period 7,8,15,34,35 . Careful patient selection, combined with expertise and close postoperative monitoring, are essential for obtaining optimal surgical outcomes while minimizing complications. CONCLUSION Although not all neuro-arthropathic feet can be prevented, the progression and subsequent destruction of the foot can be attenuated through early detection and appropriate management. This requires a thorough under- standing of the underlying pathophysiology, natural history and accepted standards of management. The ultimate goal of treatment is to maintain a useful extremity, free from ulceration, which will allow the patient to function as normally as possible throughout his/her lifetime. While longitudinal studies have not been forthcoming regarding the survival of these patients, they are certainly at risk for numerous other complications of diabetes. Prevention of ulceration and subsequent amputation is therefore a key objective in managing persons with this disorder. Constant vigilance on the part of both patient and health care providers is necessary to ensure that, once healed, the neuro-arthropathic foot is protected from further injury through appropriate footwear and careful attention to preventive foot 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, Kosofsky EM, Paul RA, Kozak GP. Neuro-neuroarthropathy (Charcot's joints) in diabetes mellitus following revascularization surgery: three case 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, 2nd edn. Philadelphia: WB Saunders, 1995; 88±97. 4. Harris JR, Brand PW. Patterns of disintegration of the tarsus in the anaesthetic foot. J Bone Joint Surg 1966; 48B: 4±16. 5. Newman JH. Spontaneous dislocation in diabetic neuropathy. J Bone Joint Surg 1979; 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: Mosby Yearbook, 1993; 149±80. 7. Sanders LJ, Frykberg RG. Diabetic neuropathic neuroarthropathy: the Charcot foot. 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 arthropathy a late sequela of osteoporosis in patients with diabetes mellitus? J Foot Ankle Surg 1998; 37: 437±9. 258 The Foot in Diabetes 10. Cundy TF, Edmonds ME, Watkins PJ. Osteopenia and metatarsal fractures in diabetic 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, Selby PL, 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. Lower Extremity 1995; 2: 207±14. 14. Eichenholtz SN. Charcot Joints. Spring®eld, IL: Charles C Thomas, 1966. 15. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The natural history of acute Charcot's arthropathy in a diabetic foot specialty clinic. Diabet Med 1997; 14: 357±63. 16. Clohisy DR, 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 neuroarthropathy in 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 reso- nance imaging: dif®culty of diagnosing osteomyelitis in patients with neuropathic neuroarthropathy. J Nucl Med 1990; 31: 549±56. 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) in diabetes mellitus: clinical study of 101 cases. Medicine 1972; 52: 191±210. 21. Caputo GM, Ulbrecht J, Cavanagh PR, Juliano P. The Charcot foot in diabetes: six key points. 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. Radiographic abnormalities 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 of bone radiopharmaceutical in diabetic neuropathy. Q J Med (New Ser) 1985; 57: 843±55. 25. Johnson JE, Kennedy EJ, Shereff MJ, Patel NC, Collier BD. Prospective study of bone, indium-111-labeled white blood cell, and gallium-67 scanning for 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. Combined bone scintigraphy and indium-111 leukocyte scans in neuropathic foot disease. J Nucl Med 1988; 29: 1651±5. 27. Longmaid HE, Kruskal JB. Imaging infections in diabetic patients. Infect Dis Clin N Am 1995; 9: 163±182. 28. Beltran J, Campanini S, Knight C, McCalla M. The diabetic foot: magnetic resonance imaging evaluation. Skel Radiol 1990; 19: 37±41. 29. Lesko P, Maurer RC. Talonavicular dislocations and midfoot arthropathy in neuropathic diabetic feet: natural course and principles of treatment. Clin Orthop Rel Res 1989; 240: 226±31. Charcot Foot 259 30. Kathol MH, El-Koury GY, Moore TE. Calcaneal insuf®ciency avulsion fractures 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 activity in patients with acute and chronic diabetic Charcot neuroarthropathy. Diabet Med 1997; 14: 527±31. 32. Selby PL, Young MJ, Boulton AJM. Bisphosphonates: a new treatment for diabetic Charcot neuroarthropathy? Diabet Med 1994; 11: 28±31. 33. Mehta JA, Brown C, Sargeant N. Charcot restraint orthotic walker. Foot Ankle Int 1998; 19: 619±23. 34. Myerson MS, Henderson MR, Saxby T, Short KW. Management of midfoot diabetic neuroarthropathy. Foot Ankle Int 1994; 15: 233±41. 35. Sammarco GJ, Conti SF. Surgical treatment of neuroarthropathic foot deformity. Foot Ankle Int 1998; 19: 102±9. 260 The Foot in Diabetes 18 Prophylactic Orthopaedic SurgeryÐIs There A Role? PATRICK LAING Wrexham Maelor Hospital, Wrexham, UK Prophylactic surgery in the diabetic foot is normally categorized as non- emergency surgery. The complications of diabetic foot ulceration can be so devastating that the concept of such surgery to prevent ulceration, or re- ulceration, is inviting. All too frequently we see feet which are suffering from repeated breakdown and creeping amputation. Surgery, though, is most often used in the acute situation as a reaction to infection or gangrene and less rarely in an elective attempt to prevent future problems. Although classi®ed as non-emergency surgery, early aggressive surgery in the acute situation, which limits the extent of amputation and avoids more proximal limb loss, is regarded by some as equally prophylactic 1 . Neuropathy and ischaemia are the two main risk factors for development of diabetic foot ulceration. However, the initiating factor in ulceration is usually 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 blood supply but lacks protective sensation. The neuropathic foot is frequently cavus in shape with clawed toes and callosities under the heel and metatarsal heads in which high pressures develop. The clawing of the toes leads to dorsal friction and increased pressures as the protruding interphalangeal joints rub against the toe box of the shoe. In a normal foot the toes take 30% and sometimes up to 50% of the load transmitted through the foot, but with severe clawing the toes become non- weightbearing, increasing the load under the metatarsal heads. In The Foot in Diabetes, 3rd edn. Edited by A. J. M. Boulton, H. Connor and P. R. Cavanagh. & 2000 John Wiley & Sons, Ltd. The Foot in Diabetes. Third Edition. Edited by A.J.M. Boulton, H. Connor, P.R. Cavanagh Copyright  2000 John Wiley & Sons, Inc. ISBNs: 0-471-48974-3 (Hardback); 0-470-84639-9 (Electronic) Ellenberg's 2 series 90% of diabetic ulcers occurred under pressure-bearing areas of the foot. Studies such as that by Veves et al 3 have shown that high plantar pressures are predictive of plantar ulceration. In their group of 86 diabetic patients, plantar ulceration occurred in 35% of those with high foot pressures but in none of those with normal pressures. Yet, despite such studies, it is not possible to predict with absolute accuracy which patients will develop ulceration. Two-thirds of Veves' group of patients with high pressures did not develop ulceration. In a large-scale screening of over 1000 patients 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 ulceration 4 . Our screening methods are, therefore, generally highly sensitive but low in speci®city. Even if we could identify with accuracy those patients with high pressures 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. Insoles and shoes can redistribute pressure over the whole foot and reduce peak pressures at critical points. Surgery is normally ablative to some degree and will reduce the total area of the foot, thus increasing the overall pressure. Transfer lesions may then occur, leading to further surgery and a spiral of events. However, shoes and insoles have a signi®cant failure rate in preventing primary ulceration or re-ulceration. Edmonds 5 found a 25% recurrence rate in both neuropathic and ischaemic ulcers, even with patients who accepted and 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 the diabetic foot largely occurs because of pressure on the at-risk foot and, unless those pressures are adequately modi®ed, then re-ulceration will occur. The risks of recurrent ulceration are ascending infection, osteomye- litis, wet and dry gangrene and amputation. Helm 6 noted that nearly half the ulcer recurrences in his series were secondary to an underlying biomechanical problem or bony prominence. Myerson 7 found 19 of 22 ulcer recurrences had an underlying ®xed deformity or osseous prominence. Before considering surgery it is important to assess the patient as a whole and also to consider the underlying aetiology of the recurrent ulceration. In assessing any ulceration we use the Liverpool classi®cation (Table 18.1) as this is a practical way of approaching the problem. Primarily we must consider whether the underlying aetiology is neuropathic, ischaemic or neuro-ischaemic, i.e. a combination of both and accurate assessment of vascular status, as described in Chapter 16, is essential. It is vitally important not to proceed with any surgery unless there is a good expectation that any wound will heal. The foot shown in Figure 18.1 was referred from another hospital, having already undergone three operations, 262 The Foot in Diabetes 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 problem was peripheral vascular disease. The amount of blood supply required to heal a surgical 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 ulcer was present over the medial aspect of the ®rst metatarsophalangeal joint in a middle-aged diabetic patient with neuropathy. This, however, is a classic site for ischaemic ulceration and the ulcer was caused by pressure from the shoe 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 his ankle brachial pressure index was signi®cantly low. An arteriogram Prophylactic Orthopaedic Surgery 263 Table 18.1 Liverpool classi®cation of diabetic foot ulcers Primary Neuropathic Ischaemic Combination of both, i.e. neuro-ischaemic Secondary Uncomplicated 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 pressure index improved to 1.07. We were then able to debride the ulcer down to good bleeding bone and heal it (Figure 18.3). Improving the blood supply prior to surgery can be vitally important in avoiding, or limiting the extent of, any subsequent amputation and ensuring that wounds such as this one will heal and not simply end up as a larger non-healing wound. In this case the necrotic ulcer was stable, with no cellulitis or spreading infection. If acute infection is present, then urgent surgery is required to control infection and prevent it spreading. If that can be achieved it may then be possible to improve the circulation prior to performing any de®nitive closure or distal amputation. Second, if ulceration is present, we must assess whether the ulcer is uncomplicated or complicated, i.e. whether cellulitis or deep infection, such as an abscess or osteomyelitis, is present. It should be noted that a positive wound swab from an ulcer does not necessarily imply infection because all ulcers 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 any bony resection. Although it has been suggested that osteomyelitis can be successfully treated with antibiotics alone 8 , it has been our experience that it is dif®cult to eradicate true osteomyelitis without resecting the infected bone. This has been the experience of others 9 and studies comparing 264 The Foot in Diabetes Figure 18.2 Necrotic ischaemic ulcer over ®rst metatarsophalangeal joint being debrided conservative surgery and medical treatment alone have shown bene®t from surgery 10 . The controversy arises from the dif®culties in diagnosing osteomyelitis with any certainty from plain radiographs. The changes of diabetic osteopathy, which include periosteal reactions, osteoporosis, juxta- articular cortical defects and osteolysis, can mimic the changes of osteomyelitis (see Chapter 15). Which patients then may bene®t from surgery? Our main indication for elective prophylactic surgery in the diabetic foot is recurrent ulceration in the presence of a ®xed deformity. The ®xed deformity may be clawed toes with recurrent ulceration or it may be intractable ulceration under the metatarsal heads due to gross forefoot deformity (Figure 18.4). In neuro- arthropathic feet it may be recurrent plantar midfoot ulceration due to a rocker bottom deformity. Often the most dif®cult patient to treat successfully with shoes and insoles is the middle-aged patient who is overweight and still very active, trying to hold down a manual job. Such a patient has frequently had previous ulceration and surgery and may already have lost some toes. What is often noticeable about these feet is how the plantar skin under the metatarsal heads has lost the elasticity seen in a normal foot and how the fat pads under the metatarsal heads have been drawn forward and atrophied. The loss of elasticity is due partly to the glycosylation of collagen in the skin and partly to scar tissue from previous ulceration. Scar tissue lacks the elasticity of normal skin and is more prone to break down with shearing forces. Prophylactic Orthopaedic Surgery 265 Figure 18.3 Ulcer in Figure 18.2 following debridement and now with good bleeding base For the patient with intractable plantar ulceration under the metatarsal heads, we may do a forefoot arthroplasty with resection of the metatarsal heads. The foot is approached through 2±3 dorsal incisions between the metatarsal heads and the metatarsal heads resected. The undersurface of the metatarsal neck is chamfered to provide a smooth surface when weightbearing and pushing off. Figure 18.5 shows this being done in a patient who required a forefoot arthroplasty with amputation of his remaining toes. The site of chronic ulceration can be left open to drain and heal and Figure 18.6 shows the end result. When fashioning skin ¯aps, it is important to leave suf®cient plantar skin to cover the end of the foot, as the plantar skin is best adapted for withstanding the stresses of weightbearing. In resecting the metatarsal heads one aims for a gentle crescent along the resected heads (Figure 18.7). If the majority of toes are still present, then 266 The Foot in Diabetes Figure 18.4 X-ray showing deformed forefoot with dislocated toes and previous partial 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 same time, because otherwise they will inevitably protrude and be liable to further injury. When assessing patients with intractable forefoot ulceration Prophylactic Orthopaedic Surgery 267 Figure 18.5 Forefoot arthroplasty with chamfering of metatarsal necks Figure 18.6 End result forefoot arthroplasty with resection of remaining toes [...]... gangrene) in persons with diabetes mellitus The initiating aetiology is most often a normal bony prominence The Foot in Diabetes, 3rd edn Edited by A J M Boulton, H Connor and P R Cavanagh & 2000 John Wiley & Sons, Ltd  280 The Foot in Diabetes combined with sensory neuropathy and inappropriate footwear, producing ulcerations which penetrate the full thickness of the skin into the bones and joints of the foot. .. through a lateral or medial incision away from the weightbearing plantar surface Late deformity, such as that in Figure 18. 12 in the hindfoot, may warrant surgery to stabilize the foot in a plantigrade Figure 18. 11 Neuro-arthropathic foot with midfoot plantar bony prominence 274 The Foot in Diabetes Figure 18. 12 Neuro-arthropathic ankle with hindfoot varus and recurrent ulceration on the lateral border position... quickly determine the options available for foot salvage Nonetheless, the surgeon cannot be certain of the full proximal extent of an infective process or the viability of remaining tissues at the beginning of debridement The patient and family must understand that the procedure is, therefore, somewhat exploratory in nature and, based upon further information obtained during the exploration, the surgeon... relatively painless, degenerative process affecting the weightbearing joints of the foot The patient will often present with a hot, swollen, erythematous foot Such a foot 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 main danger is that it will be mistaken for infection and osteomyelitis, and operated on inappropriately... arthrodesis, in intractable diabetic neuropathic arthropathy of the foot and ankle J Bone Joint Surg 1993; 75A: 1056±66 27 Sammarco GJ, Conti SF Surgical treatment of neuroarthropathic foot deformity Foot Ankle Int 19 98; 19: 102±9 The Foot in Diabetes Third Edition Edited by A.J.M Boulton, H Connor, P.R Cavanagh Copyright  2000 John Wiley & Sons, Inc ISBNs: 0-4 7 1-4 89 7 4-3 (Hardback); 0-4 7 0 -8 463 9-9 (Electronic)... achievable By 288 The Foot in Diabetes only narrowing the foot, rather than shortening it, postoperative ®tting of shoes is greatly simpli®ed Conversely, the surgeon should also consider the distinct possibility that a failed forefoot amputation done for infection may forfeit the chance for a Syme ankle disarticulation, so he/she must be reasonably sure that a partial foot amputation is the logical initial... affected are the midtarsal joints (60% of patients), the metatarsophalangeal (30%) and the ankle joint (10%) In the acute neuro-arthropathic foot, i.e Eichenholtz Stage I, surgery is almost always contra-indicated The bone is osteopenic and the literature abounds with cases of internal ®xation which have failed in the acute neuro-arthropathic foot The one exception to this may be the acute midfoot dislocation,... weightbearing, the metatarsal heads move forward and the lesser metatarsal heads also move laterally These changes are probably less pronounced in the severe diabetic foot because of generalized stiffness, but some ¯attening will occur The insole in Figure 18. 9 shows the position of the weight-relieving window and the actual position of the metatarsal head Prophylactic Orthopaedic Surgery 271 Figure 18. 9 Insole... catheter is passed into the depths of the wound from an adjacent site by means of its integral needle The catheter is sutured to the skin and connected to a bag of normal saline solution The ¯uid exits the wound between widely-spaced simple skin sutures and is collected in an absorbent dressing The irrigation continues for 3 days at the rate of 1 litre/24 hours The outer layers only of the dressing are changed... a racquet incision to disarticulate the toe (Figure 18. 8) and then leave the wound open to heal by secondary intention Primary closure of an infected diabetic wound generally leads to chronic infection If the associated metatarsal is involved with osteomyelitis, then it may be Figure 18. 8 Disarticulation of gangrenous toe using racquet incision 270 The Foot in Diabetes necessary to do a partial ray . ¯attening will occur. The insole in Figure 18. 9 shows the position of the weight-relieving window and the actual position of the metatarsal head. 270 The Foot in Diabetes It can be seen that the window. our orthotist, pressure-relieving windows in insoles may not be in the correct place. The normal foot changes considerably in shape between a non- weightbearing and a weightbearing position. As the plantar. heal. The foot shown in Figure 18. 1 was referred from another hospital, having already undergone three operations, 262 The Foot in Diabetes starting with the amputation of an infected toe. The