Aetiology

CVI is caused by functional abnormalities in lower extremity veins. The abnormality is usually reflux, but it can also be chronic obstruction or a combination of the two. It occurs in as many as 50% of people within 5-10 years of an episode of deep vein thrombosis (DVT).[9] Congenital absence of the venous valves is a less common cause, and isolated primary varicose veins (pure superficial incompetence) uncommonly causes severe CVI.

Pathophysiology

Normal venous return from the extremities to the heart requires the presence of normal calf and foot muscle pumps, patent veins, and competent valves. Theoretically, problems with any of these systems can result in venous insufficiency.

Severe CVI usually results from chronic valvular reflux, less commonly from venous obstruction, and frequently from a combination of both. These pathophysiological changes produce ambulatory venous hypertension. While walking, people with normal venous function have a relatively low extremity venous pressure (<20 mmHg). This can more than double in people with deep system incompetence.

The typical constellation of findings that ensue include oedema, lipodermatosclerosis, and eventual ulceration. Lipodermatosclerosis characteristically results from capillary proliferation, fat necrosis, and fibrosis of the skin and subcutaneous tissues. Hyperpigmentation (usually a reddish-brown discoloration) of the ankle and lower leg is also known as brawny oedema. It results from extravasation of blood and deposition of haemosiderin in the tissues due to long-standing ambulatory venous hypertension.

The fibrin cuff hypothesis of Burnand suggests that the problem is venous hypertension with resultant extravasation of plasma proteins and fibrinogen into the soft tissue, resulting in a fibrin cuff around the capillaries and tissue hypoxia. The white cell trapping theory of Coleridge-Smith suggests that white cells are trapped in capillaries due to venous hypertension, with secondary escape of proteins into the interstitial space and resultant diminished tissue oxygenation.[10]

Classification

2020 update of the Clinical, Etiological, Anatomical, and Pathophysiological (CEAP) classification system​[1]

The CEAP classification is an internationally recognised standard for describing patients with chronic venous disorders, originally developed in 1993 and updated in 1996, 2004, and 2020. It is based on clinical manifestations, aetiology, involved anatomy, and the underlying venous pathology.[1]

This staging system is extensive, but the clinical class is the only aspect in common use.

Clinical class

  • C0: no visible or palpable signs of venous disease

  • C1: telangiectasias or reticular veins

  • C2: varicose veins

  • C2r: recurrent varicose veins

  • C3: oedema

  • C4: changes in skin and subcutaneous tissue secondary to chronic venous disease (now divided into three subclasses to better define the differing severity of venous disease)

    • C4a: pigmentation or eczema

    • C4b: lipodermatosclerosis or atrophie blanche

    • C4c: corona phlebectatica

  • C5: healed venous ulcer

  • C6: active venous ulcer

  • C6r: recurrent active venous ulcer.

Each clinical class may be sub-characterised as:

  • S: symptomatic (including ache, pain, tightness, skin irritation, heaviness, muscle cramps, and other complaints attributable to venous dysfunction)

  • A: asymptomatic.

Aetiological class

  • Ec: congenital

  • Ep: primary

  • Es: secondary

    • Esi: secondary - intravenous

    • Ese: secondary - extravenous

  • En: no venous cause identified.

Anatomical class

  • As: superficial veins

  • Ap: perforator veins

  • Ad: deep veins

  • An: no venous location identified.

Pathophysiological class (accompanied by the anatomical location)

  • Pr: reflux

  • Po: obstruction

  • Pr,o: reflux and obstruction

  • Pn: no venous pathophysiology identifiable.

CVI corresponds with C3 to C6 of the CEAP classification.[2]

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