Prevention and Treatment of Leg and Foot Ulcers in Diabetes Mellitus
DEFINITION
An ulcer is defined as a breakdown in the skin that may extend to involve the subcutaneous tissue or even to the level of muscle or bone. These lesions are common, particularly on the lower extremities. Leg and foot ulcers have many causes that may further define their character.
PREVALENCE
The prevalence of leg ulceration is approximately 1% to 2%, and is slightly higher in the older adult population.1 Venous ulcers are the most common form of leg ulcers, accounting for almost 80% of all lower extremity ulcerations.2 Peak prevalence is between 60 and 80 years.3 Approximately one third of patients with chronic venous insufficiency will develop venous ulceration before the age of 40 years.2 In addition, venous ulcers may have a prolonged duration and are associated with a high rate of recurrence, which contributes to their prevalence.
Approximately 15% of persons with diabetes will develop foot ulceration during their lifetime.4 Most lower extremity amputations in the United States are preceded by a foot ulcer.5
PATHOPHYSIOLOGY
Neurotrophic Ulcers
The development of neurotrophic foot ulcers in patients with diabetes mellitus has several components, including neuropathy, biomechanical pressure, and vascular supply. Peripheral neuropathy is clearly the dominant factor in the pathogenesis of diabetic foot ulcers.
The neuropathy associated with diabetes is a distal symmetrical sensorimotor polyneuropathy. There is a clear correlation between the presence of hyperglycemia and the development of neuropathy. The mechanism by which this occurs, although extensively studied, continues to be investigated. Much attention has been focused on the polyol pathway. This pathway may result in the deposition of sorbitol within peripheral nerves. In addition, oxygen radicals may be produced, which may contribute to nerve damage. Vascular disease of nerve-supplying vessels may contribute to neuropathy. More recently, increased susceptibility to compression in diabetic patients as a contributor to the development of neuropathy has been postulated.6
The motor component of neuropathy can lead to atrophy of the intrinsic musculature of the foot, resulting in digital contractures and areas of elevated pressure on the plantar foot. In addition, weakness of the anterior leg musculature may contribute to equinus deformity with lack of adequate dorsiflexion at the ankle joint, leading to elevated plantar pressures in the forefoot.
Autonomic neuropathy may occur, with loss of sympathetic tone and arteriovenous shunting of blood in the foot. Sweat glands may also be affected; the resultant anhidrosis leads to dry, cracked skin and predisposes the skin to breakdown.
There is a well-established association between diabetes and increased risks for the development of atherosclerosis and peripheral arterial disease. This is more likely to occur in smokers. This is not microvascular but macrovascular disease, predominantly of the infragenicular (tibial and peroneal arteries) vessels, with sparing of the vessels in the foot. Ischemia may therefore contribute at least in part to the development or persistence of foot ulcers in diabetic patients.
Venous Ulcers
Venous ulceration is the eventual result of venous hypertension. This has multiple causes, but the most common cause is venous valvular incompetence or insufficiency, which may be congenital or acquired. Failure of the venous or muscle pump or venous obstruction may also contribute to venous hypertension. The end result is transmission of elevated venous pressure from the deep to superficial system of the veins, with local effects leading to ulceration. Although it is accepted that venous hypertension plays a dominant role in the development of ulceration, there are multiple hypotheses attempting to explain the direct cause of ulceration.
The fibrin cuff theory, proposed by Browse and colleagues,7 has asserted that as a result of increased venous pressure, fibrinogen is leaked from capillaries. This results in the formation of pericapillary fibrin cuffs that serve as a barrier to the diffusion of oxygen and nutrients. This theory has lost favor as the sole cause, because fibrin is probably not as significant a barrier to diffusion as previously believed.
The trapping of white cells to capillary endothelium is another hypothesis. Venous hypertension results in decreased flow in the capillaries, resulting in the accumulation of white cells. These white cells may then release proteolytic enzymes, as well as interfere with tissue oxygenation.8
A different trap hypothesis has been proposed. This suggests that venous hypertension causes various macromolecules to leak into the dermis and trap growth factors. These growth factors are then unavailable for repair of damaged tissue.9
Arterial Ulcers
Atherosclerosis is the most common cause of peripheral arterial occlusive disease. This predominantly affects the superficial femoral and popliteal vessels, reducing blood flow to the lower extremities. When the ischemia is severe enough, ulceration will develop.
Thromboangiitis obliterans (Buerger’s disease) is an inflammatory segmental thrombotic disease of the medium and small vessels of the extremities usually associated with smoking. This is a cause of peripheral arterial disease and ulceration.
Atheroembolism may cause peripheral arterial occlusion when proximal plaques break off and travel distally. This is referred to as cholesterol emboli or blue toe syndrome.
SIGNS AND SYMPTOMS
Venous Ulcers
Patients with venous ulcers may complain of tired, swollen, aching legs. These ulcers may be painful but not as severe as those seen with ischemic ulcers. The legs will typically be edematous, often with hyperpigmentation of the lower legs from chronic venous stasis. The skin around the ulcer is hyperpigmented. These ulcers are usually on or near the malleoli, usually the distal medial leg. The margins of the ulcers are irregular, with a shallow base. Lipodermatosclerosis may be present, a condition of the skin whereby it becomes indurated and fibrotic in a circumferential pattern, resembling an inverted champagne bottle.
Neurotrophic Ulcers
With neuropathy being the underlying cause of ulceration, many patients complain of burning, tingling, or numbness of the feet on presentation. The ulcer is usually on the plantar foot, most commonly under the great toe or first metatarsal head. Because of pressure, it is often surrounded by a rim of hyperkeratotic tissue, which may even cover the ulcer and give the illusion that the ulcer has healed, when it in fact has not. Infected ulcers may be associated with cellulitis, lymphangitis, adenopathy, calor, edema, foul odor, and purulent drainage. Systemic signs such as fever and chills may be related, but are often absent, even in the presence of severe infection. There may be foot deformity or prominent areas of pressure associated with the ulcer.
Arterial Ulcers
Arterial ulcers are almost always painful. Patients may relate intermittent claudication, pain in the extremities or buttocks with activity that is relieved with rest. If occlusion is severe enough, there may be pain even at rest. A familiar complaint is pain in the legs when lying in bed at night that is relieved by dangling the legs off the side of the bed. Physical examination reveals diminished or absent lower extremity pulses, trophic changes in the skin, decreased hair growth, and nails that may be thickened or ridged. The skin may be shiny, smooth, cool, and demonstrate pallor or a reddish-blue discoloration. The ulcers have a predilection for the lateral aspect of the leg, posterior heel, distal aspects of the digits, medial aspect of the first metatarsal head, and lateral aspect of the fifth metatarsal. The ulcer itself will often have a dry, dark base of eschar. Gangrene may be present. The lesions are often punched out, with a well-demarcated border.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
