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Pathophysiology of chronic venous disease

Authors
Patrick C Alguire, MD, FACP
Barbara M Mathes, MD, FACP, FAAD
Section Editors
John F Eidt, MD
Joseph L Mills, Sr, MD
Deputy Editor
Kathryn A Collins, MD, PhD, FACS

INTRODUCTION

Chronic venous disease is a common medical problem that can result in significant morbidity and mortality. The clinical presentation of this disorder spans a spectrum from asymptomatic but cosmetically troublesome small blue ectatic veins and varicosities, to severe fibrosing panniculitis, dermatitis, edema, and ulceration. (See "Clinical manifestations of lower extremity chronic venous disease".)

The final common pathway that leads to chronic venous insufficiency is the development of venous hypertension. In most cases, venous hypertension results from obstruction to venous flow, dysfunction of venous valves, and/or failure of the "venous pump." In these situations, flow is directed abnormally from the deep to the superficial system, producing local tissue inflammation fibrosis, and occasionally ulceration.

This topic will review normal venous anatomy and physiology, and the pathophysiology of venous hypertension with its clinical consequences. Other aspects of chronic venous insufficiency are discussed separately.

NORMAL VENOUS ANATOMY AND PHYSIOLOGY

Three major vascular pathways are responsible for draining blood away from the superficial vessels of the skin and subcutaneous fat and include (see "Classification of lower extremity chronic venous disorders", section on 'Anatomy (The "A" component of CEAP)'):

Superficial veins – The superficial veins are a network of subcutaneous veins that are superficial to the deep muscular fascia and include the great saphenous and small saphenous veins (figure 1 and figure 2).

        

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Literature review current through: Mar 2017. | This topic last updated: Mar 16, 2017.
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