The Foot in Diabetes - part 8 pdf

Figure 18.2 shows a foot with hallux valgus in which an ulcerwas present over the medial aspect of the ®rst metatarsophalangeal joint in a middle-aged diabetic patient with neuropathy..

period7,8,15,34,35 Careful patient selection, combined with expertise andclose postoperative monitoring, are essential for obtaining optimalsurgical outcomes while minimizing complications.

CONCLUSIONAlthough not all neuro-arthropathic feet can be prevented, the progressionand subsequent destruction of the foot can be attenuated through earlydetection and appropriate management This requires a thorough under-standing of the underlying pathophysiology, natural history and acceptedstandards of management The ultimate goal of treatment is to maintain auseful extremity, free from ulceration, which will allow the patient tofunction as normallyas possible throughout his/her lifetime Whilelongitudinal studies have not been forthcoming regarding the survival ofthese patients, theyare certainlyat risk for numerous other complications ofdiabetes Prevention of ulceration and subsequent amputation is therefore akeyobjective in managing persons with this disorder Constant vigilance onthe part of both patient and health care providers is necessaryto ensurethat, once healed, the neuro-arthropathic foot is protected from furtherinjurythrough appropriate footwear and careful attention to preventivefoot care

REFERENCES

1 Charcot J-M Sur quelques arthropathies qui paraissent dependre d'une lesion

du cerveau ou de la moelle epiniere Arch Physiol Norm Pathol 1868; 1: 161±78

2 Edelman SV, KosofskyEM, Paul RA, Kozak GP Neuro-neuroarthropathy(Charcot's joints) in diabetes mellitus following revascularization surgery: threecase reports and a review of the literature Arch Intern Med 1987; 147: 1504±8

3 Frykberg RG, Kozak GP The diabetic Charcot foot In Kozak GP, Campbell DR,Frykberg RG, Habershaw GM (eds), Management of Diabetic Foot Problems, 2ndedn Philadelphia: WB Saunders, 1995; 88±97

4 Harris JR, Brand PW Patterns of disintegration of the tarsus in the anaestheticfoot J Bone Joint Surg 1966; 48B: 4±16

5 Newman JH Spontaneous dislocation in diabetic neuropathy J Bone Joint Surg1979; 61B: 484±8

6 Sanders LJ, Frykberg RG Charcot foot In Levin ME, O'Neal LW, Bowker JH(eds), The Diabetic Foot, 5th edn St Louis, MI: MosbyYearbook, 1993; 149±80

7 Sanders LJ, Frykberg RG Diabetic neuropathic neuroarthropathy: the Charcotfoot In Frykberg RG (ed.), The High Risk Foot in Diabetes Mellitus New York:Churchill Livingstone, 1991; 297±338

8 Sanders LJ, Mrdjenovich D Anatomical patterns of bone and joint destruction

in neuropathic diabetics Diabetes 1991; 40(suppl 1): 529A

9 Childs M, Armstrong DG, Edelson G Is Charcot arthropathya late sequela ofosteoporosis in patients with diabetes mellitus? J Foot Ankle Surg 1998; 37: 437±9

10 CundyTF, Edmonds ME, Watkins PJ Osteopenia and metatarsal fractures indiabetic neuropathy Diabet Med 1985; 2: 461±4.

11 Forst T, P¯itzner A, Kann P, Schehler B, Lobmarm R, Schafer H, Andreas J,Bockisch A, Beyer J Peripheral osteopenia in adult patients with insulin-dependent diabetes mellitus Diabet Med 1995; 12: 874±9

12 Young MJ, Marshall A, Adams JE, SelbyPL, Boulton AJM Osteopenia,neurological dysfunction, and the development of Charcot neuroarthropathy.Diabet Care 1995; 18: 34±8

13 Frykberg RG Biomechanical considerations of the diabetic foot LowerExtremity 1995; 2: 207±14

14 Eichenholtz SN Charcot Joints Spring®eld, IL: Charles C Thomas, 1966

15 Armstrong DG, Todd WF, LaveryLA, Harkless LB, Bushman TR The naturalhistoryof acute Charcot's arthropathyin a diabetic foot specialtyclinic DiabetMed 1997; 14: 357±63

16 ClohisyDR, Thompson RC Fractures associated with neuropathic arthropathy

in adults who have juvenile-onset diabetes J Bone Joint Surg 1988; 70A:1192±200

17 Co®eld RH, Morison MJ, Beabout JW Diabetic neuroarthropathyin the foot:patient characteristics and patterns of radiographic change Foot Ankle 1983; 4:15±22

18 Seabold JE, Flickinger FW, Kao S, Gleason TJ, Kahn D, Nepola J, Marsh

JL Indium-111 leukocyte/technetium-99m-MDP bone and magnetic nance imaging: dif®cultyof diagnosing osteomyelitis in patients withneuropathic neuroarthropathy J Nucl Med 1990; 31: 549±56

reso-19 Klenerman L The Charcot joint in diabetes Diabet Med 1996; 13: S52±4

20 Sinha S, Munichoodappa C, Kozak GP Neuro-arthropathy(Charcot joints) indiabetes mellitus: clinical studyof 101 cases Medicine 1972; 52: 191±210

21 Caputo GM, Ulbrecht J, Cavanagh PR, Juliano P The Charcot foot in diabetes:six keypoints Am Fam Phys 1998; 57: 2705±10

22 Newman JH Non-infective disease of the diabetic foot J Bone Joint Surg 1981;63B: 593±6

23 Cavanagh PR, Young MJ, Adams JE, Vickers KL, Boulton AJM Radiographicabnormalities in the feet of patients with diabetic neuropathy Diabet Care 1994;17: 201±9

24 Edmonds ME, Clarke MB, Newton S, Barrett J, Watkins PJ Increased uptake ofbone radiopharmaceutical in diabetic neuropathy Q J Med (New Ser) 1985; 57:843±55

25 Johnson JE, KennedyEJ, Shereff MJ, Patel NC, Collier BD Prospectivestudyof bone, indium-111-labeled white blood cell, and gallium-67 scanningfor the evaluation of osteomyelitis in the diabetic foot Foot Ankle Int 1996; 7:10±16

26 Schauwecker DS, Park HM, Burt RW, Mock BH, Wellman HN Combinedbone scintigraphyand indium-111 leukocyte scans in neuropathic foot disease JNucl Med 1988; 29: 1651±5

27 Longmaid HE, Kruskal JB Imaging infections in diabetic patients Infect DisClin N Am 1995; 9: 163±182

28 Beltran J, Campanini S, Knight C, McCalla M The diabetic foot: magneticresonance imaging evaluation Skel Radiol 1990; 19: 37±41

29 Lesko P, Maurer RC Talonavicular dislocations and midfoot arthropathyinneuropathic diabetic feet: natural course and principles of treatment Clin OrthopRel Res 1989; 240: 226±31

30 Kathol MH, El-KouryGY, Moore TE Calcaneal insuf®ciencyavulsionfractures in patients with diabetes mellitus Radiology 1991; 180: 725±9.

31 Gough A, Abraha H, Li F, Purewal TS, Foster AVM, Watkins PJ, Moniz C,Edmonds ME Measurement of markers of osteoclast and osteoblast activityinpatients with acute and chronic diabetic Charcot neuroarthropathy Diabet Med1997; 14: 527±31

32 SelbyPL, Young MJ, Boulton AJM Bisphosphonates: a new treatment fordiabetic Charcot neuroarthropathy? Diabet Med 1994; 11: 28±31

33 Mehta JA, Brown C, Sargeant N Charcot restraint orthotic walker Foot AnkleInt 1998; 19: 619±23

34 Myerson MS, Henderson MR, Saxby T, Short KW Management of midfootdiabetic neuroarthropathy Foot Ankle Int 1994; 15: 233±41

35 Sammarco GJ, Conti SF Surgical treatment of neuroarthropathic footdeformity Foot Ankle Int 1998; 19: 102±9

18 Prophylactic Orthopaedic SurgeryÐIs There A Role?

PATRICK LAING

WrexhamMaelor Hospital, Wrexham, UK

Prophylactic surgery in the diabetic foot is normally categorized as emergency surgery The complications of diabetic foot ulceration can be sodevastating that the concept of such surgery to prevent ulceration, or re-ulceration, is inviting All too frequently we see feet which are sufferingfromrepeated breakdown and creeping amputation Surgery, though, ismost often used in the acute situation as a reaction to infection or gangreneand less rarely in an elective attempt to prevent future problems Althoughclassi®ed as non-emergency surgery, early aggressive surgery in the acutesituation, which limits the extent of amputation and avoids more proximallimb loss, is regarded by some as equally prophylactic1

non-Neuropathy and ischaemia are the two main risk factors for development

of diabetic foot ulceration However, the initiating factor in ulceration isusually pressure of some description In a foot with a poor blood supply,ischaemic ulcers may develop due to quite low pressures Conversely,higher pressures are required in a neuropathic foot that has a good bloodsupply but lacks protective sensation The neuropathic foot is frequentlycavus in shape with clawed toes and callosities under the heel andmetatarsal heads in which high pressures develop The clawing of the toesleads to dorsal friction and increased pressures as the protrudinginterphalangeal joints rub against the toe box of the shoe In a normalfoot the toes take 30% and sometimes up to 50% of the load transmittedthrough the foot, but with severe clawing the toes become non-weightbearing, increasing the load under the metatarsal heads InThe Foot in Diabetes, 3rd edn Edited by A J M Boulton, H Connor and P R Cavanagh.

& 2000 John Wiley & Sons, Ltd.

Copyright  2000 John Wiley & Sons, Inc ISBNs: 0-471-48974-3 (Hardback); 0-470-84639-9 (Electronic)

Ellenberg's2series 90% of diabetic ulcers occurred under pressure-bearingareas of the foot Studies such as that by Veves et al3have shown that highplantar pressures are predictive of plantar ulceration In their group of 86diabetic patients, plantar ulceration occurred in 35% of those with high footpressures but in none of those with normal pressures Yet, despite suchstudies, it is not possible to predict with absolute accuracy which patientswill develop ulceration Two-thirds of Veves' group of patients with highpressures did not develop ulceration In a large-scale screening of over 1000patients in a diabetic clinic in Liverpool, about 25% of patients were deemed

``at risk'' of ulceration but only 2.8% had a history of previous ulceration4.Our screening methods are, therefore, generally highly sensitive but low inspeci®city Even if we could identify with accuracy those patients with highpressures under the foot who were certain to ulcerate, the initial treatment

or protection should always be conservative, i.e non-operative It must also

be remembered that pressure is de®ned as force divided by area Insolesand shoes can redistribute pressure over the whole foot and reduce peakpressures at critical points Surgery is normally ablative to some degree andwill reduce the total area of the foot, thus increasing the overall pressure.Transfer lesions may then occur, leading to further surgery and a spiral ofevents

However, shoes and insoles have a signi®cant failure rate in preventingprimary ulceration or re-ulceration Edmonds5found a 25% recurrence rate

in both neuropathic and ischaemic ulcers, even with patients who acceptedand wore special shoes and insoles For those who wore their own shoes,over half the neuropathic group and 83% of the ischaemic group re-ulcerated This is not surprising because, as already noted, ulceration in thediabetic foot largely occurs because of pressure on the at-risk foot and,unless those pressures are adequately modi®ed, then re-ulceration willoccur The risks of recurrent ulceration are ascending infection, osteomye-litis, wet and dry gangrene and amputation Helm6noted that nearly halfthe ulcer recurrences in his series were secondary to an underlyingbiomechanical problem or bony prominence Myerson7found 19 of 22 ulcerrecurrences had an underlying ®xed deformity or osseous prominence.Before considering surgery it is important to assess the patient as a wholeand also to consider the underlying aetiology of the recurrent ulceration Inassessing any ulceration we use the Liverpool classi®cation (Table 18.1) asthis is a practical way of approaching the problem Primarily we mustconsider whether the underlying aetiology is neuropathic, ischaemic orneuro-ischaemic, i.e a combination of both and accurate assessment ofvascular status, as described in Chapter 16, is essential It is vitallyimportant not to proceed with any surgery unless there is a goodexpectation that any wound will heal The foot shown in Figure 18.1 wasreferred fromanother hospital, having already undergone three operations,

starting with the amputation of an infected toe The failure of each wound

to heal was followed by more radical surgery, producing the ``lobster foot''illustrated, which was still not healing because the underlying problemwasperipheral vascular disease The amount of blood supply required to heal asurgical wound is several times that required to keep the skin intact in the

®rst place Figure 18.2 shows a foot with hallux valgus in which an ulcerwas present over the medial aspect of the ®rst metatarsophalangeal joint in

a middle-aged diabetic patient with neuropathy This, however, is a classicsite for ischaemic ulceration and the ulcer was caused by pressure from theshoe on his hallux valgus deformity Pressure from a shoe upper is highest

at the points where the radius of curvature is lowest, i.e over the ®rst and

®fth metatarsal heads The ulcer had a necrotic appearance to it and hisankle brachial pressure index was signi®cantly low An arteriogram

Table 18.1 Liverpool classi®cation of diabetic foot ulcers

Complicated, i.e presence of cellulitis, abscess or osteomyelitis

Figure 18.1 ``Lobster foot'' following multiple surgery

showed a stenosis amenable to angioplasty, following which his pressureindex improved to 1.07 We were then able to debride the ulcer down togood bleeding bone and heal it (Figure 18.3) Improving the blood supplyprior to surgery can be vitally important in avoiding, or limiting the extent

of, any subsequent amputation and ensuring that wounds such as this onewill heal and not simply end up as a larger non-healing wound In this casethe necrotic ulcer was stable, with no cellulitis or spreading infection Ifacute infection is present, then urgent surgery is required to controlinfection and prevent it spreading If that can be achieved it may then bepossible to improve the circulation prior to performing any de®nitiveclosure or distal amputation

Second, if ulceration is present, we must assess whether the ulcer isuncomplicated or complicated, i.e whether cellulitis or deep infection, such

as an abscess or osteomyelitis, is present It should be noted that a positivewound swab froman ulcer does not necessarily imply infection because allulcers become colonized with bacteria, both aerobic and anaerobic Clearly,deep infection requires immediate treatment but identi®cation of under-lying osteomyelitis is important, as this will in¯uence the amount of anybony resection Although it has been suggested that osteomyelitis can besuccessfully treated with antibiotics alone8, it has been our experience that it

is dif®cult to eradicate true osteomyelitis without resecting the infectedbone This has been the experience of others9 and studies comparing

Figure 18.2 Necrotic ischaemic ulcer over ®rst metatarsophalangeal joint beingdebrided

conservative surgery and medical treatment alone have shown bene®t fromsurgery10 The controversy arises fromthe dif®culties in diagnosingosteomyelitis with any certainty from plain radiographs The changes ofdiabetic osteopathy, which include periosteal reactions, osteoporosis, juxta-articular cortical defects and osteolysis, can mimic the changes ofosteomyelitis (see Chapter 15).

Which patients then may bene®t from surgery? Our main indication forelective prophylactic surgery in the diabetic foot is recurrent ulceration inthe presence of a ®xed deformity The ®xed deformity may be clawed toeswith recurrent ulceration or it may be intractable ulceration under themetatarsal heads due to gross forefoot deformity (Figure 18.4) In neuro-arthropathic feet it may be recurrent plantar midfoot ulceration due to arocker bottom deformity Often the most dif®cult patient to treatsuccessfully with shoes and insoles is the middle-aged patient who isoverweight and still very active, trying to hold down a manual job Such apatient has frequently had previous ulceration and surgery and mayalready have lost some toes What is often noticeable about these feet is howthe plantar skin under the metatarsal heads has lost the elasticity seen in anormal foot and how the fat pads under the metatarsal heads have beendrawn forward and atrophied The loss of elasticity is due partly to theglycosylation of collagen in the skin and partly to scar tissue frompreviousulceration Scar tissue lacks the elasticity of normal skin and is more prone

to break down with shearing forces

Figure 18.3 Ulcer in Figure 18.2 following debridement and now with goodbleeding base

For the patient with intractable plantar ulceration under the metatarsalheads, we may do a forefoot arthroplasty with resection of the metatarsalheads The foot is approached through 2±3 dorsal incisions between themetatarsal heads and the metatarsal heads resected The undersurface ofthe metatarsal neck is chamfered to provide a smooth surface whenweightbearing and pushing off Figure 18.5 shows this being done in apatient who required a forefoot arthroplasty with amputation of hisremaining toes The site of chronic ulceration can be left open to drain andheal and Figure 18.6 shows the end result When fashioning skin ¯aps, it isimportant to leave suf®cient plantar skin to cover the end of the foot, as theplantar skin is best adapted for withstanding the stresses of weightbearing.

In resecting the metatarsal heads one aims for a gentle crescent along theresected heads (Figure 18.7) If the majority of toes are still present, then

Figure 18.4 X-ray showing deformed forefoot with dislocated toes and previouspartial ray amputation

these can usually be preserved If there is gross deformity or only a couple

of defunctioned toes are left, then it is better to amputate these at the sametime, because otherwise they will inevitably protrude and be liable tofurther injury When assessing patients with intractable forefoot ulceration

Figure 18.5 Forefoot arthroplasty with chamfering of metatarsal necks

Figure 18.6 End result forefoot arthroplasty with resection of remaining toes

it is important to look at the tendo achilles, as equinus deformity ortightness of this tendon restricts ankle joint dorsi¯exion and leads to greaterpressure under the metatarsal heads during the toe-off phase of walking.Lengthening a tight tendo achilles can facilitate ulcer healing and result in alower rate of recurrence11.

Individual toe problems may be addressed in different ways, depending

on the pathology Clawing usually affects all the lesser toes but sometimes

an individual toe will be clawed or hammered, causing chronic ulceration.Our ®rst line of treatment will be to try to improve the diabetic footwearand provide suf®cient space in the toe-box of the shoe If surgery isrequired, then the toe can be straightened by an interphalangeal fusion, orsimply by resection of the head of the proximal phalanx, along with atenotomy of the extensor tendon and a dorsal capsulotomy of the

Figure 18.7 X-ray of forefoot arthroplasty showing gentle crescent of resectedmetatarsal heads (note previous surgery to metatarsals)

metatarsophalangeal joint If the toe is markedly subluxed or dislocated atthe metatarsophalangeal joint, then it will be more appropriate to do aStainsby-type procedure with a proximal hemiphalangectomy of theproximal phalanx of the toe If there is a ®xed mallet deformity of the toe,then a terminal Syme procedure with resection of the distal phalanx issometimes indicated It is not unusual for a patient to present with digitalgangrene which is sometimes associated with ulceration and soft tissue gas

on the X-ray, indicating spreading infection Soft tissue gas does notnecessarily mean clostridial infection, as many organisms, both aerobic andanaerobic, produce soft tissue gas in diabetic patients12 In neuropathic feetthe overall circulation may be good but septic thrombi in digital vessels cancause gangrene Dry gangrene of the toe can be left to demarcate andproceed to autoamputation, but wet gangrene, as in this case, requiresprompt amputation to stop infection spreading Infection in the foot canspread along the tissue planes of tendons and in diabetic patients infectioncan often spread with great rapidity, particularly if the patient continueswalking The effectiveness of the in¯ammatory response may be reduced indiabetic patients Microvascular studies have shown an impaired response

to minor thermal injury, and leukocyte action may also be impaired13,14

We usually use a racquet incision to disarticulate the toe (Figure 18.8) andthen leave the wound open to heal by secondary intention Primary closure

of an infected diabetic wound generally leads to chronic infection If theassociated metatarsal is involved with osteomyelitis, then it may be

Figure 18.8 Disarticulation of gangrenous toe using racquet incision

necessary to do a partial ray amputation Ray amputations are discussed inChapter 19.

In the past the literature has suggested that prophylactic surgery indiabetic patients carries a high rate of complications Gudas15did a 5 yearretrospective study of 32 procedures considered to be prophylactic surgery

in diabetic patients His complication rate was over 30% and occurredlargely in areas where ulceration had previously been present for one yearunder a metatarsal head Petrov et al16 looked at the results of removal

of all the metatarsal heads in 12 diabetic patients and 15 rheumatoidpatients There was an ulcer recurrence rate of 25% in the diabetic patients,marginally less than in the rheumatoid patients In the diabetic patients,recurrence was most frequent under the third and fourth metatarsal headsand occurred between 1 and 2 years following surgery This is a signi®cantcomplication rate, as any revision surgery will shorten the foot further andproduce more complications Quebedeaux et al17 looked at unilateral ®rstray amputations in 25 diabetic patients at a mean of approximately 3 yearsfollowing surgery Prior to amputation the lesser toes on the operated sidehad been normal At follow-up there were signi®cantly more deformities ofthe lesser toes of the ipsilateral foot and more new ulcerations than in thecontralateral foot with an intact ®rst ray Murdoch et al18 reviewed thesubsequent course after 90 great toe and ®rst ray amputations in diabeticpatients; 60% of all patients had a second amputation at a mean of 10months after the ®rst and 17% subsequently had a below-knee and 11% atransmetatarsal amputation These ®gures partly re¯ect the progress of thedisease, but on the contralateral side only 5% had a below-knee ortransmetatarsal amputation As you reduce the weightbearing area of thefoot you shift the pressure elsewhere Armstrong et al19, however, carriedout a retrospective review of resectional arthroplasty on single lesser toesand compared the results in 31 diabetic patients with 33 non-diabeticpatients At a mean of 3 years postoperatively, only one of the diabeticpatients had re-ulcerated However, diabetic patients with a previoushistory of ulceration were more likely to have a postoperative infection thannon-diabetic patients or those with no history of ulceration

Before considering surgery, it is also important to consider why operative treatment has failed Although we work closely with ourorthotist, pressure-relieving windows in insoles may not be in the correctplace The normal foot changes considerably in shape between a non-weightbearing and a weightbearing position As the plantar arch ¯attens onweightbearing, the metatarsal heads move forward and the lessermetatarsal heads also move laterally These changes are probably lesspronounced in the severe diabetic foot because of generalized stiffness, butsome ¯attening will occur The insole in Figure 18.9 shows the position ofthe weight-relieving window and the actual position of the metatarsal head

non-It can be seen that the window is not under the ulcer and the edge effectfromthe window can create ulceration in itself.

Recurrent ulceration and osteomyelitis of the calcaneum pose a particularproblem The heel is not so easy to unload, with either a plaster cast orfootwear and insoles, as the forefoot It is dif®cult keeping the pressure offthe heel, even in a resting position, and patients with neuropathy are notalways very compliant because of a lack of sensory feedback Ulceration istherefore dif®cult to heal, becomes chronic and often leads to underlyingosteomyelitis Because of these problems, many patients have ended upwith a below-knee amputation A surgical alternative, however, can be apartial or even total calcanectomy through a midline plantar incision,known as Gaenslen's incision (Figure 18.10) It is necessary to removesuf®cient calcaneumto either clear existing osteomyelitis or provideenough slack to allow approximation of the skin following ulcer excision.Extensive excision of the calcaneum will also remove the distal attachment

of the tendo achilles which, in any case, may be necrotic if involved in theulcerated area The tendon is debrided and allowed to retract proximally.Postoperatively, patients will usually require a moulded ankle±foot orthosisbut generally are able to mobilize well, with much lower energyrequirements than if a below-knee amputation had been performed.Although originally described by Gaenslen in 1931, there have been fewseries reporting results of these procedures in diabetic patients The

Figure 18.9 Insole with weight relieving window placed too proximallyÐactualsite of ulcer is cross-hatched and indicated with arrow

operation failed in eight of the 18 diabetic patients reported by Crandall andWagner20 More recently Smith et al21 reported that six of their sevendiabetic patients went on to complete wound healing with no loss of theirpre-operative ability to walk Baumhauer et al22 reported a series of eightpatients undergoing total calcanectomy for calcaneal osteomyelitis, ofwhomsix were diabetic Five of the diabetic patients healed and onerequired a below-knee amputation The minimum acceptable pre-operativeankle brachial pressure index in both Smith's and Baumhauer's series wasgreater than 0.45.

The neuro-arthropathic foot is a special challenge It develops in lessthan 1% of diabetic patients, and is a chronic, relatively painless,degenerative process affecting the weightbearing joints of the foot Thepatient will often present with a hot, swollen, erythematous foot Such afoot is not entirely painless, but the pain experienced is not in proportion

to the degree of swelling or bony changes apparent on X-ray The maindanger is that it will be mistaken for infection and osteomyelitis, andoperated on inappropriately Radiological investigations can be mislead-ing, as the appearances on plain radiographs and magnetic resonanceimaging scans of the neuro-arthropathic foot can be mistaken for infection

It is possible to have an infected neuro-arthropathic foot, but this is veryrare in the acute presentation The neuro-arthropathic foot goes throughthree stages, described by Eichenholtz23 In Stage I there is acute

Figure 18.10 Gaenslen's incision for partial calcanectomy showing the exposedcalcaneum

in¯ammation associated with hyperaemia and erythema, the bonedissolves and fragments and fractures and dislocations are common InStage II there is bony coalescence, decreasing swelling, and radiographicevidence of periosteal new bone formation is present In Stage III, bonyconsolidation and healing occurs This whole process is variable, but maytake 2±3 years to run its full course The joints most commonly affected arethe midtarsal joints (60% of patients), the metatarsophalangeal (30%) andthe ankle joint (10%) In the acute neuro-arthropathic foot, i.e EichenholtzStage I, surgery is almost always contra-indicated The bone is osteopenicand the literature abounds with cases of internal ®xation which have failed

in the acute neuro-arthropathic foot The one exception to this may be theacute midfoot dislocation, which is severe and unstable Myerson24 hasreported that this can be reduced and ®xed, provided no bonyfragmentation is present Prophylactic surgery is therefore almostexclusively con®ned to the late stages of the disease, to treat recurrentulceration due to bony prominences or to stabilize a foot which isunbraceable The neuro-arthropathic foot frequently ends up with a rockerbottom deformity with a bony prominence prone to ulceration (Figure18.11) A deformity such as this can be treated with excision of the bonyexostosis through a lateral or medial incision away from the weightbearingplantar surface Late deformity, such as that in Figure 18.12 in thehindfoot, may warrant surgery to stabilize the foot in a plantigrade

Figure 18.11 Neuro-arthropathic foot with midfoot plantar bony prominence

position This patient had recurrent ulceration along the lateral border ofhis foot which was impossible to keep healed in footwear Prior to surgeryhis ulceration was healed in a plaster cast, as there is a higher rate ofinfection when operating with open ulceration He then had an openfusion of his ankle joint, correcting the marked varus deformity andallowing the whole foot to be swung round into a plantigrade position(Figure 18.13) Although a good blood supply is a prerequisite for theinitial development of a neuro-arthropathic foot, it is still important toassess the vascular state before surgery, as ischaemia may havesupervened by the time such a foot has reached the chronic stage.Surgery on neuro-arthropathic feet is not without complications In thepast there have been few series of diabetic patients with signi®cant numbersbut many complications and pseudarthroses have been reported Stuart andMorrey25 reported a series of hindfoot and midfoot fusions in 13 diabeticpatients, nine of whomhad neuro-arthropathy Of these nine, two had non-unions, two had below-knee amputations and there were three deepinfections Papa26 reported on 29 diabetic patients with neuro-arthropathywho all underwent fusion of the ankle, subtalar or transverse tarsal joints.Although salvage was successful in 93% of their patients (in that they didnot undergo amputation), there were 20 complications in 19 of the patientsand 10 pseudarthroses However, the majority of these pseudarthroses were

Figure 18.12 Neuro-arthropathic ankle with hindfoot varus and recurrentulceration on the lateral border

stable and presumably not painful because of the underlying pathy Most recently, Sammarco27 has reported results in 26 patients (21diabetic) with neuro-arthropathic fracture leading to signi®cant deformityand requiring reconstruction All feet were improved and no patientsubsequently required amputation However, there were six non-unionsplus other complications Surgery of the neuro-arthropathic foot is thus notfor the occasional foot surgeon, but nowadays can be a viable alternative toamputation for failed non-operative care.

neuroarthro-In conclusion, prophylactic surgery in the diabetic foot has a valuableplace but should always follow adequate non-operative treatment It should

be apparent that our general philosophy with diabetic foot surgery is topreserve as much of the foot as possible in order to maximize theweightbearing area The ultimate prophylaxis is not surgery but re®ned

Figure 18.13 Post-operative X-ray of Figure 18.12 showing ankle fusion held withthree large cancellous screws