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VARICOSE VEINS

A Comprehensive Lecture for Medical Students


1. DEFINITION AND OVERVIEW

A vein is called varicose when it is permanently dilated, tortuous, and elongated. While varicosity can affect veins in several locations (spermatic veins → varicocele; oesophageal veins; haemorrhoidal veins), the term "varicose veins" in clinical practice almost exclusively refers to the superficial veins of the lower limb.
  • Prevalence: affects up to 30% of women and 15% of men in Western populations
  • The condition represents a penalty of erect posture - not seen in quadrupeds
  • It is a spectrum ranging from minor cosmetic telangiectasia to severe chronic venous disease with ulceration

2. RELEVANT ANATOMY

The Superficial Venous System

VeinAbbreviationTermination
Great saphenous veinGSVSaphenofemoral junction (SFJ) in the groin
Small saphenous veinSSVSaphenopopliteal junction (SPJ) in the popliteal fossa
Anterior accessory GSVAAGSVSFJ or direct into femoral vein

Perforating (Communicating) Veins

These connect superficial to deep veins, traversing the deep fascia. Normally, valves allow one-way flow from superficial to deep. When incompetent, they allow bidirectional flow, raising superficial venous pressure.
Key perforators:
  • Hunterian (mid-thigh)
  • Dodd's (lower thigh)
  • Boyd's (upper calf)
  • Cockett's (medial lower leg) - most clinically important; responsible for venous ulcers

The Deep Venous System

Runs within muscle compartments: tibial veins → popliteal → femoral → common femoral → external iliac → inferior vena cava. Competent deep veins are a prerequisite before treating superficial incompetence.

Calf Muscle Pump

During walking, calf muscle contraction empties the deep veins, dropping venous pressure from 80-100 mmHg (standing) to 20-30 mmHg. Failure of this pump (immobility, ankle fusion, paralysis) causes venous hypertension.

3. PATHOPHYSIOLOGY

Normal Venous Return

Venous return against gravity depends on:
  1. Calf muscle pump
  2. Competent valves preventing retrograde flow
  3. Respiratory pressure gradient (negative intrathoracic pressure)

Venous Hypertension

The fundamental problem in varicose veins is ambulatory venous hypertension - failure of venous pressure to fall adequately during walking. Causes include (Table 62.1, Bailey & Love):
Pressure gradient dysfunction:
  • Increased intra-abdominal/thoracic pressure (COPD, pregnancy, obesity, large tumours, constipation)
  • Decreased calf muscle pump (immobility, ankle joint fusion, paralysis)
Venous structural dysfunction:
  • Valvular incompetence, valvular agenesis
  • Venous dilatation, tortuosity, loss of wall compliance
  • Arteriovenous fistula
  • Venous occlusion (thrombosis), venous compression (May-Thurner syndrome)

Vein Wall Changes

The initiation of varicose vein formation is still incompletely understood. It is no longer thought that valvular failure causes vein wall changes - rather, primary vein wall pathology may come first. Histological changes include:
  • Inflammatory cell infiltration and activation
  • Dysfunctional smooth muscle cell proliferation
  • Collagen deposition
  • Decreased elastin content
  • Increased matrix metalloproteinases
  • These lead to loss of vein wall compliance and tone, venous dilatation, and secondary valvular dysfunction
The result is a vicious cycle: vein wall changes → valvular incompetence → reflux → venous hypertension → more vein wall damage.

4. AETIOLOGY AND CLASSIFICATION

Primary (Idiopathic) Varicose Veins

The most common form. No identifiable secondary cause. Likely represents an inherent weakness of vein wall connective tissue.
Risk factors:
  • Age: Middle-aged individuals most affected, though any age can be affected
  • Sex: Women > men (ratio ~10:1 in some studies); progesterone relaxes smooth muscle
  • Pregnancy: Directly increases risk - both hormonal (progesterone) and mechanical (pelvic venous compression) effects
  • Family history: Strong evidence of familial susceptibility; likely polygenic
  • Obesity: Increases intra-abdominal pressure
  • Occupation: Prolonged standing (police, teachers, surgeons) - though evidence is inconclusive as to whether this causes varicose veins or merely exacerbates symptoms
  • Ethnicity: Less common in African and East Asian primitive civilisations; likely related to dietary fibre, posture, and lifestyle differences

Secondary Varicose Veins

An identifiable cause:
  1. Obstruction to venous outflow:
    • Pregnancy, fibroid uterus, ovarian cyst
    • Pelvic cancers (cervix, uterus, ovary, rectum)
    • Abdominal lymphadenopathy, ascites
    • Iliac vein thrombosis, retroperitoneal fibrosis
    • May-Thurner syndrome (left iliac vein compression by right iliac artery)
  2. Destruction of deep vein valves from deep vein thrombosis (post-thrombotic syndrome)
  3. High-pressure flow from arteriovenous fistula (congenital or traumatic)
    • Klippel-Trenaunay syndrome (capillary malformation + varicose veins + limb hypertrophy)

5. CLINICAL FEATURES

History

Symptoms (Bailey & Love):
  • Aching, heaviness, throbbing, burning or bursting sensation over affected areas or the whole limb
  • Symptoms worsen throughout the day and with prolonged standing
  • Relieved by leg elevation or compression hosiery
  • Itching (more common when complications are present)
  • Ankle swelling
  • Cosmetic concerns (often the primary complaint in younger women)
  • Bursting pain during walking may indicate deep vein involvement
Important to ask:
  • Duration and progression
  • Previous DVT, thrombophlebitis, trauma
  • Pregnancy history (number of pregnancies)
  • Family history of varicose veins or DVT
  • Occupation and activity level
  • Previous injection treatment or surgery (recurrent varicose veins behave differently)
  • Symptoms of secondary causes: pelvic mass, change in bowel habit
Key point: The severity of symptoms does NOT correlate with the degree of venous incompetence or presence of varicose tributaries. Some patients with minimal visible veins have severe symptoms; others with gross varicosities are asymptomatic.

Signs

Inspection (patient standing):
  • Tortuous, dilated, subcutaneous veins - usually clinically obvious
  • Distribution indicates which system is affected:
    • Medial thigh and calf → GSV incompetence (60% of cases)
    • Posterolateral calf → SSV incompetence (~20% of cases)
    • Anterolateral thigh and calf → AAGSV incompetence
Skin changes (in order of severity):
  1. Telangiectasia / spider veins (fine red intradermal vessels, <1 mm)
  2. Reticular veins (blue-green, 1-3 mm, tortuous, subdermal)
  3. Varicose veins (>3 mm, dilated, tortuous)
  4. Corona phlebectatica: fan-shaped intradermal veins at the ankle (ankleflare) - sign of deep venous hypertension
  5. Oedema: pitting, worse at end of day, initially pitting then later brawny
  6. Eczema (varicose/stasis dermatitis): erythematous dermatitis with itching; may progress to blistering and weeping
  7. Pigmentation (haemosiderosis): brownish skin discolouration around the ankle from red cell extravasation and haemosiderin deposition; usually permanent
  8. Lipodermatosclerosis (LDS): chronic inflammation and fibrosis of skin and subcutaneous tissues; "woody" or "inverted champagne bottle" leg; occasionally causes Achilles tendon contracture; sign of severe chronic venous disease
  9. Atrophie blanche: localised areas of atrophic, white, avascular skin surrounded by telangiectasia and pigmentation; sign of severe chronic venous disease
  10. Venous ulcer: full-thickness skin loss, usually over the medial gaiter area (especially over Cockett's perforators), failing to heal spontaneously
Saphena Varix: A dilated GSV at the SFJ presenting as a (usually painless) lump in the groin, disappearing when recumbent. May be mistaken for a femoral hernia. A cough impulse is present. Diagnosed by duplex ultrasound.
Abdominal Examination: Must be performed in every patient to exclude secondary causes (pelvic mass, abdominal lymphadenopathy, ascites, pregnant uterus).

Clinical Tests (Largely Historical)

TestPrincipleCurrent status
Trendelenburg testIdentifies SFJ incompetenceNow superseded by duplex
Tourniquet test (Trendelenburg + multiple tourniquets)Localises incompetent perforatorsNow superseded by duplex
Perthes' testAssesses deep vein patencyNow superseded by duplex
Hand-held Doppler (Brodie-Trendelenburg with probe)Detects reflux at SFJ/SPJSuperseded by duplex
Pratt's testIdentifies perforatorsHistorical
All tourniquet tests and hand-held Doppler have now been abandoned in favour of duplex ultrasound scanning.

6. INVESTIGATIONS

Duplex Ultrasound Scanning (Gold Standard)

Now recommended for all patients with varicose veins being considered for treatment. It provides:
  1. Detection of reflux in deep and superficial systems
  2. Exact distribution and extent of reflux, including affected junctions and perforators
  3. Presence of obstruction in the deep venous system
  4. Suitability of incompetent veins for different treatment modalities (diameter, extent, tortuosity)
  5. Presence of thrombus within superficial veins
  6. Indication of pelvic source of reflux
Technical details:
  • High-frequency linear array transducer (7.5-13 MHz)
  • Patient examined standing to optimise measurements
  • Reflux definition: retrograde flow ≥0.5 seconds in superficial/crural veins; ≥1 second in proximal deep veins
  • Blue = antegrade (towards heart); Red = retrograde (reflux) by convention
  • Reflux elicited by: calf squeeze release, Valsalva manoeuvre, pneumatic cuff deflation

Venography (Phlebography)

Largely replaced by duplex. Occasionally used:
  • Pre-operative mapping of complex anatomy
  • Assessment of deep vein patency when duplex inadequate
  • Ascending venography: contrast injected into foot dorsal vein, visualises deep system
  • Descending venography: contrast injected at SFJ, demonstrates reflux with Valsalva

Other Investigations

  • CT/MRI abdomen and pelvis: if secondary varicose veins suspected (pelvic mass, May-Thurner syndrome, pelvic congestion syndrome)
  • Blood tests: not routinely required for primary varicose veins
  • Duplex of deep veins: specifically if DVT suspected or post-thrombotic syndrome considered

7. CLASSIFICATION - CEAP SYSTEM

The CEAP (Clinical-Aetiology-Anatomy-Pathophysiology) classification is the internationally accepted system for chronic venous disorders:

Clinical Classification (C0-C6):

ClassDescription
C0No visible or palpable signs of venous disease
C1Telangiectasia or reticular veins
C2Varicose veins (≥3 mm diameter)
C3Oedema
C4aPigmentation and/or eczema
C4bLipodermatosclerosis and/or atrophie blanche
C4cCorona phlebectatica
C5Healed venous ulcer
C6Active venous ulcer
Each class is further designated S (symptomatic) or A (asymptomatic).

Aetiological Classification:

  • Ec - Congenital
  • Ep - Primary (idiopathic)
  • Es - Secondary (post-thrombotic, post-traumatic)
  • En - No identifiable aetiology

Anatomical Classification:

  • As - Superficial veins
  • Ad - Deep veins
  • Ap - Perforating veins
  • An - No anatomical location identified

Pathophysiological Classification:

  • Pr - Reflux
  • Po - Obstruction
  • Pro - Reflux and obstruction
  • Pn - No identifiable pathophysiology
Example: A patient with symptomatic varicose veins (C2S), primary aetiology (Ep), superficial venous system (As), with reflux (Pr) = C2S, Ep, As, Pr

8. COMPLICATIONS OF VARICOSE VEINS

8.1 Haemorrhage

  • May occur from minor trauma to a dilated superficial vein
  • Can be profuse due to high pressure within incompetent veins
  • The patient is often alarmed by the volume; it looks worse than it is
  • First aid: elevate the limb and apply direct pressure
  • Simple elevation does a great deal to stop the bleeding

8.2 Superficial Thrombophlebitis (Superficial Vein Thrombosis - SVT)

  • Inflammatory thrombosis of a varicose vein
  • May occur spontaneously or secondary to minor trauma
  • Clinical features: tender, firm, red, warm cord along a varicose vein; pyrexia, malaise
  • Important: SVT can propagate into the deep system (up to 25% in some series) - DVT/PE risk
  • Management: NSAIDs for pain, consider low-molecular-weight heparin (LMWH) for 6 weeks if close to SFJ or in SSV (prevents proximal extension)
  • Treat the underlying varicose veins once the acute episode settles

8.3 Venous Ulceration

The most important complication:
  • Occurs predominantly over the medial gaiter area (over Cockett's perforators)
  • Not necessarily caused by varicose veins alone - post-thrombotic deep vein incompetence is often the underlying cause
  • Mechanism: sustained venous hypertension → capillary fibrin deposition → pericapillary fibrin cuff → tissue hypoxia
  • Features of venous ulcer:
    • Shallow, flat base
    • Sloping, pale purple-blue edges
    • Floor: pink granulation tissue (or white fibrous tissue in chronic cases)
    • Discharge: seropurulent with trace of blood
    • Surrounding skin: pigmentation, lipodermatosclerosis, eczema
    • Location: medial lower leg, never above the middle third junction
    • Multiple ulcers common
  • Marjolin's ulcer: malignant transformation (squamous cell carcinoma) in long-standing venous ulcer - suspect when edges become raised and everted, or inguinal lymphadenopathy develops

8.4 Skin Changes (Chronic Venous Insufficiency)

  • Eczema (stasis dermatitis)
  • Pigmentation (haemosiderosis) - usually permanent
  • Lipodermatosclerosis - "inverted champagne bottle" leg
  • Atrophie blanche
  • These changes may be partially or completely irreversible, even after successful venous treatment

8.5 Other Complications

  • Calcification of varicose veins (phleboliths) - visible on X-ray
  • Saphena varix (see above) - mistaken for femoral hernia
  • Secondary varicose eczema - can cause contact sensitivity to topical treatments

9. MANAGEMENT

9.1 Conservative Treatment

Indications: Patients with mild symptoms, those unfit for/declining intervention, pregnancy (defer treatment until 3 months post-delivery), contraindications to treatment.
Measures:
  1. Compression hosiery: First-line non-interventional treatment
    • Graduated compression: highest pressure at ankle, reducing proximally
    • Classes: Class I (light, 14-17 mmHg), Class II (medium, 18-24 mmHg), Class III (strong, 25-35 mmHg)
    • Relieves symptoms by reducing ambulatory venous pressure
    • Does NOT cure varicose veins - symptoms return on discontinuation
    • Compliance is often poor (hot, uncomfortable, difficult to apply)
  2. Lifestyle modifications:
    • Avoid prolonged standing
    • Leg elevation when seated/resting
    • Exercise (especially walking) to activate calf muscle pump
    • Weight reduction
  3. Venoactive drugs (e.g., micronised purified flavonoid fraction - Daflon): modest evidence for symptom relief; not widely used in UK practice

9.2 Interventional Treatment

Indications (NICE guidelines for NHS treatment):
  • Symptomatic varicose veins with reflux confirmed on duplex
  • Skin changes (C4-C5-C6) are strong indications
  • Note: treatment for cosmesis alone is not funded by the NHS
Principles common to all interventions:
  • Aim to ablate the refluxing axial vein (GSV, SSV, AAGSV)
  • Perforator incompetence may also need to be addressed
  • Treatment of varicose tributaries (phlebectomy, foam) as adjunct

A. Endovenous Thermal Ablation (PREFERRED TECHNIQUE)

Endovenous Laser Ablation (EVLA / EVLT)
  • A laser fibre is introduced into the vein lumen via a percutaneous needle under duplex guidance
  • Entry point is typically at the lowest extent of reflux in the calf
  • Tumescent local anaesthetic (dilute lidocaine in saline) is injected perivenously under duplex guidance - this provides anaesthesia, compresses the vein around the fibre, and protects surrounding tissue from heat damage
  • Energy delivery ~60-80 J/cm as the fibre is withdrawn
  • The laser (810-1470 nm wavelengths used) generates heat causing endothelial destruction, fibrosis, and vein obliteration
  • Technique: catheter tip positioned just distal to the SFJ (2 cm below SFJ by convention)
Radiofrequency Ablation (RFA)
  • Same principle but uses electromagnetic current (radiofrequency energy) to create thermal damage
  • Most popular device: ClosureFast™ (Medtronic)
    • Wire coil on catheter end; generator heats coil to 120°C maintained for 20-second cycles
    • Coil withdrawn by 3 cm or 7 cm for each cycle
    • Also requires perivenous tumescent anaesthesia
  • Comparable efficacy to EVLA; some studies show less bruising and post-operative pain
Advantages of endothermal ablation over surgery:
  • Day-case procedure under local anaesthetic
  • Immediate return to normal activity
  • Lower complication rates than open surgery
  • Comparable long-term occlusion rates
Disadvantages:
  • Requires tumescent anaesthesia (multiple injections)
  • Suitable only for straight veins of adequate diameter
  • Requires duplex scanning expertise

B. Foam Sclerotherapy

Liquid sclerotherapy: injection of a sclerosant (e.g., sodium tetradecyl sulphate, polidocanol) into the vein, causing endothelial damage, inflammation, and fibrosis. Used mainly for telangiectasia and small reticular veins.
Ultrasound-Guided Foam Sclerotherapy (UGFS):
  • Sclerosant is mixed with air/CO₂ to create foam (Tessari technique: 3-4 parts gas:1 part liquid)
  • Foam is more viscous, displaces blood, and maximises endothelial contact
  • Injected under duplex guidance
  • Advantages:
    • No tumescent anaesthesia required (less painful procedure)
    • Can treat tortuous veins unsuitable for thermal ablation
    • Can treat calf veins with overlying skin damage/ulceration (no need to pierce damaged skin)
    • Very low consumable cost
  • Disadvantages:
    • Lower efficacy than endothermal ablation outside specialist centres
    • Higher reintervention rates
    • Complications: phlebitis (10-15%), pigmentation, visual disturbances (rare), stroke (rare - especially with patent foramen ovale)
    • Maximum safe foam volume per session: 12 ml (UK) or 10 ml (European guidelines)
    • UGFS is therefore often used as an adjunct to endothermal ablation (e.g., for tributaries)

C. Mechanochemical Ablation (MOCA)

  • Device (e.g., ClariVein) deploys an angled rotating wire that physically damages endothelium while simultaneously infusing liquid sclerosant
  • No tumescent anaesthesia required in most cases
  • Good choice for patients with needle phobia
  • Comparable early efficacy to endothermal ablation but increased medium/long-term recanalisation rates compared to thermal ablation
  • Treating long veins challenging due to catheter length and safe sclerosant dose limits
  • Advantage lost when combined with phlebectomy (both become equally painful)

D. Endovenous Cyanoacrylate Glue (VenaSeal™)

  • Cyanoacrylate adhesive is injected endoluminally to obliterate the vein
  • No tumescent anaesthesia; no compression hosiery required post-procedure
  • Short-term efficacy comparable to endothermal ablation
  • Risk of hypersensitivity/foreign body reaction (cyanoacrylate glue reaction): can occur months to years later; presents as nodules, erythema, induration along treated vein
  • Systematic review (Athavale et al., 2023; PMID 37054883) has documented this as a significant concern
  • Good option for patients unable to tolerate tumescent anaesthesia

E. Open Surgery (Traditional - Now Reserved for Selected Cases)

Open surgery has largely been replaced by endovenous techniques, but remains applicable for:
  • Recurrent varicose veins with complex anatomy
  • When endovenous access is not feasible
  • Patient preference
High ligation and stripping (Trendelenburg operation):
  1. Groin incision: ligation of GSV at SFJ, dividing all tributaries ("flush ligation")
  2. Stripping: removal of GSV from groin to knee (stripping below knee associated with higher saphenous nerve injury risk - not recommended)
  3. Phlebectomies/avulsions: multiple stab incisions (2-3 mm) along varicose tributaries; tributaries avulsed with hook
  4. Performed under general or spinal anaesthesia; day-case or overnight stay
Complications of open varicose vein surgery:
  • Haematoma
  • Wound infection
  • Nerve injury: saphenous nerve (medial leg numbness) from GSV stripping below knee; sural nerve from SSV surgery
  • Deep vein thrombosis/pulmonary embolism
  • Lymphocele (especially in groin)
  • Recurrence (neovascularisation at SFJ - major cause of recurrence; tributaries of residual stump re-establish connections with femoral vein)
Phlebectomy / ambulatory phlebectomy (Muller's phlebectomy):
  • Multiple 2-3 mm stab incisions; varicosities avulsed with fine hook
  • Used as standalone procedure for tributaries or adjunct to axial ablation
  • Local anaesthesia; day case

F. Subfascial Endoscopic Perforator Surgery (SEPS)

  • Endoscopic identification and ligation of incompetent perforators under the fascia
  • Used when perforator incompetence is the primary cause (e.g., post-thrombotic ulcers)
  • Less commonly performed now; often replaced by foam sclerotherapy of perforators

9.3 Treatment of Venous Ulcers

  1. Four-layer compression bandaging: primary treatment for venous ulcers
    • Produces sustained graduated compression (40 mmHg at ankle)
    • Reduces ambulatory venous hypertension, promotes healing
  2. Wound care: moist wound healing; debridement; antimicrobials only if infected
  3. Treat the underlying venous incompetence: Cochrane meta-analysis (Cai et al., 2023; PMID 37497816) confirms that endovenous ablation for venous leg ulcers significantly improves healing rates and reduces recurrence compared to compression alone
  4. Pentoxifylline: can be used as adjunct (improves microcirculation)
  5. Skin grafting: for large, slow-healing ulcers (split-thickness grafts)

10. CURRENT GUIDELINES (2023-2024)

The 2022-2024 SVS/AVF/AVLS Clinical Practice Guidelines (Gloviczki et al., PMID 36326210 and 37652254) make the following key recommendations:
  • Duplex ultrasound is recommended for all patients before treatment
  • Endovenous thermal ablation (EVLA or RFA) is the preferred first-line treatment for GSV incompetence over open surgery (Grade 1A)
  • Foam sclerotherapy is recommended when thermal ablation is not feasible (Grade 1B)
  • Compression therapy alone is recommended for patients who are not candidates for intervention
  • For venous ulcers with confirmed superficial reflux, early endovenous ablation (rather than delaying until ulcer heals) is recommended
  • MOCA and cyanoacrylate closure are acceptable alternatives when thermal ablation is not suitable

11. SPECIAL SCENARIOS

Varicose Veins in Pregnancy

  • Often appear or worsen during pregnancy
  • Defer treatment until at least 3 months post-delivery (many improve spontaneously)
  • Use compression stockings throughout pregnancy
  • Avoid injections and surgery during pregnancy

Recurrent Varicose Veins

  • Common (up to 30% at 5 years after surgery)
  • Causes: technical failure, neovascularisation (at groin), progression of disease in residual segments
  • Require careful duplex mapping before re-treatment
  • Treatment: foam sclerotherapy is often preferred (surgery in scarred field carries higher complication risk)

Bilateral Varicose Veins

  • Treat each leg separately (reduces post-operative complications)
  • Treat the more symptomatic or advanced leg first

12. DIFFERENTIAL DIAGNOSIS

Varicose veins must be distinguished from:
  • Deep vein thrombosis (DVT): calf swelling, tenderness, Homans sign, Moses sign; confirmed by duplex
  • Chronic venous insufficiency (post-thrombotic syndrome): history of DVT, deep venous reflux or obstruction on duplex
  • Lymphoedema: non-pitting oedema, does not improve overnight, skin changes different
  • Arteriovenous malformation / Klippel-Trenaunay syndrome: limb hypertrophy, port-wine stain, atypical distribution
  • Lipoma or soft tissue tumour (distinguished from saphena varix by: saphena varix disappears when recumbent, has cough impulse)
  • Femoral hernia (distinguished from saphena varix by: saphena varix disappears when recumbent; duplex confirms venous nature)

13. SUMMARY - HIGH-YIELD POINTS FOR EXAMS

TopicKey Fact
Most common affected veinGreat saphenous vein (60% of cases)
Investigation of choiceDuplex ultrasound (replaced all clinical tests)
Preferred treatment (guidelines)Endovenous thermal ablation (EVLA/RFA)
CEAP class for active ulcerC6
Site of venous ulcerMedial gaiter area (over Cockett's perforators)
Cause of recurrence after surgeryNeovascularisation at saphenofemoral junction
Saphena varix mistaken forFemoral hernia
Reflux duration defining incompetence≥0.5 s (superficial veins), ≥1.0 s (proximal deep veins)
Complication of GSV stripping below kneeSaphenous nerve injury (medial leg numbness)
Complication of SSV surgerySural nerve injury
Malignant change in venous ulcerMarjolin's ulcer (SCC)
Trendelenburg operationHigh ligation + stripping
RFA device temperature120°C for 20-second cycles
MOCA deviceClariVein

14. SOURCES

  • Bailey & Love's Short Practice of Surgery (28th Edition), Chapter 62: Chronic venous disease of the lower limb
  • S. Das: A Manual on Clinical Surgery (13th Edition), Chapter 7: Varicose Veins
  • Gloviczki P et al. (2023). SVS/AVF/AVLS Clinical Practice Guidelines for varicose veins, Part I. J Vasc Surg Venous Lymphat Disord. [PMID: 36326210]
  • Gloviczki P et al. (2024). SVS/AVF/AVLS Clinical Practice Guidelines for varicose veins, Part II. J Vasc Surg Venous Lymphat Disord. [PMID: 37652254]
  • Cai PL et al. (2023). Endovenous ablation for venous leg ulcers. Cochrane Database Syst Rev. [PMID: 37497816]
  • Athavale A et al. (2023). Cyanoacrylate glue reactions: A systematic review. J Vasc Surg Venous Lymphat Disord. [PMID: 37054883]
  • Jiang W et al. (2024). Endovenous RFA vs laser ablation in lower extremity varicose veins: A meta-analysis. J Vasc Surg Venous Lymphat Disord. [PMID: 38316290]
---That's your complete, comprehensive varicose vein lecture. Here's a quick roadmap of what was covered:

Lecture Structure at a Glance:
  1. Definition & Overview - what varicose means; prevalence
  2. Anatomy - GSV/SSV/perforators/calf pump
  3. Pathophysiology - venous hypertension, vein wall changes, the vicious cycle
  4. Aetiology & Classification - primary vs secondary causes; risk factors
  5. Clinical Features - full history-taking guide + signs in order of severity (C0 through C6 skin changes); clinical tests (and why they're now obsolete)
  6. Investigations - duplex ultrasound (gold standard) with technical detail; venography; CT/MRI
  7. CEAP Classification - full table with all 4 domains (C, E, A, P)
  8. Complications - haemorrhage, SVT, ulceration (Marjolin's), skin changes
  9. Management - conservative → EVLA → RFA → foam → MOCA → cyanoacrylate glue → open surgery; venous ulcer management
  10. 2023-2024 Guidelines - SVS/AVF/AVLS key recommendations
  11. Special Scenarios - pregnancy, recurrence, bilateral disease
  12. Differential Diagnosis - DVT, lymphoedema, saphena varix vs hernia
  13. High-Yield Summary Table - exam-ready facts
The notes are sourced from Bailey & Love (28th ed.), S. Das Clinical Surgery (13th ed.), and the latest 2023-2024 SVS practice guidelines.
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