Glucose, a type of sugar, is the main source of energy for your cells. Glucose comes from the food you eat and travels in the bloodstream to your cells. When the uptake of glucose from the blood into your cells is impaired glucose accumulates in the blood. Having too much glucose in your blood, a circumstance called hyperglycemia, can cause health problems such as diabetic neuropathy and foot problems such as a callus.
Peripheral neuropathy, nerve dysfunction, is the essential cause of diabetic foot disease. The neuropathy produced by diabetes mellitus is a symmetric polyneuropathy in which motor, sensory, and autonomic functions are affected. Dysfunction of the leg nerves produces muscle atrophy, thus favours limited joint mobility and foot deformities. Theses deformities are sites of elevated pressure on the sole of the foot. Diabetic neuropathy is associated with atrophy and qualitative defects of the sub-metatarsal fat pad. The mechanical stress on the plantar surface is even greater when there is a hypotrophia of soft tissue between bones and skin. This may decrease the resistance to shear stress. The focal increase in pressure in the foot sole leads to the formation of hyperkeratosis i.e. callus formation. The hyperkeratinisation may result in a breakdown of skin and tissue integrity. Neuropathic diabetic patients have in the absence of pain no warning of impending tissue breakdown because of loss of pain sensation. In such patients the callus continues to develop, and consecutively the mechanical stimulus increases constantly. A vicious cycle is thereforc established and this mechanical traumatism contributes to soft tissue destruction. For such patients the removal of callus plays a crucial role in prevention of foot ulceration. Peripheral neuropathy with a loss of protective pain sensation is the most important factor.
Diabetic neuropathy impairs sensations so that the diabetic patient can experience foot injury without an appreciation of foot discomfort. Autonomic nervous system dysfunction causes impaired microvascular thermoregulation with anhidrosis, the inability to sweat normally on the feet. The skin becomes dry and prone to fissuring, which diminishes its effectiveness as a barrier to micro-organism invasion, becoming susceptible to infection of the foot skin.
Diabetic foot is one of the most common complications of diabetes. Podiatric attending to toenail care and callus removal are an important part of ulcer prevention. Callus is one of the leading causes of diabetic foot ulcers. Callus formation precedes ulcer formation of patients with diabetic foot ulcers. The prevention of callus leads to the prevention of diabetic foot ulcers. Callus is a diffuse area of relatively even thickness. The keratinisation in a healthy subject is defined as a normal physlological process which maintains the Stratum corneum as a protective cover. This process becomes stimulated to overactivity under the influence of intermittent compression. The result is a hypertrophy of the Stratum comeum called hyperkeratosis. Hyperkeratosis not only participates to the increase of plantar pressure but also incrcases the duration of pressure at each step.
Callus formation is known to contribute to high plantar foot pressures and ulcers are frequently seen beneath such lesions. The treatment of callus by its podiatric removal is associated with a significant fall in foot pressure. All patients presenting with callus should be seen by a podiatrist for this to be removed.
The epidermis in callosities has a higher rate of cell division than normal plantar skin and the resulting cells do not stay within the epidermis for a sufficient time to mature and differentiate fully. The renewal time of the stratum corneum is longer in case of callus. Thomas et al. have seen a renewal time of 26 days for callosities compared to 16 days for normal plantar stratum corneum. The repetitive, systematic removal of callus every 3-4 weeks is therefore mandatory, even more frequently if the diabetic patient suffers from diabetic neuropathy and peripheral vascular disease. The role of callus on the foot of diabetics is deleterious and of early and regular removal of this hyperkeratotic tissue is important. Callus may act as a foreign body elevating plantar pressures. Significant reduction in pressure is achieved by local podiatry treatment.
Callus by producing a plantar prominence, contributes to the elevation of high dynamic plantar pressure. Removal of callus can restore this pressure towards normal. The additional rise in plantar pressures produced by callus may explain the common finding of plantar ulcers forming beneath untreated callus. Mechanism for this would be that the elevated plantar pressures at the callus-floor interface are transmitted through the plaque, causing autolysis of the underlying skin. Beneath prominent metatarsal heads denuding these bony prominences reduces their surface area. This leads to an increase in pressure, removing the otherwise beneficial effect of callus debridement at these sites.
Hyperglycemia induces skin dysfunctions and disturbs keratinocyte homeostasis with increased layers of the stratum corneum. In addition hyperglycemia disturbs skin barrier function. The epidermal cell number is significantly reduced, epidermal differentiation is disturbed, and the proliferation/differentiation process of keratinocytes in the diabetic patient is disrupted.
Skin physiologically has the outside-in barrier that blocks the invasion of harmful substances and pathogenic microorganisms from the outside into the epidermis. Another skin function is the inside-out skin barrier, through which water evaporation from epidermis is adequately regulated in order to maintain biological body fluid homeostasis. The term xerosis is used to describe dryness in the epidermal layers of the skin.
Xerosis, abnormaly dry skin, is an example where barrier functions are impaired. The skin commonly observed in diabetic patients is characterized by dryness, scaling, flaking and persistent itching. Risk factors for xerosis include friction, low humidity, and use of soap. The plantar area of the foot is particularly susceptible, due to its reliance on sweat secretions to remain hydrated.
The treatment for dry skin is the repeated use of moisturizers to hydrate the skin. Their use is based on evidence of the importance of maintaining the skin’s water content. Although the skin on the plantar surface of the foot is very thick, it is highly visco-elastic and copes with high levels of frictional, compressive and shear stresses applied to it by being supple and well hydrated. Problems arise when the skin becomes dry and loses its elastic properties. Fissures can occur which are often painful and can act as portals for infection.
It is important to adequately manage xerosis so that epidermal barrier function is maintained, serving to protect underlying tissues and structures from infection and physical damage. Topical moisturisers are of benefit in managing dry skin in diabetics. Moisturising products achieve their hydrating and/or moisture barrier properties from active ingredients in- cluded in the formulation such as occlusives, humectants, emollients or rejuvenators. Treatments containing urea as a primary active ingredient are the most prolifically researched for treating symptoms of dry skin in the foot of the diabetic patient.