Venous and Lymphatic Disorders

Varicose Veins – Pathophysiology and Assessment

Definition, Classification, and Epidemiology

Varicose veins are defined as dilated (>3 mm in diameter), incompetent superficial veins of the lower limb visible on standing. They are classified as primary (idiopathic valve failure) or secondary (from prior DVT or external compression). Primary varicose veins result from idiopathic valve failure caused by structural weakness of the valve leaflets—the leaflets are thin, floppy, and collagen-deficient. Genetic predisposition plays a major role: if both parents have varicose veins, offspring have approximately 90% risk of developing them. This autosomal dominant inheritance with variable penetrance suggests that genetic factors are more important than environmental factors in most cases.

Hormonal influences increase venous distensibility in women: female sex hormones (oestrogen, progesterone) increase venous wall compliance and valve laxity. Pregnancy dramatically increases varicose vein risk (9-fold increased risk with each pregnancy) due to progesterone-induced smooth muscle relaxation combined with increased venous pressure from the gravid uterus and increased plasma volume. Oral contraceptives (especially older, higher-dose formulations) increase risk approximately 2–3 fold through oestrogen effects. Standing occupations, obesity (increased abdominal pressure), and constipation (raised intra-abdominal pressure) are contributory factors that increase venous hypertension but are less important than genetics in primary disease. Secondary varicose veins develop when the deep venous system is compromised: post-thrombotic syndrome from prior DVT causes valve destruction by the thrombus, making secondary varicose veins the most clinically important cause (and severest form); pelvic tumour or gravid uterus compressing the external iliac vein; AVF (arteriovenous fistula) dilates veins through high-flow shunting; congenital venous anomalies such as Klippel-Trenaunay syndrome have abnormal lateral embryonic vein persistence.

Anatomy and Nomenclature

The great saphenous vein (GSV, or long saphenous vein, LSV) arises from the medial foot, runs along the medial lower leg and thigh, and joins the femoral vein at the saphenofemoral junction (SFJ) located 3.5 cm below and lateral to the pubic tubercle. The small saphenous vein (SSV) arises from the lateral foot, runs along the posterior calf, and joins the popliteal vein at the saphenopopliteal junction (SPJ). The variability in SPJ level (3–15 cm above the popliteal crease) is clinically important. The GSV is affected in approximately 70–80% of varicose vein cases; the SSV in 10–15%; non-saphenous tributaries (branches off the main trunks) in the remainder. Recurrent varicosities after previous treatment are distinct and require separate assessment.

Clinical Assessment: History and Examination

Patient history focuses on symptomatic complaints: aching and heaviness, worse at end of day and improved by elevation (classic venous symptoms from increased venous hypertension when dependent), night cramps (muscle cramps triggered by venous hypertension and hypoxia), itching (often from varicose eczema and haemosiderin deposition), skin changes, and cosmetic concern (often the primary complaint in young patients). Important to ask about previous leg swelling, skin changes, or ulceration. Family history of varicose veins is clinically relevant.

Physical examination must be performed with the patient standing, examining both legs completely—medial thigh, medial leg, posterior calf (particularly important area for SSV), and lateral thigh. The examiner should look for the location and distribution of varicosities, skin changes, and scar from previous treatment. EXAMINE THE GROIN: the saphenofemoral junction is critical. Look and feel for a saphenous varix (localized dilatation of the GSV at the SFJ—transilluminates, disappears on lying—a sign of SFJ incompetence). Look for a cough impulse palpable at the SFJ (patient coughs and you feel the thrill of blood surging cephalad through the incompetent junction)—this is a cardinal sign of SFJ incompetence.

The Tourniquet test assesses the location of venous incompetence: with the patient supine, elevate the leg and milk blood from the varicosities, then apply a tourniquet at the level of the SFJ (over the groin). Ask the patient to stand. If varicosities immediately fill from below (before the cuff is removed) = distal incompetence (perforators or SPJ). If filling occurs only after releasing the cuff = SFJ incompetence (blood flowing down from above). Trendelenburg test: compress the SFJ with a finger while the patient stands, preventing upward drainage. If varicosities empty and remain empty while the SFJ is occluded = SFJ incompetence is controlled. If varicosities remain full despite SFJ compression = perforator or SPJ incompetence (distal source). Perthes test checks deep vein patency: apply a tourniquet at mid-thigh to compress the superficial veins, then ask the patient to exercise vigorously (walk, marching in place). If varicosities empty = deep veins are patent and functioning normally. If varicosities fill more or become more prominent = deep vein obstruction or severe valvular insufficiency (contraindication to LSV stripping because the superficial veins are vital collaterals).

Duplex Ultrasound Assessment

Duplex ultrasound is the gold-standard investigation. It maps the GSV and SSV throughout their course, identifying the location of reflux (backward flow) at the SFJ, SPJ, and perforators. Reflux is defined as >0.5 seconds of backward (caudal) flow on Valsalva release or pneumatic cuff deflation. The examiner identifies the diameter of the veins (important for assessing severity and suitability for ablation), the location of reflux onset (above or below the knee, above or below the ankle), assesses for thrombus within the veins, and crucially, assesses deep vein patency (femoral vein, popliteal vein, tibial veins). Pre-operative marking is critical: the GSV course is marked with duplex guidance using a skin pen on the day of surgery (accounts for anatomical variability between individuals). The SPJ level must be marked under duplex guidance (variable level—3–15 cm above popliteal crease—marking without ultrasound can lead to missed pathology or incorrect surgery).

Complications of Untreated Varicose Veins

Superficial thrombophlebitis: varicosities are prone to thrombosis. A patient develops a painful, hot, tender, indurated cord along the course of a varicose vein (usually the GSV). Inflammation and partial or complete thrombosis of the vein occurs. Treatment is NSAIDs (ibuprofen, naproxen) and elastic compression; in most cases, the thrombosis remains localized and resolves over 4–6 weeks. However, if thrombophlebitis extends to within 3 cm of the SFJ, there is risk of propagation into the deep venous system (DVT) through the incompetent junction. Such cases require anticoagulation (LMWH or DOAC for 3 months) to prevent this proximal propagation and reduce the risk of PE. Variceal bleeding: acute, copious, dark venous bleeding from a bleed point on a varicose vein (often from trauma or from superficial thrombophlebitis erosion). Treat with direct pressure and elevation; bleeding is usually minor but can be alarming to patients. Recurrent or massive bleeding is an indication for elective variceal treatment. Skin changes from chronic venous insufficiency: haemosiderin deposition (brown/orange discolouration of the skin from iron-containing macrophages), lipodermatosclerosis (firm induration and fibrosis of the skin and subcutis—inverted champagne bottle appearance), varicose eczema (dermatitis from venous irritation), corona phlebectatica malleoli (fan-shaped telangiectasias at the ankle—sign of severe CVI). Venous ulceration (C6 CEAP): the ultimate complication, developing in areas of severe valvular insufficiency and microangiopathy.