Aetiology

Although many factors such as gender, pregnancy, occupation, weight, and race have been implicated as predisposing factors for varicose veins, only a previous episode of deep vein thrombosis and genetic links may be causative factors. The exact primary cause of varicose veins remains elusive.[4][6]

Venous valve incompetence is the most common aetiology.[10] Because veins work against gravity, their valves work by compartmentalising the blood, leading to better equalisation of pressures throughout the veins and preventing reflux. Blood pools when valves do not function properly, leading to increased pressure and distension of the veins.[11] However, it is not clear whether the valves fail because of vein dilation or whether the veins dilate due to valve failure.

Progesterone is believed to lead to passive venous dilation, which may then lead to valvular dysfunction. Oestrogen produces collagen fibre changes and smooth muscle relaxation, which both lead to vein dilation.[4]

Pathophysiology

The venous system acts as both a reservoir and a conduit in the return of blood to the heart and lungs for oxygenation and re-circulation. End capillary venous pressure is low (20 mmHg). Veins are thin-walled and lack the muscular walls of arteries. Therefore, veins require assistance in blood return. This is provided by valves and muscle pumps - as one walks, the muscle pumps contract and push blood against gravity, and as the muscle pump relaxes, the fall of the blood is stopped by the valve system. When one of these factors is not functioning properly, venous hypertension and insufficiency can ensue, possibly leading to varicose veins.

A normal vein wall has three smooth muscle layers that all help to maintain its tone. Varicose veins demonstrate marked proliferation of collagen matrix as well as decreased elastin, leading to distortion and disruption of muscle fibre layers.[6]

Classification

Clinical, Etiological, Anatomical, and Pathophysiological (CEAP) classification for chronic venous disorders[2]

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.[2]

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 - telangiectasis or reticular vein

  • C2 - varicose veins

  • C2r - recurrent varicose veins

  • C3 - oedema

  • C4 - changes in skin and subcutaneous tissue secondary to cardiovascular 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.

Aetiology class

  • Ep - primary

  • Es - secondary

    • Esi - secondary intravenous

    • Ese - secondary extravenous

  • Ec - congenital

  • En - no venous cause identified

Anatomy class

  • As - superficial veins

    • sites of reflux identified by abbreviation

  • Ap - perforator veins

    • sites of reflux identified by abbreviation

  • Ad - deep veins

    • sites of reflux identified by abbreviation

  • An - no location identified

Pathophysiology class (accompanied by the anatomical location)

  • Pr - reflux

  • Po - obstruction

  • Pro - reflux and obstruction

  • Pn - no pathophysiology identified.

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