First published May 2007, updated December 2021

Key points:

  • Diabetic foot care requires a team approach.
  • Annual screening must include assessment of pulses and sensation.
  • Refer ulcers, ischaemia or new swelling.
  • All ulcers are contaminated and are portals of entry for deep infection.
  • Swelling equals Charcot arthropathy until proven otherwise.
  • Routine swabs are not helpful in the management of ulcers.

Diabetes affects 200 million people worldwide, and by 2030 this figure is expected to double1. The life-threatening cardiac and renal complications are prevented by primary and secondary care physicians through optimal blood glucose control. Limb threatening complications, consequent upon vascular insufficiency and/or neuropathy, are also best treated by prevention2. Ulcers, infection and Charcot arthropathy are potentially devastating problems that on occasion require surgical treatment. Careful surveillance and patient education programmes keep morbidity to a minimum. Diabetic foot care is best managed through a team approach (Tables 1 and 2)3.

Diabetic neuropathy

Foot problems are the reason for 20 per cent of hospital admissions in patients with diabetes. The majority of these patients have infections from ulceration attributable to their neuropathy. The lifetime risk of ulceration has been estimated at 15– 25 per cent4. Of the 40,000 diabetic amputations each year, 85 per cent follow from non-healing ulcers. Approximately half of all these are considered preventable5.

Pathophysiology — cellular

 The cellular mechanisms underlying neuronal injury are complex and subject to much ongoing research endeavour. Reactive oxygen species (nitric oxide, H2 O2 and superoxide ions) are affected by hyperglycaemia, resulting in chronic ischaemia from vasoconstriction6; poor myelination results from diminished phospholipid production7; and reduced neurotrophic factor production (insulinderived growth factor and nerve growth factor) impairs neuron homeostasis8.

Painful neuropathy and mononeuropathy

These mechanisms, along with chronic hypoxia due to microvascular changes, can damage large and small fibre nerves in the lower extremity and elsewhere. Symmetrical polyneuropathy affects sensorimotor and autonomic nerves. This may produce a painful, rather than the classical painless, neuropathy. It is important to distinguish this from other causes of lower limb pain, such as plantar fascitis or fracture.

Pain from vascular insufficiency must also be considered. More proximally, compressive mononeuropathy of the common peroneal nerve causes foot-drop in the same way that carpal tunnel and cubital tunnel syndromes may present in diabetic patients from compression of median and ulnar nerves, respectively. Treatment of neuropathic pain is best organised through the pain clinic. Newer agents such as pregabalin are useful for some, but by no means all, cases of painful neuropathy.

Table 1. Primary care pathway

Primary care:

  • General practitioner
  • Community podiatrist

Annual check:

  • 10g monofilament
  • Pulses
  • Deformity
  • Footwear

When to refer:

  • New ulcer
  • New swelling
  • New ischaemia


Table 2. Multidisciplinary team

Secondary care:

  • Secondary care podiatrist
  • Diabetologist
  • Microbiologist
  • Vascular surgeon
  • Orthopaedic surgeon
  • Amputation rehabilitation
  • Plaster technicians
  • Surgical appliances

Charcot arthropathy

In the diabetic foot, sensory neuropathy and autonomic disturbance combine to cause development of Charcot arthropathy. Poor sensation and proprioception allow repetitive minor injuries to ‘go unnoticed’; autonomically controlled blood fl ow to the bones is also altered reducing the strength of the subchondral plate. The effect is dislocation and fracture, commonly of the midfoot9. Deformity and subsequent ulceration are inevitable sequelae in untreated cases.

Eichenholz classified the stages of Charcot arthropathy. In Stage I, bone fragmentation predominates. The clinical picture is of swelling, warmth and erythema. It is important to distinguish this presentation from cellulitis and deep vein thrombosis. In contrast to cutaneous infection, the erythema of a Charcot foot will reduce with elevation of the extremity10.

Stage II is the stage of coalescence, with reduced swelling and erythema. In Stage III, attempts at repair may produce a stable but often deformed foot — in effect a malunion after a fracture. Continuing instability leads to progressive skeletal destruction and disability. Bony prominences then predispose to ulceration.

Recognition is the key to successful management of the Charcot foot and ankle. Stage I limbs can be treated by total contact casting and strict non-weight bearing. The aim is to prevent collapse of the foot. Compliance is a major problem and patient education is essential for success. Weekly cast changes become less frequent as Stage I progresses to Stage II, but until the foot is cool and there is radiological evidence of coalescence non-weight bearing must be continued.

During the period of casting regular radiological surveillance allows consideration to be given to surgical stabilisation. In selected cases timely intervention to prevent loss of normal bony architecture is indicated11.

Once the foot is cool and stable, attention turns to prevention of ulceration. Bony prominences are common even after successful total contact casting. Provision of a total contact insole, to increase the area over which weight is borne by the foot, is essential12. There should be no interval between contact cast and contact insole. This requires close co-operation between the providers of each. Accommodative footwear is usually required as well, since ordinary shoes will seldom hold both the foot and the orthotic. Prescription shoes allow extra room for insoles, and are available in wide fittings with deep toe-boxes to accommodate even severe toe deformities. Patients should be reassured that the modern hospital shoe can be aesthetically very satisfactory.

Neuropathic ulcers

Ulcers are present in 84 per cent of diabetic patients undergoing amputation. The prevalence of neuropathic ulcers is as high as 15 per cent in diabetic patients over 65 years of age10. Counterintuitively, the majority of neuropathic foot ulcers occur in type 2 diabetics. Sensory neuropathy is the most important risk factor. Ulcers develop in response to pressure and often begin where tissue necrosis occurs because of shear forces acting on skin and subcutaneous tissues.

These areas of necrosis may be hidden beneath calluses. Neuropathic ulcers classically form under the first or fifth metatarsal heads or the heel, as these are the weight-bearing parts of the foot. A contracture of the Achilles tendon, or an isolated gastrocnemius contracture, increases plantar forefoot pressures and is a surgically correctable cause of ulceration13. Ulcers may, however, develop rapidly on the dorsum, for example hammer-toes, in response to ill-fitting shoes.

Ulcer treatment is guided by classification

Traditionally ulcers have been classified according to their depth and the extent to which the limb is ischaemic (depth–ischaemia classification). The Wagner classification is best known, but has been subsequently modified10. The PEDIS system is currently used to help guide management of ulcers and associated infections (Table 3).

Location of the lesion in the forefoot or hind foot is also relevant. Heel ulcers respond slowly because of the relative hypovascularity of the specialised tissues of the heel pad. Forefoot ulcers that are slow to heal may benefit from surgical debridement of the underlying bony prominence; e.g., shaving medial sesamoid or condylectomy fifth metatarsal head.

The established treatment of a neuropathic ulcer is to off-load the pressure area. Total contact casting is the gold standard method for this, although it is not entirely free of risk of iatrogenic complications14. An Achilles lengthening operation (usually performed percutaneously and in established neuropathy without any anaesthetic requirement) can reduce plantar forefoot pressure. The contracture may, however, recur13.

Table 3. PEDIS ulcer classification

  • Perfusion
  • Extent
  • Depth
  • Infection
  • Sensation


All ulcers are contaminated and are portals of entry for deep infection. Not all ulcers require antibiotic treatment, however. Only if there is underlying bone exposed or significant (>2cm) surrounding cellulitis, should treatment be started15. Established infections are commonly polymicrobial. Swabs cannot be relied upon. Probing the depth of an ulcer gives an indication of the likelihood of underlying osteomyelitis, but not the causative organism(s).

In the presence of Charcot arthropathy neither plain x-rays, nor bone scans nor magnetic resonance imaging are sufficiently specific to reliably diagnose osteomyelitis. Biopsy and culture of deep tissues is the investigation of choice16. Expert microbiology advice then determines the best antibiotic regimen.

Soft tissue infection, usually in the intermetatarsal spaces, requires drainage. The ever-increasing array of sophisticated dressings are useful means of promoting healing, but only after proper debridement has removed all necrotic tissue. Vacuum-assisted wound healing is an excellent means of reducing the time taken for healthy granulation tissue to develop17,18.

Preventing recurrence

Once an infection or ulcer is healed the question of preventing recurrence must be addressed, and the following surgical questions asked:

  • is there a contracture of the Achilles/ gastrocnemius?
  • do weight bearing x-rays demonstrate bony spurs on the plantar surface beneath the ulcer?
  • are foot or toe deformities so pronounced that surgical correction should be considered?

These ‘local’ questions should be addressed in tandem with review of blood glucose control and vascular status.

Multidisciplinary team

 Identifying neuropathy and managing the sequelae is beyond the remit of any one group within the medical community. Primary care screening pathways form the cornerstone of prevention19, but require accessible support from the hospital. Expertise is required from several quarters in the hospital and good lines of communication are the key to successful management.

Vascular and orthopaedic foot and ankle surgical advice is best sought early, to allow limb sparing surgery to be considered when non-operative treatments have failed11. With a coordinated team approach the morbidity associated with chronic ulcers and deep infections can be reduced.


  1. Statistics 2007. (Accessed 25/02/2007, 2007, at http://
  2. Levin ME. Preventing amputation in the patient with diabetes. Diabetes care 1995; 18(10): 1383-94
  3. Edmonds ME, Blundell MP, Morris ME et al. Improved survival of the diabetic foot: the role of a specialized foot clinic. The Quarterly journal of medicine 1986; 60(232): 763–71
  4. Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA 2005; 293(2): 217–28
  5. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention. Diabetes Care 1990; 13(5): 513–21
  6. Vincent AM, Russell JW, Low P, Feldman EL. Oxidative stress in the pathogenesis of diabetic neuropathy. Endocrine Reviews 2004; 25(4): 612–28
  7. Ferreira LD, Huey PU, Pulford BE et al. Sciatic nerve lipoprotein lipase is reduced in streptozotocin-induced diabetes and corrected by insulin. Endocrinology 2002; 143(4): 1213–7
  8. Brewster WJ, Fernyhough P, Diemel LT et al. Diabetic neuropathy, nerve growth factor and other neurotrophic factors. Trends in neurosciences 1994; 17(8): 321–5
  9. Herbst SA, Jones KB, Saltzman CL. Pattern of diabetic neuropathic arthropathy associated with the peripheral bone mineral density. Journal of Bone and Joint Surgery 2004; 86(3): 378–83
  10. Brodsky J. The Diabetic Foot. In: Coughlin&Mann, ed. Surgery of the Foot and Ankle. 7th ed. St Louis: Mosby; 1999: 895–969
  11. Brodsky JW. Evaluation of the diabetic foot. Instructional Course Lectures 1999; 48: 289–303
  12. Cavanagh PR, Owings TM. Nonsurgical strategies for healing and preventing recurrence of diabetic foot ulcers. Foot Ankle Clin 2006; 11(4): 735–43
  13. Mueller MJ, Sinacore DR, Hastings MK et al. Effect of Achilles tendon lengthening on neuropathic plantar ulcers. A randomized clinical trial. J Bone Joint Surg Am 2003; 85- A(8): 1436–45
  14. Guyton GP. An analysis of iatrogenic complications from the total contact cast. Foot & Ankle International / American Orthopaedic Foot and Ankle Society [and] Swiss Foot and Ankle Society 2005; 26(11): 903–7
  15. Pinzur MS, Slovenkai MP, Trepman E, Shields NN. Guidelines for diabetic foot care: recommendations endorsed by the Diabetes Committee of the American Orthopaedic Foot and Ankle Society. Foot & Ankle International / American Orthopaedic Foot and Ankle Society [and] Swiss Foot and Ankle Society Ankle Society 2005;26(1): 113–9
  16. Brodsky JW, Schneidler C. Diabetic foot infections. The Orthopedic Clinics of North America 1991; 22(3): 473–89
  17. Andros G, Armstrong DG, Attinger CE et al. Consensus statement on negative pressure wound therapy (V.A.C. Therapy) for the management of diabetic foot wounds. Ostomy Wound Manage 2006; Suppl: 1–32
  18. Armstrong DG, Lavery LA. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomised controlled trial. Lancet 2005;366(9498): 1704–10
  19. NICE Guideline. Type 2 Diabetes: prevention and management of foot problems. 2004. guidance/CG10/niceguidance/ pdf/English/download.dspx.)