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The diabetic foot: current best management

Jude Smith
BSc PGCE DipMan
Podiatrist
Selby and York Primary Care Trust
Diabetes Centre
York District Hospital
E:judith.a.smith@excha.yhs-tr. northy.nhs.uk

The complications of diabetes are not limited to the foot; they can affect the eyes (cataracts, retinopathy or neurological disturbances, which particularly affect the eye muscles) or the kidneys (due to sclerotic renal disorder peculiar to diabetes). Diabetes renders patients more prone to pulmonary tuberculosis, Candida skin infections and other opportunistic infections.(3) People with diabetes are between 15 and 70 times more likely to undergo lower limb amputations.(4) In Scotland, prevalence of amputations due to diabetes (excluding loss of toes or single metatarsals) is proportionally 1% of people with diabetes(4); the total UK figure is thought to be similar.(5) 
When it comes to diabetic foot ulcers (DFUs), there is uncertainty regarding their true incidence and prevalence, as much of the treatment is delivered within the community and outpatient departments, where data collection is patchy and surveillance limited. The cost of the amputation is only a small part of the total care, since most patients have many admissions before and after surgery, with an average length of stay over 200 days.(5) The cost to the NHS is about 9m per year,(2) but this does not take into account the personal costs to the patient, such as a reduction in ability to work, time taken off work, altered body image, continual worry about the threat of amputation, dressings regimes and hospital visits.
 
Aetiology of DFUs
The breakdown of the diabetic foot has traditionally been considered to be the result of peripheral vascular disease (PVD), peripheral neuropathy and infection. More recently, other contributory causes have been implicated, such as psychosocial factors, abnormalities of pressures and loads under the foot.(6)

Vascular pathology
Disease of blood vessels is a major cause of complications in diabetes and affects all types of vessel.(7) The Framingham study reported that more than 50% of men and women with diabetes had absent foot pulses.(8) PVD tends to occur at a younger age in people with diabetes and is more likely to involve smaller blood vessels further away from the heart. Reports from the USA, UK and Finland  have confirmed that PVD is a major contributory factor in the pathogenesis of foot ulceration and subsequent major amputations.(6,9-11)

Neuropathy
Impairment of nerve function is a frequent complication of diabetes. All types of fibres are involved, so that motor, sensory and autonomic functions are affected. Patients with impaired nerve function in the foot are at risk of the complication of neuropathy whether or not they are aware of its presence. Neuropathy is one of the major factors leading to the development of DFUs.(12)

Pathway to ulceration
Despite the presence of predisposing factors, such as PVD and peripheral neuropathy, an uninjured foot may not develop serious problems. However, physical trauma is a potent cause of trouble  a puncture wound, localised pressure, repeated mechanical trauma, heat or chemical injury.(13) Where there is sensory impairment (loss of sensation), a small lesion may progress because it is not recognised and the source of injury not removed. Impairment of the blood supply may result in delayed healing. Infection is an important factor, responsible for increasing the amount of damaged tissue.(7) 
An ulcer results from a break in the dermal barrier and subsequent erosion of subcutaneous tissue. In severe cases, the breach may be extended to muscle and bone. Lack of sensation allows damage to progress to ulceration. The progression to ulceration can be attributed to an impaired arterial supply, neuropathy, musculoskeletal deformities, or a combination of these factors.(14)

Management of DFUs
Rapid intervention and aggressive management by a multidisciplinary team is essential. Management should address the following:(15)

Mechanical control
Ideally the wound site should not bear any weight and should remain completely rested until the ulcer is healed. However, asking patients to remain nonweight-bearing is both impractical and unrealistic. There are various methods and devices available that will allow patients to bear weight without affecting the wound site. Examples of pressure-relieving devices include: the scotch cast boot, the total contact cast, the diabetic pneumatic walker (such as that manufactured by Aircast), weight-relieving shoes with deflective insoles, wedge shoes for heel or forefoot problems (such as those manufactured by Darco), or more commonly used methods such as wheelchairs, Zimmer frames or crutches.

Wound control
Wound control in the neuropathic and neuroischaemic ulcer is based upon debridement of the wound and the application of dressings.(15) It is widely believed that sharp debridement of an ulcer, including the removal of callus that may surround or "roof over" the ulcer, and of all devitalised tissue, is essential to healing (see Figure 1).(16)

[[NIP08_fig1_74]]

The promotion of a local wound environment conducive to healing through the judicious use of wound dressings is an essential component of diabetic foot ulcer (DFU) treatment.(17) One systematic review summarised the available evidence on wound dressings for DFUs and concluded that due to the small number of patients included in the trials there is insufficient evidence of effect, rather than evidence of no effect.(18) With the lack of any hard evidence, the choice of dressing should be based on clinical characteristics and the needs of the wound  dressings should promote moist healing, absorb exudate, be cost-effective or have ease of removal. With the increased risk of infection and the lack of protective sensation associated with DFUs, these wounds need to be closely monitored to prevent deterioration.

Microbiological control
Once the protective layer of skin is broken there is a portal of entry for bacteria. The lethal combination of ischaemia, neuropathy and high blood sugars leaves DFUs at a high risk of becoming infected. There is a distinct lack of consensus as to how to best manage DFU infection. Published evidence on antibiotics suggests that they are not necessary in the management of ulcers that are clinically clean,(19) although Foster et al have claimed clinical benefits with more widespread prescribing (particularly in the presence of ischaemia).(20) Table 1 lists the recommended antibiotics for diabetic neuropathic ulcerations.

[[NIP08_table1_74]]

The involvement of bone and subsequent osteo-myelitis is all too common with DFUs. The identification of the presence of osteomyelitis can be problematic.(22) Radiographic evidence may not detect bone infection at the early stages.(23) There is some evidence, however, that if a sterile probe penetrates to bone the presence of bone infection is likely.(24) Initial treatment for osteomyelitis is a minimum six-week course of a bone-penetrating antibiotic (such as clindamycin 300mg four times daily).

Vascular control
A thorough assessment of vascular status is needed at the initial stage and should be closely monitored throughout the patient's treatment (see Figure 2). The main reason why some neuroischaemic DFUs fail to heal, despite receiving textbook care, is their ischaemic element. If there is suspicion of critical limb ischaemia, ulcer healing may not be achievable. Referral to specialist vascular services or a vascular surgeon may be required. Arteriography will illustrate the extent of any arterial occlusion.(25)

[[NIP08_fig2_74]]

Metabolic control
Wound healing and the response to infection can be affected by systemic, metabolic and nutritional status. It is important that glycaemia control is closely monitored; various blood tests should be performed, such as full blood count, serum creatinine and liver function tests. Referral to dietetics may be indicated if the patients' diet is thought to be poor and impairing wound healing.

Educational control
The patient must understand the importance of the ulceration, they should be encouraged to rest the area, elevate the limb when possible, and return to either the podiatry clinic or the nurse or GP if the foot shows any signs of infection such as heat, pain, redness, malodour or swelling.
 
New developments
The last few years have welcomed many different products and techniques, which aim to increase or improve healing rates:

  • Growth factors - such as platelet-derived growth factor. This stimulates fibroblasts and other connective tissue found in the skin. The benefit lies in the process of cell growth and repair.(26)
  • Larval (maggot) therapy - the sterile maggots of the green bottle fly Lucilia sericata are placed directly onto the affected area and held in place by a close net dressing. The larvae have a ferocious appetite for necrotic material while actively avoiding newly formed healthy tissue. Their benefit lies in their ability to clean the wound (see Figure 3).(27)
  • Dermagraft(TM) (Smith & Nephew) - this is a bioengineered human dermis that works as a skin graft but replaces a patient's own dermis.(28)

[[NIP08_fig3_74]]

Conclusion
The healing of a DFU is dependent upon a sound multidisciplinary team; success relies heavily on each professional adopting a holistic approach and considering all intrinsic and extrinsic factors that will affect the outcome. The long-awaited NSF may well provide us with a treatment gold standard; however, no matter how exceptional the guidelines are, there is no replacement for a diabetic foot service that is seamless between all its members, whether they are in primary or secondary care, and a team that is rich in knowledge and skill.

Practice pointers

  • Ideally the wound site should not bear any weight and should remain completely rested until the ulcer is healed.
  • It is widely believed that sharp debridement of an ulcer, including the removal of callus that may surround or "roof over" the ulcer, and of all devitalised tissue, is essential to healing.
  • The lethal combination of ischaemia, neuropathy and high blood sugars leaves diabetic foot ulcers (DFUs) at a high risk of becoming infected.
  • The main reason why some neuroischaemic DFUs fail to heal, despite receiving textbook care, is their ischaemic element.
  • The successful healing of a DFU is dependent upon a sound multidisciplinary team.


References

  1. Calman K. On the state of the public health: the annual report of the chief medical officer of the Department of Health for the year 1997. London: The Stationery Office; 1998.
  2. Spencer S. Pressure relieving interventions for preventing and treating diabetic foot ulcers (Cochrane Review). In: The Cochrane Library. Issue 4. Oxford: Update Software; 2000.
  3. Davies M. Metabolic disorders. In: Neale D, Adams I, editors. Common foot disorders. 3rd ed. Edinburgh: Churchill Livingstone; 1989. p. 353-61.
  4. Scottish Intercollegiate Guidelines Network. Management of diabetic foot disease. Implementation of the St Vincent Declaration. The care of patients in Scotland. Edinburgh: SIGN; 1997.
  5. Macleod AF, Williams DR, Sonksen PH, Boulton AJ. Diabetologia 1991;34 Suppl:A39.
  6. Boulton A. The pathway to ulceration: aetiopathogenesis. In: Boulton A, Connor H, Cavanagh PR, editors. The foot in diabetes. 3rd ed. Chichester: John Wiley & Sons Ltd; 2000. p. 19-31.
  7. Faris I. Vascular disease. In: Faris I, editor. The management of the diabetic foot. 2nd ed. Edinburgh: Churchill Livingstone; 1991. p. 9-40.
  8. Abbott RDF, Brand FN, Kannel WB. Am J Med 1990;88:76-81.
  9. Pecoraro RE, Reiber GE, Burgess EM. Diabet Care 1990;13:513-21.
  10. Reiber GE, et al. Diabet Care 1999;22:157-62.
  11. Siitonen OI, Niskanen LK, Laakso M, Siitonen JF, Pyorala K. Diabet Care 1993;16:16-20.
  12. Le Quesne P, Parkhouse N, Faris I. Neuropathy. In: Faris I, editor. The management of the diabetic foot. 2nd ed. Edinburgh: Churchill Livingstone; 1991. p. 41-64.
  13. Faris I. Mechanisms for the development of foot lesions. In: Faris I, editor. The management of the diabetic foot. 2nd ed. Edinburgh: Churchill Livingstone; 1991. p. 5-9.
  14. Bauer ES. Foot ulcers. Primary Care 2000;343:787-93.
  15. Edmonds M, Foster A. Stage 3: the ulcerated foot. In: Edmonds M, Foster A. Managing the diabetic foot. London: Blackwell Science; 2000. p. 45-76.
  16. Cavanagh P, Ulbrecht J, Caputo G. What the practising physician should know about diabetic foot biomechanics. In: Boulton A, Connor H, Cavanagh PR, editors. The foot in diabetes. 3rd ed. 2000. Chichester: John Wiley & Sons Ltd; 2000. p. 33-59.
  17. Cullum N, Majid M, O'Meara S, Sheldon T. Use of dressings: is there an evidence base? In: Boulton A, Connor H, Cavanagh PR, editors. The foot in diabetes. 3rd ed. Chichester: John Wiley & Sons Ltd; 2000. p. 153-68.
  18. O'Meara S, Cullum N, Majid M, Sheldon T. Health Technol Assess 2000;4:21.
  19. Jeffcoate W. The Diabetic Foot 2000;2(4):132-5.
  20. Foster A, McColgan M, Edmonds M. Diabet Med 1998;15 Suppl 2:S10.
  21. Sharman DL, Kerr D. The Diabetic Foot 2000;3(2):49-54.
  22. Embil J. The Diabetic Foot 2000;3(3):76-84.
  23. Schauwocker DS. Am J Roentgenol 1992;158:9-18.
  24. Grayson ML, Balaugh K, Levin E, Karchmer AW. JAMA 1995;273:721-3.
  25. McInnes A. The Diabetic Foot 2001;4:S1-11.
  26. Dahn MS. Fed Pract 1998;July:14-19.
  27. Rayman A, Stansfield G, Woolard T, Mackie A, Rayman G. The Diabetic Foot 1998;1:7-13.
  28. Gentzkow G, et al. Diabet Care 1996;19:350-4.

Resources
The Diabetic Foot (journal)
W:www.diabeticfootjournal.com