Venous Insufficiency Ulcers

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Basics

  • Venous insufficiency is a condition that occurs when the venous wall and/or valves in the leg veins are not working effectively, making it difficult for blood to return to the heart and causing stasis.
  • Signs of chronic venous insufficiency include edema, bulging veins, hyperpigmentation, dermatitis, woody fibrosis, lipodermatosclerosis, and ulcers.
  • Venous stasis ulcers are the most serious consequence of chronic venous insufficiency. In the United States, up to 35% of adults have chronic venous insufficiency.
  • Venous stasis ulcers affect up to 3% of adults in developed countries at some point during their lives.
  • The annual estimated treatment cost of chronic venous ulcers is 2.5 to 3.5 billion dollars per year.

Description

  • Full-thickness shallow skin defect with surrounding hyperpigmentation and well-defined borders
  • Most frequently located in the lower leg or ankle over the bony prominences
  • Present for >30 days and fails to heal spontaneously
  • May only have mild pain unless infected

Epidemiology

Up to 80% of leg ulcers are caused by venous disease, whereas arterial disease accounts for 10–25%, and these disorders may coexist.

Incidence
  • The overall incidence of venous ulcers is 18/100,000 persons.
  • They are more common in women than men (20.4 vs. 14.6/100,000).
  • The incidence increases with age in both men and women.
Prevalence
  • Venous ulcers are seen in ~1% of the adult population and up to 4% in adults ≥80 years old in industrialized countries.
  • Point prevalence underestimates the extent of the disease due to common recurrences (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)
  • Venous pressure transmitted to capillaries leads to venous hypertensive microangiopathy and 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 the hypoxic areas and increase local inflammation.
  • Prolonged chronic inflammation and bacterial infection promote the persistence of ulcers.

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 BMI
  • Congestive heart failure (CHF)
  • History of deep venous thrombosis (DVT)
  • Failure of the calf muscle pump (e.g., ankle fusion, inactivity)
  • Previous varicose vein surgery or ulcers
  • Smoking
  • Prolonged standing
  • Pregnancy
  • Family history

General Prevention

  • Primary prevention after symptomatic DVT: Prescribe compression hose as soon as feasible, to be used 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 RCTs showed that ulcers were more likely to recur in those who stopped wearing a compression hose.
  • Avoiding lower leg trauma may help to prevent ulceration, because 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.

-- To view the remaining sections of this topic, please or --

Basics

  • Venous insufficiency is a condition that occurs when the venous wall and/or valves in the leg veins are not working effectively, making it difficult for blood to return to the heart and causing stasis.
  • Signs of chronic venous insufficiency include edema, bulging veins, hyperpigmentation, dermatitis, woody fibrosis, lipodermatosclerosis, and ulcers.
  • Venous stasis ulcers are the most serious consequence of chronic venous insufficiency. In the United States, up to 35% of adults have chronic venous insufficiency.
  • Venous stasis ulcers affect up to 3% of adults in developed countries at some point during their lives.
  • The annual estimated treatment cost of chronic venous ulcers is 2.5 to 3.5 billion dollars per year.

Description

  • Full-thickness shallow skin defect with surrounding hyperpigmentation and well-defined borders
  • Most frequently located in the lower leg or ankle over the bony prominences
  • Present for >30 days and fails to heal spontaneously
  • May only have mild pain unless infected

Epidemiology

Up to 80% of leg ulcers are caused by venous disease, whereas arterial disease accounts for 10–25%, and these disorders may coexist.

Incidence
  • The overall incidence of venous ulcers is 18/100,000 persons.
  • They are more common in women than men (20.4 vs. 14.6/100,000).
  • The incidence increases with age in both men and women.
Prevalence
  • Venous ulcers are seen in ~1% of the adult population and up to 4% in adults ≥80 years old in industrialized countries.
  • Point prevalence underestimates the extent of the disease due to common recurrences (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)
  • Venous pressure transmitted to capillaries leads to venous hypertensive microangiopathy and 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 the hypoxic areas and increase local inflammation.
  • Prolonged chronic inflammation and bacterial infection promote the persistence of ulcers.

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 BMI
  • Congestive heart failure (CHF)
  • History of deep venous thrombosis (DVT)
  • Failure of the calf muscle pump (e.g., ankle fusion, inactivity)
  • Previous varicose vein surgery or ulcers
  • Smoking
  • Prolonged standing
  • Pregnancy
  • Family history

General Prevention

  • Primary prevention after symptomatic DVT: Prescribe compression hose as soon as feasible, to be used 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 RCTs showed that ulcers were more likely to recur in those who stopped wearing a compression hose.
  • Avoiding lower leg trauma may help to prevent ulceration, because 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.

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