Every diabetic foot at stage 2 will be classiﬁed as neuropathic or neuroischaemic. It is necessary to emphasize that there is a great divide between the neuropathic foot, which lacks protective pain sensation but has a good blood supply, and the neuroischaemic foot with a combination of neuropathy and ischaemia, because the treatment will be different in the two groups and because the neuro ischaemic foot offers no leeway for error. The neuro ischaemic foot is an unforgiving foot and even well-managed diabetic patients with neuroischaemic feet sometimes come to a major amputation.
When renal impairment develops in the diabetic patient it is accompanied by ﬂuid retention with peripheral oedema, anaemia, reduced microvascular blood ﬂow and increased susceptibility to skin breakdown: thus, the addition of such renal impairment in the patient with a neuropathic or neuroischaemic foot leads to a situation of extreme risk in diabetic patients, and this syndrome is often referred to as the diabetic renal foot and has the worst prognosis of all diabetic feet.
The following components of multidisciplinary care are important at stage 2:
- Mechanical control
- Vascular control
- Metabolic control
Wound control and microbiological control are not needed as the feet have intact skin.
To maintain mechanical control, deformity must be accommodated by footwear. Callus, dry skin and ﬁssures are treated.
Deformities in the neuropathic foot may include a raised medial longitudinal arch leading to high pressure points on the sole of the foot, which develops callus and ulceration unless protected by a special insole. The insole will usually need to be accommodated in a bespoke shoe. The neuroischaemic foot is prone to develop ulcers upon its margins, often over the side of the 1st and 5th metatarsal heads, and 5th metatarsal base. Patients should be advised to wear a sufﬁciently wide and deep shoe to protect the vulnerable margins of the foot.
Customized or bespoke shoes. These accommodate the shape of the foot which cannot be ﬁtted within stock or modular shoes. The more abnormal the foot shape the greater the need for bespoke shoes. These may also be necessary if previous ulceration has resulted in scarring, depletion of ﬁbrofatty padding under the metatarsal heads, or bound down plantar tissues leading to high plantar pressures. Bespoke shoes can house moulded insoles which redistribute high plantar pressures in the neuropathic foot. In some cases of ankle deformity, bespoke boots may be necessary.
Insoles are made from a variety of polyethylene foams, microcellular rubbers and ethyl vinyl acetate foams, and can be ﬂat-bed (usually one layer, provided in stock shoes) or moulded. Moulded insoles are usually made from two or three layers of differing densities. Insoles are used to reduce or redistribute areas of high pressure, friction and shear in the following ways:
- By loading areas of the sole which are not normally in contact with the ground, such as the medial longitudinal arch, a total contact effect can be achieved, relieving local areas of high pressure
- By extending the insole up the sides of the foot, a cradle effect will reduce friction (so-called cradled insoles)
- Under particularly high-pressure areas, such as prominent metatarsal heads, areas of the insole can be excavated out to form a ‘sink’
- Extra cushioning or padding can be used to compensate for reduced ﬁbrofatty padding over the metatarsal heads
- Silicone gel plantar inserts can be used to reduce shear and this material also comes in the form of heel cups, ﬂat-bed insoles and sleeves for individual toes.
Management of speciﬁc deformities
Deformity and limited joint mobility subject the feet to abnormal mechanical forces which can lead to ulceration unless managed carefully. Some of the most common problems seen in people with diabetes are claw toes, prominent metatarsal heads, ﬁbrofatty padding depletion and displacement, hallux rigidus/limitus, hallux valgus, foot drop and rigid plantar-ﬂexed foot.
They should be accommodated in shoes with a wide, deep toe box to reduce pressure on the dorsum of the toes. This may be achieved in high-street shoes, but often extradepth shoes or bespoke shoes are needed. If the deformity is not ‘ﬁxed’ a silicone rubber device (toe prop) can correct toe position and off-load the apices.
Prominent metatarsal heads
These can be accommodated in an extra-depth stock shoe with a cushioning insole. However, where the medial longitudinal arch is high and the metatarsal heads are extremely prominent, a cradled insole with sinks and bespoke shoes will be needed.
Fibrofatty padding depletion
Where ﬁbrofatty padding is absent or greatly diminished or displaced, a cushioned insole, or felt padding can reduce plantar pressures. Patches of silicone gel can be applied over the metatarsal heads. When it is associated with raised arch and clawed toes, a cradled insole in a bespoke shoe will be needed. Felt padding should not be applied to the diabetic foot long term: removable devices are safer.
This is a very common cause of neuropathic ulceration in barefoot and sandal-wearing populations. Callus develops under the big toe and if not removed regularly an ulcer develops. A rocker sole can be applied to the sole of a shoe or sandal by an orthotist to reduce pressure at the end of the walking cycle when the toe leaves the ground. This condition may require surgical correction. Callus should be regularly debrided.
Extra-width stock shoes or bespoke shoes will be needed to protect the medial prominence.Night splints can also be used for correction of deformity.
Plantar callus is a characteristic feature of the neuropathic foot and its potential for causing ulcers should never be underestimated. It is the most important marker of a foot at risk of neuropathic ulceration. Callus concentrates pressure on the plantar aspect and increases the risk of ulceration more than 11-fold. Callus is the most important preulcerative lesion in the stage 2 foot. On the neuropathic foot it is usually hard and dry because of reduced sweating due to autonomic neuropathy. When neglected and allowed to accumulate, it causes pressure necrosis and ulceration of the underlying tissues. Good blood ﬂow is probably necessary for exuberant callus formation.
Callus also develops on the neuroischaemic foot, where it is thin and ‘glassy’ and rarely causes ulceration. We do not recommend that areas of thin glassy callus on ischaemic feet be debrided unless they develop rough areas which can catch on clothing, are causing pain or develop signs of underlying problems. The practitioner must be aware that the layer of callus may be very thin, that the texture of ischaemic callus is glazed and slippery and that without great care the scalpel blade may slip. Callus in nail sulci should also be cleared with great care when patients are ischaemic. It is very important not to traumatize the ischaemic foot: underoperating should be the rule.
Clear warning signs become apparent when callus becomes too thick and ulceration is imminent. These include:
- Small speckles of blood within callus where individual capillaries are damaged by pressure and begin to leak
- A deeper layer of white, macerated callus within callus only exposed by sharp debridement of the superﬁcial layers
- An intraepidermal bulla full of clear ﬂuid, but the underlying tissue is intact.
Emergency treatment to remove callus and reduce the excessive mechanical forces by means of footwear adaptations should be undertaken without delay.
Fissures are a complication of dry neuropathic skin. Regular application of emollient helps to prevent ﬁssures. The edges of deep ﬁssures should be cleared of callus and the crevice can be held together with Steri-strips to speed healing.
The majority of patients will be asymptomatic and ischaemia will be diagnosed on screening examination. Ischaemia should never be taken lightly. All patients with absent foot pulses should have their pressure index measured to conﬁrm ischaemia and to provide a baseline, so that subsequent deterioration can be detected before the patient presents with irreversible lesions.
Antiplatelet agents signiﬁcantly reduce myocardial infarction and stroke in high-risk patients. Thus all diabetic patients with evidence of peripheral vascular disease will beneﬁt from antiplatelet agents: 75 mg aspirin daily, or if this cannot be tolerated, clopidogrel 75 mg daily.Diabetic patients with peripheral vascular disease should also be given statin therapy. The Heart Protection Study has shown that simvastatin reduced the rate of major vascular events in a wide range of high-risk patients including those with peripheral arterial disease or diabetes. In addition patients should be encouraged to stop smoking and blood pressure should be tightly controlled. Patients who are above 55 years old and have peripheral vascular disease should also beneﬁt from an angiotensin-converting enzyme (ACE) inhibitor to prevent further vascular episodes (as indicated by the Heart Outcomes Prevention Evaluation [HOPE] and micro HOPE study). ACE inhibitors protect the vasculature in diabetic patients who have evidence of atherosclerotic disease.
When symptoms do develop in the foot with ischaemia, there are three main clinical presentations:
- Intermittent claudication
- Severe chronic ischaemia with or without rest pain
- Acute ischaemia.
The classical site of claudication is the calf, although it may occur in the thigh and buttocks in aortoiliac disease. Claudication is less common in diabetic patients compared with non-diabetic patients because of peripheral neuropathy and the very distal site of atherosclerosis in the tibial vessels of the diabetic leg. Patients with claudication rarely have vascular intervention and operative intervention is required in only 1% of diabetic patients per year although it may be indicated when the claudication is severe Patients with claudication should enter an exercise programme. Pharmacological treatment with cilostazol can now be prescribed at a dosage of 100 mg twice daily but it should not be prescribed in patients with heart failure.
Severe chronic ischaemia
With increasing severity of occlusive arterial disease, patients may develop a pink, painful pulseless foot The colour of the skin is a strikingly bright pink and the foot is cold.The amount of pain will be related to the severity of the disease and the degree of peripheral neuropathy. When neuropathy is mild, patients will have classical rest pain, which is a constant pain, often worse at night and relieved by hanging the leg down outside the bed at night. It is important not to mistake the pink painful ischaemic foot for an infected cellulitic foot. The pink painful ischaemic foot is an indication of severe arterial disease. There is no time to be lost. Urgent vascular investigations will be necessary with a view to vascular intervention. The ankle brachial pressure index will nearly always be less than 0.5, although medial calciﬁcation may give an erroneously high value. It is wise to proceed to further investigations including transcutaneous oxygen tension and toe pressure measure ments. A level below 30 mmHg conﬁrms severe ischaemia in both tests. It may be necessary to treat the ischaemia by revascularization with angioplasty if possible, as well as managing the painful neuropathy.
A sudden occlusion of a major artery, usually popliteal or superﬁcial femoral, will result in a pale, painful cold foot with purplish mottling. Initially the skin is intact, but if treatment is delayed digital necrosis will develop.
Unless the patient is profoundly neuropathic he will complain of sudden onset of pain in the leg and foot. If a hand is run down the leg a ‘cut-off ’ point will be found where the temperature of the skin suddenly decreases.
Symptoms may include:
- Blueish-grey discolouration with mottling or ‘bruised’appearance
Acute ischaemia is a clinical emergency associated with severe morbidity and mortality. If the leg is to be saved it is necessary to reperfuse it as a matter of urgency. Immediate vascular intervention is needed.
Even though neuropathy or ischaemia may now be present, progression may be checked by tight control of blood glucose, blood pressure and blood lipids, and stopping smoking as described for patients with stage 1 feet. All patients with peripheral arterial disease should take aspirin 75 mg daily.
Oedema may complicate both the neuropathic and the neuroischaemic foot and it is an important factor pre- disposing to ulceration. Its main cause will be impaired cardiac and renal function which should be investigated and treated. Venous insufﬁciency can cause swelling of the leg and foot and should be investigated with duplex scanning, treated with support hose and referred for a vascular opinion as to the need for vein surgery. Neuropathic oedema may respond to ephedrine starting at a dose of 10 mg tds but this may need to be increased up to 30–60 mg tds.