Describe Varicose Veins in detail.

The Concept

Varicose veins are dilated, tortuous, elongated superficial veins of the leg (in the long and short saphenous systems). They arise from incompetence of the venous valves, which allows blood to reflux backwards and pool in the superficial veins, raising the pressure within them (venous hypertension). This single mechanism — failed valves → reflux → venous hypertension → dilated veins and skin damage — explains the whole condition.

Pathophysiology & Causes

Normally, valves and the calf muscle pump return blood upward against gravity. When valves become incompetent — at the saphenofemoral or saphenopopliteal junctions or the perforating veins — blood refluxes, distending the superficial veins. Incompetence may be primary (idiopathic, often familial) or secondary (to a previous DVT, pelvic mass, or pregnancy).

Clinical Features & Complications

Patients have visible dilated tortuous veins with aching, heaviness, itching and swelling that worsen on standing and towards the end of the day. The important complications of chronic venous insufficiency are:

• Skin changes — haemosiderin pigmentation, venous eczema, lipodermatosclerosis (woody induration), and atrophie blanche.
• Venous ulceration — classically in the 'gaiter' area around the medial malleolus.
• Bleeding from a ruptured varix and superficial thrombophlebitis.

Examination & Investigation

The patient is examined standing. Traditional bedside tests (the Trendelenburg/tourniquet test to locate the level of incompetence, the tap test, and a cough impulse for a saphena varix) have largely been superseded by duplex ultrasound, which is the investigation of choice — it demonstrates the sites of reflux and, importantly, excludes deep venous obstruction (DVT) before any treatment.

Management

• Conservative — compression stockings, leg elevation, weight loss and exercise.
• Interventional — endovenous ablation (radiofrequency or laser), foam sclerotherapy, or surgery (saphenofemoral ligation and stripping).
• Venous ulcers — treated with graduated compression bandaging, but only after excluding arterial disease with an ABPI (compression on an ischaemic leg is dangerous).

The Calf Muscle Pump & Venous Hypertension

Understanding the calf muscle pump makes venous disease clear. During walking, calf muscle contraction squeezes the deep veins and, with competent valves, drives blood upward toward the heart while preventing backflow. When valves fail (or the deep veins are obstructed after a DVT), each contraction instead transmits high pressure back into the superficial system — sustained venous hypertension. It is this chronic pressure at the ankle that damages the skin and produces the pigmentation, lipodermatosclerosis and ulceration of chronic venous insufficiency.

Ceap & the Venous Ulcer

Venous disease is classified by the CEAP system (Clinical, Etiological, Anatomical, Pathophysiological), the clinical grades running from simple telangiectasia through varicose veins and skin changes to healed and active venous ulceration. The venous ulcer is the end-stage: a shallow, exudative ulcer in the gaiter area, treated by graduated compression bandaging (which counteracts the venous hypertension) once an ABPI has confirmed the arterial supply is adequate. Treating the underlying reflux (ablation) reduces recurrence.

A Note on Secondary Varicose Veins

It is important to identify secondary varicose veins, because they change management. Varicosities that follow a previous DVT (with deep venous damage), or that are caused by pelvic obstruction (a mass or pregnancy), must be recognised on duplex, since the deep system may be the patient's main venous drainage — stripping the superficial veins could then be harmful. This is another reason duplex ultrasound, which assesses both deep and superficial systems, is mandatory before intervention.

A Note on Superficial Thrombophlebitis

A common complication worth noting is superficial thrombophlebitis — thrombosis and inflammation of a superficial varicose vein, presenting as a tender, red, cord-like segment. Though usually self-limiting and treated with analgesia, compression and anti-inflammatories, extensive thrombophlebitis of the long saphenous vein near the saphenofemoral junction can propagate into the deep system and cause a DVT, so it is assessed with duplex and sometimes anticoagulated — a reminder that the superficial and deep systems are connected.

• Cause: valvular incompetence (saphenofemoral/saphenopopliteal junctions, perforators) → reflux → venous hypertension.
• Venous ulcer: gaiter area/medial malleolus; skin changes: haemosiderin pigmentation, lipodermatosclerosis, atrophie blanche.
• Duplex ultrasound is the investigation of choice; compression for venous ulcers only after checking ABPI (exclude arterial disease).

Ulcers occur in the gaiter area above the medial malleolus.

• Varicose veins = dilated tortuous superficial leg veins from valvular incompetence → reflux → venous hypertension.
• Primary (idiopathic/familial) or secondary (DVT, pelvic mass, pregnancy); worse on standing/end of day.
• Complications: skin changes (haemosiderin pigmentation, lipodermatosclerosis, atrophie blanche), venous ulcer (gaiter area/medial malleolus), bleeding, thrombophlebitis.
• Duplex ultrasound is the investigation of choice (also excludes DVT).
• Compression + elevation + exercise; endovenous ablation/sclerotherapy/surgery; venous ulcers need compression (check ABPI first to exclude arterial disease).