Description

• Full-thickness shallow skin defect with surrounding pigmentation and well defined borders
• Most frequently located in ankle region of lower leg over bony prominences
• Present for >30 days and fails to heal spontaneously
• May only have mild pain unless infected
• Other signs of chronic venous insufficiency include bulging veins, edema, hyperpigmentation, dermatitis, woody fibrosis, lipodermatosclerosis.

Epidemiology

Up to 80% of leg ulcers are caused by venous disease; whereas arterial disease accounts for 10–25%, which may coexist with venous disease.

• Overall incidence of venous ulcers is 18/100,000 persons.
• Prevalent sex: women > men (20.4 vs. 14.6/100,000 for venous ulcer); increased with age for both sexes

• Seen in ~1% of adult population in industrialized countries; increased to 4% in patients ≥80 years old
• Prevalence studies only available for Western countries
• Point prevalence underestimates the extent of the disease because ulcers often recur.
• 70% of ulcers recur within 5 years of closure.

Etiology and Pathophysiology

• In a diseased venous system, venous pressure in the deep system fails to fall with ambulation, causing venous hypertension.
• Venous hypertension comes from the following:
  • Venous obstruction
  • Incompetent venous valves in the deep or superficial system
  • Inadequate muscle contraction (e.g., arthritis, myopathies, neuropathies) so that the calf pump is ineffective
• Venous pressure transmitted to capillaries leading to venous hypertensive microangiopathy and extravasation of red blood cells (RBCs) and proteins (especially fibrinogen)
• Increased RBC aggregation leads to reduced oxygen transport, slowed arteriolar circulation, and ischemia at the skin level, contributing to ulcers.
• Leukocytes aggregate to hypoxic areas and increase local inflammation.
• Factors promoting persistence of venous ulcers
  • Prolonged chronic inflammation
  • Bacterial infection, critical colonization

Genetics
Research suggests the presence of genetic influences in the pathology of venous disease, the profile of the genes involved remain poorly understood (FOXC2 is the first gene in which mutations are strongly associated with primary venous valve failure).

Risk Factors

• History of leg injury
• Age ≥55 years
• High body mass index (BMI)
• Congestive heart failure (CHF)
• History of deep venous thrombosis (DVT)
• Failure of calf muscle pump (e.g., ankle fusion, inactivity) is a strong independent predictor of poorly healing wounds.
• Previous varicose vein surgery or ulcers
• Family history

General Prevention

• Primary prevention after symptomatic DVT: Prescribe compression hose to be used as soon as feasible for at least 2 years (≥20 to 30 mm Hg compression).
• Secondary prevention of recurrent ulceration includes compression, correction of the underlying problem, and surveillance.
• Circumstantial evidence from two randomized controlled trials showed that in those who stopped wearing compression hose ulcers were more likely to recur.
• Avoiding lower leg trauma may help to prevent ulceration, as most ulcers develop from trauma.

Commonly Associated Conditions

Up to 50% of patients have allergic reactions to topical agents commonly used for treatment.

• Contact sensitivity was more common in patients with stasis dermatitis (62% vs. 38%).
• Avoid triple antibiotic ointment, including anything containing neomycin sulfate.