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Occlusion of the Great and Small Saphenous Vein Using Copolymeric Glue Based on N-Butyl Cyanoacrylate and Methacryloxy Sulfolane
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Microvascular changes in chronic venous insufficiency--a review

A J Leu1, H J Leu, U K Franzeck

  • 1Department of Internal Medicine, University Hospital, Zurich, Switzerland.

Cardiovascular Surgery (London, England)
|June 1, 1995
PubMed
Summary

Chronic venous insufficiency stems from impaired veins, leading to microvascular damage. This causes swelling, skin changes, and potentially venous ulcers due to compromised blood flow.

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Area of Science:

  • Vascular Biology
  • Dermatology
  • Pathophysiology

Background:

  • Chronic venous insufficiency (CVI) results from impaired venous conduits.
  • Elevated venous pressure drives microvascular alterations in CVI.
  • Capillary changes include dilation, tortuosity, and endothelial injury.

Purpose of the Study:

  • To elucidate the microvascular mechanisms underlying chronic venous insufficiency.
  • To explain the pathophysiology of clinical manifestations like edema and skin changes.
  • To identify the role of microcirculatory dysfunction in venous ulceration.

Main Methods:

  • The study is based on a review of existing literature and pathophysiological understanding.
  • Analysis of microvascular changes in CVI patients.
  • Correlation of microcirculatory alterations with clinical findings.

Main Results:

  • Capillary injury leads to increased extravasation, edema, and hyperpigmentation (hemosiderin deposition).
  • Microthrombosis and microinfarction contribute to skin necrosis.
  • Reduced nutritional capillary perfusion and microvascular ischemia are key factors in trophic changes and ulceration.

Conclusions:

  • Microvascular dysfunction is central to the pathogenesis of chronic venous insufficiency.
  • The progression from CVI to lipodermatosclerosis, atrophy, and ulceration is driven by sustained microcirculatory damage.
  • Understanding these microvascular changes is crucial for managing CVI and preventing ulceration.