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Causes of diabetic foot lesions


The causal pathways to diabetic foot disease and tobacco use and foot ulcer or amputation has not been
amputation have been studied extensively. Many conrmed in all studies.2,6
patients and health-care workers believe that diabetic Ulceration of the foot does not develop spontaneously
foot problems are caused solely by impaired blood but usually follows trauma, which may be unnoticed
supply,1 whereas neuropathy, trauma, and infection are, because of part or complete loss of pain sensation.
if anything, of even greater importance.2 Other risk Common causes of trauma include ill-tting footwear,11
factors include previous foot ulcer, improper footwear, unnoticed foreign objects in the shoes, use of improper
unobtainable or low-quality chiropody service, poor instruments for foot care, application of corn cures and
metabolic control, psychological factors, tobacco agents for removing hard skin, injuries from walking
smoking, old age, and low socioeconomic status. Foot barefoot, and scalds from washing with water that is too
complications usually develop from an interplay of hot. Surprisingly, the daily level of physical activity does
several causes, of which neuropathy may be the most not seem to increase the risk of new or recurrent foot
important. Diabetic neuropathy can involve sensory, ulceration.12,13 Infection can complicate any type of
motor, or autonomic nerves, and is usually insidious in diabetic foot ulcer and is one of the most common
onset and therefore unnoticed. It renders the feet deaf causes of hospital admission of diabetic patients. The
and blind to stimuli that normally arouse a feeling of portal of entry is usually a site of skin trauma or
pain or discomfort. Motor neuropathy leads to muscle ulceration. Local and systemic signs of inammation are
atrophy, foot deformity (gure), altered biomechanics often reduced by the presence of associated peripheral
of walking, and redistribution of foot pressures during arterial disease. The infected foot is usually painless as a
standing and walking. Abundant callus formation on result of neuropathy, and in most patients, including
pressure points, together with thinning of the sub- those with serious infections, there is no increase in
metatarsal head fat-pads, additionally increases the temperature, white-blood-cell count, or C-reactive
force of plantar pressure and ultimately results in foot protein. For these reasons, diabetic foot infections are
ulceration.3 Autonomic neuropathy results in loss of easily overlooked.14,15
sweating, which leaves the skin dry and vulnerable to The effects of social and economic factors on add-
cracks and ssures, and altered neurogenic regulation of itional risk have not been conrmed.16,17 However, fear
cutaneous blood ow. The acute Charcots foot is a rare of limb loss and failure to recognise early warning signs
but severe limb-threatening complication of neuro-
pathy, in which complex causes lead to gross dis-
organisation of the bones of the foot.4
Diabetes mellitus is associated with a 23-fold excess
risk of accelerated atherosclerosis.5 Beside well-known
risk factors (hyperlipidaemia, hypertension, and cigar-
ette smoking, advancing age, heredity, obesity, and
physical inactivity), hyperglycaemia might contribute to
the increased risk, but its role is still not well estab-
lished.6 Whereas Moss and colleagues7 found a signi-
cantly increased amputation risk associated with poor
metabolic control, large intervention studies such as
DCCT8 and UKPDS9 only showed delayed progression of
microangiopathic complications with improved meta-
bolic control. Nevertheless, a recent analysis of the DCCT
data suggested a favourable effect of intensive insulin
treatment on intima media thickness of coronary and
carotid arteries.10 A direct causal relation between Figure: Claw-hammer toes, due to motor neuropathy and muscle atrophy

www.thelancet.com Vol 366 November 12, 2005 1675


Comment

of a limb-threatening disease are common, and often 5 Brand FN, Abbott RD, Kannel WB. Diabetes, intermittent claudication, and
risk of cardiovascular events. Diabetes 1989; 38: 50409.
lead to unnecessary delays in seeking medical help. 6 Grundy SM, Benjamin IJ, Burke GL, et al. Diabetes and cardiovascular
Psychological factors may be as equally important for disease: a statement for healthcare professionals from the American Heart
Association. Circulation 1999; 100: 113446.
the development and delayed healing of diabetic 7 Moss SE, Klein R, Klein BE. The prevalence and incidence of lower extremity
foot ulcers as physical ones. Emotional support and amputation in a diabetic population. Arch Intern Med 1992; 152: 61016.
8 Diabetes Control and Complications Trial Research Group. The effect of
structured education on foot care, provided by a doctor intensive treatment of diabetes on the development and progression of
or nurse, may be benecial. One of the basic messages long-term complications in insulin-dependent diabetes mellitus.
N Engl J Med 1993; 329: 97786.
for the patient should be to seek professional advice as 9 UKPDS Study Group. Intensive blood glucose control with sulphonylureas
or insulin compared with conventional treatment and risk of
soon as possible, to minimise the risk of toe or limb complications in patients with type 2 diabetes. Lancet 1998; 352: 83753.
amputation. One of the basic messages for health-care 10 Nathan DM, Lachin J, Cleary P, et al. Intensive diabetes therapy and carotid
intima-media thickness in type 1 diabetes mellitus. N Engl J Med 2003;
professionals is to always examine the feet of patients 348: 2294303.
with diabetes who are at risk. 11 Chantelau E, Gede A. Foot dimensions of elderly people with and without
diabetes mellitusa data basis for shoe design. Gerontology 2002; 48:
24144.
Vilma Urbancic-Rovan 12 Armstrong DG, Lavery LA, Holtz-Neiderer K, et al. Variability in activity
may precede diabetic foot ulceration. Diabetes Care 2004; 27: 198084.
Department of Endocrinology, Diabetes and Metabolic Diseases, 13 Lemaster JW, Reiber GE, Smith DG, Heagerty PJ, Wallace C. Daily
University Medical Centre, 1525 Ljubljana, Slovenia weight-bearing activity does not increase the risk of diabetic foot ulcers.
vilma.urbancic@kclj.si Med Sci Sports Exerc 2003; 35: 109399.
14 Lipsky BA, International Consensus Group on Diagnosing and Treating the
I declare that I have no conict of interest. Infected Diabetic Foot. A report from the international consensus on
1 Ulbrecht JS, Cavanagh PR, Caputo GM. Foot problems in diabetes: diagnosing and treating the infected diabetic foot. Diabetes Metab Res Rev
an overview. Clin Infect Dis 2004; 39 (suppl 2): S7382. 2004; 20 (suppl 1): S6877.
2 Boyko EJ, Ahroni JH, Stensel V, Forsberg RC, Davignon DR, Smith DG. 15 Lipsky BA, Berendt AR, Embil J, De Lalla F. Diagnosing and treating diabetic
A prospective study of risk factors for diabetic foot ulcer: the Seattle foot infections. Diabetes Metab Res Rev 2004; 20 (suppl 1): S5664.
Diabetic Foot Study. Diabetes Care 1999; 22: 103642. 16 Eldor R, Raz I, Ben Yehuda A, Boulton AJ. New and experimental
3 Pataky Z, Golay A, Faravel L, et al. The impact of callosities on the approaches to treatment of diabetic foot ulcers: a comprehensive review
magnitude and duration of plantar pressure in patients with diabetes of emerging treatment strategies. Diabet Med 2004; 21: 116173.
mellitus. Diabetes Metab 2002; 28: 35661. 17 Peters EJ, Lavery LA, Armstrong DG. Diabetic lower extremity infection:
4 Sanders LJ. The Charcot foot: historical perspective 18272003. inuence of physical, psychological, and social factors.
Diabetes Metab Res Rev 2004; 20 (suppl 1): S48. J Diabetes Complications 2005; 19: 10712.

Preventing foot ulcers and amputations in diabetes


Over the past 25 years, researchers have identied causal the most common complication of diabetes. Sub-
pathways and risk factors for foot ulcers and ampu- sequently, a registry was established to follow up
tations in people with diabetes. Single interventions 639 diabetic individuals through four phases spanning
targeting modiable risk factors can reduce the in- 14 years.4,5 During the rst 4 years (198689), no
cidence of ulcers or amputations.1,2 Although specic change was made to the organisation of care, and the
activities or products may modestly benet individuals observed amputation rate was 29 per 1000 person-
in certain risk strata, there is no single magic bullet or years. During the second 4-year period (199093), the
intervention sufciently robust for long-term pre- delivery system was strategically changed, with modi-
vention of such problems in all patients in all health-care cations in self-management support and consistent
settings. education for patients, with prophylactic foot care and
By contrast, integrated patients, providers, and footwear for those judged to be at highest risk. The
system interventions tested in different settings show amputation rate during this phase was 21 per 1000
signicant improvements in prevention and processes person-years. During the next 3 years, further rene-
of care, and a reduction in ulcers and amputations.38 For ments (including access to a multidisciplinary foot-care
example, Rith-Najarian and colleagues prospective team in primary care, better communication and
intervention in a US population of Native Americans coordination, therapeutic targets, treatment options,
substantially lowered rates of amputation.4,5 After a and improved foot-care monitoring) were undertaken
needs assessment of diabetic residents in a reservation within an overall conceptual framework (Staged Dia-
community in Minnesota, amputation was identied as betes Management), and the amputation rate fell to

1676 www.thelancet.com Vol 366 November 12, 2005