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Diabetic Ulcers

Author: Richard M Stillman, MD, FACS, Honorary Medical Staff, Northwest Medical Center; Former Chief of Staff and Medical Director, Wound Healing Center, Department of Surgery, Northwest Medical Center
Contributor Information and Disclosures

Updated: Jun 30, 2008

Introduction

Background

Diabetic foot ulcers occur as a result of various factors. Such factors include mechanical changes in conformation of the bony architecture of the foot, peripheral neuropathy, and atherosclerotic peripheral arterial disease, all of which occur with higher frequency and intensity in the diabetic population. Nonenzymatic glycosylation predisposes ligaments to stiffness. Neuropathy causes loss of protective sensation and loss of coordination of muscle groups in the foot and leg, both of which increase mechanical stresses during ambulation.

Pathophysiology

Diabetic persons, like people who are not diabetic, may develop atherosclerotic disease of large-sized and medium-sized arteries, such as aortoiliac and femoropopliteal atherosclerosis. However, significant atherosclerotic disease of the infrapopliteal segments is particularly common in the diabetic population. Underlying digital artery disease, when compounded by an infected ulcer in close proximity, may result in complete loss of digital collaterals and precipitate gangrene. The reason for the prevalence of this form of arterial disease in diabetic persons is thought to result from a number of metabolic abnormalities, including high low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) levels, elevated plasma von Willebrand factor, inhibition of prostacyclin synthesis, elevated plasma fibrinogen levels, and increased platelet adhesiveness.

Overall, people with diabetes have a higher incidence of atherosclerosis, thickening of capillary basement membranes, arteriolar hyalinosis, and endothelial proliferation. Calcification and thickening of the arterial media (Mönckeberg sclerosis) are also noted with higher frequency in the diabetic population, although whether these factors have any impact on the circulatory status is unclear.

The pathophysiology of diabetic peripheral neuropathy is multifactorial and is thought to result from vascular disease occluding the vasa nervorum; endothelial dysfunction; deficiency of myoinositol-altering myelin synthesis and diminishing sodium-potassium adenine triphosphatase (ATPase) activity; chronic hyperosmolarity, causing edema of nerve trunks; and effects of increased sorbitol and fructose1

The result of loss of sensation in the foot is repetitive stress; unnoticed injuries and fractures; structural foot deformity, such as hammertoes, bunions, metatarsal deformities, or Charcot foot (see Image 3); further stress; and eventual tissue breakdown. Unnoticed excessive heat or cold, pressure from a poorly fitting shoe, or damage from a blunt or sharp object inadvertently left in the shoe may cause blistering and ulceration. These factors, combined with poor arterial inflow, confer a high risk of limb loss on the patient with diabetes.

Frequency

United States

According to The National Institute of Diabetes and Digestive and Kidney Diseases, "an estimated 16 million Americans are known to have diabetes, and millions more are considered to be at risk for developing the disease." Diabetic foot lesions are responsible for more hospitalizations than any other complication of diabetes. Among patients with diabetes, 15% develop a foot ulcer, and 12-24% of individuals with a foot ulcer require amputation. Indeed, diabetes is the leading cause of nontraumatic lower extremity amputations in the United States. "In fact, every year approximately 5% of diabetics develop foot ulcers and 1% require amputation." Diabetic peripheral neuropathy, present in 60% of diabetic persons and 80% of diabetic persons with foot ulcers, confers the greatest risk of foot ulceration; microvascular disease and suboptimal glycemic control contribute.

Even after successful management resulting in ulcer healing, the recurrence rate in that patient population is 66% and the amputation rate rises to 12%. Half of all nontraumatic amputations are a result of diabetic foot complications, and the 5-year risk of needing a contralateral amputation is 50%.2

Mortality/Morbidity

• Limb loss: Unfortunately, limb loss is a significant risk in patients with diabetic foot ulcers, particularly if treatment has been delayed.³
• Charcot foot: Sensory neuropathy involving the feet may lead to unrecognized episodes of trauma due to ill-fitting shoes. Motor neuropathy, causing intrinsic muscle weakness and splaying of the foot on weight bearing, compounds this trauma. The result is a convex foot with a rocker-bottom appearance. Multiple fractures are unnoticed until bone and joint deformities become marked. This is termed a Charcot foot (neuropathic osteoarthropathy) and most commonly is observed in diabetes mellitus, affecting about 2% of diabetic persons. If neglected, ulceration may occur at pressure points, particularly the medial aspect of the navicular bone and the inferior aspect of the cuboid bone. Sinus tracts progress from the ulcerations into the deeper planes of the foot and into the bone. Charcot change can also affect the ankle, causing displacement of the ankle mortise and ulceration, which can lead to the need for amputation.
• Mortality: Mortality in people with diabetes and foot ulcers is often the result of associated large vessel arteriosclerotic disease involving the coronary or renal arteries.

Race

The issue of diabetic foot disease is of particular concern in the Latino communities of the Eastern United States, African Americans⁴ , and in Native Americans, who tend to have the highest prevalence of diabetes in the world.

Age

Diabetes occurs in 3-6% of Americans. Of these, 10% have type 1 diabetes and are usually diagnosed when they are younger than 40 years. Among Medicare-aged adults, the prevalence of diabetes is about 10% (of these, 90% have type 2 diabetes). Diabetic neuropathy tends to occur about 10 years after the onset of diabetes, and, therefore, diabetic foot deformity and ulceration occur sometime thereafter.

Clinical

History

• Peripheral neuropathy: The symptoms of peripheral neuropathy include the following:
  • Hypesthesia
  • Hyperesthesia
  • Paresthesia
  • Dysesthesia
  • Radicular pain
  • Anhydrosis
• Peripheral arterial insufficiency
  • Most people harboring atherosclerotic disease of the lower extremities are asymptomatic; others develop ischemic symptoms. Some patients attribute ambulatory difficulties to old age and are unaware of the existence of a potentially correctible problem.
  • Patients who are symptomatic may present with intermittent claudication, ischemic pain at rest, nonhealing ulceration of the foot, or frank ischemia of the foot.
  • Cramping or fatigue of major muscle groups in one or both lower extremities that is reproducible upon walking a specific distance suggests intermittent claudication. This symptom increases with ambulation until walking is no longer possible, and it is relieved by resting for several minutes. The onset of claudication may occur sooner with more rapid walking or walking uphill or up stairs. The claudication of infrainguinal occlusive disease typically involves the calf muscles, while symptoms that occur in the buttocks or thighs suggest aortoiliac occlusive disease.
  • Discomfort, cramping, or weakness in the calves or feet is particularly common in the diabetic population because they tend to have tibioperoneal atherosclerotic occlusions. Calf muscle atrophy may also occur. Rest pain is less common in the diabetic population. In some cases, a fissure, ulcer, or other break in the integrity of the skin envelope is the first sign that loss of perfusion has occurred. When a diabetic patient presents with gangrene it is often the result of infection.

Physical

Physical examination of the extremity having a diabetic ulcer can be divided into 3 broad categories: (1) examination of the ulcer and general condition of the extremity, (2) assessment of the possibility of vascular insufficiency5 and (3) assessment for the possibility of peripheral neuropathy. Remember that diabetes is a systemic disease. Hence, a comprehensive physical examination of the entire patient is also vital.

Extremity examination

• Diabetic ulcers tend to occur in the following areas:  
  • Areas most subjected to weight bearing, such as the heel, plantar metatarsal head areas, the tips of the most prominent toes (usually the first or second), and the tips of hammer toes (Ulcers also occur over the malleoli because these areas commonly are subjected to trauma.)
  • Areas most subjected to stress, such as the dorsal portion of hammer toes
• Other physical findings include the following: 
  • Hypertrophic calluses
  • Brittle nails
  • Hammer toes
  • Fissures

Peripheral arterial insufficiency

• Physical examination discloses absent or diminished peripheral pulses below a certain level.
• Although diminished common femoral artery pulsation is characteristic of aortoiliac disease, infrainguinal disease alone is characterized by normal femoral pulses at the level of the inguinal ligament and diminished or absent pulses distally.
• Specifically, loss of the femoral pulse just below the inguinal ligament occurs with a proximal superficial femoral artery occlusion. Loss of the popliteal artery pulse suggests superficial femoral artery occlusion, typically in the adductor canal. Loss of pedal pulses is characteristic of disease of the distal popliteal artery or its trifurcation.
• However, be aware that absence of the dorsalis pedis pulse may be a normal anatomic variant that is noted in about 10% of the pediatric population. On the other hand, the posterior tibial pulse is present in 99.8% of persons aged 0-19 years. Hence, absence of both pedal pulses is a more specific indicator of peripheral arterial disease.
• Other findings suggestive of atherosclerotic disease include a bruit heard overlying the iliac or femoral arteries, skin atrophy, loss of pedal hair growth, cyanosis of the toes, ulceration or ischemic necrosis, and pallor of the involved foot followed by dependent rubor after 1-2 minutes of elevation above heart level.
• For further details, see Infrainguinal Arterial Occlusive Disease.

Peripheral neuropathy

• Signs of peripheral neuropathy include loss of vibratory and position sense, loss of deep tendon reflexes (especially loss of the ankle jerk), trophic ulceration, foot drop, muscle atrophy, and excessive callous formation, especially overlying pressure points such as the heel.
• The nylon monofilament test helps diagnose the presence of sensory neuropathy6 A 10-gauge monofilament nylon is pressed against each specific site of the foot just enough to bend the wire. If the patient does not feel the wire at 4 or more of these 10 sites, the test is positive for neuropathy. General use filaments can be obtained from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), or the clinician can use the professional Semmes-Weinstein filaments described here.

Causes

The etiologies of diabetic ulceration include neuropathy,⁷ arterial disease,⁸ pressure,⁹ and foot deformity.¹⁰

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