Description

• Full-thickness skin defect with surrounding pigmentation and dermatitis
• Most frequently located in ankle region of lower leg (“gaiter region”)
• Present for >30 days and fails to heal spontaneously
• May only have mild pain unless infected
• Other signs of chronic venous insufficiency include edema/brawny edema and chronic skin changes (i.e., hyperpigmentation and/or fibrosis).

Epidemiology

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

• Overall incidence of venous ulcers is 18/100,000 person-years.
• Women > Men (20.4 vs. 14.6 per 100,000 for venous ulcer); increased with age for both sexes

• Seen in ~1% of adult population
• 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.

Risk Factors

• History of leg injury
• Obesity
• 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
• Family history

General Prevention

• Primary prevention (1)[A] after symptomatic DVT shown in randomized, controlled trials (RCTs): Prescribe compression hose to be used as soon as feasible for at least 2 years (≥20–30 mm Hg compression).
• Secondary prevention of recurrent ulceration includes compression, correction of the underlying problem, and surveillance. Circumstantial evidence from 2 RCTs showed those who stopped wearing compression hose were more likely to have recurrence (1)[A].
• Since most ulcers develop following some type of trauma, avoiding lower leg trauma may help to prevent ulceration.

Pathophysiology

• In a diseased venous system, venous pressure in the deep system fails to fall with ambulation, causing venous hypertension.
• Venous hypertension comes from:
  • 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, extravasation of 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

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 neomycin sulfate in particular (including triple antibiotic ointment).