Annals of the Royal College of Surgeons of England (1991) vol. 73, 170-175
Amputations
in diabetics
William S L Stebbings
MChir FRCS Lecturer in SurgerylHonorary Senior Registrar
Richard F M Wood
MD FRCS
Professor of Surgery
Professorial Surgical Unit, St Bartholomew's Hospital, London
Incidence
There are three major factors causing foot problems in the diabetic patient which may subsequently lead to a need for amputation. These are neuropathy (2), arterial insufficiency (3), and infection. Ischaemia and neuropathy contribute to the failure of healing of local injury owing to mechanical trauma. These wounds then have an increased potential of becoming infected.
diabetic. The tibial vessels are particularly prone to be affected while there is often relative sparing of the proximal arterial tree. This frequently results in presentation with peripheral gangrene and infection, despite the presence of a popliteal pulse. The question of whether microvascular changes are important in causing foot lesions is one of the unresolved problems in diabetes. Although microangiopathy, which involves thickening of the basement membrane of capillaries and arterioles, can be found in about 50% of diabetic patients with foot ulcers, the balance of opinion suggests that these changes are not responsible for the development of either ulcers or gangrene (4). However, digital and metatarsal artery disease may be relevant. Diabetics have a greater fall in blood pressure between the ankle and the toe than non-diabetics, and this gradient is most pronounced in patients who develop foot ulcers and gangrene (5).
Neuropathy
Infection
Patients who have had diabetes for 10 to 15 years are likely to have neuropathy. This is usually a diffuse distal polyneuropathy particularly affecting the motor nerves to the small muscles of the feet and leading to deformity and redistribution of the weight-bearing areas. All modalities of sensation can be impaired and approximately 30% of patients with sensorimotor neuropathy will also have an autonomic neuropathy involving both the parasympathetic and sympathetic systems.
Diabetic patients are more prone to develop infection than non-diabetics, and this is possibly due to an inadequate immune response (6). A variety of defects in leucocyte function have been demonstrated, as well as impaired cell-mediated immunity with a reduction in interleukin 2 production. Thickening of the arteriolar and capillary basement membranes may affect leucocyte migration into areas of sepsis, decreasing resistance to infection. The bacteriology of infected lesions in diabetics tends to be different from non-diabetics, in that a wide range of organisms are encountered, even in relatively minor infections. Gangrene is 53 times more frequent in diabetic men and 71 times more frequent in diabetic women over 40 years of age than in non-diabetic atherosclerotic individuals (7).
Diabetes mellitus is the disease process responsible for limb loss in one-quarter of all amputations of the leg for arterial insufficiency. In England, Wales and Northern Ireland in 1986, 4852 legs were amputated for vascular disease, of which 1156 were due to the complications of diabetes (1).
Aetiology
Arterial insufficiency The large- and medium-sized arteries of the diabetic are affected by atherosclerosis that is morphologically indistinguishable from that found in the non-diabetic. However, the indicence of atherosclerosis is increased and the site prevalence is different to that in the nonCorrespondence to: Professor R F M Wood, Professorial Surgical Unit, St Bartholomew's Hospital, West Smithfield, London ECIA 7BE
Presentation of the diabetic foot The typical presentation of the diabetic foot is with digital gangrene (Fig. 1) or ulceration of the sole of the foot. The characteristic lesion of the neuropathic foot is
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Figure 1. Digital gangrene which in the well-vascularised foot can be treated solely by amputation of the toe.
the mal perforans ulcer (Fig. 2). These ulcers are most common beneath the metatarsal heads and are usually painless. Neuropathy of the intrinsic small muscles of the foot alters the normal equilibrium between the flexor and the extensor muscle groups, which maintain correct weight distribution during walking. This alteration results in excess load being transmitted to the metatarsal heads. This initially causes hyperkeratosis and callus formation. The callus formed is abnormal since hyperglycaemia is known to cause glycosylation of keratin resulting in rigidity. Shear forces lead to cavitation under the callus which, in the presence of infection, will break down to form the classic mal perforans ulcer. Infection can spread along the tendon sheaths into the deep tissues of the foot leading to plantar abscesses. Neuropathy affecting the small muscles also results in clawing of the toes. This deformity leads to ulceration over the dorsum of the proximal interphalangeal joints, where the toes rub on the inside of the shoe. Ulcers may also develop on the tip of the toes, and on the sides of the toes due to pressure from adjacent toes or toe nails. Gangrene can occur in a neuropathic foot which is apparently well vascularised owing to digital vessel thrombosis. Gangrene can also be caused by large vessel occlusion, particularly tibial artery disease, which may result in dry gangrene of the digits or forefoot. The patient will present with rest pain (if not masked by neuropathy) and will have the clinical signs of an ischaemic leg with absent distal pulses. Infection can be difficult to diagnose in the neuropathic foot with absence of pain sensation. Swelling and redness are important signs of deep infection. Swelling can occur in the interdigital clefts, over the dorsum of the foot and in the toes. Separation of the toes owing to diffuse oedema of the deep tissues of the foot almost always signifies a deep collection of pus.
Investigation of the diabetic foot Any diabetic presenting with a foot lesion has to be assessed clinically to determine the presence or absence
Figure 2. Neuropathic or mal perforans ulcer overlying the second metatarsal head.
of neuropathy, vascular insufficiency, and the extent and severity of infection. It is important to assess the peripheral pulses to exclude an inflow problem in the aortoiliac segment. The ankle/brachial Doppler pressure index should be measured, but it must be remembered that medial calcification with vessel rigidity can lead to falsely high ratios. If there is evidence of significant impairment of Doppler ratios, angiography will be required. It is important to make an adequate assessment of the distal run-off, including views of the vessels in the feet. A detailed neurological examination should be performed to assess the extent of neuropathy. Examination of the posture of the foot is important; clawing of the toes and prominence of the metatarsal heads suggesting
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Figure 4. Tarsal Charcot osteoarthropathy in a neuropathic diabetic foot.
Treatment of the diabetic foot
Figure 3. Osteomyelitis of the first metatarsophalangeal joint.
neuropathy of the small muscles. Sensory neuropathy can result in impairment of light touch sensation, loss of vibration sense and reduced awareness of pain. Autonomic involvement is suggested by a warm, dry foot, and can be assessed at the bedside by demonstrating postural hypotension. Plain radiographs of the foot should be taken to search for evidence of deep infection, osteomyelitis (Fig. 3), septic arthritis, gas in the subcutaneous tissues suggesting spreading anaerobic infection, Charcot joints (Fig. 4), and foreign bodies. Radiologically, it can sometimes be difficult to distinguish between neuropathic and infective changes. If there is clinical evidence of infection in the foot bone, destruction should be assumed to be caused by infective processes. Swabs should be sent for bacteriological culture. A wide range of organisms may be isolated including Gram-positive aerobes (Staphylococci, Streptococci, Enterococci, and Diphtheroids), Gram-negative aerobes (E. coli, Proteus, Klebsiella) and anaerobes (Clostridium perfringens, Bacteroides and anaerobic cocci). Anaerobic infections should be suspected when there is a fetid discharge, crepitus and subcutaneous gas present on plain radiographs.
Initial management of the diabetic foot is usually concentrated on controlling infection. Careful management in the early stages will undoubtedly reduce the need for major amputation. If not critically ischaemic, the leg should be elevated to remove oedema. Broad-spectrum antibiotics with aerobic and anaerobic activity are started. Antibiotic therapy should be changed as necessary according to the results of bacteriological culture. Superficial ulcers and cellulitis may respond to this regimen alone. More severe infections will require surgical incision and drainage. If the foot has a good blood supply the major principle of treatment is radical debridement. Extensive drainage, excision and debridement of all infected and necrotic tissue should be performed. The amount of tissue requiring debridement is normally much greater than was initially suspected at clinical examination, and digital or ray amputations may be required at this stage. The primary aim of treatment is to control sepsis and if this results in a functionally useless foot a formal amputation at a higher level will be required. Medial and lateral plantar space abscesses should, if possible, be drained dorsal to the 'print line' of the foot to avoid scar formation on the weight-bearing part of the sole. In treating a central plantar abscess the incision is extended proximally towards the heel if there is evidence of spreading infection in the tendon sheaths. A guillotine amputation just above the ankle joint should be considered in patients presenting with severe spreading infections with so much devitalised tissue that the foot cannot be saved. This particularly applies to cases where there is evidence of spreading anaerobic infection. A formal below-knee amputation can then be carried out after 5-6 days of parenteral antibiotics to eradicate the
infection. In parallel with measures to control infection, assessment should be made of the need for a revascularisation procedure. Ideally, autogenous vein should be used below the inguinal ligament as vascular reconstruction
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may have to be performed in the presence of residual distal infection. Skin grafting may be required to aid the healing of foot lesions once good granulation tissue has been achieved. This may be successful on the dorsum of the foot, but is inappropirate on the sole of the foot as the graft will inevitably break down under the pressure of walking. Heel ulcers can sometimes be encouraged to heal if the patient is put in a 'scotch cast' boot to relieve pressure (8). If healing of foot problems requires a long period of immobilisation, the patient's rehabilitation may be compromised and additional problems such as fixed flexion contractures of the knee may develop. Therefore, in the case of major infection affecting the sole of the foot or a large heel ulcer, it may be best to consider a primary below-knee amputation.
Amputations Toe amputation The indications for amputation of a toe include gangrene of a single digit, deformity of the toe, and penetrating ulcers affecting the tip of the toe or the interphalangeal joints. Multiple amputations for gangrenous toes can be performed as long as the gangrene does not extend onto the forefoot. Before performing a local amputation of the toe, the measurement of Doppler ankle/brachial ratios should have ensured that the foot has a good vascular supply. The skin is incised at the junction of the living and dead tissue and plantar and dorsal flaps fashioned. The soft tissues are stripped from the proximal phalanx and this is divided at its base. Otherwise the digit can be disarticulated at the metatarsophalangeal joint. In this situation the articular cartilage should be removed to promote healing. If there is doubt about the cleanliness of the wound it can be left open for subsequent delayed closure.
Ray amputation The indications for ray amputation include an infected metatarsophalangeal joint in the well-vascularised foot, gangrene or osteomyelitis affecting a toe and involving the metatarsophalangeal joint, and infection spreading along the deep flexor tendon sheaths. The amputation involves excision of the phalanx and the head and distal half of the metatarsal shaft. The skin incision encircles the base of the toe and then extends proximally towards the medial side of the calcaneum on the sole of the foot. The toe is disarticulated at the metatarsophalangeal joint, and the incision on the sole is deepened down to the metatarsal shaft, which is freed from its surrounding soft tissue structures. The metatarsal shaft is divided obliquely from dorsal distally to plantar proximally. All dead and devitalised tissue is excised (Fig. 5). Particular attention is paid to the flexor tendons and sheaths, which are the most common site for proximal extension of infection. Pockets in the depth of the wound should be avoided as this can give rise to further spread of infection
Figure 5. Ray amputation. and failure to heal. The wound is dressed daily with a saline-soaked gauze, and may require repeated surgical debridement if further necrotic or infected areas develop.
Transmetatarsal amputation If there is gangrene involving more than two toes, a transmetatarsal amputation is considered by many to be the operation of choice, leaving the patient with a relatively functional extremity. The procedure should not be attempted in the presence of rest pain, and tends to be less successful if gangrene is extending on to the forefoot (9). Infection, if present, should be localised. The skin incision dorsally is at the level of the midshaft of the metatarsals and the plantar incision is at the crease at the base of the toes, so that the plantar flap will eventually cover the end of the foot (Figs 6 and 7). The flaps should bleed well at the margins and not contain inflamed tissue; the plantar flap should contain as much soft tissue as possible. The anterior flap should not be undermined, dividing the tendons down to the level of the bone along the line of the incision. An oblique line of division of the metatarsals spreads the load for weight bearing and reduces the risk of subsequent ulceration (10). If there is infection deep in the foot, delayed closure of the wound should be performed. This operation is also
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WS L Stebbings and R F M Wood
satisfactory, and are no longer recommended by experts in the field. They result in muscle imbalance owing to loss of extensor action which causes an equinovarus deformity. The instability makes walking difficult and tendon Achilles lengthening procedures will be required, plus the services of a skilled prosthetist.
Figure 6. Transmetatarsal amputation demonstrating the figuration of the skin flaps.
con-
indicated in those patients who have undergone successful revascularisation procedures, and gangrene has then localised to the toes and forefoot. Transtarsal amputation Transtarsal disarticulation amputation (Lisfranc) and the mid-tarsal amputation (Chopart) are not particularly
Syme's amputation In this operation the calcaneum is dissected from the heel pad which is then rotated to cover the ends of the tibia and fibula, divided transversely just above the malleoli. The end bearing stump has reasonable proprioception and the procedure can be useful in patients with visual disturbances and others who would do poorly with crutches and prostheses. In the past this operation has not been favoured since it shortens the limb by about 5 cm and leaves a stump which traditionally has been difficult to fit with a prosthesis. However, there have been recent improvements in available prostheses. A point of technique in this operation is that it is essential to preserve the branches of the posterior tibial artery which supply the heel flap. These vessels are closely applied to the posterior ligament of the ankle joint and therefore great care is required in the dissection of the calcaneum. A two-stage Syme's amputation can be undertaken even in the presence of gross sepsis. The first stage involves a simple disarticulation through the ankle; the second stage involving removal of the malleoli is performed 6 weeks later.
High amputations A higher amputation will be necessary when there is major arterial occlusion unsuitable for reconstructive surgery or where there is extensive tissue destruction. It should be possible to preserve the knee joint in about 80% of diabetics, and this will result in greater rehabilitation potential. With below-knee amputations, 70-90% of diabetics should walk with a prosthesis compared to only 30-40% of those with above-knee amputations. The outlook for diabetics undergoing major amputations is poor, and mortality rates of up to 20% have been reported. For example, in one study 15% died during their hospital stay, 8% required re-amputation and only 25% were alive 4 years later (11). Data from the Danish Amputation Register has shown that at 4 years 53% of diabetic amputees had undergone amputation of the contralateral limb (12).
Figure 7. Healed transmetatarsal amputation.
Below-knee amputation The long posterior flap below-knee amputation is the procedure most widely used (13). More recently Robinson et al. described the skew flap myoplastic technique (14). The claimed advantages include the ease of fashioning the flaps and the avoidance of the bulbous end and 'dog ears' often associated with the long posterior flap; this results in earlier prosthesis fitting. If the popliteal pulse is present, a below-knee amputation will
Amputations in diabetics usually heal, but healing can also occur when the pulse is absent; an ankle/brachial ratio in excess of 0.45 will normally ensure healing at a below-knee site.
Through-knee amputation A through-knee amputation should be considered if the patient is unlikely to be able to use a prosthesis because of paralysis, knee contracture or general infirmity and age. It is an easy and quick operation to perform, and therefore is of value in diabetics if the general condition of the patient is poor and the anaesthetic risk is high. Healing rates are good if long medial and lateral flaps are fashioned. Acceptable prostheses are now available if the general condition of the patient improves sufficiently.
Rehabilitation Active rehabilitation is vitally important in returning diabetic patients to the community. A major limb amputation may follow a prolonged period of relative immobility and previous surgical procedures which had attempted to achieve limb salvage. The amputee may therefore be both physically and mentally debilitated. Rehabilitation therefore requires a team approach from surgeons, physicians, nurses, physiotherapists, occupational therapists, social workers, prosthetists and not least the patient's friends and relatives. The artificial limb and appliance centres do not provide prostheses for patients who have undergone forefoot and ray amputations. Appropriate footwear, supports and insoles can usually be obtained either through the chiropody department or through the local orthotist. The chiropodist may be able to measure foot pressure profiles and produce moulded insoles to relieve pressure and thereby readjust the weight-bearing characteristics of the foot. These techniques can also be applied to diabetics with incipient foot problems where redistribution of the pressurebearing areas may prevent ulceration developing, particularly over the heads of the metatarsals. For patients with a transmetatarsal amputation a toe filler is required plus a shoe with a braced steel bar and rocker sole to prevent 'shoe toe' brake.
Prophylaxis The clinician's aim should be to try to prevent foot problems from occurring, and it is therefore essential that diabetic patients are taught the importance of foot care. This involves wearing wool or cotton socks with no seams, washing the feet daily and drying carefully, especially between the toes. Shoes must be well fitting, and particular care must be taken in 'breaking in' new palrs of shoes. Toe nails should be trimmed so that the
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distal edge is straight, and the corners are not rounded. Diabetic patients should not use hot-water bottles on their feet, especially if they are known to have peripheral neuropathy. Medical advice must be sought at an early stage if the foot becomes tender or if colour changes develop, especially if associated with swelling or cracks in the skin.
Conclusion Early and effective local treatment of diabetic foot problems will reduce the need for major amputations. With vigorous measures to control infection and the use of revascularisation procedures where appropriate, digital or ray amputations may be effective in patients where the initial impression is that a proximal amputation is inevitable.
References I DHSS. Amputation Statistics for England, Wales and N Ireland, 1976-1986. Statistics and Research, 1987. 2 Delbridge L, Ctercteko G, Fowler C, Reeve TS, LeQuesne LP. The aetiology of diabetic neuropathic ulceration of the foot. Br J Surg 1985;72:1-6. 3 Garda OP. Pathogenesis of macrovascular disease in the human diabetic. Diabetes 1980;29:931-42. 4 LoGerfo FW, Coffman JD. Vascular and microvascular disease of the foot in diabetes: Implications for foot care. N EnglJ Med 1984;311:1615-19. 5 Faris I. Small and large vessel disease in the development of foot lesions in diabetics. Diabetologia 1975;11:249-53. 6 Casey JI. Host defense and infections in diabetes mellitus. In: Ellenberg M, Rifkin H eds. Diabetes Mellitus. Theory and Practice, 3rd edition. New York: Medical Examination Publishing Co Inc, 1983:667-8. 7 Bell ET. Incidence of gangrene of the extremities in nondiabetic and in diabetic persons. Arch Pathol 1950;49:46973. 8 Burden AG, Jones GR, Jones R, Blandford RL. Use of the 'Scotchcast Boot' in treating diabetic foot ulcers. Br Med J
1983;286: 1555-7. 9 McKittrick LS, McKittrick JB, Risley TS. Transmetatarsal amputations for infection or gangrene in patients with diabetes mellitus. Ann Surg 1949;130:826-42. 10 Corson JD, Jacobs RL, Karmody AM, Leather RP, Shah DM. The diabetic foot. Curr Probl Surg 1986;10:769. 11 Ecker ML, Jacobs BS. Lower extremity amputations in
diabetic patients. Diabetes 1970;19: 189-95. 12 Ebskov B, Josephsen P. Incidence of re-amputation and death after gangrene of the lower extremity. Prosthet Orthot Int 1980;4:77-80. 13 Burgess EM. The below knee amputation. Bull Pros Res BRP. 1968;10:15-19. 14 Robinson KP, Hoile R, Coddington T. Skew flap myoplastic below knee amputation: a preliminary report. BrJ Surg
1982;69:554-7.
Amputations
in diabetics
William S L Stebbings
MChir FRCS Lecturer in SurgerylHonorary Senior Registrar
Richard F M Wood
MD FRCS
Professor of Surgery
Professorial Surgical Unit, St Bartholomew's Hospital, London
Incidence
There are three major factors causing foot problems in the diabetic patient which may subsequently lead to a need for amputation. These are neuropathy (2), arterial insufficiency (3), and infection. Ischaemia and neuropathy contribute to the failure of healing of local injury owing to mechanical trauma. These wounds then have an increased potential of becoming infected.
diabetic. The tibial vessels are particularly prone to be affected while there is often relative sparing of the proximal arterial tree. This frequently results in presentation with peripheral gangrene and infection, despite the presence of a popliteal pulse. The question of whether microvascular changes are important in causing foot lesions is one of the unresolved problems in diabetes. Although microangiopathy, which involves thickening of the basement membrane of capillaries and arterioles, can be found in about 50% of diabetic patients with foot ulcers, the balance of opinion suggests that these changes are not responsible for the development of either ulcers or gangrene (4). However, digital and metatarsal artery disease may be relevant. Diabetics have a greater fall in blood pressure between the ankle and the toe than non-diabetics, and this gradient is most pronounced in patients who develop foot ulcers and gangrene (5).
Neuropathy
Infection
Patients who have had diabetes for 10 to 15 years are likely to have neuropathy. This is usually a diffuse distal polyneuropathy particularly affecting the motor nerves to the small muscles of the feet and leading to deformity and redistribution of the weight-bearing areas. All modalities of sensation can be impaired and approximately 30% of patients with sensorimotor neuropathy will also have an autonomic neuropathy involving both the parasympathetic and sympathetic systems.
Diabetic patients are more prone to develop infection than non-diabetics, and this is possibly due to an inadequate immune response (6). A variety of defects in leucocyte function have been demonstrated, as well as impaired cell-mediated immunity with a reduction in interleukin 2 production. Thickening of the arteriolar and capillary basement membranes may affect leucocyte migration into areas of sepsis, decreasing resistance to infection. The bacteriology of infected lesions in diabetics tends to be different from non-diabetics, in that a wide range of organisms are encountered, even in relatively minor infections. Gangrene is 53 times more frequent in diabetic men and 71 times more frequent in diabetic women over 40 years of age than in non-diabetic atherosclerotic individuals (7).
Diabetes mellitus is the disease process responsible for limb loss in one-quarter of all amputations of the leg for arterial insufficiency. In England, Wales and Northern Ireland in 1986, 4852 legs were amputated for vascular disease, of which 1156 were due to the complications of diabetes (1).
Aetiology
Arterial insufficiency The large- and medium-sized arteries of the diabetic are affected by atherosclerosis that is morphologically indistinguishable from that found in the non-diabetic. However, the indicence of atherosclerosis is increased and the site prevalence is different to that in the nonCorrespondence to: Professor R F M Wood, Professorial Surgical Unit, St Bartholomew's Hospital, West Smithfield, London ECIA 7BE
Presentation of the diabetic foot The typical presentation of the diabetic foot is with digital gangrene (Fig. 1) or ulceration of the sole of the foot. The characteristic lesion of the neuropathic foot is
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Figure 1. Digital gangrene which in the well-vascularised foot can be treated solely by amputation of the toe.
the mal perforans ulcer (Fig. 2). These ulcers are most common beneath the metatarsal heads and are usually painless. Neuropathy of the intrinsic small muscles of the foot alters the normal equilibrium between the flexor and the extensor muscle groups, which maintain correct weight distribution during walking. This alteration results in excess load being transmitted to the metatarsal heads. This initially causes hyperkeratosis and callus formation. The callus formed is abnormal since hyperglycaemia is known to cause glycosylation of keratin resulting in rigidity. Shear forces lead to cavitation under the callus which, in the presence of infection, will break down to form the classic mal perforans ulcer. Infection can spread along the tendon sheaths into the deep tissues of the foot leading to plantar abscesses. Neuropathy affecting the small muscles also results in clawing of the toes. This deformity leads to ulceration over the dorsum of the proximal interphalangeal joints, where the toes rub on the inside of the shoe. Ulcers may also develop on the tip of the toes, and on the sides of the toes due to pressure from adjacent toes or toe nails. Gangrene can occur in a neuropathic foot which is apparently well vascularised owing to digital vessel thrombosis. Gangrene can also be caused by large vessel occlusion, particularly tibial artery disease, which may result in dry gangrene of the digits or forefoot. The patient will present with rest pain (if not masked by neuropathy) and will have the clinical signs of an ischaemic leg with absent distal pulses. Infection can be difficult to diagnose in the neuropathic foot with absence of pain sensation. Swelling and redness are important signs of deep infection. Swelling can occur in the interdigital clefts, over the dorsum of the foot and in the toes. Separation of the toes owing to diffuse oedema of the deep tissues of the foot almost always signifies a deep collection of pus.
Investigation of the diabetic foot Any diabetic presenting with a foot lesion has to be assessed clinically to determine the presence or absence
Figure 2. Neuropathic or mal perforans ulcer overlying the second metatarsal head.
of neuropathy, vascular insufficiency, and the extent and severity of infection. It is important to assess the peripheral pulses to exclude an inflow problem in the aortoiliac segment. The ankle/brachial Doppler pressure index should be measured, but it must be remembered that medial calcification with vessel rigidity can lead to falsely high ratios. If there is evidence of significant impairment of Doppler ratios, angiography will be required. It is important to make an adequate assessment of the distal run-off, including views of the vessels in the feet. A detailed neurological examination should be performed to assess the extent of neuropathy. Examination of the posture of the foot is important; clawing of the toes and prominence of the metatarsal heads suggesting
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Figure 4. Tarsal Charcot osteoarthropathy in a neuropathic diabetic foot.
Treatment of the diabetic foot
Figure 3. Osteomyelitis of the first metatarsophalangeal joint.
neuropathy of the small muscles. Sensory neuropathy can result in impairment of light touch sensation, loss of vibration sense and reduced awareness of pain. Autonomic involvement is suggested by a warm, dry foot, and can be assessed at the bedside by demonstrating postural hypotension. Plain radiographs of the foot should be taken to search for evidence of deep infection, osteomyelitis (Fig. 3), septic arthritis, gas in the subcutaneous tissues suggesting spreading anaerobic infection, Charcot joints (Fig. 4), and foreign bodies. Radiologically, it can sometimes be difficult to distinguish between neuropathic and infective changes. If there is clinical evidence of infection in the foot bone, destruction should be assumed to be caused by infective processes. Swabs should be sent for bacteriological culture. A wide range of organisms may be isolated including Gram-positive aerobes (Staphylococci, Streptococci, Enterococci, and Diphtheroids), Gram-negative aerobes (E. coli, Proteus, Klebsiella) and anaerobes (Clostridium perfringens, Bacteroides and anaerobic cocci). Anaerobic infections should be suspected when there is a fetid discharge, crepitus and subcutaneous gas present on plain radiographs.
Initial management of the diabetic foot is usually concentrated on controlling infection. Careful management in the early stages will undoubtedly reduce the need for major amputation. If not critically ischaemic, the leg should be elevated to remove oedema. Broad-spectrum antibiotics with aerobic and anaerobic activity are started. Antibiotic therapy should be changed as necessary according to the results of bacteriological culture. Superficial ulcers and cellulitis may respond to this regimen alone. More severe infections will require surgical incision and drainage. If the foot has a good blood supply the major principle of treatment is radical debridement. Extensive drainage, excision and debridement of all infected and necrotic tissue should be performed. The amount of tissue requiring debridement is normally much greater than was initially suspected at clinical examination, and digital or ray amputations may be required at this stage. The primary aim of treatment is to control sepsis and if this results in a functionally useless foot a formal amputation at a higher level will be required. Medial and lateral plantar space abscesses should, if possible, be drained dorsal to the 'print line' of the foot to avoid scar formation on the weight-bearing part of the sole. In treating a central plantar abscess the incision is extended proximally towards the heel if there is evidence of spreading infection in the tendon sheaths. A guillotine amputation just above the ankle joint should be considered in patients presenting with severe spreading infections with so much devitalised tissue that the foot cannot be saved. This particularly applies to cases where there is evidence of spreading anaerobic infection. A formal below-knee amputation can then be carried out after 5-6 days of parenteral antibiotics to eradicate the
infection. In parallel with measures to control infection, assessment should be made of the need for a revascularisation procedure. Ideally, autogenous vein should be used below the inguinal ligament as vascular reconstruction
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173
may have to be performed in the presence of residual distal infection. Skin grafting may be required to aid the healing of foot lesions once good granulation tissue has been achieved. This may be successful on the dorsum of the foot, but is inappropirate on the sole of the foot as the graft will inevitably break down under the pressure of walking. Heel ulcers can sometimes be encouraged to heal if the patient is put in a 'scotch cast' boot to relieve pressure (8). If healing of foot problems requires a long period of immobilisation, the patient's rehabilitation may be compromised and additional problems such as fixed flexion contractures of the knee may develop. Therefore, in the case of major infection affecting the sole of the foot or a large heel ulcer, it may be best to consider a primary below-knee amputation.
Amputations Toe amputation The indications for amputation of a toe include gangrene of a single digit, deformity of the toe, and penetrating ulcers affecting the tip of the toe or the interphalangeal joints. Multiple amputations for gangrenous toes can be performed as long as the gangrene does not extend onto the forefoot. Before performing a local amputation of the toe, the measurement of Doppler ankle/brachial ratios should have ensured that the foot has a good vascular supply. The skin is incised at the junction of the living and dead tissue and plantar and dorsal flaps fashioned. The soft tissues are stripped from the proximal phalanx and this is divided at its base. Otherwise the digit can be disarticulated at the metatarsophalangeal joint. In this situation the articular cartilage should be removed to promote healing. If there is doubt about the cleanliness of the wound it can be left open for subsequent delayed closure.
Ray amputation The indications for ray amputation include an infected metatarsophalangeal joint in the well-vascularised foot, gangrene or osteomyelitis affecting a toe and involving the metatarsophalangeal joint, and infection spreading along the deep flexor tendon sheaths. The amputation involves excision of the phalanx and the head and distal half of the metatarsal shaft. The skin incision encircles the base of the toe and then extends proximally towards the medial side of the calcaneum on the sole of the foot. The toe is disarticulated at the metatarsophalangeal joint, and the incision on the sole is deepened down to the metatarsal shaft, which is freed from its surrounding soft tissue structures. The metatarsal shaft is divided obliquely from dorsal distally to plantar proximally. All dead and devitalised tissue is excised (Fig. 5). Particular attention is paid to the flexor tendons and sheaths, which are the most common site for proximal extension of infection. Pockets in the depth of the wound should be avoided as this can give rise to further spread of infection
Figure 5. Ray amputation. and failure to heal. The wound is dressed daily with a saline-soaked gauze, and may require repeated surgical debridement if further necrotic or infected areas develop.
Transmetatarsal amputation If there is gangrene involving more than two toes, a transmetatarsal amputation is considered by many to be the operation of choice, leaving the patient with a relatively functional extremity. The procedure should not be attempted in the presence of rest pain, and tends to be less successful if gangrene is extending on to the forefoot (9). Infection, if present, should be localised. The skin incision dorsally is at the level of the midshaft of the metatarsals and the plantar incision is at the crease at the base of the toes, so that the plantar flap will eventually cover the end of the foot (Figs 6 and 7). The flaps should bleed well at the margins and not contain inflamed tissue; the plantar flap should contain as much soft tissue as possible. The anterior flap should not be undermined, dividing the tendons down to the level of the bone along the line of the incision. An oblique line of division of the metatarsals spreads the load for weight bearing and reduces the risk of subsequent ulceration (10). If there is infection deep in the foot, delayed closure of the wound should be performed. This operation is also
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satisfactory, and are no longer recommended by experts in the field. They result in muscle imbalance owing to loss of extensor action which causes an equinovarus deformity. The instability makes walking difficult and tendon Achilles lengthening procedures will be required, plus the services of a skilled prosthetist.
Figure 6. Transmetatarsal amputation demonstrating the figuration of the skin flaps.
con-
indicated in those patients who have undergone successful revascularisation procedures, and gangrene has then localised to the toes and forefoot. Transtarsal amputation Transtarsal disarticulation amputation (Lisfranc) and the mid-tarsal amputation (Chopart) are not particularly
Syme's amputation In this operation the calcaneum is dissected from the heel pad which is then rotated to cover the ends of the tibia and fibula, divided transversely just above the malleoli. The end bearing stump has reasonable proprioception and the procedure can be useful in patients with visual disturbances and others who would do poorly with crutches and prostheses. In the past this operation has not been favoured since it shortens the limb by about 5 cm and leaves a stump which traditionally has been difficult to fit with a prosthesis. However, there have been recent improvements in available prostheses. A point of technique in this operation is that it is essential to preserve the branches of the posterior tibial artery which supply the heel flap. These vessels are closely applied to the posterior ligament of the ankle joint and therefore great care is required in the dissection of the calcaneum. A two-stage Syme's amputation can be undertaken even in the presence of gross sepsis. The first stage involves a simple disarticulation through the ankle; the second stage involving removal of the malleoli is performed 6 weeks later.
High amputations A higher amputation will be necessary when there is major arterial occlusion unsuitable for reconstructive surgery or where there is extensive tissue destruction. It should be possible to preserve the knee joint in about 80% of diabetics, and this will result in greater rehabilitation potential. With below-knee amputations, 70-90% of diabetics should walk with a prosthesis compared to only 30-40% of those with above-knee amputations. The outlook for diabetics undergoing major amputations is poor, and mortality rates of up to 20% have been reported. For example, in one study 15% died during their hospital stay, 8% required re-amputation and only 25% were alive 4 years later (11). Data from the Danish Amputation Register has shown that at 4 years 53% of diabetic amputees had undergone amputation of the contralateral limb (12).
Figure 7. Healed transmetatarsal amputation.
Below-knee amputation The long posterior flap below-knee amputation is the procedure most widely used (13). More recently Robinson et al. described the skew flap myoplastic technique (14). The claimed advantages include the ease of fashioning the flaps and the avoidance of the bulbous end and 'dog ears' often associated with the long posterior flap; this results in earlier prosthesis fitting. If the popliteal pulse is present, a below-knee amputation will
Amputations in diabetics usually heal, but healing can also occur when the pulse is absent; an ankle/brachial ratio in excess of 0.45 will normally ensure healing at a below-knee site.
Through-knee amputation A through-knee amputation should be considered if the patient is unlikely to be able to use a prosthesis because of paralysis, knee contracture or general infirmity and age. It is an easy and quick operation to perform, and therefore is of value in diabetics if the general condition of the patient is poor and the anaesthetic risk is high. Healing rates are good if long medial and lateral flaps are fashioned. Acceptable prostheses are now available if the general condition of the patient improves sufficiently.
Rehabilitation Active rehabilitation is vitally important in returning diabetic patients to the community. A major limb amputation may follow a prolonged period of relative immobility and previous surgical procedures which had attempted to achieve limb salvage. The amputee may therefore be both physically and mentally debilitated. Rehabilitation therefore requires a team approach from surgeons, physicians, nurses, physiotherapists, occupational therapists, social workers, prosthetists and not least the patient's friends and relatives. The artificial limb and appliance centres do not provide prostheses for patients who have undergone forefoot and ray amputations. Appropriate footwear, supports and insoles can usually be obtained either through the chiropody department or through the local orthotist. The chiropodist may be able to measure foot pressure profiles and produce moulded insoles to relieve pressure and thereby readjust the weight-bearing characteristics of the foot. These techniques can also be applied to diabetics with incipient foot problems where redistribution of the pressurebearing areas may prevent ulceration developing, particularly over the heads of the metatarsals. For patients with a transmetatarsal amputation a toe filler is required plus a shoe with a braced steel bar and rocker sole to prevent 'shoe toe' brake.
Prophylaxis The clinician's aim should be to try to prevent foot problems from occurring, and it is therefore essential that diabetic patients are taught the importance of foot care. This involves wearing wool or cotton socks with no seams, washing the feet daily and drying carefully, especially between the toes. Shoes must be well fitting, and particular care must be taken in 'breaking in' new palrs of shoes. Toe nails should be trimmed so that the
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distal edge is straight, and the corners are not rounded. Diabetic patients should not use hot-water bottles on their feet, especially if they are known to have peripheral neuropathy. Medical advice must be sought at an early stage if the foot becomes tender or if colour changes develop, especially if associated with swelling or cracks in the skin.
Conclusion Early and effective local treatment of diabetic foot problems will reduce the need for major amputations. With vigorous measures to control infection and the use of revascularisation procedures where appropriate, digital or ray amputations may be effective in patients where the initial impression is that a proximal amputation is inevitable.
References I DHSS. Amputation Statistics for England, Wales and N Ireland, 1976-1986. Statistics and Research, 1987. 2 Delbridge L, Ctercteko G, Fowler C, Reeve TS, LeQuesne LP. The aetiology of diabetic neuropathic ulceration of the foot. Br J Surg 1985;72:1-6. 3 Garda OP. Pathogenesis of macrovascular disease in the human diabetic. Diabetes 1980;29:931-42. 4 LoGerfo FW, Coffman JD. Vascular and microvascular disease of the foot in diabetes: Implications for foot care. N EnglJ Med 1984;311:1615-19. 5 Faris I. Small and large vessel disease in the development of foot lesions in diabetics. Diabetologia 1975;11:249-53. 6 Casey JI. Host defense and infections in diabetes mellitus. In: Ellenberg M, Rifkin H eds. Diabetes Mellitus. Theory and Practice, 3rd edition. New York: Medical Examination Publishing Co Inc, 1983:667-8. 7 Bell ET. Incidence of gangrene of the extremities in nondiabetic and in diabetic persons. Arch Pathol 1950;49:46973. 8 Burden AG, Jones GR, Jones R, Blandford RL. Use of the 'Scotchcast Boot' in treating diabetic foot ulcers. Br Med J
1983;286: 1555-7. 9 McKittrick LS, McKittrick JB, Risley TS. Transmetatarsal amputations for infection or gangrene in patients with diabetes mellitus. Ann Surg 1949;130:826-42. 10 Corson JD, Jacobs RL, Karmody AM, Leather RP, Shah DM. The diabetic foot. Curr Probl Surg 1986;10:769. 11 Ecker ML, Jacobs BS. Lower extremity amputations in
diabetic patients. Diabetes 1970;19: 189-95. 12 Ebskov B, Josephsen P. Incidence of re-amputation and death after gangrene of the lower extremity. Prosthet Orthot Int 1980;4:77-80. 13 Burgess EM. The below knee amputation. Bull Pros Res BRP. 1968;10:15-19. 14 Robinson KP, Hoile R, Coddington T. Skew flap myoplastic below knee amputation: a preliminary report. BrJ Surg
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