Varicose vein anatomy

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Varicose Vein Anatomy

Varicose veins are abnormally dilated, tortuous, elongated superficial veins resulting from prolonged increased intraluminal pressure and subsequent incompetence of venous valves. They occur most commonly in the lower limbs.

The Venous System of the Lower Limb

The lower limb has two interconnected venous systems:

1. Deep venous system Lies within the muscle compartments, enclosed by deep fascia. Includes the femoral vein (thigh), popliteal vein (behind the knee), and the anterior/posterior tibial and peroneal veins (leg). These veins carry approximately 90% of venous return from the leg.

2. Superficial venous system Lies in the subcutaneous fat, superficial to the deep fascia. Drains only skin and subcutaneous tissue. The two major trunks are:

Great Saphenous Vein (GSV) - also called the long saphenous vein. Originates from the medial end of the dorsal venous arch of the foot, passes anterior to the medial malleolus, runs up the medial aspect of the calf and thigh, and terminates by passing through the saphenous opening (cribriform fascia) in the upper thigh to join the common femoral vein at the saphenofemoral junction (SFJ) - also called the saphena varix.
Small Saphenous Vein (SSV) - also called the short saphenous vein. Runs up the posterior calf and drains into the popliteal vein in the popliteal fossa at the saphenopopliteal junction (SPJ).

3. Perforating (communicating) veins Connect the superficial to the deep system by traversing the deep fascia. Normally have one-way valves directing flow from superficial to deep. The clinically important perforators include:

Midthigh perforator - connecting the GSV to the femoral vein
Calf perforators (Cockett's perforators) - connecting the GSV tributaries to the posterior tibial veins, located at 5, 10, and 15 cm above the medial malleolus

Normal Venous Return Mechanism

Blood in the superficial veins is driven into the deep veins via perforators, then propelled toward the heart by:

Calf muscle pump - contraction of the soleus and gastrocnemius squeezes the deep veins, generating pressures up to 200 mmHg
Respiratory pressure changes - negative intrathoracic pressure on inspiration aids venous return
Competent venous valves - bicuspid valves prevent retrograde flow (reflux) between contractions

Anatomy of Valvular Incompetence - How Varicose Veins Form

Calf muscle pump anatomy and hemodynamics in normal vs varicose veins

Fig: Normal (left) vs. abnormal (right) calf vein hemodynamics. With incompetent perforating veins, high-pressure deep venous blood refluxes into the unsupported superficial veins, causing dilation. - Fitzpatrick's Dermatology, Fig. 148-15

When venous valves become incompetent, blood refluxes retrograde under the influence of gravity. This raises pressure in distal valves, causing a cascade of progressive incompetence. Blood flows in the opposite direction - from the deep system back into the superficial system through incompetent perforators. The superficial veins, unsupported by muscle or fascia, cannot withstand the elevated pressure and dilate, elongate, and become tortuous.

Venous pressure in these superficial veins can rise to up to 10 times normal in prolonged dependent posture. - Robbins & Cotran

Key Anatomical Sites of Valvular Incompetence

According to Gray's Anatomy for Students, the typical sites where incompetent valves cause marked varicosities are:

Site	Structures Involved
Saphena varix	Saphenofemoral junction - GSV joining femoral vein
Midthigh perforator	GSV to femoral vein
Calf (Cockett's) perforators	5, 10, 15 cm above medial malleolus - GSV to deep calf veins
Popliteal junction	SSV to popliteal vein

The GSV system is affected in ~60% of cases; the SSV system in ~20%. - Bailey and Love's, p. 1052

Clinical Photo

Clinical appearance: extensive varicose veins on the calf and thigh. - Fitzpatrick's Dermatology

Classification

Primary varicose veins - result from intrinsic weakness of the venous wall (faulty collagen/smooth muscle development), with no prior deep vein thrombosis. Genetic predisposition is well recognised.

Secondary varicose veins - result from pre-existing deep or superficial venous insufficiency, most commonly following deep vein thrombosis (DVT). When thrombus incorporates the valve cusps and the clot is lysed by plasmin, the valve leaflets are destroyed, rendering them permanently incompetent. This is the post-phlebitic (post-thrombotic) syndrome.

CEAP classification places varicose veins at C2 (visible varicose veins ≥3 mm diameter).

Consequences of Anatomical Disruption

Once perforating vein valves fail, high-pressure deep venous blood refluxes into the unsupported superficial veins. The resulting chronically elevated venous pressure causes:

Capillary hypertension - fluid and proteins leak into the interstitium - oedema
Red cell extravasation - haemolysis produces haemosiderin - brown skin pigmentation
Fibrin cuff formation - fibrinogen leaks around capillaries, potentially impairing tissue nutrition
White cell trapping - leads to soft-tissue inflammation and fibrosis - lipodermatosclerosis
Venous ulceration - particularly around the medial malleolus (the "gaiter area"), where perforators are most numerous and reflux pressure is highest

Notably, embolism from superficial varicose veins is very rare, in contrast to deep vein thrombosis. - Robbins & Cotran, p. 60

Surgical Anatomy Points

The saphenous nerve runs alongside the GSV in the lower leg and can be injured during stripping. In the popliteal fossa, the SSV junction with the popliteal vein is variable - it may enter higher than expected, and the common peroneal nerve and sural nerve lie in close proximity, explaining why nerve injury is a recognised complication of SPJ surgery.

Sources: Gray's Anatomy for Students (4th Ed.) | Bailey and Love's Short Practice of Surgery (28th Ed.) | Robbins, Cotran & Kumar Pathologic Basis of Disease | Schwartz's Principles of Surgery (11th Ed.) | Fitzpatrick's Dermatology

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