The foot is not simply an organ used for movement: it is a complex organ which carries out its functions by supplying information to the brain in the form of sensations, receiving motor commands from it in return.
Sensory information warns us of the temperature and the roughness of the ground over which we are walking, of the pressure exerted on the foot and of the stresses which cause it to experience pain.
Walking about is the conseguence of commands from the brain which arrange for the muscles of the foot to move in synchrony by contracting or relaxing, in synergy with all the muscles of the body, in accordance with requirements relating to taking steps or adopting a particular posture.
Maintaining temperature, skin hydration and trophism take place via the nerve fibres which do not depend on the person’s wishes but which work independently, without the person making any conscious decisions.
Diabetic neuropathy affects the sensory nerves (sensory neuropathy) the motor nerves (motor neuropathy) and the vegetative nerves (autonomic neuropathy); the neuropathic foot is therefore a foot in which the diabetic neuropathy has altered the equilibrium of the muscles, the perception of stimuli, vegetative autoregulation, namely all three nerve components.

Sensory neuropathy
Sensory neuropathy affects the nerve fibres which send sensations to the brain.
The most serious consequence is the lowering of the pain threshold which can involve various levels of seriousness; indeed some patients have feet which are not very sensitive whereas others lose sensitivity to such a degree that they are able to endure surgery without any anaesthetic.
The lack of pain stimuli, which may initially seem an advantage, actually proves to be a curse because pain is a symptom which warns us that something is harming us.
For example, it is pain which warns us that a shoe is too tight, prompting us to take it off; if there is no pain we will continue to wear the shoes all day and, when we take them off, we realise too late that an ulcerated wound has formed.
This example is not a random one: medical literature states that over 30% of foot ulcers in diabetic patients are caused by unsuitable shoes.
Likewise, it is pain which warns us if our feet are too close to the fireside or if the sand on which we are walking is full of broken glass or shells which hurt us.
Sensory neuropathy is therefore a pathology which allows a trauma to continue for sufficient time to cause a wound without the person noticing any warning signal.
Today there are simple diagnostic methods, which are not very costly, harmless and rapidly applicable which can give early warning of the presence of sensory neuropathy ( Figure 4).
One method is to evaluate pressure sensitivity using the Semmes-Weinstein monofilament (5.07 - 10 g).
This simple instrument, which fits conveniently into a doctor’s coat pocket, consists of a nylon thread which is free at one end and anchored to a rigid "stick" at the opposite end.
This filament is placed on certain points on the foot, on the plantar and dorsal areas, and is pressed until bending (flexing) is established.
The filament normally used bends when a pressure in excess of 10 grams is applied; a reduction or even the disappearance of the ability to recognise the pressure of the monofilament on all the points of the foot being tested tells us that the patient has compromised pressure sensitivity.
The diapason and the biotensiometer, which are also low cost instruments, easy to use and small in size, transmit a vibration of variable intensity to the foot.
If the subject does not feel the vibration or only feels it at a high threshold (in excess of 25 V) this means that he or she has a vibratory sensitivity deficit.
If there is no tactile and vibratory sensitivity we can be certain that the subject we are testing has a high risk of ulceration of the foot and as such must be closely monitored in time.

Motor neuropathy
Motor neuropathy affects the nerve fibres which innervate the muscles of the foot.
These nerve fibres are sent to direct the brain’s commands to the muscles, therefore determining movements.
If a nerve which goes to a muscle is damaged, this same muscle will suffer, reacting with an involution: this will be expressed in terms of hypotrophy and atrophy.
The atrophy of a muscle or a group of muscles will result in an imbalance between muscles or groups of muscles.
Typically in a diabetic patient with motor neuropathy an imbalance is created between the extensor and the flexor muscles with a consequent imbalance between the various tendinous structures which will in turn cause an imbalance in the relating joints.
In simpler terms, if a muscle "retracts" because it is atrophying, the tendon of that muscle will drag the joint to which it is joined backwards.
The end result will be hammer toes (these will behave in a way reminiscent of animal claws), prominence of the metatarsal heads or accentuation of the flat feet, etc. ( Figure 5).
These deformities can coexist in the same foot and, in some cases worsen the deformity already present (e.g. a bunion which worsens the actual level of the valgus condition).
All this leads to deformation of the foot and to a change in plantar support with the consequente change in the supporting surface which will be reduced to particular points (e.g. metatarsal heads, heel).
This disruption of the foot’s support leads to an excessive load (point of greatest support, therefore greatest pressure) in some areas and a reduced load in others.
In attempting to protect itself from this excess load the organism strengthens the most superficial layer of skin, the corneal layer, in the areas in which greater pressure develops: this is the typical picture of callosity on the sole of the foot, defined using the medical term "hyperkeratosis" ( Figure 6).
Hyperkeratosis is an extreme attempt on the part of the foot to defend itself from excess load, but it is a defence which is short-lived: if hyperpressure is not reduced at that point, in the long term a hematoma caused by squashing will form and, if the excess load lasts, inevitably an ulcer will be formed ( Figure 7).
Hyperkeratosis is visible when the foot is inspected, but a peak of hyperpressure at specific points of the foot, even without hyperkeratosis, can be diagnosed using the appropriate podobarographic charts or platforms which provide a visible and/or numerical image of plantar pressures (Figure 8).

Autonomic neuropathy
The influence of autonomic neuropathy is much less well known and, probably, less relevant in comparison with the devastating impact of sensory and motor neuropathy.
The consequence of autonomic neuropathy which is most immediately visible is dryness (anhydrosis) of the foot due to poor functioning of the nerve fibres which regulate the activities of the secretory glands of the skin.
The dryness can cause fissuring (small cuts) of the skin ( Figure 9), especially of the heel, and these provide easy entry for germs, additionally because of the different pH (level of acidity of the skin) which is created on account of anhydrosis.
Another clinical aspect which is easy to see in a neuropathic foot and attributed to autonomic neuropathy is edema of the leg and foot; this aspect seems to be linked with a change in microcirculation regulation.
Physiologically the sympathetic autonomic system causes vasoconstriction in the arterioles and controls the blood flow to the skin via arterio-venous anastomosis (connection vessels).
Autonomic neuropathy results in a loss of sympathetic tone with the relating change in circolatory flow in this area.
It actually increases the influx of blood to the skin which is revealed clinically by an increase in temperature; it also increases capillary permeability on account of the increased hydrostatic pressure in the microcirculation: this is the mechanism by means of which edema of the lower limbs occurs ( Figure 10).
Finally it would seem that autonomic neuropathy is the cause of calcification of the arterial wall in the tunica media (so-called Monckeberg sclerosis); this aspect must be borne in mind in particular when searching for a concomitant arteriopathy of the lower limbs (Figure 11).
The rigidity of the arterial vessel, in fact, results in its inability to be compressed which, in screening for arteriopathy, can produce a false result for the data obtained from measurements taken using the ABI (Ankle Brachial Index) with Doppler and consequently lead the operator to believe that a foot which is actually neuroischemic is neuropathic (for additional information on this subject see the section on the ischemic foot).

Treatment of the plantar ulcer
The ideal would be to identify all those diabetic patients suffering from neuropathy and from deformation of the feet in order to implement a prevention programme which could succeed in reducing the risk of an ulcerative wound occurring.
In spite of attempting to apply effective prevention, and more so if s is not implemented, a neuropathic foot can become ulcerated.
The problem at this point is to treat the ulcer in the best possible way and consequently to heal it as soon as possible.
Fundamentally the treatment of the neuropathic plantar ulcer is based on three points:

• local treatment of the wound (i.e. cleaning the ulcer plus dressing)
• the treatment of any infections
• the removal of the ulcerative wound (i.e. preventing this worsening on account of the weight of the body while the subject is walking)

It is of fundamental importance to point out the fact that the failure to implement even one of these therapeutic stages drastically reduces the likelihood of the ulcerative wound healing, with, on the the other hand, the added risk of it worsening in time.
The neuropathic ulcer, for the reasons indicated above, is in most cases located on the sole of the foot.
The treatment of a plantar ulcer, as with all ulcers, must ensure not only healing of the wound but also elimination of its cause, in our case hyperpressure.
The first step will therefore be what is known as "debridement" of the ulcer which consists of removing all the non-vital tissues down to clearly bleeding tissues ( Figure 12).
This approach is frequently poorly understood and therefore not willingly accepted by the patient who, prior to debridement, had a wound which was not bleeding and was small in size ( Figure 13).
In fact debridement, by removing non-vital callous tissue, reveals the underlying ulcer, hidden by the hyperkeratosis, which is considerably larger in size.
This treatment stage is however essential: hyperkeratosis is not a tissue capable of regenerating living cells but on the contrary tends to “suffocate” the underlying living tissue needed for healing; if the hyperkeratosis is not removed the ulcer will never heal.
But debridement is only the first step in the treatment of the ulcer: even if we have carried out careful debridement and applied "advanced" latest generation dressings but then put the medicated foot back into any shoe (Figure 14). we will not have eliminated the cause which led to the ulcer, namely hyperpressure and friction.
This shoe will continue to damage the ulcer, even if it has been dressed, hindering the healing process.
It has actually been demonstrated in an Italian study that if the fibroblasts (the cells needed for the ulcer to heal) are traumatised by a load cannot correctly fulfil their regenerative functions, unlike those protected by an adequate off-bearing device.
An essential step will therefore be removing the load from the ulcerative wound; this can easily be obtained by bed-rest or by using a wheelchair.
However an ulcer takes a long time to heal and staying in bed for 2-3 months is not simply difficult to put into effect but could prove harmful for the organism (thinking, for example, of the possible formation of new bedsores on the heel or in the sacral regions).
Even recourse to a wheelchair cannot be proposed because of the resulting discomfort; from the minimum movements needed to carry out the patient’s own physiological needs to the limitations imposed by the need to deal with stairs or architectural features which deny access to handicapped people.
The optimum treatment, defined in medical terms as "gold standard", is an "ankle boot" which allows the weight to be completely taken off the foot while allowing relative mobility.
This treatment approach has been known for several years but has barely been used basically because of the possibility of the ankle boot causing further ulcers caused by pressure or friction.
These consequences were due to the rigidity of the material used, the ordinary orthopedic plaster cast ("Plaster of Paris"); Italian research must take credit for having identified new materials whose rigidity can be varied in order to cancel out these negative effects (Figure 15).
Off-bearing apparatus produced using these materials (fibreglass) is used in Centres specialising in the treatment of the diabetic foot, allowing a high percentage of plantar ulcers to be healed in relatively short periods (Film sequence "Off-Bearing Apparatus").
In subjects for whom the use of off-bearing apparatus is contraindicated (patients who have difficulty in walking, for example as a result of a stroke or a major amputation of the other limb, patients with poor vision, with varicose veins, etc.) a preformed shoe can be used, characterised by a sole which has been "hollowed out" in an appropriate way to correspond to the ulcerated zone; this footwear has been designed so that it can also hold a foot which has been "abundantly" medicated (Figure 16).
Recent studies, some of which have been published and others still under preparation, are describing good effectiveness using a removable plastic pneumatic boot as an off-bearing device (Aircast®).

The neuropathic diabetic foot is frequently a foot to which is visibly deformed on account of hammer toes, flat feet, bone prominences; these deformities are very serious, particularly if they lead to the reappearance of ulcers (recurrence), it may be appropriate to correct these surgically.
More specifically bunions, hammer toes and flat feet are frequently encountered deformities which can be corrected surgically ( Figure 17 and Figure 18).

Once again it is important to stress the fact that it is a priority to exclude any arteriopathy before subjecting a patient to an intervention to correct deformities in order to avoid the failure of the surgical procedure ( Figure 19).