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Diabetes mellitus is a common metabolic dysfunction, which is increasing in prevalence among Indians. Among the long-term complications of diabetes, involvement of the foot is a dreaded prospect.
Management of the diabetic foot requires commitment from the medical team and the patient as well. Preventive care is nowhere more important than in diabetic foot care. Advances in investigation and intervention have occurred in many countries, and have perhaps percolated to some Indian centres. However to the vast majority of Indian doctors caring for diabetics, such sophistication is beyond their reach.
The attempt of this presentation is to review what can be achieved in our setting, without access to vascular diagnosis and surgery. In addition, we also look at some of the exciting prospects that could reach us in future.
Disorders of the foot in persons with diabetes can be classed as:
(a) infections, eg cellulitis, ulcers, abscesses, osteomyelitis;
(b) vascular, peripheral vascular disease with intermittent claudication, ischemic ulcers, gangrene and acute ischemia such as thrombosis
(c) neuropathic, Charcots joints, neuropathiculcer and deformities such as hallux valgus.
The basic disorder usually arises from neuropathy, which impairs the sense of
pain in the feet. While pain in normal limbs acts as a protection in leading to
subtle changes of posture that relieve abnormal pressure, impaired sensation
removes this protection. As a result, weight is borne despite there being an
injury, especially over bony prominences. This leads to discontinuity in the
skin. Healing is poor due to inadequate blood supply to the lower limbs and the
overlying skin. Infection can then supervene leading to the typical diabetic
foot which is unfortunately all too common. Studies from our country have shown
that predominant infection in the diabetic foot forms a significant disease
burden.
Can neuropathy be prevented or reversed ? Results from the Diabetes Control and
Complications Trial (DCCT) have shown that tight glycemic control can indeed
prevent neuropathy, or at least slow its progression. Although the study was
carried out in IDDM patients, it is likely that similar results can be obtained
in NIDDM also.
In fact, an earlier study showed tight glycemic control can prevent worsening of nerve conduction velocity in newly diagnosed diabetic subjects.
In India, rat bites are an unusual though not uncommon cause of foot lesions in persons with diabetes. In addition, ants are known to bury into anesthetic feet. Precautions such as adequate hygiene and use of mosquito nets at nights can help prevent such problems.
Studies from the West have shown that certain factors predispose to the risk of developing diabetic foot ulcers: eg, increasing duration of diabetes, poor sense of light touch, low pain perception, absent dorsalis pedis artery and the presence of retinopathy. As we have a large corpus of patients with diabetic foot lesions, multicentric studies can pool the data so that practical information can be generated in our own country, so that helpful clinical guidelines can be given for primary care physicians.
Use of topical agents to aid in the healing of foot ulcers in diabetes has been
practised. The older surgeons and physicians applied a drop or two of
conventional insulin over the wound. Advances today have seen application of
growth factors, growth hormone itself, or pharmacological agents such as
phenytoin topically to hasten the process of ulcer healing.
Among the risk factors for diabetic foot lesions is loss of sweating over the
feet. Local dysautonomia leading to dryness can be identified by the use of
local acetylcholine to document this cause of dryness. Once the risk factor is
identified, prophylactic measures are applied aggressively.
Parenteral drugs that can help in management of diabetic foot include the
hemorheological agent pentoxifylline. Given in a dose of 400 mg three times a
day, it improves red cell deformibility, and studies have shown improvement in
claudication distance. Although not an elixir of cure for all foot ulcers, it
could be additional help.
In this age of high-tech investigations, it is surprising that the plain old x
-ray of the foot can give invaluable information, such as presence of
(a) Osteoporosis and osteosclerosis
(b) osteolysis
(c) bone necrosis, new bone formation
(d) spontaneous fractures
(e) subluxation and
(f) neuropathic Artiritis.
Certain practical measures such as the use of moulded insoles and deep shoes can
help in both prevention of foot ulcers, as well as aid in early healing of
established ulcers in diabetes. It is possible to train local cobblers and to
provide them with raw materials to manufacture shoes that are helpful in
diabetic neuropathy.
It is theoretically possible for a physician to take adequate care of the feet in all diabetic patients, at all visits. Given the work-load most of us face, this may be a counsel of perfection. The next best alternative is to set aside a particular space and time for foot-care, or, establishing a diabetic foot clinic. Studies have conclusively shown that such clinics result in earlier detection and treatment of potential and actual foot lesions. The ideal combination is an orthopedic surgeon, a vascular surgeon and an endocrinologist.
Osteomyelitis is a serious complication in diabetic foot, and usually requires aggressive surgery. Osteomyelitis has been shown to be identified by using a blunt probe to examine the base of the ulcer; presence of bone at the base suggests osteomyelitis. More sophisticated measures can be used to identify bone involvement and the direction of pus, by magnetic resonance imaging. Where this facility is available, and affordable, MRI can aid the surgeon in identifying pockets of pus, and in draining all foci, in addition to visualising osteomyelitis. Advances in nuclear techniques have provided radio nuclide tagging of leucocytes, which concentrate at the site of osteomyelitis. External scanning can provide a measure of the tagged leucocyte concentration, and indirectly of the degree of focal infection. Once infection begins to resolve, the hot spot also reduces. This procedure has been used to monitor the progress of focal infection in diabetic feet.
Use of non invasive instruments such as optical pedobarograph to measure foot pressure can also aid in identifying feet at risk of developing ulcers.
Down the line, local gene therapy can come to the aid of managing diabetic peripheral vascular disease. Technology is advancing so that it is possible to transfer genes into the vascular cells that produce proteins which can ensure patency of the vessel wall. Instead of pharmacologic agents, transitorily functioning genes may be introduced in the management of vascular insufficiency, in addition to procedures such as angioplasty.
It has now been recognised that polymicrobial infections are common in diabetic foot; an average of three organisms are usually isolated. Anaerobes are more common, and staphyloccus aureus is less commonly isolated. Proper precautions must be therefore employed in the collection and culture of samples from diabetic foot infections.
While chemotherapy depends on the results of culture and sensitivity, empiric initial antibiotic treatment must be started awaiting the lab reports. The following schedule has been suggested:
Local spectrum of antibiotic sensitivity and organisms must be generated.
Good glycemic control, education of the patient and family about foot care, early evaluation of foot lesions by treating physicians, and referral to specialist centres when appropriate, all go in saving the legs of diabetic patients; nowhere is patient empowerment more important than in the prevention of foot lesions. Avoidance of bare-foot walking, meticulous examination of feet, early presentation to doctor and stopping smoking, are all very much possible, and not expensive at all.
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