Venous Leg Ulcer: Causes

Pathogenesis (development of disease)

Venous leg ulcer is the result of chronic venous insufficiency (CVI). Chronic venous insufficiency represents an obstruction of outflow in the venous system of the lower extremity.

It occurs due to hypertension (high blood pressure) in the venous system with hypervolemia, which leads to circulatory disorders due to damage to the capillaries. Venous valve insufficiency (weakness of venous valve closure) is most often the triggering factor, but obstruction (occlusion), such as by thrombosis (complete or partial occlusion of a blood vessel by blood clots), may also be causative.

Etiology (causes) of leg ulcer (UC)

Biographic causes

  • Age of life – increasing age

Disease-related causes

Cardiovascular system (I00-I99)

Other causes of chronic leg ulcer (UC) include:

  • Genetic defects: e.g., factor V mutation, Klinefelter syndrome, spina bifida.
  • Alcohol abuse
  • Diseases
    • Dermatoses (skin diseases): e.g., pyoderma gangraenosum, lupus erythematosus, morphea, necrobiosis lipoidica, systemic scleroderma,
    • Endocrinological diseases (disease of hormone-producing glands): e.g., diabetes mellitus (about 30% of all cases of UC).
    • Vascular diseases, arterial → ulcus cruris arteriosum (approx. 10-15% of all ulcers):
      • Angiopathy (vascular disease).
      • Angiodysplasias – vascular malformations of arteries, veins, or lymphatic vessels.
      • Hypertension / high blood pressure (Ulcus hypertonicum Martorell).
      • Peripheral arterial occlusive disease (pAVK) – progressive stenosis (narrowing) or occlusion (closure) of the arteries supplying the arms / (more often) legs, usually due to atherosclerosis (arteriosclerosis, arteriosclerosis).
      • Thrombangiitis obliterans (synonyms: endarteritis obliterans, Winiwarter-Buerger disease, Von Winiwarter-Buerger disease, thrombangitis obliterans) – vasculitis (vascular disease) associated with recurrent (recurring) arterial and venous thrombosis (blood clot (thrombus) in a blood vessel); symptoms: Exercise-induced pain, acrocyanosis (blue discoloration of body appendages), and trophic disturbances (necrosis/tissue damage resulting from cell death and gangrene of fingers and toes in advanced stages); more or less symmetrical occurrence; young patients (< 45 years).
      • Thromboembolism (e.g., in aneurysms).
      • Vasculitides – inflammatory rheumatic diseases characterized by a tendency to inflammation of the (mostly) arterial blood vessels.
    • Hematological diseases, eg.
      • Hypercoagulopathies (pathological increased clotting time of the blood): factor V Leiden (APC resistance), protein C or protein S deficiency, ATIII deficiency, antiphospholipid syndrome.
      • Sickle cell disease
    • Infections: S. aureus, gram-negative pathogens, rare infections (leishmaniasis, mycoses, mycobacteriosis, sporotrichiosis).
    • Neoplasms: e.g., basal cell carcinoma (BCC; basal cell carcinoma), squamous cell carcinoma of the skin; rarely: Lymphoma, sarcoma, metastases.
    • Metabolic diseases: calcifying uremic arteriolopathy (calciphylaxis), gout, dysproteinemia (disorder of protein balance in the blood).
  • Drugs, e.g. hydroxyurea, phenprocoumon.
  • Exogenous factors, e.g., manipulation, thermal effects/burns, pressure sores, radiation sequelae, trauma (injuries).

Approximately 18% of all crural ulcers are arterial-venous ulcers.