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Pathomechanism of chronic venous insufficiency and leg ulcer

T Sándor1

  • 12nd Department of Surgery, Semmelweis University, Budapest, Hungary. dr.sandor.tamas@axelero.hu

Acta Physiologica Hungarica
|October 16, 2004
PubMed

Insights

Chronic venous insufficiency (CVI) stems from venous hypertension, leading to microcirculation issues and skin changes. Leukocyte activation and inflammation are key factors in the development of venous leg ulcers.

Area of Science:

  • Vascular Medicine
  • Dermatology
  • Pathophysiology

Background:

  • Chronic venous diseases, particularly chronic venous insufficiency (CVI), are prevalent functional disorders of the lower limb venous system.
  • CVI is characterized by venous hypertension, resulting from valvular insufficiency and reflux, potentially combined with venous outflow obstruction.
  • The pathology manifests in various forms (epifascial, subfascial, transfascial), often coexisting in clinical practice.

Purpose of the Study:

  • To elucidate the pathophysiological mechanisms underlying chronic venous insufficiency and venous leg ulceration.
  • To explore the role of microcirculatory alterations and inflammatory processes in CVI progression.
  • To understand the contribution of endothelial dysfunction and cellular interactions in the development of venous ulcers.

Main Methods:

  • Review of current understanding of CVI pathophysiology.
  • Analysis of the proposed mechanisms involving microcirculation, leukocytes, and endothelium.
  • Examination of inflammatory markers such as tissue metalloproteinases, leukocyte infiltration, and fibrin cuffs.

Main Results:

  • Consistent venous hypertension initiates microcirculatory changes, leading to skin alterations and ulceration.
  • A leading hypothesis implicates activated leukocytes in capillaries, releasing destructive enzymes and free radicals.
  • The endothelium plays an active role, with increased tissue metalloproteinase expression observed in periulcer skin.
  • Perivascular leukocyte infiltration and fibrin cuffs indicate an inflammatory process contributing to CVI stages.

Conclusions:

  • Chronic venous insufficiency is driven by sustained venous hypertension, impacting microcirculation and skin integrity.
  • Leukocyte activation and endothelial dysfunction are central to the inflammatory cascade leading to venous leg ulceration.
  • The clinical stages of CVI are likely manifestations of a systemic inflammatory response to chronic venous hypertension.

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