Point-Counterpoint: Active Charcot: Should You Proceed With Surgery?

By Peter M. Wilusz, DPM, Guy R. Pupp, DPM, and Molly Judge, DPM

Yes, these authors say early identification of the Charcot process and prompt surgical intervention can prevent progression of the deformity and related complications. By Peter M. Wilusz, DPM and Guy R. Pupp, DPM    The presentation of Charcot neuroarthropathy has been historically problematic for the foot and ankle surgeon. Acute Charcot has traditionally been treated with conservative therapy as most attempts at treatment involve immobilization and removal of weightbearing forces from the involved foot. Many surgeons do not surgically address the acute Charcot foot due to the immunocompromised status of the patient, non-compliance issues and the progressive nature of the deformity.    In the past, most surgical approaches have consisted of “lump and bump” exostectomies, which are performed after the gross deformity has occurred, in an attempt to prevent ulceration from osseous deformities producing pressure points. To achieve success in treating the acute Charcot foot, early recognition and aggressive treatment of deforming contractures is essential. Such contractures would otherwise lead to limb threatening complications with deformation, the potential for ulcer formation and an eventual battle with infection.

Voicing Concerns Over Conservative Care

   The goals of resolving the acute Charcot foot have traditionally been immobilization and offloading of the involved foot. Immobilization in a nonweightbearing cast or a total contact cast in our clinic has averaged between seven and 16 weeks. However, when one looks back and reevaluates casting for acute Charcot treatment, there is the concern of cast disease and the potential development of osteopenia in an already threatened osseous integrity of a limb. Keep in mind that making the transition from the cast to shoes, with or without bracing, often frustrates both the patient and physician with recurrence of an acute Charcot foot.    It is our belief that patient education, strict glycemic control and aggressively treating the deforming forces causing the Charcot arthropathy are key for successful salvage of the at-risk limb. Early surgical treatment of the Charcot foot can avoid the progression of major deforming forces and limb threatening complications.

What The Literature Reveals About Early Surgical Intervention

   In order to consider whether surgical intervention is appropriate, one should review the classification of the stages of Charcot neuroarthropathy. In 1966, Eichenholtz described Charcot in three stages.1 Stage 1, often described as the “hot phase,” usually presents with edema, hyperemia and often pain. Stage 2, which is referred to as the coalescence phase, radiographically demonstrates the absorption of cartilaginous and osseous debris with larger fragments fusing to the joint surfaces. Stage 3 is the remodeling phase and displays a fusion of bone and joint. With their respective articles in 1990 and 1999, Shibata and Sella added stage 0, which does not display radiographic changes but presents clinically with warmth, edema and pain in an often otherwise anesthetic foot.2,3    A few reports have supported early surgical correction during the acute developmental phase of Charcot when there are structural changes. In 2000, Simon reported success in restoring the anatomic alignment and improving function in acute Charcot with open reduction and internal fixation.4 As early as 1966, Harris and Brand suggested performing arthrodesis early in the disease process.5 A paper by Newman in 1981 suggested that early arthrodesis and a period of immobilization of the involved joint(s) can prevent further deformity.6 In 2003, Wang presented surgical goals to achieve a stable, reliable foot early in the Charcot process with external fixation and closed reduction of the deformity.7 We have had similar experiences utilizing open reduction and external fixation.    No published papers specifically address surgical intervention of the Charcot foot in Stage 0 or early Stage 1 before deformation exists. Many Charcot feet present in the category of stage 1, 2 or 3. However, critical evaluation of a stage 0 foot should include surgical intervention.    A patient with diabetes who presents with Stage 0 Charcot often has significant equinus. Due to the existing contractures, these patients place more stress on the insensate foot. In addition to the various neurological and vascular etiological theories about the development of Charcot, researchers have discussed the process of glycosylation and the formation of Advanced Glycated End-Products (AGE).8,9,10    In 1997, Grant, et. al., published a study, supporting the theory that tendon fiber organization is altered whereby the functional characteristics of soft tissues are decreased in diabetic tissues.11 They studied the Achilles tendon in diabetic and non-diabetic patients. The tendon specimens from all of the patients with diabetes showed abnormalities in fibrillar structure. In short, the marked alteration in the structure of tendon results in a resistance to stretching and contractures within the tendon. This can lead to the major architectural deformation one sees in Charcot collapse.    The Achilles tendon is the most important tendon affecting foot function. When it comes to patients with neuropathy due to diabetes, a tight Achilles tendon, combined with sensory loss, will contribute to altered gait patterns. This eventually results in dermal ulceration and Charcot joint collapse.9-11

Key Insights On Surgical Management Of Acute Charcot

   In our opinion, surgical management of the acute Charcot foot starts with early identification of the process. One should obtain and evaluate radiographs when one suspects a Charcot deformity. In the absence of fractures or subluxation, biomechanical evaluation of the weightbearing lateral radiograph supports the clinical evidence of equinus. If one corrects the equinus component in Stage 0 or early Stage 1, and protects the foot and ankle with a cast or brace, then clinicians can arrest significant progressive deformities of the foot. In fact, the Charcot inflammatory process has been shown to subside within a shorter period of time.    Depending on patient expectations and their given level of activity, one may pursue numerous approaches for lengthening the Achilles tendon. Percutaneous Achilles tenotomy, percutaneous multiple incision Achilles tendon lengthening and open Achilles tendon lengthening have all produced consistent and reproducible results in preventing the progression of Charcot foot when it is treated before severe fragmentation and gross deformity ensues.    Managing the patient with diabetes and Charcot, regardless of the presenting Charcot stage, can be more successful with adjunctive modalities. Stringent management of glycemic control by an endocrinologist, co-management with a certified diabetic nurse practitioner, weight management and concomitant use of bisphosphonates to slow the resorption of bone are all part of the multidisciplinary approach to treating patients with diabetes who present with Charcot complications.

Final Thoughts

   Early identification of acute Charcot in the diabetic patient is important and surgical treatment can be safe and reliable. The majority of Charcot feet develop from a combination of several factors. These factors include: chronic elevation of blood glucose; the development of AGEs; and the progression of contractures that increase plantar forces and can eventually exceed the strength of collagenous structures in the foot. These factors can lead to structural failure and joint collapse.    Early recognition of contractures and appropriate surgical treatment can prevent significant progression of the Charcot process. Granted, there is still much to be learned concerning diagnosis, treatment and management of the Charcot foot. However, we have utilized early diagnosis and aggressive treatment of the Charcot components to attain a more predictable result and to avoid limb- or life-threatening complications. Dr. Wilusz is a Clinical and Surgical Instructor at the Foot and Ankle Clinic at the Southeastern Michigan Surgical Hospital in Warren, Mich. He is an Associate of the American College of Foot and Ankle Surgeons, and is in private practice in Dearborn, Mich. Dr. Pupp is the Clinical Director of the Foot and Ankle Clinic at the Southeastern Michigan Surgical Hospital in Warren, Mich. He is a Fellow of the American College of Foot and Ankle Surgeons, and is also the Clinic Director at the Sinai Grace Diabetic Foot Center in Detroit. Editor’s Note: For related articles, see “External Fixation: Is It The Answer For Diabetic Limb Salvage?” in the July 2004 issue or “Is Rocker Bottom Reconstruction A Viable Option For Limb Preservation?” in the December 2004 issue. For other articles on Charcot, check out the archives at www.podiatrytoday.com. References 1. Eichenholz SN. Charcot Joints. Springfield, IL: Charles C. Thomas; 1966. 2. Shibata T, Tada K, Hashizume C. The result of arthrodesis of the ankle for leprotic neuropathy. J Bone Joint Surg Am 1990;72:749-56. 3. Sella EJ, Barrette C. Staging of Charcot neuroarthropathy along the medial column of the foot in the diabetic patient. J Foot Ankle Surg 1999;38(1):34-40. 4. Simon SR, Tejwani SG, Wilson DL, et. al. Arthrodesis as an early alternative to nonoperative management of Charcot arthropathy of the diabetic foot. J Bone Joint Surg 2000;82(7);939-50. 5. Harris JR, Brand PW. Patterns of disintegration of the tarsus in the anesthetic foot. J Bone Joint Surg Br 1966;48(1):4-16. 6. Newman JH. Non-infective diseases of the diabetic foot. J Bone Joint Surg Br 1981;63:593. 7. Wang JC. Use of external fixation in the reconstruction of the Charcot foot and ankle. Clin Pod Med Surg 2003(20);97-117. 8. Crisp A, Heathcoate J. Connective tissue abnormalities in diabetes mellitus. J R Coll. Physicians Lon. 18:132-140, 1984. 9. Brownless M, Vlassara H, Cerami A. Non-enzymatic glycosylation and the pathogenesis of diabetic complications. Ann. Intern. Med. 101:527-537, 1984. 10. Bai P, Keng P, Hardt T, Cernada M, Brodsky B. Glycation alters collagen fibril organization. Connect. Tissue Res. 28:1-12, 1992. 11. Grant WP, Sullivan R, Soneshine DE, Adam M, Slusser JH, Carson KA, Vinik AI. Electron microscopic investigation of the effects of diabetes mellitus on the Achilles tendon. J Foot Ankle Surg 1997: 272-278. No, this author says conservative treatment is often effective for these patients. She says patient compliance is a particularly significant hurdle and discusses various risks that surgery can pose for patients with Charcot. By Molly Judge, DPM    The reported incidence of Charcot neuroarthropathy has slowly been on the rise. This is not necessarily because of an increased incidence but as a result of increased physician awareness of the “at-risk” population, particularly diabetic patients with peripheral neuropathy. There has also been an increased appreciation for the harbingers of an acute Charcot joint flare. It is now more likely these patients will be diagnosed more expediently and treated in a fashion more likely to preserve health and orthopedic function.1    One can accomplish this purely with conservative interventions in many, if not most, cases. Conservative therapy is the mainstay in addressing the Charcot foot. In exceptional cases, surgical intervention is required. Therapy for this condition principally focused upon major reconstructive efforts in the 1970s and 1980s and we spent the early 1990s looking back at what we had accomplished by these surgeries.    Numerous surgical complications and enhanced morbidity and mortality from those surgeries have been taken very seriously. This shifted the pendulum of care toward a conservative philosophy, which continues to be exercised whenever possible. In fact, we realized that a majority of Charcot cases present in later stages of the disease. Therefore, they are not actively progressing and are amenable to the conservative approach. The pendulum continued to swing and by the mid- to late 1990s, there was a new emphasis on the use of external fixation and the Ilizarov technique. While there is a renewed surgical emphasis for treating the Charcot foot, it should still only be applied in certain select cases.

How Staging And Practice Standards Guide Appropriate Treatment Decisions

   Charcot neuroarthropathy presents itself in a spectrum of degenerative change that can be generically described as sub-acute (a.k.a. stage 0), acute or chronic in nature. As a result, numerous authors have designed staging or grading criteria to describe the condition of the Charcot foot.1-4    The advent of such staging systems began with Eichenholtz in 1966.3 In 2002, Schon, et. al., researched the reliability and reproducibility of a modified staging system that takes into account radiographic changes as well as the overall appearance of the foot.2 Each of these systems is meant to guide clinicians in determining the extent of the degenerative process as well as to prognosticate morbidity and disability.    Many cases of Charcot foot are diagnosed well after the onset of pathology and it is common to meet these patients after they have entered into a chronic phase of the neuroarthropathy with deformity in a stage of coalescence or consolidation. The extremity is often ready for bracing at this point. Even in the event one identifies an acute Charcot flare, the goals in intervention are to halt the progression of the degenerative process and stabilize the leg, ankle and foot. These goals can often be achieved via nonweightbearing immobilization and followed by external, non-interventional stabilizers such as an ankle foot orthosis (AFO).    A clinical practice pathway is a standard approach to the Charcot foot and has been published by the American College of Foot and Ankle Surgeons.5 This document emphasizes the evaluation and conservative management for this disease state. Both acute and chronic phases of Charcot degeneration are amenable to conservative measures. These measures are geared at stabilizing the part and eliminating the ill effects of hyperemia and edema. One can even make a profoundly deformed foot plantargrade and fit it for an AFO of some type. There is a wide range of prosthetic devices that one can employ to offload the aberrant lower extremity to varying degrees. Some of the most commonly used devices are simple AFOs, customized healing boots, CROW walkers and patellar weightbearing braces.

Do The Potential Risks Of Surgery Outweigh The Benefits?

   That said, even trivial trauma, including elective orthopedic surgery, has been associated with the initiation and/or perpetuation of the degenerative changes of a Charcot foot.6-9 Therefore, there is an expressed risk in surgery for the Charcot patient beyond that of other elective orthopedic candidates. The risk of exacerbating this rapidly degenerative osteolytic process has very grave ramifications and ultimately increases the risk of limb loss.    The risks of surgery in the Charcot foot are naturally compounded by hyperglycemia. The presence of autonomic dysfunction that is commonly associated with this process has a profound impact on the general health of the patient. These patients suffer from numerous secondary effects of diabetes including renal vascular dysfunction, cardiovascular and peripheral vascular disease and gastrointestinal dysfunction that increases the potential morbidity of those who undergo surgery.    It is obvious that subjecting this patient population to prolonged anesthesia experiences increases the risk of postoperative complications and some say this extended anesthesia exposure actually reduces the life expectancy of the patient.    One should also be aware that the negative effects of diabetes on bone healing have been investigated, described and discussed in the literature.10,11 Levin, et. al., used photon absorptometry to study bone mineral density in both juvenile and adult onset diabetes, revealing a defect in fracture healing potential due to a loss of bone mineral density.12

Key Considerations For Treating These Patients

   When deliberating whether to perform surgery for a Charcot patient, one must consider the whole health picture of the patient. Allen Jacobs, DPM, detailed a guide to perioperative considerations in management of the diabetic patient in 1984 and there has not been a more detailed document since.10 To facilitate design of a therapeutic plan for the Charcot foot, Alan Banks, DPM, published a guide to the management of the Charcot foot long before it became an in-vogue topic in medicine and surgery.13 This chapter detailed a scheme for clinical evaluation and a thorough rationale in treatment of both acute and chronic conditions that placed a strong emphasis on the conservative management of these patients.    Actually, the first decision point in the care of the Charcot foot is not whether the patient is a viable candidate for surgery, but whether one’s practice can tolerate the stress of the Charcot patient population. It is well known these patients increase the overhead of the office in terms of both time and materials. As a consequence, not all physicians choose to accept these cases and there is nothing wrong with that. However, if there is a delay in referring these patients out, it can be deleterious to the patient if end-stage degeneration and collapse occurs in the interim. Such a delay can put the physician at an increased medical/legal liability. Therefore, one should promptly make referrals to specialists and thoroughly document correspondence with referring physicians in the medical record.

Understanding And Conveying The Importance Of Patient Compliance

   The second decision point, when an active form of Charcot degeneration presents, is one that only the patient can make. Will the patient take ownership in the treatment plan and assume the role of a compliant patient? It is always prudent to pursue a formal consultation regarding the seriousness of the condition and the need for immediate, complete immobilization.    Emphasize that conservative therapy is the only thing that separates the patient from requiring surgical intervention or even amputation. This is a sort of litmus test in patient compliance. If the patient comes in for the next visit and shows signs of weightbearing such as a soiled or broken down short leg cast, he or she has essentially failed the litmus test. Accordingly, the patient is at high risk for suffering the worst of consequences for this condition, namely limb loss.    If noncompliance is evident in the early pursuit of conservative care, it is likely this patient will not be compliant after surgical intervention. One may have identified a patient who is a hazard to him- or herself, and is at risk for complications in management. At this point, one must continue to educate the patient regarding the gravity of his or her condition and further document patient noncompliance in the medical record.    Clinicians should also consider certain character traits that can make it difficult to work with patients with Charcot. These traits may include depression, anxiety and the tendency to be apathetic. Apathy regarding one’s diabetic condition and denial of one’s neuropathic disease are perhaps the most important as these states of mind are often associated with noncompliance. The reality is that despite very pointed consultations describing the high degree of morbidity, mortality and potential limb loss associated with the Charcot foot, these patients often fail to understand the gravity of their condition. Unfortunately, apathy is the character trait that often leads to limb loss.

Learning From The Serious Surgical Complications Of The Past

   Even in the conservative management of the Charcot foot, there is a risk for medical and orthopedic complications. In general, however, these risks are pale in comparison to the risks faced by patients who have undergone an extensive surgical reconstruction and lengthy anesthesia experience.    Some of the most renowned physicians who perform reconstructive surgery in Charcot patients admit that in the 1970s and 1980s, the outcomes in treating a Charcot foot were less than stellar and had shifted first-line therapy in a definitive way to conservative management. This is a direct result of the myriad of serious complications that have been reported in the postoperative period, including:    • failure of major reconstructions and arthrodesis procedures;    • the development of osteomyelitis;    • deep vein thrombosis (DVT);    • silent myocardial infarction;    • stroke; and    • bone healing complications leading to lower limb amputation and death.    Some will extrapolate that a prolonged anesthesia experience reduces the life expectancy in these patients and that is a strong consideration when debating surgical versus conservative therapies. In essence, definitive care can be defined as maintaining a stable, plantargrade foot and preventing ulceration and infection. One can often accomplish these goals through a conservative approach.

In Conclusion

   As most of the cases that I have encountered over time have been either Stage 0 Charcot or chronic stages of Charcot degeneration, I have found conservative management to be effective and rewarding but it requires due diligence and close follow-up care. Overall, I feel the conservative approach is, in a majority of cases, the most reasonable form of care and best preserves the health of the patient. If one provides conservative therapy promptly and subsequently monitors the patient closely, the outcome of these cases can be very successful.    I do believe the actively progressing, unstable Charcot foot stages ultimately require surgical intervention and those are the minority of cases that typically report to my office.    There are many adjunctive therapies one should consider when dealing with the Charcot foot conservatively or otherwise. These include medicinal and physical interventions such as bisphosphonate therapy, external bone stimulation, DVT prophylaxis and the medical management of all existing secondary manifestations of diabetes in addition to enhanced glycemic control. A successful care plan mandates an enormous amount of patient education and extensive communication to ensure the team approach is implemented and that the most reasonable care plan is being pursued.    The medical community at large needs to understand that prompt referral of these patients should be made to a lower extremity specialist who is educated in the management of the Charcot foot to prevent limb loss and higher morbidity. This can only be achieved by educating the physicians within your area as to the special expertise that board certified foot and ankle surgeons possess. These surgeons are the most skilled at identifying and treating this complicated condition of the Charcot foot.    To find a board-certified foot and ankle surgeon to refer Charcot patients to, check out www.acfas.org, the official Web site of the American College of Foot and Ankle Surgeons (ACFAS). Dr. Judge is a Fellow of the American College of Foot and Ankle Surgeons. She is board-certified in foot, ankle and reconstructive rearfoot and ankle surgery by the American Board of Podiatric Surgery. Dr. Judge is a certified nuclear medicine technologist and has private practices in Toledo and Port Clinton, Ohio. She is the official foot and ankle physician for the Jamie Farr Owens Corning LPGA Classic and the Toledo Storm hockey team. References 1. Yu GV and Hudson JR. Evaluation and Treatment of Stage 0 Charcot’s Neuroarthropathy of the Foot and Ankle. JAPMA 2002 April; 92(4): 210-220. 2. Schon LC, Easley ME, Cohen I, Lam PWC et al. Foot & Ankle Int 2002 January; 23 (1):30 – 36. 3. Eichenholtz SN: Charcot Joints, Springfield Illinois, Charles C. Thomas, 1966. 4. Cofield RH, Morrison MJ, and Beabout JW. Diabetic Neuroarthropathy in the Foot: Patient Characteristics and Patterns of Radiographic Change. Foot & Ankle 1983; 4 (1): 15 – 22. 5. ACFAS. Diabetic Foot Disorders CHARCOT FOOT: A Clinical Practice Pathway. A Supplement to the Journal of Foot and Ankle Surgery. 6. De-yong X, Lai-bin C, Cheng L, A-lai Z and Wei-hua F. Neuroarthropathy, Clinico-Radiologic Analysis of 115 Cases. Chinese Medical Journal, 1992 Oct; 105(10):860-865. 7. Fishco WD. Surgically Induced Charcot’s Foot. JAPMA 2001; September, 91(8): 388 – 393. 8. Sanders LJ and Frykberg RG. The Diabetic Foot / Marvin E. Levin, Lawrence W. O’Neal, John Bowker; St. Louis; Mosby Year Book, c1993, 5th ed Charcot Foot Chapter 7 Pg. 149-179. 9. Frykberg RG and Kozak G. The Diabetic Charcot Foot. WB Saunders Company, West Washington Square, Philadelphia PA, 1984, Chapter 11 Pg. 103 -112. 10. Jacobs AM and Oloff LM: The Diabetic Foot. In Marcus SA (ed): Complications in Foot Surgery, ed 2. Baltimore, Williams & Wilkins, 1984, pp. 309-356 11. Cozen L. Does Diabetes Delay Fracture Healing? Clin Orthop 82: 134 – 140, 1972. 12. Levin ME et al. Effects of Diabetes Mellitus on Bone Mass in Juvenile and Adult Onset Diabetes. N Eng J Med 294:241-244, 1976. 13. Banks AS. A Clinical Guide to the Charcot Foot. In Stephen J. Kominsky (ed): Medical and Surgical Management of the Diabetic Foot, St. Louis; Mosby, c1994, Pg. 115 – 143. Editor’s Note: For a related article, see “Using Serologic Screening To Identify And Monitor At-Risk Charcot Patients” in the August 2004 issue or check out the archives at www.podiatrytoday.com.

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