- Email: [email protected]
Surgical off-loading of the diabetic foot
Surgical off-loading of the diabetic foot Robert G. Frykberg, DPM, MPH,a Nicholas J. Bevilacqua, DPM,b and Geoffrey Habershaw, DPM,c Phoenix, Ariz; Los Angeles, Calif; and Boston, Mass Surgical intervention for chronic deformities and ulcerations has become an important component in the management of patients with diabetes mellitus. These patients are no longer relegated to wearing cumbersome braces or footwear for deformities that might otherwise be easily corrected. Although surgical intervention in these often high-risk individuals is not without risk, the outcomes are fairly predictable when patients are properly selected and evaluated. In this brief review, we discuss the rationale and indications for diabetic foot surgery, focusing on the surgical decompression of deformities that frequently lead to foot ulcers. ( J Vasc Surg 2010;52:44S-58S.)
Foot deformities, including contracture of the gastrocnemius-soleus complex, are clinically significant risk factors that commonly lead to diabetic foot ulceration.1-3 In fact, deformity in association with peripheral neuropathy and trauma were the three most common component causes in the pathway leading to foot ulceration.3 Structural alterations in the architecture of the foot often lead to abnormally high plantar foot pressures, as well as increased dorsal, medial, or lateral pressures when snugly fitting footwear is worn.4,5 These high pedal pressures consequently place the foot at risk for ulceration.6-8 Although deformities such as hammer toes and bunions are quite common in the nondiabetic population, they also frequently develop in persons with diabetes but without significant consequence. It is the presence of peripheral neuropathy, however, that confers the attendant risk for ulceration in diabetic individuals. A recent study of patients undergoing foot and ankle surgery has shown that diabetes without complications imparts no greater risk for postoperative infection than that for persons without diabetes. However, when diabetic patients with complications (including neuropathy) were compared with those without diabetes, there was a tenfold risk for developing postoperative infection.9 Although this study’s focus was on postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant predictor of foot ulceration.3,7,10-12 From the Carl T. Hayden VA Medical Center, Phoenix;a Valley Presbyterian Hospital, Los Angeles;b and Boston University Medical Center, Boston.c Competition of interest: none. This article is being co-published in the Journal of Vascular Surgery® and the Journal of the American Podiatric Medical Association. Correspondence: Robert G. Frykberg, DPM, Carl T. Hayden VA Medical Center, 650 E Indian School Rd, Phoenix, AZ 85012-1892 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery and the American Podiatric Medical Association. doi:10.1016/j.jvs.2010.06.008
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Neuropathy not only predisposes to foot ulcer in the presence of deformity and trauma but can also lead to the development of deformity in the diabetic foot.4,8,13 The Charcot foot is the most classic example of a deformity primarily related to peripheral neuropathy of any cause.14,15 Neuropathy affects the sensory nerves of the lower extremities and the motor as well as autonomic fibers.16-19 Consequently, motor neuropathy leads to muscle dysfunction, dynamic contractures, and even paresis (ie, foot drop). Ankle equinus, caused by a contracture of the gastrocnemius-soleus muscle complex and Achilles’ tendon, is often found in patients with diabetes and has been associated with high forefoot plantar pressures.20-22 The clinical effects of motor neuropathy are also seen in the form of intrinsic muscle atrophy.23 The “intrinsic minus” foot is typified by such atrophy on the dorsal forefoot in concert with the development of hammer toes or claw toes (Fig 1).8,24 In severe cases, the intrinsic minus foot will develop a cavus appearance and associated high plantar pressures under the prominent metatarsal heads. Shoes are an important cause of trauma to the neuropathic foot, especially in individuals with structural deformity. Therefore, the provision of properly fitted therapeutic footwear is considered a key component of an ulcer and amputation prevention program.13,25-27 Unfortunately, over-the-counter shoes often cannot accommodate severe foot deformities, including high plantar pressures. In some situations, custom footwear is indicated to protect severely misshapen feet. Nonetheless, any footwear is only as good as the patients’ adherence to wearing the shoes as prescribed. To this end, even in the ulcerated foot where strict adherence to off-loading modalities are critical, one study showed that patients had poor compliance and wore the prescribed off-loading devices only 28% of the time.28 Nonetheless, several studies have shown that patients fitted with therapeutic footwear suffer significantly fewer primary or recurrent ulcerations compared with diabetic patients who were not given such footwear.29-32 Surgical intervention should be considered when recurrent ulceration or preulcerative lesions develop despite
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Fig 1. Intrinsic minus foot. Note the high arched, thin foot with little muscle mass in this patient with advanced peripheral neuropathy. Flexible hammer toes (claw toes) usually accompany this deformity as well.
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Fig 2. Acquired second hammer toe after great toe amputation with dorsal ulcer. This is easily treated by a digital arthroplasty or joint resection with excision of the ulceration. A metatarsophalangeal joint release is also usually required for rigid deformities.
Table. Classification of diabetic foot surgery40 ● Class I: Elective. Reconstructive procedures on patients who do not have loss of protective sensation (LOPS) ● Class II: Prophylactic. Reconstructive procedures performed to reduce the risk of ulceration or reulceration in patients who have LOPS and do not have a wound present ● Class III: Curative. Procedures performed to assist in healing of open wounds ● Class IV: Emergent. Procedures performed to arrest or limit progression of infection
concerted efforts to prevent such lesions. Once considered ill-advised, corrective or reconstructive foot surgery has assumed an important role in the management of patients with chronic or recurrent foot ulcerations.13,33-38 Of course, such patients need to be carefully selected and evaluated to ensure that adequate vascularity is present and that major comorbidities, including renal insufficiency, unstable cardiovascular disease, and congestive heart failure, are adequately controlled. Because peripheral arterial disease (PAD) is often asymptomatic in persons with diabetes, we follow the American Diabetes Association recommendation that an ankle-brachial index (ABI) be measured in such persons who are aged ⬎50 years.2,39 Furthermore, we routinely recommend obtaining a preoperative ABI (with toe pressures and waveforms) in diabetic patients with foot ulcers in the absence of clearly bounding pulses. In 2003, Armstrong and Frykberg38,40 revised a risk-based scheme for classifying the types of foot surgery performed in diabetic patients largely depending on the presence of open wounds and their acuity. Fundamentally, the classes of foot surgery are distinguished by their progressive risks for subsequent proximal levels of amputation (Table):
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Elective surgery (class I) represents reconstructive procedures performed to correct deformities or high plantar pressures in persons without neuropathy. Prophylactic (class II) procedures are those performed in patients with neuropathy (loss of protective sensation) to reduce the risk of ulceration or recurrent ulceration when no open wounds are present. Curative surgery (class III) is often performed when open wounds are present to effect a cure by removing underlying bony prominences (surgical decompression), osteomyelitis, or by draining underlying abscesses. Obviously, such procedures are at higher risk for nonhealing or infection than are the first two classes. Emergent procedures (class IV) are performed for severe infections (wet gangrene, necrotizing fasciitis, etc) to control the progression of infection. As the name implies, these procedures are performed emergently and often consist of open amputations at the foot level combined with fasciotomies of the leg.
Armstrong et al41 later validated this classification scheme in subsequent risk for proximal amputation and infection. They found a significant trend toward increasing risk of ulceration/reulceration, postoperative infection, alllevel amputation, and major amputation with increasing class of foot surgery (P ⬍ .01 for all complications). As would be expected, the greatest frequency of major amputation was in class IV procedures. Specific types of operations or procedures are not restricted to single classes of surgery as described above. To the contrary, many procedures are used in operations performed across multiple foot surgery categories. For example, a hammer toe repair might be performed as an elective, prophylactic, or a curative procedure depending on the presence of neuropathy and the presence or absence of an open wound (Fig 2) A tendo-Achilles’
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Fig 3. Reconstruction for correction of unstable Charcot ankle. A, Preoperative clinical view demonstrates ankle deformity. B, A preoperative radiograph shows osteolysis of the talar dome. C, Circular external fixator in place after talectomy and fusion. D, Postoperative radiograph.
lengthening (TAL) would be indicated under the same situations. A first ray amputation might be performed to cure chronic osteomyelitis even in the absence of an open wound (prophylactic), in the presence of a chronic draining ulcer (curative), or as an emergent procedure to control the spread of an acute necrotizing infection. A midfoot osteotomy or arthrodesis of an ulcerated Charcot deformity is commonly performed as a curative operation (class III), but is just as frequently performed to reconstruct a deformed nonulcerated foot and thereby offer surgical decompression to reduce plantar pressures (class II; Fig 3).15,42,43 This review will focus on those procedures commonly used by foot and ankle surgeons to address deformities that are causing abnormal pressure gradients. As already noted, many of these procedures can be used in elective, prophylactic, or curative situations depending on the presence (or absence) of neuropathy or ulceration. Although we will not discuss amputations or specific management of infection, a brief discussion of those procedures used to correct the Charcot foot will be presented.
DIGITAL DEFORMITIES Common digital deformities, such as hammer toe, claw toe, and mallet toe, are known to increase pressures and are associated with neuropathic ulceration. Correcting the structural deformity with a resection arthroplasty may augment healing and reduce the risk of ulcer recurrence.44 Alternatively, a percutaneous flexor tenotomy offers a less invasive approach and may afford the necessary intrinsic pressure modulation to augment healing. Distal tip ulcers, in a flexible hammer toe, may be managed with a flexor digitorum longus tenotomy. A blade or 18-gauge needle is introduced 1 cm proximal to the proximal plantar flexural crease of the toe (Fig 4). The ankle is held in a dorsiflexed position with the patient actively holding all toes in a flexed position. The toe is manually straightened, and the blade is moved across the taught tendon, making ease of the tenotomy. The long extensor tendon will now hold the toe straight. A postoperative shoe can be used for limited ambulation. Overex-
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Fig 4. Flexor tenotomy. A, The toe is flexible and ulcer is at the tip. B, Lidocaine is injected at the site of entry, and the patient is asked to dorsiflex the ankle and actively flex all the toes. This makes the long flexor tendon very taught, and can easily be tenotomized as shown here with a #61 Beaver blade. No suture is needed. C, Shows all three middle toes that have had flexor tenotomies. The fourth toe had resection of osteomyelitis, 4 weeks postoperatively, done in the office setting.
tension of the toe can be managed with an extensor longus tenotomy at a later date. Laborde45 retrospectively reviewed 18 patients presenting with plantar toe ulcers treated with a flexor tenotomy. All patients had a flexible claw toe deformity with ulcers on the distal plantar aspect of the hallux or lesser toes. The incision and the ulcer healed in all patients. Two patients underwent a repeat procedure for ulcer recurrence and remained ulcer free at 17 and 34 months. Tamir et al46 retrospectively reviewed the outcomes of 14 patients (24 toes) treated with percutaneous flexor tenotomies for a claw toe deformity to off-load the tip of the toe for ulcer healing. The authors performed an osteoclasis in select patients to correct rigid contractures at the proximal interphalangeal joint. All patients healed with no significant complications noted. Although the methodologic quality of both studies was poor, their results support the ability of a percutaneous
flexor tenotomy of the hallux and lesser toes to heal neuropathic toe ulceration secondary to toe contracture in persons with diabetes.47 A rigid hammer toe is best treated with an arthroplasty at the level of the distal or proximal interphalangeal joint. However, a percutaneous flexor tenotomy may be attempted in the nonflexible deformity before resorting to an open arthroplasty. On those occasions where a hallux ulcer is not due to a limitation of motion at the metatarsophalangeal joint (MTPJ), this same procedure can be used on this digit (Fig 5). LESSER METATARSALS Neuropathic ulcerations under the metatarsal heads are a challenging problem and may lead to infection and amputation.48 Various metatarsal procedures have been de-
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Fig 5. Arthroplasty of the hallux for surgical off-loading of a chronic hallux ulceration. A, The ulcer is adjacent to the head of the proximal phalanx. B, Incision placement. C, The head of the phalanx is removed, and the long extensor tendon is repaired. D, The wound closed primarily. Early ambulation is possible with a postoperative shoe.
scribed, including metatarsal head osteotomies and resections.38,49,50 An isolated metatarsal osteotomy should be considered for a chronic, nonundermining, nontunneling, ulcer below a specific metatarsal head. It can be performed through a dorsal incision with a doubleaction bone cutter or an oscillating saw. The osteotomy can be done at the surgical or anatomic neck of the metatarsal (Fig 6). A collar of bone may be removed if shortening of the metatarsal is desired. Such procedures are generally performed when the plantar ulceration does not penetrate to bone. A tunneling ulcer should be appropriately débrided to remove all undermining. A metatarsal head resection may be performed to assist in healing by internally off-loading the ulcer (Fig 7). Armstrong et al51 evaluated the outcomes of an isolated fifth metatarsal head resection for ulcerations beneath the fifth metatarsal head and compared it with nonsurgical care. They reported more rapid healing and a lower recurrence rate in the surgical group. The surgeon must be cognizant of maintaining a nearly normal metatarsal parabola. The second, third, and fourth metatarsals function as a single unit and any disruption in metatarsal length or height may result in a transfer callus or ulceration. If an ulcer occurs, further metatarsal osteotomy may be necessary. Osteotomies should be performed on the remaining two metatarsals, and if not, additional ulceration is likely to develop over the remaining metatarsal, necessitating a third procedure. This scenario is especially likely to
occur after one of the metatarsal heads has been removed due to infection. Multiple metatarsal head resections or a panmetatarsal head resection may be considered for nonhealing ulcers in the presence of an abnormal metatarsal parabola (Fig 8).52 Hamilton et al48 proposed combining lesser metatarsal head resections with gastrocnemius recession and a peroneus longus-to-brevis tendon transfer in patients with chronic, neuropathic forefoot ulcerations. All ulcers were located beneath lesser metatarsal heads, allowing the authors to preserve the first MTPJ. They adjunctively managed the equinus deformity with a gastrocnemius recession and alleviated pressure beneath the first metatarsal with the peroneus longus-to-brevis transfer. The authors reported ulcer healing in 10 patients (100%), with no ulcer recurrence at a mean 14.2 months of follow-up.48 KELLER ARTHROPLASTY Limited range of motion at the MTPJ is a common forefoot deformity that contributes to ulcer formation beneath the hallux. This limitation in joint range of motion leads to increased pressure on the hallux during ambulation. Pressure reduction is essential and usually consists of an external device to off-load the area.53 This does not correct the underlying deformity, however. The associated biomechanical abnormality still exists after the off-loading device is removed, and ulcer recurrence may occur. Identifying and correcting the underlying struc-
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Fig 6. Metatarsal osteotomy, now performed in the office setting when possible, can be done with simple instruments: bone cutter, hemostat, and freer elevator as a probe. A, Through a dorsal incision, the metatarsal neck is grasped with a large hemostat. B, A double-action bone cutter is introduced adjacent to the hemostat. C, The bone is osteotomized at the metatarsal neck level. D, Multiple osteotomies shown here are all in the proper location, between the anatomic and surgical neck of each metatarsal.
tural deformity may assist in healing and also reduce ulcer recurrence. Armstrong et al54 compared the safety and efficacy of a first MTPJ arthroplasty (Keller-type procedure) with nonsurgical management for wounds at the plantar aspect of the hallux interphalangeal joint (Fig 9). They included 41 patients, with 21 undergoing a first MTPJ arthroplasty to augment ulcer healing. Patients in the surgery group healed significantly faster than patients in the nonsurgery group. Care after healing was identical in both groups, and the surgery group had fewer ulcer recurrences during the 6-month follow-up. There was a very high prevalence of postoperative infections in the surgery group (40%), but this was compared with the 38% of patients in the control group who required treatment for infection during the period of therapy. The results of this study suggest that a first MTPJ arthroplasty is a safe and effective procedure in the treatment of noninfected, nonischemic wounds beneath the hallux.54
FIRST MTPJ RESECTION The excision of the first MTPJ should be considered if the metatarsal head has osteomyelitis, after failed sesamoidectomy, or for a chronic ulcer probing to the joint but with a viable hallux.38 The incision may incorporate and excise the ulcer or be placed dorsally to avoid the ulcer altogether. The incision is made directly to bone, with no undermining of the soft tissue. The dissection is at the level of the ligaments and periosteum. The metatarsal is cut and beveled plantarly to reduce any bone prominences. The base of the phalanx is removed as in a Keller bunionectomy. Both sesamoids should be removed because a fibrous union to the metatarsal stump may occur if they are left and become a future source of ulceration (Fig 10). This is also necessary in cases of open joint involvement or infection, wherein the infected or contaminated sesamoids will become a source for continued infection.
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Fig 7. A, Undermining ulceration that probes into deep tissues (including bone or joint) is not appropriate for standard metatarsal osteotomy. B, The ulcer is excised and the adjacent metatarsal is removed. C, Primary closure with a proximal drain is acceptable as long as there is no active sepsis. The drain is pulled in 24 hours, and the patient is kept non-weight bearing for 4 weeks.
TAL LENGTHENING Limited ankle joint mobility, as seen clinically as a tight Achilles’-gastrocnemius-soleus complex, is a deforming force and a causative factor in plantar forefoot ulcerations.21 During normal gait, 10° of dorsiflexion at the ankle is required, and anything less will increase plantar pressures in the forefoot and impede healing of the wound. To alleviate the pressure, several authors have suggested percutaneous TAL.55-58 Armstrong et al21 confirmed that plantar pressures are reduced after percutaneous TAL. Lin
et al59 reported results of percutaneous TAL in 15 patients with plantar forefoot ulcers that did not heal despite 9 weeks of total contact casting. All but one ulcer healed (93%), with no ulcer recurrence noted after a mean 17.3month follow-up. Mueller et al22 conducted a randomized control trial comparing the combined treatment of total contact cast and percutaneous TAL against a total contact cast alone. Initial healing rates were similar in both groups, but the significant difference was noted when the ulcer recur-
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Fig 8. Pan metatarsal head resection. A, Failed metatarsal surgeries with transfer ulcer subsecond. B, Transmetatarsal amputation could be done, but the toes are viable. Surgical off-loading can be accomplished through a dorsal or plantar approach; here, a dorsal approach is planned. C, Excision of metatarsal head through a dorsal incision. D, Radiograph several months after procedure.
rence rate was compared. After 2 years, the ulcer recurrence rate was 81% in the group treated with a total contact cast alone compared with 38% in those treated with a total contact cast and TAL. A gastrocnemius recession may be used as an alternative for relief of forefoot pressure60 and has also been described as an effective treatment for midfoot ulcers (Fig 11).60,61 CHARCOT FOOT Charcot arthropathy, perhaps the most characteristic deformity attributed to the diabetic foot, occurs in only 1% of the diabetic population as a whole and in approximately 30% of individuals with peripheral neuropathy.62-64 Originally described by Charcot as the pied tabétiques in persons with tertiary syphilis,65 the Charcot foot is now most commonly encountered in persons with
diabetes.66 Several studies have indicated that diabetic patients with Charcot foot deformities have an increased risk for ulceration and subsequent amputation and higher mortality compared with diabetic persons without this complication.67-69 The classic “rocker-bottom” deformity (Fig 12) is the result of a collapse of the midfoot architecture generally due to injury and continued weight bearing on the insensate foot. With the continued stress of weight bearing, a vicious cycle ensues that exaggerates local inflammation and leads to more fractures, dislocations, and deformity.14,70 Abnormally concentrated pressures develop in the midfoot during ambulation on the deformed foot, and ulceration frequently ensues.71 When the ankle joint is the primary site of involvement (Sanders-Frykberg pattern V),14 instability and deformity become the most difficult problem to man-
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Fig 9. A, Keller arthroplasty used as a curative procedure for ulcer under a rigid hallux. B, A postoperative radiograph shows the resection of the base of the proximal phalanx to allow for unrestricted dorsiflexion. C, Healed ulceration noted 3 weeks after a Keller arthroplasty was performed.
age and all too frequently fails conservative therapy with bracing.15,64,72 Conservative care for Charcot arthropathy has been the traditional mainstay of treatment for this limb-threatening disorder,14,64,72,73 but surgical management for Charcot joints is not a recent evolution in our understanding of how this entity can be approached. Although his report dealt primarily with Charcot joints due to tabes dorsalis, Steindler74 presented a series of surgical cases including subtalar arthrodesis as early as 1931. Several other important surgical case series were published in the ensuing decades that illustrated the efficacy of a surgical approach to this arthropathy as well as its inherent difficulties and complications.75,76 Numerous descriptive studies have been published in the last 20 years detailing various surgical techniques for the management of the deformed Charcot foot.15,43,77-82 The
indications for surgery are generally to provide a more effective management strategy when conservative measures have failed. Specifically, surgery is recommended for those patients with recurrent ulceration (with or without infection), severe instability, or severe deformities not amenable to footwear therapy alone.83 Many surgical techniques have been described, including simple plantar exostectomy with or without TAL, midfoot realignment arthrodeses, hindfoot arthrodeses, and ankle arthrodeses (Fig 13). A combination of procedures is most often required because Charcot deformities are usually multilevel. Although arthrodesis using internal fixation is most often practiced, multiplanar external circular fixation using Ilizarov techniques (Fig 14) has been used with increasing frequency in recent years.43,82,84 Regardless of technique, the goals of surgery remain the same: establish a stable, plantigrade foot mitigating focal areas of increased pressure and shearing forces.
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Fig 10. First metatarsophalangeal joint resection. A, A chronic deep ulcer under the first metatarsal head. B, The joint is resected through a dorsal incision. The elevator illustrates that the plantar ulcer penetrated into the joint. C, A radiograph shows the resection of the metatarsal head, both sesamoids, and the base of proximal phalanx.
By reducing plantar prominences and their attendant high pressures, healing of open ulcers can be augmented and the risk of subsequent skin breakdown will be reduced.77 The reader is referred to the referenced citations for specific techniques of interest. CONCLUSION Surgical management of diabetic foot disorders is no longer considered an unwarranted practice. To the contrary, surgery on the ulcerated or deformed foot has assumed an increasingly important role in the management of such disorders both in the United States and
abroad. Nonetheless, these patients are indeed at a higher risk for complications than their nondiabetic counterparts, especially in those with peripheral neuropathy or ischemia. Careful patient selection and thorough evaluation of the foot as well as attendant comorbidities are the cornerstones of achieving successful results in otherwise very complicated patients. Early and ostensibly aggressive surgical intervention on the deformed foot can obviate many months of unsuccessful conservative care, especially when ulcer recidivism becomes the primary challenge. Although virtually all the procedures used in this setting are not exclusive to diabetic foot
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Fig 12. A rocker-bottom Charcot foot is shown with soft tissue visualization of large plantar midfoot ulcer under the apex of the deformity.
Fig 11. A, A gastrocnemius recession performed to augment healing of a plantar forefoot ulceration. B, An image taken 2 years postoperatively demonstrates long-term ulcer healing.
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Fig 13. A, This chronic midfoot ulcer was treated with a simple exostectomy with tendo-Achilles’ lengthening. B, Postoperative image shows a plantar incision that was closed primarily and reinforced with tape strips (tendoAchilles’ lengthening incision not shown).
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Fig 14. A, A midfoot Charcot reconstruction using an Ilizarov circular frame. B, A lateral radiograph shows the orientation of the foot and ankle in the frame. In this case, internal fixation was also used.
surgery, great care (with close follow-up) is necessary in the postoperative period to ensure optimal outcomes in these high-risk patients. REFERENCES 1. Boulton AJ, Kirsner RS, Vileikyte L. Clinical practice. Neuropathic diabetic foot ulcers. N Engl J Med 2004;351:48-55. 2. Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care 2008;31:1679-85. 3. Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care 1999;22:157-62. 4. Frykberg RG. Biomechanical considerations of the diabetic foot. Lower Extremity 1995;2:207-14. 5. Cavanagh PR. Therapeutic footwear for people with diabetes. Diabetes Metab Res Rev 2004;20(Suppl 1):S51-5. 6. Veves A, Murray HJ, Young MJ, Boulton AJ. The risk of foot ulceration in diabetic patients with high foot pressure: a prospective study. Diabetologia 1992;35:660-3.
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7. Frykberg RG, Lavery LA, Pham H, Harvey C, Harkless L, Veves A. Role of neuropathy and high foot pressures in diabetic foot ulceration. Diabetes Care 1998;21:1714-9. 8. van Schie CH. A review of the biomechanics of the diabetic foot. Int J Low Extrem Wounds 2005;4:160-70. 9. Wukich DK, Lowery NJ, McMillen RL, Frykberg RG. Postoperative infection rates in foot and ankle surgery: a comparison of patients with and without diabetes mellitus. J Bone Joint Surg Am 2010;92:287-95. 10. Fernando DJ, Masson EA, Veves A, Boulton AJ. Relationship of limited joint mobility to abnormal foot pressures and diabetic foot ulceration. Diabetes Care 1991;14:8-11. 11. Abbott CA, Carrington AL, Ashe H, Bath S, Every LC, Griffiths J, et al. The North-West Diabetes Foot Care Study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based patient cohort. Diabet Med 2002;19:377-84. 12. Boyko EJ, Ahroni JH, Stensel V, Forsberg RC, Davignon DR, Smith DG. A prospective study of risk factors for diabetic foot ulcer. The Seattle Diabetic Foot Study. Diabetes Care 1999;22:1036-42. 13. Frykberg RG, Zgonis T, Armstrong DG, Driver VR, Giurini JM, Kravitz SR, et al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg 2006;45(5 suppl):S1-66. 14. Sanders LJ, Frykberg RG. Diabetic neuropathic osteoarthropathy: The Charcot foot. In: Frykberg RG, editor. The high risk foot in diabetes mellitus. New York: Churchill Livingstone; 1991. p. 325-35. 15. Wukich DK, Sung W. Charcot arthropathy of the foot and ankle: modern concepts and management review. J Diabetes Complications 2009;23:409-26. 16. Boulton AJ. Diabetic neuropathy: classification, measurement and treatment. Curr Opin Endocrinol Diabetes Obes 2007;14:141-5. 17. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care 2003;26:1553-79. 18. Boulton AJ, Vinik AI, Arezzo JC, Bril V, Feldman EL, Freeman R, et al. Diabetic neuropathies: a statement by the American Diabetes Association. Diabetes Care 2005;28:956-62. 19. Andersen H, Gjerstad MD, Jakobsen J. Atrophy of foot muscles: a measure of diabetic neuropathy. Diabetes Care 2004;27:2382-5. 20. Lavery LA, Armstrong DG, Boulton AJ. Ankle equinus deformity and its relationship to high plantar pressure in a large population with diabetes mellitus. J Am Podiatr Med Assoc 2002;92:479-82. 21. Armstrong DG, Stacpoole-Shea S, Nguyen H, Harkless LB. Lengthening of the Achilles tendon in diabetic patients who are at high risk for ulceration of the foot. J Bone Joint Surg Am 1999;81:535-8. 22. Mueller MJ, Sinacore DR, Hastings MK, Strube MJ, Johnson JE. Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg Am 2003;85:1436-45. 23. van Schie CH, Vermigli C, Carrington AL, Boulton A. Muscle weakness and foot deformities in diabetes: relationship to neuropathy and foot ulceration in Caucasian diabetic men. Diabetes Care 2004;27:1668-73. 24. Habershaw GM, Chrzan J. Biomechanical considerations of the diabetic foot. In: Kozak GP, Campbell DR, Frykberg RG, Habershaw GM, ed. Management of diabetic foot problems, 2nd ed. Philadelphia: WB Saunders; 1995. p. 53-65. 25. International Working Group on the Diabetic Foot. International Consensus on the Diabetic Foot. Paper presented at: International Working Group on the Diabetic Foot 2003; Noordwijkerhout, Netherlands. 26. Consensus Development Conference on Diabetic Foot Wound Care: 7-8 April 1999, Boston, Massachusetts. American Diabetes Association. Diabetes Care 1999;22:1354-60. 27. American Diabetes Association. Preventive foot care in diabetes. Diabetes Care 2004;27(Suppl 1):S63-4. 28. Armstrong DG, Lavery LA, Kimbriel HR, Nixon BP, Boulton AJ. Activity patterns of patients with diabetic foot ulceration: patients with active ulceration may not adhere to a standard pressure off-loading regimen. Diabetes Care 2003;26:2595-7. 29. Uccioli L, Faglia E, Monticone G, Favales F, Durola L, Aldeghi A, et al. Manufactured shoes in the prevention of diabetic foot ulcers. Diabetes Care 1995;18:1376-8.
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30. Chantelau E, Kushner T, Spraul M. How effective is cushioned therapeutic footwear in protecting diabetic feet? A clinical study. Diabet Med 1990;7:335-9. 31. Chantelau E. Therapeutic footwear in patients with diabetes. JAMA 2002;288:1231-2. 32. Edmonds ME, Blundell MP, Morns ME, Thomas EM, Cotton LT, Watkins PJ. Improved survival of the diabetic foot: the role of a specialized foot clinic. Q J Med 1986;60:763-71. 33. Piaggesi A, Schipani E, Campi F, Romanelli M, Baccetti F, Arvia C, et al. Conservative surgical approach versus non-surgical management for diabetic neuropathic foot ulcers: a randomized trial. Diabet Med 1998; 15:412-7. 34. Armstrong DG, Lavery LA, Stern S, Harkless LB. Is prophylactic diabetic foot surgery dangerous? J Foot Ankle Surg 1996;35:585-9. 35. Catanzariti AR, Blitch EL, Karlock LG. Elective foot and ankle surgery in the diabetic patient. J Foot Ankle Surg 1995;35:23-41. 36. Nicklas BJ. Prophylactic surgery in the diabetic foot. In: Frykberg RG, editor. The high risk foot in diabetes mellitus. New York City: Churchill Livingstone; 1991. p. 537-8. 37. Frykberg RG. Diabetic foot ulcers: pathogenesis and management. Am Fam Physician 2002;66:1655-62. 38. Frykberg R, Giurini J, Habershaw G, Rosenblum B, Chrzan J. Prophylactic surgery in the diabetic foot. In: Kominsky SJ, editor. Medical and surgical management of the diabetic foot. Saint Louis: Mosby; 1993. p. 399-439. 39. American Diabetes Association. Peripheral arterial disease in people with diabetes. Diabetes Care 2003;26:3333-41. 40. Armstrong DG, Frykberg RG. Classifying diabetic foot surgery: toward a rational definition. Diabet Med 2003;20:329-31. 41. Armstrong DG, Lavery LA, Frykberg RG, Wu SC, Boulton AJ. Validation of a diabetic foot surgery classification. Int Wound J 2006;3:240-6. 42. Zgonis T, Roukis TS, Frykberg RG, Landsman AS. Unstable acute and chronic Charcot’s deformity: staged skeletal and soft-tissue reconstruction. J Wound Care 2006;15:276-80. 43. Zgonis T, Roukis TS, Lamm BM. Charcot foot and ankle reconstruction: current thinking and surgical approaches. Clin Podiatr Med Surg 2007;24:505-17, ix. 44. Kim JY, Kim TW, Park YE, Lee YJ. Modified resection arthroplasty for infected non-healing ulcers with toe deformity in diabetic patients. Foot Ankle Int 2008;29:493-7. 45. Laborde JM. Neuropathic toe ulcers treated with toe flexor tenotomies. Foot Ankle Int 2007;28:1160-4. 46. Tamir E, McLaren AM, Gadgil A, Daniels TR. Outpatient percutaneous flexor tenotomies for management of diabetic claw toe deformities with ulcers: a preliminary report. Can J Surg 2008;51:41-4. 47. Roukis TS, Schade VL. Percutaneous flexor tenotomy for treatment of neuropathic toe ulceration secondary to toe contracture in persons with diabetes: a systematic review. J Foot Ankle Surg 2009;48:684-9. 48. Hamilton GA, Ford LA, Perez H, Rush SM. Salvage of the neuropathic foot by using bone resection and tendon balancing: a retrospective review of 10 patients. J Foot Ankle Surg 2005;44:37-43. 49. Sayner LR, Rosenblum BI, Giurini JM. Elective surgery of the diabetic foot. Clin Podiatr Med Surg 2003;20:783-92. 50. Tillo TH, Giurini JM, Habershaw GM, Chrzan JS, Rowbotham JL. Review of metatarsal osteotomies for the treatment of neuropathic ulcerations. J Am Podiatr Med Assoc 1990;80:211-7. 51. Armstrong DG, Rosales MA, Gashi A. Efficacy of fifth metatarsal head resection for treatment of chronic diabetic foot ulceration. J Am Podiatr Med Assoc 2005;95:353-6. 52. Giurini JM, Habershaw GM, Chrzan JS. Panmetatarsal head resection in chronic neuropathic ulceration. J Foot Surg 1987;26:249-52. 53. Wu SC, Crews RT, Armstrong DG. The pivotal role of offloading in the management of neuropathic foot ulceration. Curr Diab Rep 2005;5: 423-9. 54. Armstrong DG, Lavery LA, Vazquez JR, Short B, Kimbriel HR, Nixon BP, et al. Clinical efficacy of the first metatarsophalangeal joint arthroplasty as a curative procedure for hallux interphalangeal joint wounds in persons with diabetes. Diabetes Care 2003;26:3284-7. 55. Barry DC, Sabacinski KA, Habershaw GM, Giurini JM, Chrzan JS. Tendo Achillis procedures for chronic ulcerations in diabetic patients
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with transmetatarsal amputations. J Am Podiatr Med Assoc 1993;83:96-100. Holstein P, Lohmann M, Bitsch M, Jorgensen B. Achilles tendon lengthening, the panacea for plantar forefoot ulceration? Diabetes Metab Res Rev 2004;20(Suppl 1):S37-40. La Fontaine J, Brown D, Adams M, VanPelt M. New and recurrent ulcerations after percutaneous Achilles tendon lengthening in transmetatarsal amputation. J Foot Ankle Surg 2008;47:225-9. Nishimoto GS, Attinger CE, Cooper PS. Lengthening the Achilles tendon for the treatment of diabetic plantar forefoot ulceration. Surg Clin North Am 2003;83:707-26. Lin SS, Lee TH, Wapner KL. Plantar forefoot ulceration with equinus deformity of the ankle in diabetic patients: the effect of tendo-Achilles lengthening and total contact casting. Orthopaedics 1996;19:465-75. Greenhagen RM, Johnson AR, Peterson MC, Rogers LC, Bevilacqua NJ. Gastrocnemius recession as an alternative to tendoAchillis lengthening for relief of forefoot pressure in a patient with peripheral neuropathy: a case report and description of a technical modification. J Foot Ankle Surgery 2010;49:159.e9-13. Laborde JM. Midfoot ulcers treated with gastrocnemius-soleus recession. Foot Ankle Int 2009;30:842-6. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. Clin Podiatr Med Surg 2008;25:17-28, v. Cofield RH, Morrison MJ, Beabout JW. Diabetic neuroarthropathy in the foot: patient characteristics and patterns of radiographic change. Foot Ankle 1983;4:15-22. Frykberg RG, Eneroth M. Principles of conservative management. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing Company; 2010. p. 93-116. Charcot J-M, Fere C. Affections osseuses et articulaires du pied chez les tabétiques (Pied tabétique). Arch Neurol 1883;6:305-19. Sanders LJ. The Charcot foot and ankle: historical perspective. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing; 2010. p. 1-12. Sohn MW, Stuck RM, Pinzur M, Lee TA, Budiman-Mak E. Lowerextremity amputation risk after Charcot arthropathy and diabetic foot ulcer. Diabetes Care 2010;33:98-100. Sohn MW, Lee TA, Stuck RM, Frykberg RG, Budiman-Mak E. Mortality risk of Charcot arthropathy compared with that of diabetic foot ulcer and diabetes alone. Diabetes Care 2009;32:816-21. Gazis A, Pound N, Macfarlane R, Treece K, Game F, Jeffcoate W. Mortality in patients with diabetic neuropathic osteoarthropathy (Charcot foot). Diabet Med 2004;21:1243-6. Bevilacqua NJ, Bowling FL, Armstrong DG. The natural history of Charcot neuroarthropathy. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing Co; 2010. p. 13-27. Cavanagh PR, Botek G, Owings T. Biomechanical factors in Charcot’s neuroarthropathy. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing; 2010. p. 131-41. 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 2005:185-90. Frykberg RG, Rogers LC. The diabetic Charcot foot: a primer on medical and surgical management. J Diabet Foot Complications 2009; 1:19-25. Steindler A. The tabetic arthropathies. JAMA 1931;96:250-6. Harris JR, Brand PW. Patterns of disintegration of the tarsus in the anaesthetic foot. J Bone Joint Surg Br 1966;48:4-16. Johnson JT. Neuropathic fractures and joint injuries. Pathogenesis and rationale of prevention and treatment. J Bone Joint Surg Am 1967;49: 1-30. Bevilacqua NJ, Rogers LC. Surgical management of Charcot midfoot deformities. Clin Podiatr Med Surg 2008;25:81-94. Pinzur MS. Neutral ring fixation for high-risk nonplantigrade Charcot midfoot deformity. Foot Ankle Int 2007;28:961-6.
Surgical off-loading of the diabetic foot Robert G. Frykberg, DPM, MPH,a Nicholas J. Bevilacqua, DPM,b and Geoffrey Habershaw, DPM,c Phoenix, Ariz; Los Angeles, Calif; and Boston, Mass Surgical intervention for chronic deformities and ulcerations has become an important component in the management of patients with diabetes mellitus. These patients are no longer relegated to wearing cumbersome braces or footwear for deformities that might otherwise be easily corrected. Although surgical intervention in these often high-risk individuals is not without risk, the outcomes are fairly predictable when patients are properly selected and evaluated. In this brief review, we discuss the rationale and indications for diabetic foot surgery, focusing on the surgical decompression of deformities that frequently lead to foot ulcers. ( J Vasc Surg 2010;52:44S-58S.)
Foot deformities, including contracture of the gastrocnemius-soleus complex, are clinically significant risk factors that commonly lead to diabetic foot ulceration.1-3 In fact, deformity in association with peripheral neuropathy and trauma were the three most common component causes in the pathway leading to foot ulceration.3 Structural alterations in the architecture of the foot often lead to abnormally high plantar foot pressures, as well as increased dorsal, medial, or lateral pressures when snugly fitting footwear is worn.4,5 These high pedal pressures consequently place the foot at risk for ulceration.6-8 Although deformities such as hammer toes and bunions are quite common in the nondiabetic population, they also frequently develop in persons with diabetes but without significant consequence. It is the presence of peripheral neuropathy, however, that confers the attendant risk for ulceration in diabetic individuals. A recent study of patients undergoing foot and ankle surgery has shown that diabetes without complications imparts no greater risk for postoperative infection than that for persons without diabetes. However, when diabetic patients with complications (including neuropathy) were compared with those without diabetes, there was a tenfold risk for developing postoperative infection.9 Although this study’s focus was on postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant predictor of foot ulceration.3,7,10-12 From the Carl T. Hayden VA Medical Center, Phoenix;a Valley Presbyterian Hospital, Los Angeles;b and Boston University Medical Center, Boston.c Competition of interest: none. This article is being co-published in the Journal of Vascular Surgery® and the Journal of the American Podiatric Medical Association. Correspondence: Robert G. Frykberg, DPM, Carl T. Hayden VA Medical Center, 650 E Indian School Rd, Phoenix, AZ 85012-1892 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery and the American Podiatric Medical Association. doi:10.1016/j.jvs.2010.06.008
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Neuropathy not only predisposes to foot ulcer in the presence of deformity and trauma but can also lead to the development of deformity in the diabetic foot.4,8,13 The Charcot foot is the most classic example of a deformity primarily related to peripheral neuropathy of any cause.14,15 Neuropathy affects the sensory nerves of the lower extremities and the motor as well as autonomic fibers.16-19 Consequently, motor neuropathy leads to muscle dysfunction, dynamic contractures, and even paresis (ie, foot drop). Ankle equinus, caused by a contracture of the gastrocnemius-soleus muscle complex and Achilles’ tendon, is often found in patients with diabetes and has been associated with high forefoot plantar pressures.20-22 The clinical effects of motor neuropathy are also seen in the form of intrinsic muscle atrophy.23 The “intrinsic minus” foot is typified by such atrophy on the dorsal forefoot in concert with the development of hammer toes or claw toes (Fig 1).8,24 In severe cases, the intrinsic minus foot will develop a cavus appearance and associated high plantar pressures under the prominent metatarsal heads. Shoes are an important cause of trauma to the neuropathic foot, especially in individuals with structural deformity. Therefore, the provision of properly fitted therapeutic footwear is considered a key component of an ulcer and amputation prevention program.13,25-27 Unfortunately, over-the-counter shoes often cannot accommodate severe foot deformities, including high plantar pressures. In some situations, custom footwear is indicated to protect severely misshapen feet. Nonetheless, any footwear is only as good as the patients’ adherence to wearing the shoes as prescribed. To this end, even in the ulcerated foot where strict adherence to off-loading modalities are critical, one study showed that patients had poor compliance and wore the prescribed off-loading devices only 28% of the time.28 Nonetheless, several studies have shown that patients fitted with therapeutic footwear suffer significantly fewer primary or recurrent ulcerations compared with diabetic patients who were not given such footwear.29-32 Surgical intervention should be considered when recurrent ulceration or preulcerative lesions develop despite
Foot deformities, including contracture of the gastrocnemius-soleus complex, are clinically significant risk factors that commonly lead to diabetic foot ulceration.1-3 In fact, deformity in association with peripheral neuropathy and trauma were the three most common component causes in the pathway leading to foot ulceration.3 Structural alterations in the architecture of the foot often lead to abnormally high plantar foot pressures, as well as increased dorsal, medial, or lateral pressures when snugly fitting footwear is worn.4,5 These high pedal pressures consequently place the foot at risk for ulceration.6-8 Although deformities such as hammer toes and bunions are quite common in the nondiabetic population, they also frequently develop in persons with diabetes but without significant consequence. It is the presence of peripheral neuropathy, however, that confers the attendant risk for ulceration in diabetic individuals. A recent study of patients undergoing foot and ankle surgery has shown that diabetes without complications imparts no greater risk for postoperative infection than that for persons without diabetes. However, when diabetic patients with complications (including neuropathy) were compared with those without diabetes, there was a tenfold risk for developing postoperative infection.9 Although this study’s focus was on postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant predictor of foot ulceration.3,7,10-12 From the Carl T. Hayden VA Medical Center, Phoenix;a Valley Presbyterian Hospital, Los Angeles;b and Boston University Medical Center, Boston.c Competition of interest: none. This article is being co-published in the Journal of Vascular Surgery® and the Journal of the American Podiatric Medical Association. Correspondence: Robert G. Frykberg, DPM, Carl T. Hayden VA Medical Center, 650 E Indian School Rd, Phoenix, AZ 85012-1892 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery and the American Podiatric Medical Association. doi:10.1016/j.jvs.2010.06.008
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Neuropathy not only predisposes to foot ulcer in the presence of deformity and trauma but can also lead to the development of deformity in the diabetic foot.4,8,13 The Charcot foot is the most classic example of a deformity primarily related to peripheral neuropathy of any cause.14,15 Neuropathy affects the sensory nerves of the lower extremities and the motor as well as autonomic fibers.16-19 Consequently, motor neuropathy leads to muscle dysfunction, dynamic contractures, and even paresis (ie, foot drop). Ankle equinus, caused by a contracture of the gastrocnemius-soleus muscle complex and Achilles’ tendon, is often found in patients with diabetes and has been associated with high forefoot plantar pressures.20-22 The clinical effects of motor neuropathy are also seen in the form of intrinsic muscle atrophy.23 The “intrinsic minus” foot is typified by such atrophy on the dorsal forefoot in concert with the development of hammer toes or claw toes (Fig 1).8,24 In severe cases, the intrinsic minus foot will develop a cavus appearance and associated high plantar pressures under the prominent metatarsal heads. Shoes are an important cause of trauma to the neuropathic foot, especially in individuals with structural deformity. Therefore, the provision of properly fitted therapeutic footwear is considered a key component of an ulcer and amputation prevention program.13,25-27 Unfortunately, over-the-counter shoes often cannot accommodate severe foot deformities, including high plantar pressures. In some situations, custom footwear is indicated to protect severely misshapen feet. Nonetheless, any footwear is only as good as the patients’ adherence to wearing the shoes as prescribed. To this end, even in the ulcerated foot where strict adherence to off-loading modalities are critical, one study showed that patients had poor compliance and wore the prescribed off-loading devices only 28% of the time.28 Nonetheless, several studies have shown that patients fitted with therapeutic footwear suffer significantly fewer primary or recurrent ulcerations compared with diabetic patients who were not given such footwear.29-32 Surgical intervention should be considered when recurrent ulceration or preulcerative lesions develop despite
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Fig 1. Intrinsic minus foot. Note the high arched, thin foot with little muscle mass in this patient with advanced peripheral neuropathy. Flexible hammer toes (claw toes) usually accompany this deformity as well.
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Fig 2. Acquired second hammer toe after great toe amputation with dorsal ulcer. This is easily treated by a digital arthroplasty or joint resection with excision of the ulceration. A metatarsophalangeal joint release is also usually required for rigid deformities.
Table. Classification of diabetic foot surgery40 ● Class I: Elective. Reconstructive procedures on patients who do not have loss of protective sensation (LOPS) ● Class II: Prophylactic. Reconstructive procedures performed to reduce the risk of ulceration or reulceration in patients who have LOPS and do not have a wound present ● Class III: Curative. Procedures performed to assist in healing of open wounds ● Class IV: Emergent. Procedures performed to arrest or limit progression of infection
concerted efforts to prevent such lesions. Once considered ill-advised, corrective or reconstructive foot surgery has assumed an important role in the management of patients with chronic or recurrent foot ulcerations.13,33-38 Of course, such patients need to be carefully selected and evaluated to ensure that adequate vascularity is present and that major comorbidities, including renal insufficiency, unstable cardiovascular disease, and congestive heart failure, are adequately controlled. Because peripheral arterial disease (PAD) is often asymptomatic in persons with diabetes, we follow the American Diabetes Association recommendation that an ankle-brachial index (ABI) be measured in such persons who are aged ⬎50 years.2,39 Furthermore, we routinely recommend obtaining a preoperative ABI (with toe pressures and waveforms) in diabetic patients with foot ulcers in the absence of clearly bounding pulses. In 2003, Armstrong and Frykberg38,40 revised a risk-based scheme for classifying the types of foot surgery performed in diabetic patients largely depending on the presence of open wounds and their acuity. Fundamentally, the classes of foot surgery are distinguished by their progressive risks for subsequent proximal levels of amputation (Table):
●
●
●
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Elective surgery (class I) represents reconstructive procedures performed to correct deformities or high plantar pressures in persons without neuropathy. Prophylactic (class II) procedures are those performed in patients with neuropathy (loss of protective sensation) to reduce the risk of ulceration or recurrent ulceration when no open wounds are present. Curative surgery (class III) is often performed when open wounds are present to effect a cure by removing underlying bony prominences (surgical decompression), osteomyelitis, or by draining underlying abscesses. Obviously, such procedures are at higher risk for nonhealing or infection than are the first two classes. Emergent procedures (class IV) are performed for severe infections (wet gangrene, necrotizing fasciitis, etc) to control the progression of infection. As the name implies, these procedures are performed emergently and often consist of open amputations at the foot level combined with fasciotomies of the leg.
Armstrong et al41 later validated this classification scheme in subsequent risk for proximal amputation and infection. They found a significant trend toward increasing risk of ulceration/reulceration, postoperative infection, alllevel amputation, and major amputation with increasing class of foot surgery (P ⬍ .01 for all complications). As would be expected, the greatest frequency of major amputation was in class IV procedures. Specific types of operations or procedures are not restricted to single classes of surgery as described above. To the contrary, many procedures are used in operations performed across multiple foot surgery categories. For example, a hammer toe repair might be performed as an elective, prophylactic, or a curative procedure depending on the presence of neuropathy and the presence or absence of an open wound (Fig 2) A tendo-Achilles’
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Fig 3. Reconstruction for correction of unstable Charcot ankle. A, Preoperative clinical view demonstrates ankle deformity. B, A preoperative radiograph shows osteolysis of the talar dome. C, Circular external fixator in place after talectomy and fusion. D, Postoperative radiograph.
lengthening (TAL) would be indicated under the same situations. A first ray amputation might be performed to cure chronic osteomyelitis even in the absence of an open wound (prophylactic), in the presence of a chronic draining ulcer (curative), or as an emergent procedure to control the spread of an acute necrotizing infection. A midfoot osteotomy or arthrodesis of an ulcerated Charcot deformity is commonly performed as a curative operation (class III), but is just as frequently performed to reconstruct a deformed nonulcerated foot and thereby offer surgical decompression to reduce plantar pressures (class II; Fig 3).15,42,43 This review will focus on those procedures commonly used by foot and ankle surgeons to address deformities that are causing abnormal pressure gradients. As already noted, many of these procedures can be used in elective, prophylactic, or curative situations depending on the presence (or absence) of neuropathy or ulceration. Although we will not discuss amputations or specific management of infection, a brief discussion of those procedures used to correct the Charcot foot will be presented.
DIGITAL DEFORMITIES Common digital deformities, such as hammer toe, claw toe, and mallet toe, are known to increase pressures and are associated with neuropathic ulceration. Correcting the structural deformity with a resection arthroplasty may augment healing and reduce the risk of ulcer recurrence.44 Alternatively, a percutaneous flexor tenotomy offers a less invasive approach and may afford the necessary intrinsic pressure modulation to augment healing. Distal tip ulcers, in a flexible hammer toe, may be managed with a flexor digitorum longus tenotomy. A blade or 18-gauge needle is introduced 1 cm proximal to the proximal plantar flexural crease of the toe (Fig 4). The ankle is held in a dorsiflexed position with the patient actively holding all toes in a flexed position. The toe is manually straightened, and the blade is moved across the taught tendon, making ease of the tenotomy. The long extensor tendon will now hold the toe straight. A postoperative shoe can be used for limited ambulation. Overex-
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Fig 4. Flexor tenotomy. A, The toe is flexible and ulcer is at the tip. B, Lidocaine is injected at the site of entry, and the patient is asked to dorsiflex the ankle and actively flex all the toes. This makes the long flexor tendon very taught, and can easily be tenotomized as shown here with a #61 Beaver blade. No suture is needed. C, Shows all three middle toes that have had flexor tenotomies. The fourth toe had resection of osteomyelitis, 4 weeks postoperatively, done in the office setting.
tension of the toe can be managed with an extensor longus tenotomy at a later date. Laborde45 retrospectively reviewed 18 patients presenting with plantar toe ulcers treated with a flexor tenotomy. All patients had a flexible claw toe deformity with ulcers on the distal plantar aspect of the hallux or lesser toes. The incision and the ulcer healed in all patients. Two patients underwent a repeat procedure for ulcer recurrence and remained ulcer free at 17 and 34 months. Tamir et al46 retrospectively reviewed the outcomes of 14 patients (24 toes) treated with percutaneous flexor tenotomies for a claw toe deformity to off-load the tip of the toe for ulcer healing. The authors performed an osteoclasis in select patients to correct rigid contractures at the proximal interphalangeal joint. All patients healed with no significant complications noted. Although the methodologic quality of both studies was poor, their results support the ability of a percutaneous
flexor tenotomy of the hallux and lesser toes to heal neuropathic toe ulceration secondary to toe contracture in persons with diabetes.47 A rigid hammer toe is best treated with an arthroplasty at the level of the distal or proximal interphalangeal joint. However, a percutaneous flexor tenotomy may be attempted in the nonflexible deformity before resorting to an open arthroplasty. On those occasions where a hallux ulcer is not due to a limitation of motion at the metatarsophalangeal joint (MTPJ), this same procedure can be used on this digit (Fig 5). LESSER METATARSALS Neuropathic ulcerations under the metatarsal heads are a challenging problem and may lead to infection and amputation.48 Various metatarsal procedures have been de-
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Fig 5. Arthroplasty of the hallux for surgical off-loading of a chronic hallux ulceration. A, The ulcer is adjacent to the head of the proximal phalanx. B, Incision placement. C, The head of the phalanx is removed, and the long extensor tendon is repaired. D, The wound closed primarily. Early ambulation is possible with a postoperative shoe.
scribed, including metatarsal head osteotomies and resections.38,49,50 An isolated metatarsal osteotomy should be considered for a chronic, nonundermining, nontunneling, ulcer below a specific metatarsal head. It can be performed through a dorsal incision with a doubleaction bone cutter or an oscillating saw. The osteotomy can be done at the surgical or anatomic neck of the metatarsal (Fig 6). A collar of bone may be removed if shortening of the metatarsal is desired. Such procedures are generally performed when the plantar ulceration does not penetrate to bone. A tunneling ulcer should be appropriately débrided to remove all undermining. A metatarsal head resection may be performed to assist in healing by internally off-loading the ulcer (Fig 7). Armstrong et al51 evaluated the outcomes of an isolated fifth metatarsal head resection for ulcerations beneath the fifth metatarsal head and compared it with nonsurgical care. They reported more rapid healing and a lower recurrence rate in the surgical group. The surgeon must be cognizant of maintaining a nearly normal metatarsal parabola. The second, third, and fourth metatarsals function as a single unit and any disruption in metatarsal length or height may result in a transfer callus or ulceration. If an ulcer occurs, further metatarsal osteotomy may be necessary. Osteotomies should be performed on the remaining two metatarsals, and if not, additional ulceration is likely to develop over the remaining metatarsal, necessitating a third procedure. This scenario is especially likely to
occur after one of the metatarsal heads has been removed due to infection. Multiple metatarsal head resections or a panmetatarsal head resection may be considered for nonhealing ulcers in the presence of an abnormal metatarsal parabola (Fig 8).52 Hamilton et al48 proposed combining lesser metatarsal head resections with gastrocnemius recession and a peroneus longus-to-brevis tendon transfer in patients with chronic, neuropathic forefoot ulcerations. All ulcers were located beneath lesser metatarsal heads, allowing the authors to preserve the first MTPJ. They adjunctively managed the equinus deformity with a gastrocnemius recession and alleviated pressure beneath the first metatarsal with the peroneus longus-to-brevis transfer. The authors reported ulcer healing in 10 patients (100%), with no ulcer recurrence at a mean 14.2 months of follow-up.48 KELLER ARTHROPLASTY Limited range of motion at the MTPJ is a common forefoot deformity that contributes to ulcer formation beneath the hallux. This limitation in joint range of motion leads to increased pressure on the hallux during ambulation. Pressure reduction is essential and usually consists of an external device to off-load the area.53 This does not correct the underlying deformity, however. The associated biomechanical abnormality still exists after the off-loading device is removed, and ulcer recurrence may occur. Identifying and correcting the underlying struc-
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Fig 6. Metatarsal osteotomy, now performed in the office setting when possible, can be done with simple instruments: bone cutter, hemostat, and freer elevator as a probe. A, Through a dorsal incision, the metatarsal neck is grasped with a large hemostat. B, A double-action bone cutter is introduced adjacent to the hemostat. C, The bone is osteotomized at the metatarsal neck level. D, Multiple osteotomies shown here are all in the proper location, between the anatomic and surgical neck of each metatarsal.
tural deformity may assist in healing and also reduce ulcer recurrence. Armstrong et al54 compared the safety and efficacy of a first MTPJ arthroplasty (Keller-type procedure) with nonsurgical management for wounds at the plantar aspect of the hallux interphalangeal joint (Fig 9). They included 41 patients, with 21 undergoing a first MTPJ arthroplasty to augment ulcer healing. Patients in the surgery group healed significantly faster than patients in the nonsurgery group. Care after healing was identical in both groups, and the surgery group had fewer ulcer recurrences during the 6-month follow-up. There was a very high prevalence of postoperative infections in the surgery group (40%), but this was compared with the 38% of patients in the control group who required treatment for infection during the period of therapy. The results of this study suggest that a first MTPJ arthroplasty is a safe and effective procedure in the treatment of noninfected, nonischemic wounds beneath the hallux.54
FIRST MTPJ RESECTION The excision of the first MTPJ should be considered if the metatarsal head has osteomyelitis, after failed sesamoidectomy, or for a chronic ulcer probing to the joint but with a viable hallux.38 The incision may incorporate and excise the ulcer or be placed dorsally to avoid the ulcer altogether. The incision is made directly to bone, with no undermining of the soft tissue. The dissection is at the level of the ligaments and periosteum. The metatarsal is cut and beveled plantarly to reduce any bone prominences. The base of the phalanx is removed as in a Keller bunionectomy. Both sesamoids should be removed because a fibrous union to the metatarsal stump may occur if they are left and become a future source of ulceration (Fig 10). This is also necessary in cases of open joint involvement or infection, wherein the infected or contaminated sesamoids will become a source for continued infection.
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Fig 7. A, Undermining ulceration that probes into deep tissues (including bone or joint) is not appropriate for standard metatarsal osteotomy. B, The ulcer is excised and the adjacent metatarsal is removed. C, Primary closure with a proximal drain is acceptable as long as there is no active sepsis. The drain is pulled in 24 hours, and the patient is kept non-weight bearing for 4 weeks.
TAL LENGTHENING Limited ankle joint mobility, as seen clinically as a tight Achilles’-gastrocnemius-soleus complex, is a deforming force and a causative factor in plantar forefoot ulcerations.21 During normal gait, 10° of dorsiflexion at the ankle is required, and anything less will increase plantar pressures in the forefoot and impede healing of the wound. To alleviate the pressure, several authors have suggested percutaneous TAL.55-58 Armstrong et al21 confirmed that plantar pressures are reduced after percutaneous TAL. Lin
et al59 reported results of percutaneous TAL in 15 patients with plantar forefoot ulcers that did not heal despite 9 weeks of total contact casting. All but one ulcer healed (93%), with no ulcer recurrence noted after a mean 17.3month follow-up. Mueller et al22 conducted a randomized control trial comparing the combined treatment of total contact cast and percutaneous TAL against a total contact cast alone. Initial healing rates were similar in both groups, but the significant difference was noted when the ulcer recur-
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Fig 8. Pan metatarsal head resection. A, Failed metatarsal surgeries with transfer ulcer subsecond. B, Transmetatarsal amputation could be done, but the toes are viable. Surgical off-loading can be accomplished through a dorsal or plantar approach; here, a dorsal approach is planned. C, Excision of metatarsal head through a dorsal incision. D, Radiograph several months after procedure.
rence rate was compared. After 2 years, the ulcer recurrence rate was 81% in the group treated with a total contact cast alone compared with 38% in those treated with a total contact cast and TAL. A gastrocnemius recession may be used as an alternative for relief of forefoot pressure60 and has also been described as an effective treatment for midfoot ulcers (Fig 11).60,61 CHARCOT FOOT Charcot arthropathy, perhaps the most characteristic deformity attributed to the diabetic foot, occurs in only 1% of the diabetic population as a whole and in approximately 30% of individuals with peripheral neuropathy.62-64 Originally described by Charcot as the pied tabétiques in persons with tertiary syphilis,65 the Charcot foot is now most commonly encountered in persons with
diabetes.66 Several studies have indicated that diabetic patients with Charcot foot deformities have an increased risk for ulceration and subsequent amputation and higher mortality compared with diabetic persons without this complication.67-69 The classic “rocker-bottom” deformity (Fig 12) is the result of a collapse of the midfoot architecture generally due to injury and continued weight bearing on the insensate foot. With the continued stress of weight bearing, a vicious cycle ensues that exaggerates local inflammation and leads to more fractures, dislocations, and deformity.14,70 Abnormally concentrated pressures develop in the midfoot during ambulation on the deformed foot, and ulceration frequently ensues.71 When the ankle joint is the primary site of involvement (Sanders-Frykberg pattern V),14 instability and deformity become the most difficult problem to man-
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Fig 9. A, Keller arthroplasty used as a curative procedure for ulcer under a rigid hallux. B, A postoperative radiograph shows the resection of the base of the proximal phalanx to allow for unrestricted dorsiflexion. C, Healed ulceration noted 3 weeks after a Keller arthroplasty was performed.
age and all too frequently fails conservative therapy with bracing.15,64,72 Conservative care for Charcot arthropathy has been the traditional mainstay of treatment for this limb-threatening disorder,14,64,72,73 but surgical management for Charcot joints is not a recent evolution in our understanding of how this entity can be approached. Although his report dealt primarily with Charcot joints due to tabes dorsalis, Steindler74 presented a series of surgical cases including subtalar arthrodesis as early as 1931. Several other important surgical case series were published in the ensuing decades that illustrated the efficacy of a surgical approach to this arthropathy as well as its inherent difficulties and complications.75,76 Numerous descriptive studies have been published in the last 20 years detailing various surgical techniques for the management of the deformed Charcot foot.15,43,77-82 The
indications for surgery are generally to provide a more effective management strategy when conservative measures have failed. Specifically, surgery is recommended for those patients with recurrent ulceration (with or without infection), severe instability, or severe deformities not amenable to footwear therapy alone.83 Many surgical techniques have been described, including simple plantar exostectomy with or without TAL, midfoot realignment arthrodeses, hindfoot arthrodeses, and ankle arthrodeses (Fig 13). A combination of procedures is most often required because Charcot deformities are usually multilevel. Although arthrodesis using internal fixation is most often practiced, multiplanar external circular fixation using Ilizarov techniques (Fig 14) has been used with increasing frequency in recent years.43,82,84 Regardless of technique, the goals of surgery remain the same: establish a stable, plantigrade foot mitigating focal areas of increased pressure and shearing forces.
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Fig 10. First metatarsophalangeal joint resection. A, A chronic deep ulcer under the first metatarsal head. B, The joint is resected through a dorsal incision. The elevator illustrates that the plantar ulcer penetrated into the joint. C, A radiograph shows the resection of the metatarsal head, both sesamoids, and the base of proximal phalanx.
By reducing plantar prominences and their attendant high pressures, healing of open ulcers can be augmented and the risk of subsequent skin breakdown will be reduced.77 The reader is referred to the referenced citations for specific techniques of interest. CONCLUSION Surgical management of diabetic foot disorders is no longer considered an unwarranted practice. To the contrary, surgery on the ulcerated or deformed foot has assumed an increasingly important role in the management of such disorders both in the United States and
abroad. Nonetheless, these patients are indeed at a higher risk for complications than their nondiabetic counterparts, especially in those with peripheral neuropathy or ischemia. Careful patient selection and thorough evaluation of the foot as well as attendant comorbidities are the cornerstones of achieving successful results in otherwise very complicated patients. Early and ostensibly aggressive surgical intervention on the deformed foot can obviate many months of unsuccessful conservative care, especially when ulcer recidivism becomes the primary challenge. Although virtually all the procedures used in this setting are not exclusive to diabetic foot
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Fig 12. A rocker-bottom Charcot foot is shown with soft tissue visualization of large plantar midfoot ulcer under the apex of the deformity.
Fig 11. A, A gastrocnemius recession performed to augment healing of a plantar forefoot ulceration. B, An image taken 2 years postoperatively demonstrates long-term ulcer healing.
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Fig 13. A, This chronic midfoot ulcer was treated with a simple exostectomy with tendo-Achilles’ lengthening. B, Postoperative image shows a plantar incision that was closed primarily and reinforced with tape strips (tendoAchilles’ lengthening incision not shown).
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Fig 14. A, A midfoot Charcot reconstruction using an Ilizarov circular frame. B, A lateral radiograph shows the orientation of the foot and ankle in the frame. In this case, internal fixation was also used.
surgery, great care (with close follow-up) is necessary in the postoperative period to ensure optimal outcomes in these high-risk patients. REFERENCES 1. Boulton AJ, Kirsner RS, Vileikyte L. Clinical practice. Neuropathic diabetic foot ulcers. N Engl J Med 2004;351:48-55. 2. Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive foot examination and risk assessment: a report of the task force of the foot care interest group of the American Diabetes Association, with endorsement by the American Association of Clinical Endocrinologists. Diabetes Care 2008;31:1679-85. 3. Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care 1999;22:157-62. 4. Frykberg RG. Biomechanical considerations of the diabetic foot. Lower Extremity 1995;2:207-14. 5. Cavanagh PR. Therapeutic footwear for people with diabetes. Diabetes Metab Res Rev 2004;20(Suppl 1):S51-5. 6. Veves A, Murray HJ, Young MJ, Boulton AJ. The risk of foot ulceration in diabetic patients with high foot pressure: a prospective study. Diabetologia 1992;35:660-3.
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7. Frykberg RG, Lavery LA, Pham H, Harvey C, Harkless L, Veves A. Role of neuropathy and high foot pressures in diabetic foot ulceration. Diabetes Care 1998;21:1714-9. 8. van Schie CH. A review of the biomechanics of the diabetic foot. Int J Low Extrem Wounds 2005;4:160-70. 9. Wukich DK, Lowery NJ, McMillen RL, Frykberg RG. Postoperative infection rates in foot and ankle surgery: a comparison of patients with and without diabetes mellitus. J Bone Joint Surg Am 2010;92:287-95. 10. Fernando DJ, Masson EA, Veves A, Boulton AJ. Relationship of limited joint mobility to abnormal foot pressures and diabetic foot ulceration. Diabetes Care 1991;14:8-11. 11. Abbott CA, Carrington AL, Ashe H, Bath S, Every LC, Griffiths J, et al. The North-West Diabetes Foot Care Study: incidence of, and risk factors for, new diabetic foot ulceration in a community-based patient cohort. Diabet Med 2002;19:377-84. 12. Boyko EJ, Ahroni JH, Stensel V, Forsberg RC, Davignon DR, Smith DG. A prospective study of risk factors for diabetic foot ulcer. The Seattle Diabetic Foot Study. Diabetes Care 1999;22:1036-42. 13. Frykberg RG, Zgonis T, Armstrong DG, Driver VR, Giurini JM, Kravitz SR, et al. Diabetic foot disorders. A clinical practice guideline (2006 revision). J Foot Ankle Surg 2006;45(5 suppl):S1-66. 14. Sanders LJ, Frykberg RG. Diabetic neuropathic osteoarthropathy: The Charcot foot. In: Frykberg RG, editor. The high risk foot in diabetes mellitus. New York: Churchill Livingstone; 1991. p. 325-35. 15. Wukich DK, Sung W. Charcot arthropathy of the foot and ankle: modern concepts and management review. J Diabetes Complications 2009;23:409-26. 16. Boulton AJ. Diabetic neuropathy: classification, measurement and treatment. Curr Opin Endocrinol Diabetes Obes 2007;14:141-5. 17. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomic neuropathy. Diabetes Care 2003;26:1553-79. 18. Boulton AJ, Vinik AI, Arezzo JC, Bril V, Feldman EL, Freeman R, et al. Diabetic neuropathies: a statement by the American Diabetes Association. Diabetes Care 2005;28:956-62. 19. Andersen H, Gjerstad MD, Jakobsen J. Atrophy of foot muscles: a measure of diabetic neuropathy. Diabetes Care 2004;27:2382-5. 20. Lavery LA, Armstrong DG, Boulton AJ. Ankle equinus deformity and its relationship to high plantar pressure in a large population with diabetes mellitus. J Am Podiatr Med Assoc 2002;92:479-82. 21. Armstrong DG, Stacpoole-Shea S, Nguyen H, Harkless LB. Lengthening of the Achilles tendon in diabetic patients who are at high risk for ulceration of the foot. J Bone Joint Surg Am 1999;81:535-8. 22. Mueller MJ, Sinacore DR, Hastings MK, Strube MJ, Johnson JE. Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg Am 2003;85:1436-45. 23. van Schie CH, Vermigli C, Carrington AL, Boulton A. Muscle weakness and foot deformities in diabetes: relationship to neuropathy and foot ulceration in Caucasian diabetic men. Diabetes Care 2004;27:1668-73. 24. Habershaw GM, Chrzan J. Biomechanical considerations of the diabetic foot. In: Kozak GP, Campbell DR, Frykberg RG, Habershaw GM, ed. Management of diabetic foot problems, 2nd ed. Philadelphia: WB Saunders; 1995. p. 53-65. 25. International Working Group on the Diabetic Foot. International Consensus on the Diabetic Foot. Paper presented at: International Working Group on the Diabetic Foot 2003; Noordwijkerhout, Netherlands. 26. Consensus Development Conference on Diabetic Foot Wound Care: 7-8 April 1999, Boston, Massachusetts. American Diabetes Association. Diabetes Care 1999;22:1354-60. 27. American Diabetes Association. Preventive foot care in diabetes. Diabetes Care 2004;27(Suppl 1):S63-4. 28. Armstrong DG, Lavery LA, Kimbriel HR, Nixon BP, Boulton AJ. Activity patterns of patients with diabetic foot ulceration: patients with active ulceration may not adhere to a standard pressure off-loading regimen. Diabetes Care 2003;26:2595-7. 29. Uccioli L, Faglia E, Monticone G, Favales F, Durola L, Aldeghi A, et al. Manufactured shoes in the prevention of diabetic foot ulcers. Diabetes Care 1995;18:1376-8.
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30. Chantelau E, Kushner T, Spraul M. How effective is cushioned therapeutic footwear in protecting diabetic feet? A clinical study. Diabet Med 1990;7:335-9. 31. Chantelau E. Therapeutic footwear in patients with diabetes. JAMA 2002;288:1231-2. 32. Edmonds ME, Blundell MP, Morns ME, Thomas EM, Cotton LT, Watkins PJ. Improved survival of the diabetic foot: the role of a specialized foot clinic. Q J Med 1986;60:763-71. 33. Piaggesi A, Schipani E, Campi F, Romanelli M, Baccetti F, Arvia C, et al. Conservative surgical approach versus non-surgical management for diabetic neuropathic foot ulcers: a randomized trial. Diabet Med 1998; 15:412-7. 34. Armstrong DG, Lavery LA, Stern S, Harkless LB. Is prophylactic diabetic foot surgery dangerous? J Foot Ankle Surg 1996;35:585-9. 35. Catanzariti AR, Blitch EL, Karlock LG. Elective foot and ankle surgery in the diabetic patient. J Foot Ankle Surg 1995;35:23-41. 36. Nicklas BJ. Prophylactic surgery in the diabetic foot. In: Frykberg RG, editor. The high risk foot in diabetes mellitus. New York City: Churchill Livingstone; 1991. p. 537-8. 37. Frykberg RG. Diabetic foot ulcers: pathogenesis and management. Am Fam Physician 2002;66:1655-62. 38. Frykberg R, Giurini J, Habershaw G, Rosenblum B, Chrzan J. Prophylactic surgery in the diabetic foot. In: Kominsky SJ, editor. Medical and surgical management of the diabetic foot. Saint Louis: Mosby; 1993. p. 399-439. 39. American Diabetes Association. Peripheral arterial disease in people with diabetes. Diabetes Care 2003;26:3333-41. 40. Armstrong DG, Frykberg RG. Classifying diabetic foot surgery: toward a rational definition. Diabet Med 2003;20:329-31. 41. Armstrong DG, Lavery LA, Frykberg RG, Wu SC, Boulton AJ. Validation of a diabetic foot surgery classification. Int Wound J 2006;3:240-6. 42. Zgonis T, Roukis TS, Frykberg RG, Landsman AS. Unstable acute and chronic Charcot’s deformity: staged skeletal and soft-tissue reconstruction. J Wound Care 2006;15:276-80. 43. Zgonis T, Roukis TS, Lamm BM. Charcot foot and ankle reconstruction: current thinking and surgical approaches. Clin Podiatr Med Surg 2007;24:505-17, ix. 44. Kim JY, Kim TW, Park YE, Lee YJ. Modified resection arthroplasty for infected non-healing ulcers with toe deformity in diabetic patients. Foot Ankle Int 2008;29:493-7. 45. Laborde JM. Neuropathic toe ulcers treated with toe flexor tenotomies. Foot Ankle Int 2007;28:1160-4. 46. Tamir E, McLaren AM, Gadgil A, Daniels TR. Outpatient percutaneous flexor tenotomies for management of diabetic claw toe deformities with ulcers: a preliminary report. Can J Surg 2008;51:41-4. 47. Roukis TS, Schade VL. Percutaneous flexor tenotomy for treatment of neuropathic toe ulceration secondary to toe contracture in persons with diabetes: a systematic review. J Foot Ankle Surg 2009;48:684-9. 48. Hamilton GA, Ford LA, Perez H, Rush SM. Salvage of the neuropathic foot by using bone resection and tendon balancing: a retrospective review of 10 patients. J Foot Ankle Surg 2005;44:37-43. 49. Sayner LR, Rosenblum BI, Giurini JM. Elective surgery of the diabetic foot. Clin Podiatr Med Surg 2003;20:783-92. 50. Tillo TH, Giurini JM, Habershaw GM, Chrzan JS, Rowbotham JL. Review of metatarsal osteotomies for the treatment of neuropathic ulcerations. J Am Podiatr Med Assoc 1990;80:211-7. 51. Armstrong DG, Rosales MA, Gashi A. Efficacy of fifth metatarsal head resection for treatment of chronic diabetic foot ulceration. J Am Podiatr Med Assoc 2005;95:353-6. 52. Giurini JM, Habershaw GM, Chrzan JS. Panmetatarsal head resection in chronic neuropathic ulceration. J Foot Surg 1987;26:249-52. 53. Wu SC, Crews RT, Armstrong DG. The pivotal role of offloading in the management of neuropathic foot ulceration. Curr Diab Rep 2005;5: 423-9. 54. Armstrong DG, Lavery LA, Vazquez JR, Short B, Kimbriel HR, Nixon BP, et al. Clinical efficacy of the first metatarsophalangeal joint arthroplasty as a curative procedure for hallux interphalangeal joint wounds in persons with diabetes. Diabetes Care 2003;26:3284-7. 55. Barry DC, Sabacinski KA, Habershaw GM, Giurini JM, Chrzan JS. Tendo Achillis procedures for chronic ulcerations in diabetic patients
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with transmetatarsal amputations. J Am Podiatr Med Assoc 1993;83:96-100. Holstein P, Lohmann M, Bitsch M, Jorgensen B. Achilles tendon lengthening, the panacea for plantar forefoot ulceration? Diabetes Metab Res Rev 2004;20(Suppl 1):S37-40. La Fontaine J, Brown D, Adams M, VanPelt M. New and recurrent ulcerations after percutaneous Achilles tendon lengthening in transmetatarsal amputation. J Foot Ankle Surg 2008;47:225-9. Nishimoto GS, Attinger CE, Cooper PS. Lengthening the Achilles tendon for the treatment of diabetic plantar forefoot ulceration. Surg Clin North Am 2003;83:707-26. Lin SS, Lee TH, Wapner KL. Plantar forefoot ulceration with equinus deformity of the ankle in diabetic patients: the effect of tendo-Achilles lengthening and total contact casting. Orthopaedics 1996;19:465-75. Greenhagen RM, Johnson AR, Peterson MC, Rogers LC, Bevilacqua NJ. Gastrocnemius recession as an alternative to tendoAchillis lengthening for relief of forefoot pressure in a patient with peripheral neuropathy: a case report and description of a technical modification. J Foot Ankle Surgery 2010;49:159.e9-13. Laborde JM. Midfoot ulcers treated with gastrocnemius-soleus recession. Foot Ankle Int 2009;30:842-6. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. Clin Podiatr Med Surg 2008;25:17-28, v. Cofield RH, Morrison MJ, Beabout JW. Diabetic neuroarthropathy in the foot: patient characteristics and patterns of radiographic change. Foot Ankle 1983;4:15-22. Frykberg RG, Eneroth M. Principles of conservative management. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing Company; 2010. p. 93-116. Charcot J-M, Fere C. Affections osseuses et articulaires du pied chez les tabétiques (Pied tabétique). Arch Neurol 1883;6:305-19. Sanders LJ. The Charcot foot and ankle: historical perspective. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing; 2010. p. 1-12. Sohn MW, Stuck RM, Pinzur M, Lee TA, Budiman-Mak E. Lowerextremity amputation risk after Charcot arthropathy and diabetic foot ulcer. Diabetes Care 2010;33:98-100. Sohn MW, Lee TA, Stuck RM, Frykberg RG, Budiman-Mak E. Mortality risk of Charcot arthropathy compared with that of diabetic foot ulcer and diabetes alone. Diabetes Care 2009;32:816-21. Gazis A, Pound N, Macfarlane R, Treece K, Game F, Jeffcoate W. Mortality in patients with diabetic neuropathic osteoarthropathy (Charcot foot). Diabet Med 2004;21:1243-6. Bevilacqua NJ, Bowling FL, Armstrong DG. The natural history of Charcot neuroarthropathy. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing Co; 2010. p. 13-27. Cavanagh PR, Botek G, Owings T. Biomechanical factors in Charcot’s neuroarthropathy. In: Frykberg RG, editor. The diabetic Charcot foot: principles and management. Brooklandville, MD: Data Trace Publishing; 2010. p. 131-41. 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 2005:185-90. Frykberg RG, Rogers LC. The diabetic Charcot foot: a primer on medical and surgical management. J Diabet Foot Complications 2009; 1:19-25. Steindler A. The tabetic arthropathies. JAMA 1931;96:250-6. Harris JR, Brand PW. Patterns of disintegration of the tarsus in the anaesthetic foot. J Bone Joint Surg Br 1966;48:4-16. Johnson JT. Neuropathic fractures and joint injuries. Pathogenesis and rationale of prevention and treatment. J Bone Joint Surg Am 1967;49: 1-30. Bevilacqua NJ, Rogers LC. Surgical management of Charcot midfoot deformities. Clin Podiatr Med Surg 2008;25:81-94. Pinzur MS. Neutral ring fixation for high-risk nonplantigrade Charcot midfoot deformity. Foot Ankle Int 2007;28:961-6.
Surgical off-loading of the diabetic foot Robert G. Frykberg, DPM, MPH,a Nicholas J. Bevilacqua, DPM,b and Geoffrey Habershaw, DPM,c Phoenix, Ariz; Los Angeles, Calif; and Boston, Mass Surgical intervention for chronic deformities and ulcerations has become an important component in the management of patients with diabetes mellitus. These patients are no longer relegated to wearing cumbersome braces or footwear for deformities that might otherwise be easily corrected. Although surgical intervention in these often high-risk individuals is not without risk, the outcomes are fairly predictable when patients are properly selected and evaluated. In this brief review, we discuss the rationale and indications for diabetic foot surgery, focusing on the surgical decompression of deformities that frequently lead to foot ulcers. ( J Vasc Surg 2010;52:44S-58S.)
Foot deformities, including contracture of the gastrocnemius-soleus complex, are clinically significant risk factors that commonly lead to diabetic foot ulceration.1-3 In fact, deformity in association with peripheral neuropathy and trauma were the three most common component causes in the pathway leading to foot ulceration.3 Structural alterations in the architecture of the foot often lead to abnormally high plantar foot pressures, as well as increased dorsal, medial, or lateral pressures when snugly fitting footwear is worn.4,5 These high pedal pressures consequently place the foot at risk for ulceration.6-8 Although deformities such as hammer toes and bunions are quite common in the nondiabetic population, they also frequently develop in persons with diabetes but without significant consequence. It is the presence of peripheral neuropathy, however, that confers the attendant risk for ulceration in diabetic individuals. A recent study of patients undergoing foot and ankle surgery has shown that diabetes without complications imparts no greater risk for postoperative infection than that for persons without diabetes. However, when diabetic patients with complications (including neuropathy) were compared with those without diabetes, there was a tenfold risk for developing postoperative infection.9 Although this study’s focus was on postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant predictor of foot ulceration.3,7,10-12 From the Carl T. Hayden VA Medical Center, Phoenix;a Valley Presbyterian Hospital, Los Angeles;b and Boston University Medical Center, Boston.c Competition of interest: none. This article is being co-published in the Journal of Vascular Surgery® and the Journal of the American Podiatric Medical Association. Correspondence: Robert G. Frykberg, DPM, Carl T. Hayden VA Medical Center, 650 E Indian School Rd, Phoenix, AZ 85012-1892 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery and the American Podiatric Medical Association. doi:10.1016/j.jvs.2010.06.008
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Neuropathy not only predisposes to foot ulcer in the presence of deformity and trauma but can also lead to the development of deformity in the diabetic foot.4,8,13 The Charcot foot is the most classic example of a deformity primarily related to peripheral neuropathy of any cause.14,15 Neuropathy affects the sensory nerves of the lower extremities and the motor as well as autonomic fibers.16-19 Consequently, motor neuropathy leads to muscle dysfunction, dynamic contractures, and even paresis (ie, foot drop). Ankle equinus, caused by a contracture of the gastrocnemius-soleus muscle complex and Achilles’ tendon, is often found in patients with diabetes and has been associated with high forefoot plantar pressures.20-22 The clinical effects of motor neuropathy are also seen in the form of intrinsic muscle atrophy.23 The “intrinsic minus” foot is typified by such atrophy on the dorsal forefoot in concert with the development of hammer toes or claw toes (Fig 1).8,24 In severe cases, the intrinsic minus foot will develop a cavus appearance and associated high plantar pressures under the prominent metatarsal heads. Shoes are an important cause of trauma to the neuropathic foot, especially in individuals with structural deformity. Therefore, the provision of properly fitted therapeutic footwear is considered a key component of an ulcer and amputation prevention program.13,25-27 Unfortunately, over-the-counter shoes often cannot accommodate severe foot deformities, including high plantar pressures. In some situations, custom footwear is indicated to protect severely misshapen feet. Nonetheless, any footwear is only as good as the patients’ adherence to wearing the shoes as prescribed. To this end, even in the ulcerated foot where strict adherence to off-loading modalities are critical, one study showed that patients had poor compliance and wore the prescribed off-loading devices only 28% of the time.28 Nonetheless, several studies have shown that patients fitted with therapeutic footwear suffer significantly fewer primary or recurrent ulcerations compared with diabetic patients who were not given such footwear.29-32 Surgical intervention should be considered when recurrent ulceration or preulcerative lesions develop despite