The lower limb venous system is divided into three compartments, separated by the deep fascia ^[1][2][3]:

The GSV is the longest vein in the body ^[1][2]:

• Origin: Arises from the medial side of the dorsal venous arch of the foot
• Course: Ascends anterior to the medial malleolus → runs up the leg posterior to the medial border of the patella → ascends obliquely along the medial aspect of the thigh
• Termination: Pierces the cribriform fascia at the saphenofemoral junction (SFJ) and drains into the common femoral vein
  • SFJ is located approximately 2.5 cm lateral and inferior to the pubic tubercle ^[1]
• Nerve companion: The saphenous nerve accompanies the GSV, especially below the knee — this is why GSV stripping below the knee risks saphenous nerve injury (numbness along medial calf/foot)

• Origin: Arises from the lateral side of the dorsal venous arch of the foot
• Course: Ascends posterior to the lateral malleolus → runs up the midline of the calf posteriorly
• Termination: Pierces the deep fascia over the popliteal fossa and drains into the popliteal vein at the saphenopopliteal junction (SPJ)
• Nerve companion: The sural nerve accompanies the SSV — SSV surgery risks sural nerve injury (numbness along posterolateral leg and lateral foot) ^[1][2]

These are valved veins that join the superficial to the deep veins at inconstant sites, allowing blood to flow from superficial → deep venous system ^[1][2]. They are critical because when their one-way valves fail, high-pressure deep venous blood refluxes into the superficial system, contributing to CVI.

Named perforators (from proximal to distal):

The Cockett perforators are particularly important because they are in the "gaiter area" (lower medial calf/ankle) — this is precisely where venous ulcers develop.

Why doesn't blood just pool in our legs when we stand up? Several mechanisms work together ^[2][3]:

1. Calf muscle pump (the "peripheral heart") — this is the major mechanism

   • Contraction of calf muscles (gastrocnemius, soleus) compresses the large venous sinuses within the muscles
   • This squeezes blood into the popliteal veins and propels it cephalad towards the heart
   • During relaxation, the deep venous pressure drops, and blood flows from the superficial system into the deep system via the perforator veins

2. One-way bicuspid valves

   • Present in all three venous systems (deep, superficial, perforator)
   • Ensure unidirectional flow: deep veins → towards the heart; superficial → towards deep; perforators → superficial to deep only
   • Valve closure is triggered by retrograde flow — when blood starts to fall back, the valve cusps fill and coapt

3. Respiratory pump

   • Decreased intrathoracic pressure during inspiration creates a pressure gradient that sucks blood from the abdomen and lower limbs into the thorax

4. Vis a tergo (force from behind) — residual arterial pressure transmitted through capillary beds

5. Venous tone — smooth muscle in venous walls maintains basal tone under sympathetic control

The risk factors make intuitive sense once you understand the physiology — anything that increases venous pressure, damages valves, or impairs the calf pump ^[1][2][3]:

The core pathophysiology of both varicose veins and CVI is venous hypertension ^[2][3].

Normal ambulatory venous pressure in the foot is ~20–25 mmHg (because the calf muscle pump effectively empties the veins during walking). In CVI, ambulatory venous pressure rises to 60–90 mmHg.

Here is the pathophysiological cascade:

1. Reflux (>80% of cases) ^[1]: When valves are incompetent, blood refluxes during relaxation of the calf pump. In the standing position, this creates a continuous column of hydrostatic pressure from the heart to the ankle, with no effective "breaks."

2. White cell trapping hypothesis (Coleridge-Smith): Venous hypertension causes leucocytes to marginate, adhere to capillary endothelium, become activated, and release inflammatory mediators (proteolytic enzymes, free radicals) → endothelial damage and tissue destruction.

3. Fibrin cuff hypothesis (Browse and Burnand): Fibrinogen leaks through distended capillaries, polymerises into pericapillary fibrin cuffs → acts as a physical barrier to O₂ and nutrient diffusion → tissue ischaemia.

4. Growth factor trapping hypothesis (Falanga and Eaglstein): Macromolecules that leak into the interstitium bind and "trap" growth factors essential for tissue repair, impeding wound healing.

In practice, all three mechanisms likely operate simultaneously.

Venous ulcers classically occur at the medial gaiter area (the zone between the lower calf and medial malleolus). Why?

• This is the site of the medial calf perforators (Cockett perforators), which connect the posterior tibial vein to the GSV tributaries
• When these perforator valves fail, high-pressure deep venous blood is transmitted directly to the superficial subcutaneous tissues in this area
• The skin here is thin and poorly vascularised to begin with, making it particularly vulnerable to venous hypertension-mediated injury ^[3]

Each C class is further subscripted as S (symptomatic) or A (asymptomatic). For example, C2S = symptomatic varicose veins.

Example: A patient with symptomatic varicose veins from primary GSV reflux would be classified as: C2S, Ep, As, Pr

Another common example: post-thrombotic CVI with deep venous reflux would fall under Esi, not the older undifferentiated Es bucket.

This is a classic exam comparison ^[3][5]:

The diagnosis requires ALL of ^[1][2]:

1. Clinical: Visible dilated, tortuous subcutaneous veins ≥ 3 mm in diameter, measured in the upright position
2. Functional: Demonstrable reflux — this is confirmed by duplex ultrasound showing retrograde flow with valve closure time > 0.5 seconds ^[1][2]

Without demonstrable reflux on duplex, a dilated vein is just that — a dilated vein. It is the reflux that makes it a "varicose vein" by definition.

CVI is defined as chronic venous disease of CEAP class C3–C6 ^[1][2]:

• Requires the presence of oedema (C3), skin changes (C4), or ulceration (C5/C6)
• Plus evidence of venous aetiology (reflux, obstruction, or both) — confirmed by duplex USG

The CEAP classification itself serves as the diagnostic framework — once you have completed your clinical assessment and investigations, you assign the full CEAP descriptor. This is the international standard for documenting and communicating the diagnosis ^[1][2][3]:

The key insight: C is clinical; E, A, and P require investigations (primarily duplex USG) to complete.

• Surgical scars — previous venous surgery (recurrence is common — 30%) ^[2]
• Location of varicosities — the single most important inspection finding for localising incompetence ^[1]:

• Signs of CVI — systematically assess for all C-class features ^[1][2]:
  • Corona phlebectatica (malleolar flare)
  • Hyperpigmentation (gaiter area)
  • Venous eczema
  • Lipodermatosclerosis (hyperpigmentation + erythema + induration + tenderness — palpate!) ^[2]
  • Atrophie blanche
  • Healed or active ulceration (medial gaiter area)

• Palpate along course of GSV and SSV and their tributaries for varicosities and tenderness ^[1][2]
• Check peripheral pulses — rule out PAD since management includes compression ^[1][2]. This is not optional — it is a safety-critical step
• Pitting oedema — confined to ankle area usually, may extend proximally ^[1]
• Saphena varix — at the inguinal region: a compressible lump with cough impulse that refills on release ^[1][2]
• Inguinal lymph nodes — if venous ulcers present, check for lymphadenopathy (infection or Marjolin transformation) ^[2]
• Neurological function — test sensation (e.g., sural nerve territory) if surgical scars present, to document pre-existing nerve damage ^[2]

This classic bedside test localises the level of valvular incompetence. Although largely superseded by duplex USG, it remains an exam favourite ^[1][2]:

Procedure ^[1]:

1. Patient lies supine → elevate leg to empty superficial veins (or stroke blood proximally)
2. Apply tourniquet tightly around the upper thigh (just below SFJ)
3. Patient stands up quickly → observe filling of varicose veins

Interpretation ^[1]:

• The test is repeated with the tourniquet at progressively lower levels: mid-thigh, above knee, below knee ^[1][2]
• Below-knee tourniquet specifically excludes SSV incompetence ^[1]

This tests deep venous patency ^[2]:

1. Apply tourniquet around the SFJ (blocking superficial reflux)
2. Ask the patient to walk (activating the calf muscle pump)
3. If the deep system is patent: walking should empty the leg via the deep veins → varicosities decrease
4. If the deep system is NOT patent: walking causes swelling and pain — blood cannot drain through the deep system and the tourniquet blocks superficial drainage → the leg is trapped

• Auscultate over varicosities for a continuous bruit — suggests AV malformation ^[1]
• Examine inguinal region for mass or lymphadenopathy causing venous outflow obstruction ^[1]
• Abdominal and PR examination — if secondary causes suspected (pelvic mass obstructing IVC/iliac veins) ^[2]
• ABPI measurement — to rule out PAD before compression therapy ^[2]

What it is: Ratio of the highest systolic BP at the ankle (dorsalis pedis or posterior tibial) to the highest brachial systolic BP, measured using a handheld Doppler and sphygmomanometer ^[1][5].

Why you need it: Compression therapy (stockings, bandaging) is the mainstay of CVI management. Applying compression to an ischaemic limb can cause tissue necrosis. ABPI is therefore a mandatory safety check before any compression or surgical planning ^[2].

• Pen-like handheld probe that detects blood flow direction using the Doppler principle ^[1]
• Helpful for screening reflux at SFJ and SPJ in the office setting ^[1]
• Limitations: Unable to quantitate reflux or provide precise anatomical information ^[1] — it tells you "there is reflux here" but not exactly which vein, how much, or whether the deep system is involved
• In modern practice, this has been largely replaced by duplex USG for definitive assessment, but remains useful as a quick bedside screening tool

• Indication: When a secondary cause is suspected ^[2] — e.g., pelvic mass (ovarian cyst, fibroid, pelvic malignancy), IVC obstruction, May-Thurner syndrome
• Look for: Pelvic masses compressing the iliac veins, lymphadenopathy, ascites
• Consider in:
  • Young patients with unexplained unilateral CVI
  • Patients with no typical risk factors
  • New-onset varicose veins with abdominal symptoms

• Not routine — reserved for complex or recurrent cases
• Indications:
  • Suspected iliocaval obstruction (May-Thurner syndrome, IVC thrombosis)
  • Pelvic venous congestion syndrome
  • Planning for deep venous reconstruction or stenting
  • Congenital venous anomalies (Klippel-Trénaunay)
• CT venography: Good spatial resolution, involves contrast and radiation
• MR venography: No radiation, excellent soft tissue contrast, but longer acquisition time and limited availability
• Intravascular ultrasound (IVUS): Increasingly used during endovascular procedures to assess iliac vein stenosis (May-Thurner) — gives cross-sectional area and degree of compression from within the vessel

Laboratory tests are not used to diagnose CVI itself but are important in the work-up of complications and differential diagnoses:

When a patient presents with a lower limb ulcer in the context of CVI:

1. Duplex USG — confirm venous aetiology and plan venous treatment
2. ABPI — exclude arterial component (mixed ulcers are common ~15%)
3. Wound swab C/ST — if signs of clinical infection (erythema, purulent discharge, cellulitis, systemic sepsis)
4. 4-quadrant biopsy + palpate groin lymph nodes — if ulcer is chronic, non-healing, or has suspicious features (raised/everted edges, bleeding easily) → exclude Marjolin's ulcer ^[2][6]
5. Bloods: CBC, CRP, albumin, HbA1c

• Daflon (micronised purified flavonoid fraction / micronised diosmin) ^[2]: A venotonic that increases venous tone and lymphatic drainage
• Mechanism: Increases venous wall contractility by modulating noradrenaline release; reduces capillary permeability; has anti-inflammatory effects (reduces leucocyte adhesion)
• Good for oedema (CEAP ≥ C3) ^[2]
• Limited role in earlier disease; used as adjunctive therapy rather than primary treatment
• Available over the counter in Hong Kong

For patients with C5/C6 disease:

1. Leg elevation and encourage mobilisation ^[6] — elevation reduces venous pressure; mobilisation activates the calf muscle pump
2. Wound swab for C/ST + antibiotics if signs of infection ^[6] — only treat clinical infection (cellulitis, purulence, systemic signs), not colonisation
3. Ulcer care: debridement of necrotic tissue, appropriate wound dressings, barrier cream for surrounding skin ^[6]
4. Four-layered graduated compression bandage (ABPI > 0.4) ^[6]
5. Treat the underlying varicose veins (intervention if appropriate)
6. If non-healing despite adequate treatment: 4-quadrant biopsy and palpate groin LN to exclude Marjolin ulcer (2% — malignant transformation to SCC, rarely BCC) ^[6]
7. Fenestrated split-thickness skin graft — for large or refractory ulcers after the wound bed is adequately prepared ^[6]

Intervention is indicated when there is documented superficial venous reflux (retrograde flow > 0.5 seconds on duplex) ^[2] AND one or more of:

Endovenous therapy and surgery appear equally effective ^[1], but there are important differences:

Surgical treatment is preferred over endovenous if ^[2]:

• Superficial varicose veins (< 1 cm deep): Risk of skin burns from thermal energy
• Tortuous veins: Endovenous catheter/fibre cannot be passed through tortuous segments
• Chronic/recurrent phlebitis: Adhesions prevent passage of endovenous devices

Surgery reduces venous volume in the limbs and thereby the effects of venous hypertension upon the cutaneous tissues ^[8]. It physically removes or disconnects the incompetent veins.

• SPJ ligation + stripping +/- below-knee stab avulsion ^[2]
• Nerve at risk: Sural nerve — runs alongside the SSV. Damage causes pain or numbness in the posterolateral leg and lateral foot ^[1][2]

• A mechanical alternative to stab avulsion
• Powered mechanical aspirator device inserted adjacent to the target vein after tumescent anaesthesia ^[8]
• Blade activated → vein aspirated into the device and destroyed ^[8]
• Advantage: Fewer incisions needed
• Disadvantage: More postoperative pain and haematoma formation ^[8]

• What it is: Pruritic, scaling skin with erosions and crusting, typically around the gaiter area ^[1][8]
• Pathophysiology: Venous hypertension → capillary distension → leakage of plasma proteins and inflammatory mediators into the dermis → chronic inflammatory response → eczematous change. The leaked fibrinogen polymerises into pericapillary fibrin cuffs, which trap growth factors and impair tissue repair, perpetuating inflammation.
• Why it matters: Itching leads to scratching → excoriation → breaks in skin barrier → portal of entry for bacteria → secondary infection (cellulitis). The eczema itself also indicates the skin is already compromised and at risk of ulceration.
• Management: Emollients, topical corticosteroids (short courses for flares), compression therapy to address the underlying venous hypertension. Avoid known contact allergens (many patients develop sensitivity to dressings, topical antibiotics like neomycin, or lanolin).

• What it is: Brown discolouration of the gaiter area skin ^[1][8]
• Pathophysiology: Venous hypertension → capillary distension → extravasation of red blood cells into the dermis → macrophages phagocytose and break down the RBCs → haemosiderin deposition (an iron-rich pigment from haemoglobin degradation) ^[1][8]
• Clinical significance: Haemosiderin staining is permanent — surgery will NOT alter existing skin changes ^[2]. This is a crucial counselling point. Treatment prevents further pigmentation but cannot reverse what is already there.
• Distribution: Commonly occurs in gaiter area (medial lower 1/3 of the leg) ^[1][8]. In severe cases, pigmentation may cover the entire lower limb ^[3]

• What it is: Fibrosing panniculitis of subcutaneous tissue due to chronic venous insufficiency ^[1][8]
• Clinical features: Hyperpigmentation + subcutaneous induration + redness + tenderness + pitting oedema ^[1][8]
• Pathophysiology: Chronic venous hypertension → sustained capillary leak → fibrinogen leak → pericapillary fibrin deposition → impaired O₂/nutrient diffusion → tissue hypoxia → chronic inflammation with release of TGF-β and other fibrogenic cytokines → progressive replacement of skin and subcutaneous fat by fibrous tissue ^[1][8]
• Consequences:
  • Classic "inverted champagne bottle" leg — the lower leg becomes narrowed and hardened while the calf above remains relatively normal
  • Fixed flexion contracture of the ankle joint — subcutaneous fibrosis and/or painful ulceration restricts ankle range of motion ^[3]. This creates a vicious cycle: reduced ankle mobility → impaired calf muscle pump → worsening venous hypertension
• Acute LDS: Painful, hot, red, and tender on the medial side of the gaiter area. Often misdiagnosed as cellulitis or acute thrombophlebitis ^[3]. The distinction matters because acute LDS does not respond to antibiotics.

• What it is: Ivory-white avascular fibrotic scars with hyperpigmented borders and telangiectasia ^[1][8]
• Pathophysiology: End-stage microvascular damage — the dermal capillaries have been obliterated by the chronic inflammatory process, leaving areas of avascular scar tissue. The surrounding hyperpigmented border represents the still-active zone of haemosiderin deposition.
• Clinical significance: Prone to secondary venous ulceration due to poor blood supply ^[1][8] — these avascular white areas have minimal capacity for repair, so even minor trauma can trigger ulceration that heals poorly.

This is the most clinically significant complication and the one that generates the greatest healthcare burden.

• Location: At the medial gaiter area — the site of medial calf perforators (Cockett perforators) ^[2]
• Characteristics: Shallow, gently sloping edges, with slough or granulation tissue at the base
• Pain: Usually painless unless infected (commonly S. aureus) ^[2]. However, acute venous ulcers in the context of active tissue sloughing can be very painful ^[3]
• Pathophysiology: The culmination of the entire venous hypertension cascade — tissue hypoxia from fibrin cuffs + white cell trapping + growth factor sequestration → skin breakdown → full-thickness skin loss (C6 = active; C5 = healed)
• Infection: Chronic venous ulcers are typically colonised by bacteria (this is expected and does not necessarily require antibiotics). Clinical infection — characterised by expanding cellulitis, purulent discharge, increased pain, or systemic features — requires wound swab for C/ST and appropriate antibiotics ^[6]
• Healing: With adequate conservative management (4-layer compression bandaging, wound care, leg elevation), 50–70% of venous ulcers heal within 3 months ^[6]
• Recurrence: High recurrence rate if the underlying venous pathology is not treated. Treating the varicose veins reduces ulcer recurrence.

• What it is: Malignant transformation of a chronic venous ulcer, usually to squamous cell carcinoma (SCC), rarely basal cell carcinoma (BCC) ^[2][6]
• Incidence: ~2% of long-standing venous ulcers ^[2]
• Why it happens: Chronic ulcers create a microenvironment of persistent inflammation, repeated tissue destruction and regeneration, and impaired immune surveillance — this promotes accumulation of genetic mutations in keratinocytes over years to decades, eventually leading to malignant transformation. This is conceptually similar to how chronic inflammation anywhere in the body increases cancer risk (e.g., Barrett's → oesophageal adenocarcinoma, ulcerative colitis → colorectal cancer).
• When to suspect: A chronic ulcer that changes character — becomes raised, develops everted or rolled edges, bleeds easily, grows rapidly, or fails to heal despite months of adequate therapy
• Investigation: 4-quadrant biopsy of the ulcer edge and palpation of groin lymph nodes for metastasis ^[6]
• Management: Wide local excision ± lymph node dissection depending on staging

• Bleeding from attenuated vein clusters ^[1] — varicose veins near the surface, especially over bony prominences (medial malleolus), can rupture with minimal trauma
• Pathophysiology: The vein wall is already weakened (decreased elastin, increased MMPs). As the vein dilates and becomes more superficial, the overlying skin thins (atrophic changes from CVI). A minor knock can rupture both the skin and the vein.
• Clinical picture: Can be dramatic — venous bleeding from a varicose vein can produce surprisingly large volumes of blood, causing alarm in patients. However, it is low-pressure venous bleeding and is readily controlled.
• Management: Elevation and direct pressure. Lay the patient down, elevate the leg above heart level, and apply firm pressure with a pad. This simple manoeuvre controls virtually all varicose vein bleeds. Once controlled, the underlying vein should be treated to prevent recurrence.

• What it is: Thrombosis and inflammation within a superficial varicose vein ^[1]
• Clinical features: Localised pain, redness, warmth, and a tender, palpable, cord-like vein
• Pathophysiology: Venous stasis within a dilated, incompetent varicose vein → activation of coagulation cascade (Virchow's triad: stasis + endothelial damage from chronic distension + hypercoagulable microenvironment) → thrombus formation → inflammatory response
• Risk: Superficial thrombophlebitis can propagate into the deep venous system via the SFJ or SPJ, or via perforator veins. If the thrombus extends to within 3 cm of the SFJ, there is a real risk of DVT and PE. Always assess with duplex USG.
• Management: Usually self-limited — compression stockings, NSAIDs for pain and inflammation. If extensive or proximal, consider anticoagulation.

• Patients with varicose veins have an increased risk of DVT — the chronic venous stasis and endothelial dysfunction create a prothrombotic environment
• DVT can also be a cause of secondary CVI (post-thrombotic syndrome), creating a bidirectional relationship
• Complication of DVT → chronic venous insufficiency and pulmonary embolism ^[10]
• Post-thrombotic syndrome: DVT damages venous valves → permanent valvular incompetence → secondary CVI → further venous hypertension. This is why DVT prophylaxis and early treatment of DVT are so important.

• In advanced CVI, chronic inflammation and fibrosis can damage lymphatic vessels running alongside the veins
• This adds a lymphatic component to the venous oedema, creating phlebo-lymphoedema — harder to treat because lymphatic damage is largely irreversible
• The skin may develop features of both CVI (pigmentation, eczema) and lymphoedema (thickening, warty changes)

• Subcutaneous fibrosis from chronic lipodermatosclerosis and/or painful ulceration may cause a fixed flexion contracture of the ankle joint ^[3]
• This impairs the calf muscle pump mechanism (which requires full ankle dorsiflexion to function efficiently) → worsening venous hypertension → a self-perpetuating vicious cycle
• Physiotherapy and early treatment of LDS can help prevent this debilitating complication

This is one of the most important specific complications to know for exams:

• This is precisely why GSV stripping is limited to the thigh only — extending below the knee significantly increases saphenous nerve injury risk without improving symptomatic relief ^[1]
• Both nerves are purely sensory, so the deficit is numbness/paraesthesia rather than motor weakness

• Occurs along the course of excised veins or in residual varicosities ^[1]
• Caused by endothelial damage and blood stasis in residual vein segments after treatment
• Self-limited and treated conservatively with compression stockings ^[1]
• NSAIDs reduce the incidence and severity (particularly after thermal ablation) ^[1]

• Complication of dissection/manipulation of venous structures ^[1]
• Risk is inherent because you are operating within the venous system — thermal energy, mechanical disruption, and blood stasis all activate coagulation
• Thromboprophylaxis should be given in high-risk individuals ^[1] — those with prior VTE, thrombophilia, malignancy, obesity, immobility
• Detection: Post-operative duplex USG at 2–3 days can screen for early DVT ^[2]
• Suspect if: Excessive pain with swelling post-operatively → urgent duplex

• Specific to EVLA and RFA
• Occurs when the vein being treated is too superficial (< 1 cm from the skin surface) or when tumescent anaesthesia is inadequately placed — the thermal energy conducts through to the skin
• This is why surgical treatment is preferred over endovenous treatment for superficial veins (< 1 cm deep) ^[2]
• Prevention: Adequate tumescent anaesthesia (acts as a heat sink and pushes the vein deeper)

• Hyperpigmentation along the treated vein — from haemosiderin deposition after sclerosant-induced vein damage and trapped blood
• Also occurs with non-thermal methods (MOCA, cyanoacrylate) due to extravasation of sclerosant or inflammatory reaction ^[2]
• Usually fades over months but can be permanent in some cases

• Rare but possible reaction to sclerosant agents (especially STS)
• Can range from minor skin rash to anaphylaxis
• Always have resuscitation equipment available when performing sclerotherapy

This is arguably the most important long-term complication:

• Recurrence rate is approximately 30% ^[2]
• More common in SSV than GSV territory ^[2]
• Causes of recurrence ^[2]:
  • Neovascularisation — new small veins grow across the ligated junction (especially at the groin), re-establishing reflux. This is a biological response to surgical disruption.
  • Reflux in residual axial vein — incomplete treatment of the trunk saphenous vein
  • New junctional reflux — development of reflux at a previously competent junction
  • Inadequate initial surgery — failure to identify and treat all sources of reflux (e.g., missed perforator incompetence, untreated tributary)
• Management of recurrent varicose veins: Repeat duplex USG to map the recurrence → tailored re-intervention (usually endovenous or sclerotherapy rather than redo surgery, as adhesions from prior surgery make dissection difficult)