15
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 ulcer- ation. 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 ulcer- ation. 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 bun- ions are quite common in the nondiabetic population, they also frequently develop in persons with diabetes but with- out 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 postop- erative infection than that for persons without diabetes. However, when diabetic patients with complications (in- cluding neuropathy) were compared with those without diabetes, there was a tenfold risk for developing postop- erative 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 ulcer- ation. 3,7,10-12 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 ex- tremities and the motor as well as autonomic fibers. 16-19 Consequently, motor neuropathy leads to muscle dys- function, dynamic contractures, and even paresis (ie, foot drop). Ankle equinus, caused by a contracture of the gastrocnemius-soleus muscle complex and Achilles’ ten- don, 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 mi- nus” 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 associ- ated high plantar pressures under the prominent meta- tarsal heads. Shoes are an important cause of trauma to the neuro- pathic foot, especially in individuals with structural defor- mity. 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 pa- tients’ 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 thera- peutic footwear suffer significantly fewer primary or recur- rent ulcerations compared with diabetic patients who were not given such footwear. 29-32 Surgical intervention should be considered when recur- rent ulceration or preulcerative lesions develop despite 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 competi- tion 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 44S

Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

  • Upload
    others

  • View
    2

  • Download
    0

Embed Size (px)

Citation preview

Page 1: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

Surgical off-loading of the diabetic footRobert G. Frykberg, DPM, MPH,a Nicholas J. Bevilacqua, DPM,b andGeoffrey 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 ofpatients with diabetes mellitus. These patients are no longer relegated to wearing cumbersome braces or footwear fordeformities that might otherwise be easily corrected. Although surgical intervention in these often high-risk individualsis not without risk, the outcomes are fairly predictable when patients are properly selected and evaluated. In this briefreview, 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 thegastrocnemius-soleus complex, are clinically significantrisk factors that commonly lead to diabetic foot ulcer-ation.1-3 In fact, deformity in association with peripheralneuropathy and trauma were the three most commoncomponent causes in the pathway leading to foot ulcer-ation.3 Structural alterations in the architecture of thefoot often lead to abnormally high plantar foot pressures,as well as increased dorsal, medial, or lateral pressureswhen snugly fitting footwear is worn.4,5 These highpedal pressures consequently place the foot at risk forulceration.6-8

Although deformities such as hammer toes and bun-ions are quite common in the nondiabetic population, theyalso frequently develop in persons with diabetes but with-out significant consequence. It is the presence of peripheralneuropathy, however, that confers the attendant risk forulceration in diabetic individuals. A recent study of patientsundergoing foot and ankle surgery has shown that diabeteswithout complications imparts no greater risk for postop-erative infection than that for persons without diabetes.However, when diabetic patients with complications (in-cluding neuropathy) were compared with those withoutdiabetes, there was a tenfold risk for developing postop-erative infection.9 Although this study’s focus was onpostoperative infection in the foot and ankle, manyprevious studies have demonstrated the importance ofneuropathy as a significant predictor of foot ulcer-ation.3,7,10-12

From the Carl T. Hayden VA Medical Center, Phoenix;a Valley PresbyterianHospital, 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 financialrelationships to disclose per the JVS policy that requires reviewers todecline review of any manuscript for which they may have a competi-tion of interest.

0741-5214/$36.00Published 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

44S

Neuropathy not only predisposes to foot ulcer in thepresence of deformity and trauma but can also lead tothe development of deformity in the diabetic foot.4,8,13 TheCharcot foot is the most classic example of a deformityprimarily related to peripheral neuropathy of any cause.14,15

Neuropathy affects the sensory nerves of the lower ex-tremities and the motor as well as autonomic fibers.16-19

Consequently, motor neuropathy leads to muscle dys-function, dynamic contractures, and even paresis (ie,foot drop).

Ankle equinus, caused by a contracture of thegastrocnemius-soleus muscle complex and Achilles’ ten-don, is often found in patients with diabetes and has beenassociated with high forefoot plantar pressures.20-22 Theclinical effects of motor neuropathy are also seen in theform of intrinsic muscle atrophy.23 The “intrinsic mi-nus” foot is typified by such atrophy on the dorsalforefoot in concert with the development of hammertoes or claw toes (Fig 1).8,24 In severe cases, the intrinsicminus foot will develop a cavus appearance and associ-ated high plantar pressures under the prominent meta-tarsal heads.

Shoes are an important cause of trauma to the neuro-pathic foot, especially in individuals with structural defor-mity. Therefore, the provision of properly fitted therapeuticfootwear is considered a key component of an ulcer andamputation prevention program.13,25-27 Unfortunately,over-the-counter shoes often cannot accommodate severefoot deformities, including high plantar pressures. In somesituations, custom footwear is indicated to protect severelymisshapen feet.

Nonetheless, any footwear is only as good as the pa-tients’ adherence to wearing the shoes as prescribed. Tothis end, even in the ulcerated foot where strict adherenceto off-loading modalities are critical, one study showed thatpatients had poor compliance and wore the prescribedoff-loading devices only 28% of the time.28 Nonetheless,several studies have shown that patients fitted with thera-peutic footwear suffer significantly fewer primary or recur-rent ulcerations compared with diabetic patients who werenot given such footwear.29-32

Surgical intervention should be considered when recur-

rent ulceration or preulcerative lesions develop despite
Page 2: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYVolume 52, Number 12S Frykberg et al 45S

concerted efforts to prevent such lesions. Once consideredill-advised, corrective or reconstructive foot surgery hasassumed an important role in the management of pa-tients with chronic or recurrent foot ulcerations.13,33-38

Of course, such patients need to be carefully selected andevaluated to ensure that adequate vascularity is presentand that major comorbidities, including renal insuffi-ciency, unstable cardiovascular disease, and congestiveheart failure, are adequately controlled. Because periph-eral arterial disease (PAD) is often asymptomatic inpersons with diabetes, we follow the American DiabetesAssociation recommendation that an ankle-brachial in-dex (ABI) be measured in such persons who are aged�50 years.2,39 Furthermore, we routinely recommendobtaining a preoperative ABI (with toe pressures andwaveforms) in diabetic patients with foot ulcers in theabsence of clearly bounding pulses.

In 2003, Armstrong and Frykberg38,40 revised arisk-based scheme for classifying the types of foot surgeryperformed in diabetic patients largely depending on thepresence of open wounds and their acuity. Fundamen-tally, the classes of foot surgery are distinguished by theirprogressive risks for subsequent proximal levels of ampu-

Fig 1. Intrinsic minus foot. Note the high arched, thin foot withlittle muscle mass in this patient with advanced peripheral neurop-athy. Flexible hammer toes (claw toes) usually accompany thisdeformity as well.

Table. Classification of diabetic foot surgery40

● Class I: Elective. Reconstructive procedures on patients whodo not have loss of protective sensation (LOPS)

● Class II: Prophylactic. Reconstructive procedures performedto reduce the risk of ulceration or reulceration in patients whohave LOPS and do not have a wound present

● Class III: Curative. Procedures performed to assist in healingof open wounds

● Class IV: Emergent. Procedures performed to arrest or limitprogression of infection

tation (Table):

● Elective surgery (class I) represents reconstructive pro-cedures performed to correct deformities or high plan-tar pressures in persons without neuropathy.

● Prophylactic (class II) procedures are those performedin patients with neuropathy (loss of protective sensa-tion) to reduce the risk of ulceration or recurrentulceration when no open wounds are present.

● Curative surgery (class III) is often performed when openwounds are present to effect a cure by removing under-lying bony prominences (surgical decompression), osteo-myelitis, or by draining underlying abscesses. Obviously,such procedures are at higher risk for nonhealing orinfection than are the first two classes.

● Emergent procedures (class IV) are performed forsevere infections (wet gangrene, necrotizing fasci-itis, etc) to control the progression of infection. Asthe name implies, these procedures are performedemergently and often consist of open amputations atthe foot level combined with fasciotomies of the leg.

Armstrong et al41 later validated this classificationscheme in subsequent risk for proximal amputation andinfection. They found a significant trend toward increasingrisk of ulceration/reulceration, postoperative infection, all-level amputation, and major amputation with increasingclass of foot surgery (P � .01 for all complications). Aswould be expected, the greatest frequency of major ampu-tation was in class IV procedures.

Specific types of operations or procedures are notrestricted to single classes of surgery as described above.To the contrary, many procedures are used in operationsperformed across multiple foot surgery categories. Forexample, a hammer toe repair might be performed as anelective, prophylactic, or a curative procedure dependingon the presence of neuropathy and the presence or

Fig 2. Acquired second hammer toe after great toe amputationwith dorsal ulcer. This is easily treated by a digital arthroplastyor joint resection with excision of the ulceration. A metatarso-phalangeal joint release is also usually required for rigiddeformities.

absence of an open wound (Fig 2) A tendo-Achilles’

Page 3: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYSeptember Supplement 201046S Frykberg et al

lengthening (TAL) would be indicated under the samesituations. A first ray amputation might be performed tocure chronic osteomyelitis even in the absence of an openwound (prophylactic), in the presence of a chronic drain-ing ulcer (curative), or as an emergent procedure tocontrol the spread of an acute necrotizing infection. Amidfoot osteotomy or arthrodesis of an ulcerated Char-cot deformity is commonly performed as a curative op-eration (class III), but is just as frequently performed toreconstruct a deformed nonulcerated foot and therebyoffer surgical decompression to reduce plantar pressures(class II; Fig 3).15,42,43

This review will focus on those procedures commonlyused by foot and ankle surgeons to address deformities thatare causing abnormal pressure gradients. As already noted,many of these procedures can be used in elective, prophy-lactic, or curative situations depending on the presence (orabsence) of neuropathy or ulceration. Although we will notdiscuss amputations or specific management of infection, abrief discussion of those procedures used to correct the

Fig 3. Reconstruction for correction of unstable Chardeformity. B, A preoperative radiograph shows osteolysitalectomy and fusion. D, Postoperative radiograph.

Charcot foot will be presented.

DIGITAL DEFORMITIES

Common digital deformities, such as hammer toe,claw toe, and mallet toe, are known to increase pres-sures and are associated with neuropathic ulceration.Correcting the structural deformity with a resectionarthroplasty may augment healing and reduce the risk ofulcer recurrence.44 Alternatively, a percutaneous flexortenotomy offers a less invasive approach and may affordthe necessary intrinsic pressure modulation to augmenthealing.

Distal tip ulcers, in a flexible hammer toe, maybe managed with a flexor digitorum longus tenotomy. Ablade or 18-gauge needle is introduced 1 cm proximal tothe proximal plantar flexural crease of the toe (Fig 4). Theankle is held in a dorsiflexed position with the patientactively holding all toes in a flexed position. The toe ismanually straightened, and the blade is moved across thetaught tendon, making ease of the tenotomy. The longextensor tendon will now hold the toe straight. A postop-

nkle. A, Preoperative clinical view demonstrates anklehe talar dome. C, Circular external fixator in place after

cot as of t

erative shoe can be used for limited ambulation. Overex-

Page 4: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYVolume 52, Number 12S Frykberg et al 47S

tension of the toe can be managed with an extensor longustenotomy at a later date.

Laborde45 retrospectively reviewed 18 patients pre-senting with plantar toe ulcers treated with a flexor tenot-omy. All patients had a flexible claw toe deformity withulcers on the distal plantar aspect of the hallux or lesser toes.The incision and the ulcer healed in all patients. Twopatients underwent a repeat procedure for ulcer recurrenceand remained ulcer free at 17 and 34 months.

Tamir et al46 retrospectively reviewed the outcomes of14 patients (24 toes) treated with percutaneous flexortenotomies for a claw toe deformity to off-load the tip ofthe toe for ulcer healing. The authors performed an oste-oclasis in select patients to correct rigid contractures at theproximal interphalangeal joint. All patients healed with nosignificant complications noted.

Although the methodologic quality of both studies was

Fig 4. Flexor tenotomy. A, The toe is flexible and ulcethe patient is asked to dorsiflex the ankle and actively fleand can easily be tenotomized as shown here with a #61toes that have had flexor tenotomies. The fourth toe hadthe office setting.

poor, their results support the ability of a percutaneous

flexor tenotomy of the hallux and lesser toes to heal neu-ropathic toe ulceration secondary to toe contracture inpersons with diabetes.47

A rigid hammer toe is best treated with an arthroplastyat the level of the distal or proximal interphalangeal joint.However, a percutaneous flexor tenotomy may be at-tempted in the nonflexible deformity before resorting to anopen arthroplasty. On those occasions where a hallux ulceris not due to a limitation of motion at the metatarsopha-langeal joint (MTPJ), this same procedure can be used onthis digit (Fig 5).

LESSER METATARSALS

Neuropathic ulcerations under the metatarsal heads area challenging problem and may lead to infection and am-

the tip. B, Lidocaine is injected at the site of entry, andhe toes. This makes the long flexor tendon very taught,r blade. No suture is needed. C, Shows all three middlection of osteomyelitis, 4 weeks postoperatively, done in

r is atx all tBeave

rese

putation.48 Various metatarsal procedures have been de-

Page 5: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

y am

JOURNAL OF VASCULAR SURGERYSeptember Supplement 201048S Frykberg et al

scribed, including metatarsal head osteotomies and resec-tions.38,49,50 An isolated metatarsal osteotomy should beconsidered for a chronic, nonundermining, nontunnel-ing, ulcer below a specific metatarsal head. It can beperformed through a dorsal incision with a double-action bone cutter or an oscillating saw. The osteotomycan be done at the surgical or anatomic neck of themetatarsal (Fig 6). A collar of bone may be removed ifshortening of the metatarsal is desired. Such proceduresare generally performed when the plantar ulceration doesnot penetrate to bone.

A tunneling ulcer should be appropriately débridedto remove all undermining. A metatarsal head resectionmay be performed to assist in healing by internallyoff-loading the ulcer (Fig 7). Armstrong et al51 evaluatedthe outcomes of an isolated fifth metatarsal head resec-tion for ulcerations beneath the fifth metatarsal head andcompared it with nonsurgical care. They reported morerapid healing and a lower recurrence rate in the surgicalgroup.

The surgeon must be cognizant of maintaining a nearlynormal metatarsal parabola. The second, third, and fourthmetatarsals function as a single unit and any disruption inmetatarsal length or height may result in a transfer callus orulceration. If an ulcer occurs, further metatarsal osteotomymay be necessary. Osteotomies should be performed on theremaining two metatarsals, and if not, additional ulcerationis likely to develop over the remaining metatarsal, necessi-

Fig 5. Arthroplasty of the hallux for surgical off-loadinghead of the proximal phalanx. B, Incision placement. Ctendon is repaired. D, The wound closed primarily. Earl

tating a third procedure. This scenario is especially likely to

occur after one of the metatarsal heads has been removeddue to infection.

Multiple metatarsal head resections or a panmetatar-sal head resection may be considered for nonhealingulcers in the presence of an abnormal metatarsal parabola(Fig 8).52 Hamilton et al48 proposed combining lessermetatarsal head resections with gastrocnemius recessionand a peroneus longus-to-brevis tendon transfer in pa-tients with chronic, neuropathic forefoot ulcerations. Allulcers were located beneath lesser metatarsal heads, al-lowing the authors to preserve the first MTPJ. Theyadjunctively managed the equinus deformity with a gas-trocnemius recession and alleviated pressure beneath thefirst metatarsal with the peroneus longus-to-brevis trans-fer. The authors reported ulcer healing in 10 patients(100%), with no ulcer recurrence at a mean 14.2 monthsof follow-up.48

KELLER ARTHROPLASTY

Limited range of motion at the MTPJ is a commonforefoot deformity that contributes to ulcer formationbeneath the hallux. This limitation in joint range ofmotion leads to increased pressure on the hallux duringambulation. Pressure reduction is essential and usuallyconsists of an external device to off-load the area.53 Thisdoes not correct the underlying deformity, however. Theassociated biomechanical abnormality still exists after theoff-loading device is removed, and ulcer recurrence may

chronic hallux ulceration. A, The ulcer is adjacent to thehead of the phalanx is removed, and the long extensor

bulation is possible with a postoperative shoe.

of a, The

occur. Identifying and correcting the underlying struc-

Page 6: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYVolume 52, Number 12S Frykberg et al 49S

tural deformity may assist in healing and also reduceulcer recurrence.

Armstrong et al54 compared the safety and efficacy of afirst MTPJ arthroplasty (Keller-type procedure) with non-surgical management for wounds at the plantar aspect ofthe hallux interphalangeal joint (Fig 9). They included 41patients, with 21 undergoing a first MTPJ arthroplasty toaugment ulcer healing. Patients in the surgery group healedsignificantly faster than patients in the nonsurgery group.Care after healing was identical in both groups, and thesurgery group had fewer ulcer recurrences during the6-month follow-up. There was a very high prevalence ofpostoperative infections in the surgery group (40%), butthis was compared with the 38% of patients in the controlgroup who required treatment for infection during theperiod of therapy. The results of this study suggest that afirst MTPJ arthroplasty is a safe and effective procedure inthe treatment of noninfected, nonischemic wounds be-

Fig 6. Metatarsal osteotomy, now performed in the officbone cutter, hemostat, and freer elevator as a probe. A, Ta large hemostat. B, A double-action bone cutter is introat the metatarsal neck level. D, Multiple osteotomies shoand surgical neck of each metatarsal.

neath the hallux.54

FIRST MTPJ RESECTION

The excision of the first MTPJ should be consideredif the metatarsal head has osteomyelitis, after failed sesa-moidectomy, or for a chronic ulcer probing to the jointbut with a viable hallux.38 The incision may incorporateand excise the ulcer or be placed dorsally to avoid theulcer altogether. The incision is made directly to bone,with no undermining of the soft tissue. The dissection isat the level of the ligaments and periosteum. The meta-tarsal is cut and beveled plantarly to reduce any boneprominences. The base of the phalanx is removed as in aKeller bunionectomy. Both sesamoids should be re-moved because a fibrous union to the metatarsal stumpmay occur if they are left and become a future source ofulceration (Fig 10). This is also necessary in cases of openjoint involvement or infection, wherein the infected orcontaminated sesamoids will become a source for con-

ing when possible, can be done with simple instruments:gh a dorsal incision, the metatarsal neck is grasped withadjacent to the hemostat. C, The bone is osteotomized

ere are all in the proper location, between the anatomic

e setthrou

ducedwn h

tinued infection.

Page 7: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYSeptember Supplement 201050S Frykberg et al

TAL LENGTHENING

Limited ankle joint mobility, as seen clinically as a tightAchilles’-gastrocnemius-soleus complex, is a deformingforce and a causative factor in plantar forefoot ulcer-ations.21 During normal gait, 10° of dorsiflexion at theankle is required, and anything less will increase plantarpressures in the forefoot and impede healing of the wound.To alleviate the pressure, several authors have suggestedpercutaneous TAL.55-58 Armstrong et al21 confirmed that

Fig 7. A, Undermining ulceration that probes into dstandard metatarsal osteotomy. B, The ulcer is excised ana proximal drain is acceptable as long as there is no activenon-weight bearing for 4 weeks.

plantar pressures are reduced after percutaneous TAL. Lin

et al59 reported results of percutaneous TAL in 15 patientswith plantar forefoot ulcers that did not heal despite 9weeks of total contact casting. All but one ulcer healed(93%), with no ulcer recurrence noted after a mean 17.3-month follow-up.

Mueller et al22 conducted a randomized control trialcomparing the combined treatment of total contact castand percutaneous TAL against a total contact cast alone.Initial healing rates were similar in both groups, but the

issues (including bone or joint) is not appropriate foradjacent metatarsal is removed. C, Primary closure with

s. The drain is pulled in 24 hours, and the patient is kept

eep td thesepsi

significant difference was noted when the ulcer recur-

Page 8: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYVolume 52, Number 12S Frykberg et al 51S

rence rate was compared. After 2 years, the ulcer recur-rence rate was 81% in the group treated with a total contactcast alone compared with 38% in those treated with a totalcontact cast and TAL. A gastrocnemius recession may beused as an alternative for relief of forefoot pressure60 andhas also been described as an effective treatment for mid-foot ulcers (Fig 11).60,61

CHARCOT FOOT

Charcot arthropathy, perhaps the most characteristicdeformity attributed to the diabetic foot, occurs in only1% of the diabetic population as a whole and in approx-imately 30% of individuals with peripheral neuropa-thy.62-64 Originally described by Charcot as the piedtabétiques in persons with tertiary syphilis,65 the Charcot

Fig 8. Pan metatarsal head resection. A, Failed metatarsamputation could be done, but the toes are viable. Surgicapproach; here, a dorsal approach is planned. C, Excisionseveral months after procedure.

foot is now most commonly encountered in persons with

diabetes.66 Several studies have indicated that diabeticpatients with Charcot foot deformities have an increasedrisk for ulceration and subsequent amputation andhigher mortality compared with diabetic persons with-out this complication.67-69

The classic “rocker-bottom” deformity (Fig 12) is theresult of a collapse of the midfoot architecture generally dueto injury and continued weight bearing on the insensatefoot. With the continued stress of weight bearing, a viciouscycle ensues that exaggerates local inflammation and leadsto more fractures, dislocations, and deformity.14,70 Abnor-mally concentrated pressures develop in the midfoot duringambulation on the deformed foot, and ulceration fre-quently ensues.71 When the ankle joint is the primary site ofinvolvement (Sanders-Frykberg pattern V),14 instability

geries with transfer ulcer subsecond. B, Transmetatarsalloading can be accomplished through a dorsal or plantaretatarsal head through a dorsal incision. D, Radiograph

al sural off-of m

and deformity become the most difficult problem to man-

Page 9: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYSeptember Supplement 201052S Frykberg et al

age and all too frequently fails conservative therapy withbracing.15,64,72

Conservative care for Charcot arthropathy has been thetraditional mainstay of treatment for this limb-threateningdisorder,14,64,72,73 but surgical management for Charcotjoints is not a recent evolution in our understanding of howthis entity can be approached. Although his report dealtprimarily with Charcot joints due to tabes dorsalis, Stein-dler74 presented a series of surgical cases including subtalararthrodesis as early as 1931. Several other important surgi-cal case series were published in the ensuing decades thatillustrated the efficacy of a surgical approach to this arthrop-athy as well as its inherent difficulties and complica-tions.75,76

Numerous descriptive studies have been published inthe last 20 years detailing various surgical techniques for the

Fig 9. A, Keller arthroplasty used as a curative procedurshows the resection of the base of the proximal phalanxnoted 3 weeks after a Keller arthroplasty was performed.

management of the deformed Charcot foot.15,43,77-82 The

indications for surgery are generally to provide a moreeffective management strategy when conservative measureshave failed. Specifically, surgery is recommended for thosepatients with recurrent ulceration (with or without infec-tion), severe instability, or severe deformities not amenableto footwear therapy alone.83 Many surgical techniques havebeen described, including simple plantar exostectomy withor without TAL, midfoot realignment arthrodeses, hind-foot arthrodeses, and ankle arthrodeses (Fig 13). A combi-nation of procedures is most often required because Char-cot deformities are usually multilevel. Although arthrodesisusing internal fixation is most often practiced, multipla-nar external circular fixation using Ilizarov techniques (Fig14) has been used with increasing frequency in recentyears.43,82,84 Regardless of technique, the goals of surgeryremain the same: establish a stable, plantigrade foot miti-

ulcer under a rigid hallux. B, A postoperative radiographllow for unrestricted dorsiflexion. C, Healed ulceration

e forto a

gating focal areas of increased pressure and shearing forces.

Page 10: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYVolume 52, Number 12S Frykberg et al 53S

By reducing plantar prominences and their attendant highpressures, healing of open ulcers can be augmented and therisk of subsequent skin breakdown will be reduced.77 Thereader is referred to the referenced citations for specifictechniques of interest.

CONCLUSION

Surgical management of diabetic foot disorders is nolonger considered an unwarranted practice. To the con-trary, surgery on the ulcerated or deformed foot hasassumed an increasingly important role in the manage-

Fig 10. First metatarsophalangeal joint resection. AB, The joint is resected through a dorsal incision. Thejoint. C, A radiograph shows the resection of the mphalanx.

ment of such disorders both in the United States and

abroad. Nonetheless, these patients are indeed at ahigher risk for complications than their nondiabeticcounterparts, especially in those with peripheral neurop-athy or ischemia. Careful patient selection and thoroughevaluation of the foot as well as attendant comorbiditiesare the cornerstones of achieving successful results inotherwise very complicated patients. Early and ostensiblyaggressive surgical intervention on the deformed footcan obviate many months of unsuccessful conservativecare, especially when ulcer recidivism becomes the pri-mary challenge. Although virtually all the procedures

chronic deep ulcer under the first metatarsal head.or illustrates that the plantar ulcer penetrated into thersal head, both sesamoids, and the base of proximal

, Aelevatetata

used in this setting are not exclusive to diabetic foot

Page 11: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

deformity.

JOURNAL OF VASCULAR SURGERYSeptember Supplement 201054S Frykberg et al

Fig 11. A, A gastrocnemius recession performed to augmenthealing of a plantar forefoot ulceration. B, An image taken 2 years

postoperatively demonstrates long-term ulcer healing.

Fig 12. A rocker-bottom Charcot foot is shown with soft tissuevisualization of large plantar midfoot ulcer under the apex of the

Page 12: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYVolume 52, Number 12S Frykberg et al 55S

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 (tendo-

Achilles’ lengthening incision not shown).
Page 13: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYSeptember Supplement 201056S Frykberg et al

surgery, great care (with close follow-up) is necessary inthe postoperative period to ensure optimal outcomes inthese high-risk patients.

REFERENCES

1. Boulton AJ, Kirsner RS, Vileikyte L. Clinical practice. Neuropathicdiabetic foot ulcers. N Engl J Med 2004;351:48-55.

2. Boulton AJ, Armstrong DG, Albert SF, et al. Comprehensive footexamination and risk assessment: a report of the task force of the footcare interest group of the American Diabetes Association, with endorse-ment by the American Association of Clinical Endocrinologists. Diabe-tes Care 2008;31:1679-85.

3. Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incidentlower-extremity ulcers in patients with diabetes from two settings.Diabetes Care 1999;22:157-62.

4. Frykberg RG. Biomechanical considerations of the diabetic foot. LowerExtremity 1995;2:207-14.

5. Cavanagh PR. Therapeutic footwear for people with diabetes. DiabetesMetab Res Rev 2004;20(Suppl 1):S51-5.

6. Veves A, Murray HJ, Young MJ, Boulton AJ. The risk of foot ulcerationin diabetic patients with high foot pressure: a prospective study. Diabe-

Fig 14. A, A midfoot Charcot reconstruction using an Ilizarovcircular frame. B, A lateral radiograph shows the orientation of thefoot and ankle in the frame. In this case, internal fixation was alsoused.

tologia 1992;35:660-3.

7. Frykberg RG, Lavery LA, Pham H, Harvey C, Harkless L, Veves A. Roleof 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 JLow Extrem Wounds 2005;4:160-70.

9. Wukich DK, Lowery NJ, McMillen RL, Frykberg RG. Postoperativeinfection rates in foot and ankle surgery: a comparison of patients withand without diabetes mellitus. J Bone Joint Surg Am 2010;92:287-95.

10. Fernando DJ, Masson EA, Veves A, Boulton AJ. Relationship of limitedjoint 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 riskfactors for, new diabetic foot ulceration in a community-based patientcohort. Diabet Med 2002;19:377-84.

12. Boyko EJ, Ahroni JH, Stensel V, Forsberg RC, Davignon DR, SmithDG. A prospective study of risk factors for diabetic foot ulcer. TheSeattle 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: TheCharcot foot. In: Frykberg RG, editor. The high risk foot in diabetesmellitus. 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 Complications2009;23:409-26.

16. Boulton AJ. Diabetic neuropathy: classification, measurement andtreatment. Curr Opin Endocrinol Diabetes Obes 2007;14:141-5.

17. Vinik AI, Maser RE, Mitchell BD, Freeman R. Diabetic autonomicneuropathy. 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 Associa-tion. Diabetes Care 2005;28:956-62.

19. Andersen H, Gjerstad MD, Jakobsen J. Atrophy of foot muscles: ameasure of diabetic neuropathy. Diabetes Care 2004;27:2382-5.

20. Lavery LA, Armstrong DG, Boulton AJ. Ankle equinus deformity andits relationship to high plantar pressure in a large population withdiabetes mellitus. J Am Podiatr Med Assoc 2002;92:479-82.

21. Armstrong DG, Stacpoole-Shea S, Nguyen H, Harkless LB. Lengthen-ing of the Achilles tendon in diabetic patients who are at high risk forulceration of the foot. J Bone Joint Surg Am 1999;81:535-8.

22. Mueller MJ, Sinacore DR, Hastings MK, Strube MJ, Johnson JE. Effectof Achilles tendon lengthening on neuropathic plantar ulcers. A ran-domized clinical trial. J Bone Joint Surg Am 2003;85:1436-45.

23. van Schie CH, Vermigli C, Carrington AL, Boulton A. Muscle weaknessand foot deformities in diabetes: relationship to neuropathy and footulceration in Caucasian diabetic men. Diabetes Care 2004;27:1668-73.

24. Habershaw GM, Chrzan J. Biomechanical considerations of the dia-betic foot. In: Kozak GP, Campbell DR, Frykberg RG, Habershaw GM,ed. Management of diabetic foot problems, 2nd ed. Philadelphia: WBSaunders; 1995. p. 53-65.

25. International Working Group on the Diabetic Foot. InternationalConsensus on the Diabetic Foot. Paper presented at: InternationalWorking Group on the Diabetic Foot 2003; Noordwijkerhout, Neth-erlands.

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. Dia-betes 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 withactive ulceration may not adhere to a standard pressure off-loadingregimen. 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.
Page 14: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYVolume 52, Number 12S Frykberg et al 57S

30. Chantelau E, Kushner T, Spraul M. How effective is cushioned thera-peutic footwear in protecting diabetic feet? A clinical study. Diabet Med1990;7:335-9.

31. Chantelau E. Therapeutic footwear in patients with diabetes. JAMA2002;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 aspecialized foot clinic. Q J Med 1986;60:763-71.

33. Piaggesi A, Schipani E, Campi F, Romanelli M, Baccetti F, Arvia C, etal. Conservative surgical approach versus non-surgical management fordiabetic neuropathic foot ulcers: a randomized trial. Diabet Med 1998;15:412-7.

34. Armstrong DG, Lavery LA, Stern S, Harkless LB. Is prophylacticdiabetic foot surgery dangerous? J Foot Ankle Surg 1996;35:585-9.

35. Catanzariti AR, Blitch EL, Karlock LG. Elective foot and ankle surgeryin 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: ChurchillLivingstone; 1991. p. 537-8.

37. Frykberg RG. Diabetic foot ulcers: pathogenesis and management. AmFam Physician 2002;66:1655-62.

38. Frykberg R, Giurini J, Habershaw G, Rosenblum B, Chrzan J. Prophy-lactic surgery in the diabetic foot. In: Kominsky SJ, editor. Medical andsurgical management of the diabetic foot. Saint Louis: Mosby; 1993. p.399-439.

39. American Diabetes Association. Peripheral arterial disease in peoplewith diabetes. Diabetes Care 2003;26:3333-41.

40. Armstrong DG, Frykberg RG. Classifying diabetic foot surgery: towarda rational definition. Diabet Med 2003;20:329-31.

41. Armstrong DG, Lavery LA, Frykberg RG, Wu SC, Boulton AJ. Valida-tion of a diabetic foot surgery classification. Int Wound J 2006;3:240-6.

42. Zgonis T, Roukis TS, Frykberg RG, Landsman AS. Unstable acute andchronic Charcot’s deformity: staged skeletal and soft-tissue reconstruc-tion. J Wound Care 2006;15:276-80.

43. Zgonis T, Roukis TS, Lamm BM. Charcot foot and ankle reconstruc-tion: current thinking and surgical approaches. Clin Podiatr Med Surg2007;24:505-17, ix.

44. Kim JY, Kim TW, Park YE, Lee YJ. Modified resection arthroplasty forinfected non-healing ulcers with toe deformity in diabetic patients. FootAnkle 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 percutane-ous flexor tenotomies for management of diabetic claw toe deformitieswith ulcers: a preliminary report. Can J Surg 2008;51:41-4.

47. Roukis TS, Schade VL. Percutaneous flexor tenotomy for treatment ofneuropathic toe ulceration secondary to toe contracture in persons withdiabetes: a systematic review. J Foot Ankle Surg 2009;48:684-9.

48. Hamilton GA, Ford LA, Perez H, Rush SM. Salvage of the neuropathicfoot by using bone resection and tendon balancing: a retrospectivereview of 10 patients. J Foot Ankle Surg 2005;44:37-43.

49. Sayner LR, Rosenblum BI, Giurini JM. Elective surgery of the diabeticfoot. 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 neuropathiculcerations. J Am Podiatr Med Assoc 1990;80:211-7.

51. Armstrong DG, Rosales MA, Gashi A. Efficacy of fifth metatarsal headresection for treatment of chronic diabetic foot ulceration. J Am PodiatrMed Assoc 2005;95:353-6.

52. Giurini JM, Habershaw GM, Chrzan JS. Panmetatarsal head resectionin chronic neuropathic ulceration. J Foot Surg 1987;26:249-52.

53. Wu SC, Crews RT, Armstrong DG. The pivotal role of offloading in themanagement of neuropathic foot ulceration. Curr Diab Rep 2005;5:423-9.

54. Armstrong DG, Lavery LA, Vazquez JR, Short B, Kimbriel HR, NixonBP, et al. Clinical efficacy of the first metatarsophalangeal joint arthro-plasty as a curative procedure for hallux interphalangeal joint wounds inpersons 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

with transmetatarsal amputations. J Am Podiatr Med Assoc1993;83:96-100.

56. Holstein P, Lohmann M, Bitsch M, Jorgensen B. Achilles tendonlengthening, the panacea for plantar forefoot ulceration? DiabetesMetab Res Rev 2004;20(Suppl 1):S37-40.

57. La Fontaine J, Brown D, Adams M, VanPelt M. New and recurrentulcerations after percutaneous Achilles tendon lengthening in trans-metatarsal amputation. J Foot Ankle Surg 2008;47:225-9.

58. Nishimoto GS, Attinger CE, Cooper PS. Lengthening the Achillestendon for the treatment of diabetic plantar forefoot ulceration. SurgClin North Am 2003;83:707-26.

59. Lin SS, Lee TH, Wapner KL. Plantar forefoot ulceration with equinusdeformity of the ankle in diabetic patients: the effect of tendo-Achilleslengthening and total contact casting. Orthopaedics 1996;19:465-75.

60. Greenhagen RM, Johnson AR, Peterson MC, Rogers LC, BevilacquaNJ. Gastrocnemius recession as an alternative to tendoAchillis length-ening for relief of forefoot pressure in a patient with peripheral neurop-athy: a case report and description of a technical modification. J FootAnkle Surgery 2010;49:159.e9-13.

61. Laborde JM. Midfoot ulcers treated with gastrocnemius-soleus reces-sion. Foot Ankle Int 2009;30:842-6.

62. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. ClinPodiatr Med Surg 2008;25:17-28, v.

63. Cofield RH, Morrison MJ, Beabout JW. Diabetic neuroarthropathy inthe foot: patient characteristics and patterns of radiographic change.Foot Ankle 1983;4:15-22.

64. Frykberg RG, Eneroth M. Principles of conservative management. In:Frykberg RG, editor. The diabetic Charcot foot: principles and man-agement. Brooklandville, MD: Data Trace Publishing Company; 2010.p. 93-116.

65. Charcot J-M, Fere C. Affections osseuses et articulaires du pied chez lestabétiques (Pied tabétique). Arch Neurol 1883;6:305-19.

66. Sanders LJ. The Charcot foot and ankle: historical perspective. In:Frykberg RG, editor. The diabetic Charcot foot: principles and man-agement. Brooklandville, MD: Data Trace Publishing; 2010. p. 1-12.

67. Sohn MW, Stuck RM, Pinzur M, Lee TA, Budiman-Mak E. Lower-extremity amputation risk after Charcot arthropathy and diabetic footulcer. Diabetes Care 2010;33:98-100.

68. Sohn MW, Lee TA, Stuck RM, Frykberg RG, Budiman-Mak E. Mor-tality risk of Charcot arthropathy compared with that of diabetic footulcer and diabetes alone. Diabetes Care 2009;32:816-21.

69. Gazis A, Pound N, Macfarlane R, Treece K, Game F, Jeffcoate W.Mortality in patients with diabetic neuropathic osteoarthropathy (Char-cot foot). Diabet Med 2004;21:1243-6.

70. Bevilacqua NJ, Bowling FL, Armstrong DG. The natural history ofCharcot neuroarthropathy. In: Frykberg RG, editor. The diabetic Char-cot foot: principles and management. Brooklandville, MD: Data TracePublishing Co; 2010. p. 13-27.

71. Cavanagh PR, Botek G, Owings T. Biomechanical factors in Charcot’sneuroarthropathy. In: Frykberg RG, editor. The diabetic Charcot foot:principles and management. Brooklandville, MD: Data Trace Publish-ing; 2010. p. 131-41.

72. Saltzman CL, Hagy ML, Zimmerman B, Estin M, Cooper R. Howeffective is intensive nonoperative initial treatment of patients withdiabetes and Charcot arthropathy of the feet? Clin Orthop Relat Res2005:185-90.

73. Frykberg RG, Rogers LC. The diabetic Charcot foot: a primer onmedical and surgical management. J Diabet Foot Complications 2009;1:19-25.

74. Steindler A. The tabetic arthropathies. JAMA 1931;96:250-6.75. Harris JR, Brand PW. Patterns of disintegration of the tarsus in the

anaesthetic foot. J Bone Joint Surg Br 1966;48:4-16.76. Johnson JT. Neuropathic fractures and joint injuries. Pathogenesis and

rationale of prevention and treatment. J Bone Joint Surg Am 1967;49:1-30.

77. Bevilacqua NJ, Rogers LC. Surgical management of Charcot midfootdeformities. Clin Podiatr Med Surg 2008;25:81-94.

78. Pinzur MS. Neutral ring fixation for high-risk nonplantigrade Charcot

midfoot deformity. Foot Ankle Int 2007;28:961-6.
Page 15: Surgical off-loading of the diabetic foot · postoperative infection in the foot and ankle, many previous studies have demonstrated the importance of neuropathy as a significant

JOURNAL OF VASCULAR SURGERYSeptember Supplement 201058S Frykberg et al

79. Catanzariti AR, Mendicino R, Haverstock B. Ostectomy for diabeticneuroarthropathy involving the midfoot. J Foot Ankle Surg 2000;39:291-300.

80. Cooper PS. Application of external fixators for management of Charcotdeformities of the foot and ankle. Semin Vasc Surg 2003;16:67-78.

81. Farber DC, Juliano PJ, Cavanagh PR, Ulbrecht J, Caputo G. Singlestage correction with external fixation of the ulcerated foot inindividuals with Charcot neuroarthropathy. Foot Ankle Int 2002;

23:130-4.

82. Burns PR, Wukich DK. Surgical reconstruction of the Charcot rearfootand ankle. Clin Podiatr Med Surg 2008;25:95-120, vii-viii.

83. Pinzur MS. Surgical management—history and general principles. In:Frykberg RG, editor. The diabetic Charcot foot: principles and manage-ment. Brooklandville, MD: Data Trace Publishing Co; 2010. p. 165-86.

84. Wukich DK, Zgonis T. Circular external fixation in Charcot neuroar-thropathy. In: Frykberg RG, editor. The diabetic Charcot foot: princi-ples and management. Brooklandville, MD: Data Trace Publishing Co;

2010. p. 231-41.