Assessing The Talectomy For Charcot Ankle Deformity

A talectomy with or without tibiocalcaneal arthrodesis may provide a viable option for patients with Charcot neuroarthropathy of the ankle. Accordingly, these authors discuss the indications and timing for talectomy, offer surgical pearls and review results from the literature.

Charcot neuroarthropathy in people with diabetes and peripheral neuropathy is associated with significant morbidity and mortality, and a decreased quality of life.^1-5 Patients with Charcot neuroarthropathy are at a higher risk for amputation without ulceration (7 percent higher risk) and with ulceration (28 percent higher risk) than patients with diabetes both with and without ulceration.⁶

Shon and colleagues showed a 2 percent lower amputation risk in Charcot neuroarthropathy patients without ulceration than patients with a diabetic foot ulcer only, but the combination of Charcot neuroarthropathy and ulceration resulted in a 12-fold higher rate of amputation in comparison to a patient with a diabetic foot ulcer only.⁷ The difficulty of this pathological entity is higher when the ankle joint is involved.⁸ The literature has described the general incidence of Charcot neuroarthropathy as being between 0.4 and 13 percent with ankle Charcot neuroarthropathy occurring in approximately 9 percent of all Charcot neuroarthropathy foot and ankle cases.^9-11 Lavery and colleagues reported a Charcot neuroarthropathy incidence of 8.5 per 1,000 patients with diabetes.¹²

Diabetes mellitus is now the main cause of Charcot neuroarthropathy although there are other causes of sensory peripheral neuropathy such as leprosy, alcoholism, tabes dorsalis (syphilis), syringomyelia, peripheral nerve injuries or congenital absence of pain sensation.^13,14 The larger joints in the lower limb are primarily affected in patients with syphilis whereas the larger joints of the upper extremity are primarily involved in those with syringomyelia.¹⁴ Diabetic Charcot neuroarthropathy typically involves the joints of the foot and ankle.^14,15

Although we do not currently understand the disease process, there are many theories with regard to the direct causes of the development of the Charcot joint with the main two being neurotraumatic and neurovascular.¹⁶

The neurovascular theory is based on increased blood flow to the limb from dilation of the blood vessels because of sympathetic denervation. The loss of vasomotor control allows blood vessels to dilate, thus increasing the peripheral blood flow. The increased blood flow increases the arteriovenous shunting, which causes hyperemia, demineralization and bone resorption.1^7,18 The neurotraumatic theory postulates that neuroarthropathy results from repetitive microtrauma secondary to overuse in the absence of normal protective sensation. The continued microtrauma causes fractures and dislocations. Researchers believe the current mechanism to be a combination of these two leading concepts.^14,19

An Overview Of Charcot Classification Systems
When it comes to Charcot neuroarthropathy, there are a number of classifications based on radiographic, anatomical or clinical presentations. According to Eichenholtz, radiographic findings were sufficient for the diagnosis of Charcot neuroarthropathy.²⁰ He postulated a primarily three-stage radiographic classification system for Charcot arthropathy with an additional prodromal stage added later.²¹

Stage 0: This acute phase is characterized by swelling, warmth, joint instability and normal radiographic anatomy of the foot and ankle.
Stage 1: The development phase is characterized by fragmentation of bones and cartilage, joint effusions, subluxation and dislocation, soft tissue edema, hyperemia, bone resorption and intra-articular fractures.
Stage 2: The coalescence phase is characterized by decreased soft tissue edema, healing of fractures and organization of bone fragments.
Stage 3: The reconstruction phase is characterized by new bone formation and remodeling of bone.

Additionally, Brodsky has described four main anatomic areas of destruction in Charcot neuroarthropathy.²²
Type 1: Midfoot is the most common location for this type, which affects approximately 60 percent of patients with Charcot neuroarthropathy.
Type 2: This type involves the rearfoot joints (the subtalar, talonavicular and calcaneocuboid joints), and affects 20 to 25 percent of patients.
Type 3: This type is divided into two subtypes. Subtype A affects the tibiotalar joint and subtype B affects the posterior calcaneus. The incidence of these subtypes is 9 and 2 percent respectively. Brodsky did not include the forefoot in his classification system but Sanders and Frykberg later expanded it, accounting for approximately 15 percent of cases.²³

A Closer Look At The Indications And Timing For Talectomy
The purpose of this article is to examine pertinent pearls for talectomy in Charcot neuroarthropathy of the ankle. Clinicians must first determine whether surgical intervention is indicated as opposed to non-surgical intervention. The indications for surgery are acute dislocation, non-healing ulceration due to instability or deformity, or uncontrolled deformity or instability.^19,24-27 Lowery and colleagues in their literature review found that ankle Charcot neuroarthropathy was the second highest Charcot location for surgical intervention at 29.3 percent.³

The second criterion that one must determine is the timing of the surgical intervention.²⁸ The Eichenholtz classification system has often been the benchmark for surgical timing of the unstable Charcot neuroarthropathy patient. Historically, the specific benchmark has been stage 3.^20,25 Authors have also described Stage 2 intervention.^29,30 Although the profession has reached no consensus on the timing of surgical intervention for patients with unstable Charcot neuroarthropathy, surgical intervention during Stage 1 is generally not recommended due to technical difficulty, complications with fixation and increased infection risk.^20,25 Generally, researchers recommend waiting for surgical intervention until erythema, edema and warmth have subsided.^14,31

The goals for surgical intervention in the ankle Charcot neuroarthropathy patient are to reestablish stability and alignment while allowing for ambulation without ulceration and with or without orthoses or bracing.²⁵ The ultimate goal of limb salvage while protecting the unaffected limb is critical in mitigating the daunting morbidity and mortality rates associated with Charcot neuroarthropathy.

The use of talectomy in foot surgery dates back to 1608.^32,33 Talectomy has primarily been an end-stage procedure in complex pediatric and adult pathologies. The use in pediatric clubfoot surgery is most often associated with severe rigid clubfoot deformities. Cooper and Capello showed a 92 percent success rate with a 20-year follow-up for patients with pediatric clubfoot.³⁴ Solund and colleagues noted an 82 percent satisfaction rate with talectomy in a pediatric population of various pathologies.³⁵ One of the more common uses in the adult population is that of the talar trauma.³⁶ Talectomy can also be an excellent choice in patients with severely deformed, unstable Charcot neuroarthropathy. In 1943, Blair first described the tibiocalcaneal arthrodesis for fracture dislocation resulting in talar avascular necrosis.³⁷

How To Perform The Talectomy
One can perform talectomy with or without tibiocalcaneal arthrodesis either in a single-stage or as a staged procedure if there is severe deformity and concern about neurovascular status with single-stage deformity correction. Typically, authors have described a long lateral incision for talectomy, starting approximately 6 cm proximal to the distal tip of the fibula and coursing along the fibula and over the sinus tarsi to the calcaneocuboid joint.²⁸ One may utilize an adjunctive medial incision starting just anterior to the medial malleolus and lying between the tibialis posterior and tibialis anterior tendons. Tom and Pupp described a medial incision with two semi-elliptical incisions to excise an ulcer over the medial talar head.³⁸

Carry dissection to the level of both the ankle and subtalar joints to expose the talus. Often, one will resect the distal 5 cm of the fibula, which allows for better visualization and can provide a bone graft if a tibiocalcaneal arthrodesis is necessary. Resection of the distal end of the fibula is helpful for alignment and congruity if one does not perform an arthrodesis. The surgeon can then excise the talus in toto or leave the head of the talus.

Equinus is often a component of ankle Charcot neuroarthropathy and may require adjunctive treatment beyond the talectomy. Check ankle joint dorsiflexion with the knee extended after excising the talus. If ankle joint dorsiflexion is less than 90 degrees with the knee extended, authors recommend a triple hemisection tendo-Achilles lengthening (TAL).²⁸ Although most Charcot neuroarthropathy cases have an associated equinus deformity, after excising the talus, there may be enough relaxation in the soft tissue to allow the equinus to resolve. Doing the TAL before excision of the talus may result in increased instability and weakness, which is obviously only a concern if one performs an arthroplasty instead of an arthrodesis. If the calcaneal inclination angle is not reducing intraoperatively, this is a sign that equinus is a significant component of the deformity that one must address.

Addressing Significant Equinus: Should You Perform A Tibiocalcaneal Arthrodesis Or Arthroplasty?
At this point, there are two available options: tibiocalcaneal arthrodesis or arthroplasty. There is literature to support either approach. The case described by Tom and Pupp did not have fusion but did have temporary fixation with a Steinmann pin, which surgeons left in for seven weeks.³⁸ The patient was ambulatory without complication at 15 months postoperatively. Coltart’s study showed better results with arthroplasty in comparison to arthrodesis.³⁹

In the pediatric study by Cooper and Capello, the two patients with unsatisfactory results were those with ankylosis of the tibia and calcaneus.³⁴ Burkhart and Peterson echoed similar results as both of these studies in the 60-year case presentation follow-up.⁴⁰ In fact, Whitman stated that the limited motion that remains with arthroplasty is beneficial to long-term outcomes.^41-43 Itokazu and colleagues demonstrated an average range of motion of the tibiocalcaneal articulation of 10 to 25 degrees with an average shortening of 2 cm (causing no clinical pathology).⁴⁴ If one is performing an arthroplasty, remove temporary fixation at six to eight weeks to prevent ankylosis, which results in increased stress on joints proximally and distally.³⁸ This is concerning in a patient predisposed to Charcot neuroarthropathy.

When performing tibiocalcaneal arthrodesis, debride the articular surfaces of the tibial plafond and calcaneus, and utilize bone grafting as necessary. Temporary fixation maintains alignment and deformity correction until permanent fixation is in place. When it comes to permanent fixation, the options have both increased and improved. Typically, the choice categories are internal fixation, external fixation or a combination of both.

In a recent article by LaPorta and colleagues, five of the six case presentations involving the use of tibiocalcaneal arthrodesis were related to diabetic neuropathy.⁴⁵ In this study, they used external fixation as either primary or secondary fixation. The different types of fixation included initial external fixation followed by intramedullary nail and tripod screw fixation (three 8.0 mm partially threaded cancellous screws with one screw oriented from the inferior central calcaneus into the medullary canal of tibia, one oriented from the posterior inferior calcaneus (tuber) to the anterior distal tibia, and one oriented from the distal lateral aspect of the cuboid to the posterior medial tibia). The study authors also used multiple forms of internal fixation in combination with external fixation.

LaPorta and co-workers used staging for infected patients.⁴⁵ For patients with stage 1 infection, they debrided all infected bone and soft tissue, and employed fixation to maintain length, alignment and rotation. Once the infection clears, one can perform arthrodesis by compression with or without bone grafting, distraction osteogenesis or bone transport. The combined use of internal and external fixation in Charcot neuroarthropathy patients without osteomyelitis has the benefit of additional stability by neutralizing stress at the arthrodesis site.

There is substantially more literature for tibiocalcaneal arthrodesis than arthroplasty. A study by Fabrin and coworkers included both tibiotalar (seven patients) and tibiocalcaneal (five patients) arthrodesis.⁴⁶ For the tibiocalcaneal group, there was one fusion, two stable fibrous nonunions, one unstable fibrous nonunion and one transtibial amputation. Their conclusion was that although tibiocalcaneal arthrodesis with external fixation was unlikely to lead to fusion, the fibrous nonunion is often acceptable.

Pelton and coworkers showed an 88 percent fusion rate in 33 patients with a tibocalcaneal arthrodesis.⁴⁷ Papa and colleagues reported on 29 patients with Charcot neuroarthropathy with 11 of these patients having a tibiocalcaneal arthrodesis.³⁰ The fixation consisted of cannulated cancellous screws with bone grafting. The results showed seven pseudarthroses, five of which were stable and asymptomatic, one that went on to a below-knee amputation and one who was unstable with limited ambulatory ability.

In a study of tibiocalcaneal arthrodesis for the treatment of non-braceable neuropathic ankle deformities, Alvarez and colleagues used a blade plate with 7.0 mm cannulated screws and bone grafting.⁴⁸ They achieved talar head and neck fusion to the anterior aspect of the tibia with all ankles fusing in an average of 5.2 months. All patients were satisfied with outcomes at an average of 26.9 months follow-up.

Myerson and coworkers examined tibiocalcaneal arthrodesis in 30 patients for a variety of pathologies using a blade plate.⁴⁹ Fusion occurred in 93 percent of the patients at an average of 16 weeks with two patients developing nonunions. This study, like that of LaPorta, Pinzur and Noonan, discussed the importance of using a longer intramedullary nail or plate that extends above the tibial metaphysis to dissipate stress concentration.^13,45,49

Myers and colleagues conducted a retrospective analysis of ankle and hindfoot fusions in both patients with diabetes and patients without diabetes.⁵⁰ Their study consisted of 74 patients in each group. Patients with diabetes had significantly higher complication rates in comparison to those without diabetes.

In Conclusion
Ankle Charcot neuroarthropathy is a difficult condition in a difficult patient population so one must carefully evaluate the cost versus benefit prior to any surgical intervention. As with any diabetic foot pathology, prevention and early intervention yield better outcomes with less risk. If the deformity progresses to a non-braceable, unstable deformity with or without ulceration/infection, then surgery becomes a viable option for limb preservation.

Talectomy can be a useful surgical procedure for ankle Charcot neuroarthropathy in this case. One must consider the decisions about timing, arthroplasty versus arthrodesis and the type(s) of fixation. One must tailor the postoperative course to the individual due to the complicated nature of these cases and a conservative approach is often warranted.

Dr. DeHeer is a Fellow of the American College of Foot and Ankle Surgeons, and a Diplomate of the American Board of Podiatric Surgery. He is also a team podiatrist for the Indiana Pacers and the Indiana Fever. Dr. DeHeer is in private practice with various offices in Indianapolis. Dr. DeHeer writes a monthly blog for Podiatry Today. One can access his blog at https://www.podiatrytoday.com/blog/289 .

Dr. Grebenyuk is an Associate of the American Board of Foot and Ankle Surgery. She is also a Fellow in the Reconstructive Foot and Ankle Surgery and International Medical Mission Program in Indianapolis.

Dr. Yeager is board certified in foot and reconstructive rearfoot/ankle surgery. He is the Immediate Past Chair of the American Society of Podiatric Surgeons and has served on both the state and national levels in such capacities as President of the Illinois Podiatric Medical Association and on the APMA Vision 2015 Path to Parity Committee. He is the Residency Director for the Katherine Shaw Bethea (KSB) Hospital Podiatric and Surgical Residency Program in Illinois.      

References

1.     Dhawan V, Spratt KF, Pinzur MS, et al. Reliability of AOFAS diabetic foot questionnaire in Charcot arthropathy: stability, internal consistency, and measurable difference. Foot Ankle Int. 2005; 26(9):717–731.
2.     Wukich DK, Sung W. Charcot arthropathy of the foot and ankle: modern concepts and management review. J Diabetes Complications. 2008; 23(6):409–426.
3.     Lowery NJ, Woods JB, Armstrong DG, Wukich DK. Surgical management of Charcot neuroarthropathy of the foot and ankle: a systematic review. Foot Ankle Int. 2012; 33(2):113–121.
4.     Richard JL, Almasri M, Schuldiner S. Treatment of acute Charcot foot with bisphosphonates: a systematic review of the literature. Diabetologia. 2012; 55(5):1258–1264.
5.     Pakarinen TK, Laine HJ, Maenpaa H, Mattila P, Lahtela J. Long-term outcome and quality of life in patients with Charcot foot. Foot Ankle Surg. 2009; 15(4):187–191.
6.     Saltzman CL, Hagy ML, Zimmerman B, Estin M, Cooper R. How effective is intensive nonoperative initial treatment of patients with diabetes and Charcot arthropathy of the feet? Clin Orthop Relat Res. 2005; 435:185–190.
7.     Sohn MW, Stuck RM, Pinzur M, et al. Lower-extremity amputation risk after charcot arthropathy and diabetic foot ulcer. Diabetes Care. 2010; 33(1):98-100.
8.     Brodsky JW. The diabetic foot. In: MJ Coughlin, RA Mann (eds.) Surgery of the Foot and Ankle, Seventh Edition, Mosby, St. Louis, 1999, pp. 895–969.
9.     Sinha S, Munichoodappa CS, Kozak GP. Neuro-arthropathy (Charcot joints) in diabetes mellitus. Medicine. 1972; 51(3):191–210.
10.     Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. Clin Podiatr Med Surg. 2008; 25(1):17–28.
11.     Leung HB, Ho YC, Wong WC. Charcot foot in Hong Kong Chinese diabetic population. Hong Kong Med J. 2009; 15(3):191–195.
12.     Lavery LA, Armstrong DG, Wunderlich RP, Tredwell J, Boulton AJ. Diabetic foot syndrome: evaluating the prevalence and incidence of foot pathology in Mexican-Americans and non-Hispanic whites from a diabetes management cohort. Diabetes Care. 2003; 26(5):1435–1438.
13.     Pinzur MS, Noonan T. Ankle arthrodesis with a retrograde femoral nail for Charcot ankle arthropathy. Foot Ankle Int. 2005; 26(7):545–549.
14.     Johnson JTH. Neuropathic fractures and joint injuries. J Bone Joint Surg. 1967; 49(1):1–30.
15.     Gupta R. A short history of neuropathic arthropathy. Clin Orthop. 1993; 296:43–49.
16.     Trepman E, Nihal A, Pinzur MS. Current topics review: Charcot neuroarthropathy of the foot and ankle. Foot Ankle Int. 2005; 26(1):46-63.
17.     Edelman SV, Kosofsky EM, Paul RA, Kozak GP. Neuro- osteoarthropathy (Charcot’s Joint) in diabetes mellitus following revascularization surgery. Arch Intern Med. 1987; 147(8):1504–1508.
18.     Edmonds ME, Roberts VC, Watkins PJ. Blood flow in the diabetic neuropathic foot. Diabetologia. 1982; 22(1):9–15.
19.     Caputo GM, Ulbrecht J, Cavanagh PR, Juliano P. The Charcot foot in diabetes: six key points. Am Fam Physician. 1998; 57(11):2705–2710.
20.     Eichenholtz SN. Charcot Joints, Charles C Thomas, Springfield, IL, 1966.
21.     Shibata T, Tada K, Hashizume C. The results of arthrodesis of the ankle for leprotic neuroarthropathy. J Bone Joint Surg Am. 1990; 72(5):749–756.
22.     Brodsky JW, Wagner FW, Kwong PK, et al. Patterns of breakdown. I. The Charcot tarsus of diabetes and relation of treatment. Presented at the American Orthopedic Foot and Ankle Society (AOFAS) 16th Annual Meeting. New Orleans, February 1986.
23.     Sanders L, Frykberg RG. The Charcot foot (Pied de Charcot). In: Bowker JH, Pfeifer MA (eds.). Levin and O’Neal’s The Diabetic Foot. Mosby Elsevier, Philadelphia, 2007, pp. 257–283.
24.     Lesko P, Maurer RC. Talonavicular dislocations and midfoot arthropathy in neuropathic diabetic feet. Clin Orthop. 1989; 240:226– 231.
25.     Johnson JE. Operative treatment of neuropathic arthropathy of the foot and ankle. J Bone Joint Surg. 1998; 80-A:1700–1709.
26.     Schon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop. 1998; 349:116–131.
27.     Stone NC, Daniels TR. Midfoot and hindfoot arthrodeses in diabetic Charcot arthropathy. Can J Surg. 2000; 43(6):449–455.

    28. Burns PR, Wukich DK. Surgical reconstruction of the Charcot rearfoot and ankle. Clin Podiatr Med Surg. 2008; 25(1):95-120.

    29. Myerson MS, Henderson MR, Saxby T, Short, KW. Management of midfoot diabetic neuroarthropathy. Foot Ankle Int. 15: 233 – 241, 1994.

    30. Papa J, Myerson M, Girard P. Salvage, with arthrodesis, in intractable diabetic neuropathic arthropathy of the foot and ankle. J Bone Joint Surg. 1993; 75(7):1056–1066.

    31. Jacobs RL. Charcot foot. In: MH Jahss (ed.) Disorders of the Foot & Ankle, WB Saunders, Philadelphia, 1991, pp. 2156–2169.

   32. Szyszkowitz R, Reschauer R, Seggl W. Eighty-five talus fractures treated by ORIF with five to eight years of follow-up study of 69 patients. Clin Orthop. 1985;199:97–107.

    33. Kelikian H, Kelikian AS. Disorders of the Ankle. W.B. Saunders Company, Philadelphia, 1985.

    34. Cooper RR, Capello W. Talectomy. A long-term follow-up evaluation. Clin Orthop. 1985; 201:32–5.

    35. Solund K, Sonne-Holm S, Kjolbye JE. Talectomy for equinovarus deformity in arthrogryposis. A 13 (2–20) year review of 17 feet. Acta Orthop Scand. 1991;62(4):372–4.

    36. Joseph TN, Myerson MS. Use of talectomy in modern foot and ankle surgery. Foot Ankle Clin. 2004; 9(4):775-785.

    37. Blair HC. Comminuted fractures and fracture dislocations of the body of the astragalus: operative treatment. Am J Surg. 1943; 59:37–47.

    38. Tom RK, Pupp GR. Talectomy for diabetic Charcot foot. An alternative to amputation. J Am Podiatr Med Assoc. 1992; 82(9):447-453.

    39. Coltart WD. Aviator’s astragalus. J Bone Joint Surg Br. 1952; 34(4):545-566.

    40. Burkhart SS, Peterson HA. Sixty-year follow-up of talectomy. J Bone Joint Surg. 1989; 71(2):325.

    41. Whitman R. The operative treatment of paralytic talipes of the calcaneus type. Am J Med Sci. 1901; 122:593.

    42. Whitman R. Further observations on the treatment of paralytic talipes calcaneus, by astragalectomy and backward displacement of the foot. Ann Surg. 1908; 47:264. 264.

    43. Whitman R. Further observations on the operative treatment of paralytic talipes of the calcaneus type. Am J Orthop Surg. 1910; 8:137.

    44. Itokazu M, Matsuna GA. Ankle arthroplasty by excision of the talar body. Foot Ankle Int. 1994; 15(4):191–6.

    45. LaPorta GA, Nasser EM, Mulhern JL. Tibiocalcaneal arthrodesis in the high-risk foot. J Foot Ankle Surg. 2014; 53(6):774-786.

    46. Fabrin J, Larsen K, Holstein PE. Arthrodesis with external fixation in the unstable or misaligned Charcot ankle in patients with diabetes mellitus. Int J Low Extrem Wounds. 2007; 6(2):102–107.

    47. Pelton K, Hofer JK, Thordarson DB. Tibiotalocalcaneal arthrodesis using a dynamically locked retrograde intramedullary nail. Foot Ankle Int. 2006; 27(10):759–763.

    48. Alvarez RG, Barbour TM, Perkins TD. Tibiocalcaneal arthrodesis for nonbraceable neuropathic ankle deformity. Foot Ankle Int. 1994;15(7):354–9.

    49. Myerson MS, Alvarez RG, Lam PW. Tibiocalcaneal arthrodesis for the management of severe ankle and hindfoot deformities. Foot Ankle Int. 2000;21(8):643–50.

    50. Myers TG, Lowery NJ, Frykberg RG, Wukich DK. Ankle and hindfoot fusions: comparison of outcomes in patients with and without diabetes. Foot Ankle Int. 2012; 33(1):20-28.

Additional References
    51. Sinha S, Munichoodappa CS, Kozak GP. Neuro-arthropathy (Charcot joints) in diabetes mellitus. Medicine. 1972; 51(3):191–210, 1972.
   52.  Micheli LJ, Solomon R. Stress fractures in dancers. In: R Solomon, SC Minton, J Solomon (eds.) Preventing Dance Injuries: An Interdisciplinary Perspective, AAHPERD Publications, Reston, VA, 1990, pp. 133–153.