Varicose Veins & Venous Insufficiency

Varicose veins are dilated, elongated and tortuous superficial veins (>3 mm) of the lower limb, resulting from sustained venous hypertension and valvular incompetence. This is a favourite NEET PG topic because it leans heavily on bedside clinical tests (Trendelenburg, Perthe's, Schwartz, Morrissey) and on the anatomy of the sapheno-femoral and sapheno-popliteal junctions.

Definition & basic anatomy

Venous return from the leg occurs through three interconnected systems:

• Superficial system — great (long) saphenous vein (GSV) and small (short) saphenous vein (SSV), lying above the deep fascia.
• Deep system — venae comitantes and the popliteal/femoral veins, below the deep fascia, propelled by the calf muscle pump.
• Perforators (communicating veins) — connect superficial to deep; valves normally direct flow superficial → deep only.

Normal venous flow is unidirectional toward the heart, maintained by bicuspid valves and the calf muscle pump ("the peripheral heart"). When valves fail, blood refluxes back down (deep → superficial via incompetent perforators), raising ambulatory venous pressure → varicosities.

High-yield: The great saphenous vein drains into the femoral vein at the sapheno-femoral junction (SFJ), ~2.5–4 cm below and lateral to the pubic tubercle. It passes anterior to the medial malleolus — a constant landmark used for venous cut-down. The GSV is accompanied by the saphenous nerve.

The SSV passes behind the lateral malleolus, ascends the back of the calf with the sural nerve, and drains into the popliteal vein at the sapheno-popliteal junction (SPJ).

Key named perforators (frequently asked):

Perforator	Location
Hunterian	Mid-thigh (adductor canal)
Dodd's	Lower thigh, just above knee
Boyd's	Just below the knee
Cockett's (I, II, III)	Medial lower leg / ankle — drain into posterior tibial vein; most important in venous ulceration

High-yield: Incompetent Cockett's perforators in the medial gaiter area are the classic cause of venous (stasis) ulcers.

Classification

Primary varicose veins (~95%) — no identifiable underlying cause; due to inherent weakness/incompetence of valves or vein wall. Strong familial tendency.

Secondary varicose veins — develop from an underlying cause that raises venous pressure:

• Deep vein thrombosis (DVT) → post-thrombotic syndrome (commonest secondary cause)
• Pelvic/abdominal mass, pregnancy, ovarian tumour
• Arteriovenous fistula
• Klippel–Trénaunay syndrome (port-wine stain + varicosities + limb hypertrophy — note: deep veins absent/hypoplastic, so varicose veins must NOT be stripped)

CEAP classification (Clinical–Etiology–Anatomy–Pathophysiology) — standard for chronic venous disease; remember the Clinical axis:

CEAP-C	Finding
C0	No visible/palpable venous disease
C1	Telangiectasia / reticular veins
C2	Varicose veins (>3 mm)
C3	Oedema
C4	Skin changes — pigmentation, eczema (C4a); lipodermatosclerosis, atrophie blanche (C4b)
C5	Healed venous ulcer
C6	Active venous ulcer

High-yield: C5 = healed ulcer, C6 = active ulcer. This sequence is a repeat one-liner question.

Etiology & pathophysiology

The unifying mechanism is chronic ambulatory venous hypertension. Two routes:

Valvular incompetence → reflux → blood pools in superficial veins → progressive dilatation (which further pulls valve cusps apart, a vicious cycle).

Outflow obstruction (e.g., post-DVT) → high distal pressure transmitted via perforators to superficial system.

Sustained venous hypertension at the skin leads to:

1. Capillary dilatation and fibrin cuff deposition around capillaries (Browse's fibrin-cuff theory) → impaired oxygen diffusion.
2. White cell trapping and activation → release of proteolytic enzymes and free radicals → tissue damage.
3. Extravasation of RBCs → haemosiderin deposition → brown pigmentation.
4. Fibrosis of dermis/subcutaneous fat → lipodermatosclerosis (inverted "champagne-bottle"/"inverted beer-bottle" leg).

Risk factors: female sex, pregnancy, prolonged standing occupation, obesity, advancing age, family history, previous DVT.

Clinical features

Symptoms are often disproportionately mild relative to appearance:

• Dull aching, heaviness, "bursting" pain on prolonged standing, relieved by elevation/walking (contrast with arterial claudication, worsened by walking).
• Night cramps, ankle swelling, itching.
• Cosmetic disfigurement, dilated tortuous veins along GSV/SSV territory.
• Venous claudication (post-thrombotic, with deep obstruction) — bursting calf pain on walking relieved by elevation.

Signs / complications of skin changes (mostly in the gaiter area — medial lower third of leg, above medial malleolus):

• Haemosiderin pigmentation, venous eczema (varicose eczema)
• Lipodermatosclerosis, atrophie blanche (white scarred avascular patches)
• Venous ulcer — typically medial gaiter area, shallow, sloping edge, granulating floor, relatively painless, with surrounding pigmentation.

High-yield: Venous ulcer = medial gaiter area, sloping edge, painless, vertical. Arterial ulcer = punched-out, painful, over pressure points/toes. Neuropathic ulcer = trophic, over weight-bearing points (sole/heel), painless with deep penetration.

Clinical tests (very high-yield)

A stepwise bedside approach: elevate to empty the veins → apply tourniquet → ask patient to stand → observe filling.

Trendelenburg test (SFJ / perforator incompetence)

Patient lies supine, leg elevated to empty veins. Apply tourniquet (or thumb) at the SFJ. Patient stands. Test I (release): veins fill rapidly from above on release → SFJ incompetence. Test II (keep occluded): veins fill from below within ~30–35 s while tourniquet stays on → incompetent perforators.

Multiple/Three-tourniquet test — localises the level of perforator incompetence by placing tourniquets at upper thigh, above knee and below knee; the segment that fills first localises the leaking perforator.

Perthe's test (deep vein patency)

Apply a tourniquet at mid-thigh with veins filled; ask patient to walk/do tip-toe exercises for ~5 min. If the calf muscle pump and deep system are patent, superficial veins empty (improve). If varicosities become more prominent and painful, the deep veins are obstructed → stripping is contraindicated.

High-yield: Perthe's test is the single most important pre-operative test — it confirms deep vein patency. Never strip the GSV if the deep system is blocked, as it is the only collateral channel.

Schwartz test — tapping a lower varix transmits an impulse felt at the SFJ (continuous column of blood = valvular incompetence).

Morrissey's cough impulse test — palpable thrill/impulse at SFJ on coughing = SFJ incompetence (a saphena varix may be mistaken for a femoral hernia, but it has a bluish hue and a fluid thrill).

Fegan's test / Modified Perthe's — used to mark the sites of incompetent perforators.

Investigation of choice

• Duplex (colour Doppler) ultrasonography — investigation of choice. It demonstrates the site of reflux, valvular incompetence (reflux > 0.5 s in superficial veins, > 1.0 s in deep/femoro-popliteal veins), perforator incompetence, and excludes DVT. Non-invasive, no contrast.
• Hand-held continuous-wave Doppler — quick OPD screening of SFJ/SPJ reflux.
• Venography (ascending/descending) — now largely obsolete, reserved for complex/recurrent cases or congenital anomalies.
• Plethysmography — quantifies venous reflux and calf pump function (research/specialised use).

High-yield: Duplex Dovenous reflux cut-offs: >0.5 s = pathological reflux in superficial veins. Memorise this number.

Flow of evaluation: History → inspection (standing) → palpation → tourniquet tests (Trendelenburg, Perthe's) → confirm with Duplex USG → plan intervention.

Management

Conservative (first line for mild disease, C1–C3)

• Graduated compression stockings (Class II, ~18–24 mmHg; pressure highest at ankle) — mainstay of conservative therapy.
• Leg elevation, regular walking/calf exercises, weight reduction, avoid prolonged standing.
• Skin care, emollients for eczema.

Sclerotherapy

Injection of a sclerosant that destroys the endothelium → fibrosis and obliteration.

• Agents: sodium tetradecyl sulphate (STDS), polidocanol, hypertonic saline.
• Foam sclerotherapy (sclerosant + air, "Tessari technique") for larger veins and as ultrasound-guided treatment of trunk veins.
• Best for small varicosities, reticular veins, telangiectasia, and residual veins post-surgery.
• Complications: pigmentation, skin necrosis (extravasation), DVT, allergic reaction, rarely stroke from air embolism (foam).

Endovenous ablation (now first-line for truncal GSV/SSV reflux)

• Endovenous laser therapy (EVLT/EVLA) and radiofrequency ablation (RFA) — minimally invasive, thermal ablation of the saphenous trunk under tumescent anaesthesia, day-care, faster recovery and less recurrence than open surgery.
• Newer non-thermal: cyanoacrylate glue closure, mechanochemical ablation (MOCA).

High-yield: EVLT/RFA have largely replaced open surgery as first-line for axial saphenous reflux. Sclerotherapy is best for small/reticular veins.

Surgery (open)

• Trendelenburg operation — flush ligation of the SFJ (juxtafemoral ligation) with division of all named tributaries: superficial circumflex iliac, superficial epigastric, superficial/deep external pudendal, posteromedial and anterolateral thigh veins — the "saphenofemoral disconnection."
• Stripping of the GSV — usually only to knee level (stripping below knee risks saphenous nerve injury → medial leg/foot paraesthesia).
• SPJ ligation — for SSV; beware sural nerve injury.
• Subfascial endoscopic perforator surgery (SEPS) — ligation of incompetent perforators, useful in advanced skin changes/ulcers.
• Stab avulsion / multiple phlebectomy (Müller's) for residual varicosities.

High-yield mnemonic — SFJ tributaries: *"Some Surgeons Prefer Pulling Nerves Apart"* → Superficial epigastric, Superficial circumflex iliac, superficial external Pudendal, deep external Pudendal, Posteromedial & anterolateral thigh veins.

Venous ulcer management

• Four-layer compression bandaging is the cornerstone (after excluding arterial disease — check ABPI; compression is safe only if ABPI > 0.8).
• Treat infection, debride, dressings; correct underlying reflux (ablation/SEPS).
• Skin grafting for large non-healing ulcers.

High-yield: Always measure ABPI before applying compression. ABPI < 0.8 → coexisting arterial disease, and compression can cause limb ischaemia/necrosis.

Complications of varicose veins

1. Haemorrhage — from a ruptured varix (treat by elevation + direct pressure, NOT tourniquet).
2. Superficial thrombophlebitis — tender, red, cord-like vein.
3. Venous eczema & lipodermatosclerosis.
4. Venous ulceration (gaiter area).
5. Calcification, periostitis, equinus deformity (chronic).
6. Marjolin's ulcer — squamous cell carcinoma arising in a long-standing (chronic) venous ulcer.
7. Deep vein thrombosis.

High-yield: A long-standing, indurated, everted-edge venous ulcer that fails to heal = suspect Marjolin's ulcer (SCC) → biopsy. Marjolin's ulcer is painless (no nerves), slow-growing, does not metastasize via lymphatics while confined to the scar.

Key differentials

Feature	Venous ulcer	Arterial ulcer	Neuropathic (trophic) ulcer
Site	Medial gaiter area	Toes, pressure points, lateral malleolus	Sole, heel, metatarsal heads
Edge	Sloping, granulating	Punched-out	Punched-out, deep
Pain	Mild	Severe (worse on elevation)	Painless
Surrounding skin	Pigmented, eczematous	Pale, cold, hairless	Callus, warm, pulses present
Pulses	Present	Absent	Present

Other differentials: lymphoedema (non-pitting late, no skin pigmentation, positive Stemmer's sign), DVT (acute unilateral swelling), saphena varix vs femoral hernia (saphena varix has cough impulse + fluid thrill, disappears on lying down, bluish), and AV malformation (continuous bruit, raised local temperature).

Recently asked / exam angle

• Trendelenburg test I vs II — distinguishing SFJ from perforator incompetence (filling from above vs below) is repeatedly tested.
• Perthe's test — interpretation: increased prominence/pain on exercise = deep vein obstruction = contraindication to stripping.
• Investigation of choice = Duplex USG; reflux cut-off >0.5 s.
• Surface marking: GSV anterior to medial malleolus, SSV behind lateral malleolus; nerves at risk — saphenous (GSV below knee), sural (SSV).
• Cockett's perforators & gaiter area in venous ulcer.
• EVLT/RFA as modern first-line; foam sclerotherapy for small veins.
• ABPI > 0.8 mandatory before compression therapy.
• Marjolin's ulcer in chronic venous ulcer.
• CEAP C5 (healed) vs C6 (active) ulcer.
• Image-based: lipodermatosclerosis "inverted champagne-bottle" leg, atrophie blanche.

Rapid revision

1. Varicose veins = dilated tortuous superficial veins (>3 mm) from venous hypertension + valve incompetence.
2. GSV → femoral vein at SFJ, 2.5–4 cm below & lateral to pubic tubercle; lies anterior to medial malleolus.
3. SSV → popliteal vein at SPJ; passes behind lateral malleolus with sural nerve.
4. Cockett's perforators (medial leg) → posterior tibial vein → key in venous ulcers.
5. Trendelenburg I = fills from above → SFJ incompetence; Trendelenburg II = fills from below → perforator incompetence.
6. Perthe's test = checks deep vein patency; pain/prominence on exercise → do NOT strip.
7. Duplex USG = investigation of choice; reflux >0.5 s is pathological.
8. Venous ulcer = medial gaiter area, sloping edge, painless; arterial ulcer = punched-out & painful.
9. EVLT/RFA = first-line for truncal reflux; foam sclerotherapy for small/reticular veins.
10. Trendelenburg operation = flush SFJ ligation; strip GSV only to knee (saphenous nerve below).
11. Check ABPI >0.8 before compression; four-layer compression is the cornerstone of ulcer care.
12. Chronic non-healing venous ulcer → suspect Marjolin's ulcer (SCC) → biopsy; never strip in Klippel–Trénaunay syndrome (deep veins absent).