T. The management of acute Charcot fracture-dislocations with the Taylor’s spatial external fixation system. Clin Podiatr Med Surg, 23(2): 467-83, viii, 2006.
44. Sayner LR and Rosenblum BI. External fixation for Charcot foot reconstruction. Curr Surg, 62(6): 618-23, 2005.
45. Wang JC. Use of external fixation in the reconstruction of the Charcot foot and ankle. Clin Podiatr Med Surg, 20(1): 97-117, 2003.
46. Wang JC, Le AW and Tsukuda RK. A new technique for Charcot’s foot reconstruction. J Am Podiatr Med Assoc, 92(8): 429-36, 2002.
47. Zgonis T, Roukis TS and Lamm BM. Charcot foot and ankle reconstruction: current thinking and surgical approaches. Clin Podiatr Med Surg, 24(3): 505-17, 2007.
48. Pinzur MS. Neutral ring fixation for high-risk nonplantigrade Charcot midfoot deformity. Foot Ankle Int 28(9):961-6, 2007.