Vericose vein

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"varicose veins"[MeSH Terms] AND treatment

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Varicose Veins

Varicose veins: (a) preoperative marking, (b) edema/skin changes, (c) tortuous dilated great saphenous vein territory
Fig. 62.3 - Bailey and Love: Varicose veins: marked for surgery (a), edema (b), and tortuous veins along the saphenous territory (c).

Definition

Varicose veins are dilated, tortuous superficial veins measuring at least 3 mm in diameter. They most commonly affect the lower limbs. The smaller reticular veins (1-3 mm, blue-green, non-protruding) and telangiectasias (spider veins, <1 mm) are related but distinct entities on the spectrum of chronic venous disease (CVD).
  • Harrison's Principles of Internal Medicine 22E, p. 2224
  • Gray's Anatomy for Students, p. 44

Epidemiology

  • Adult prevalence of visible varicose veins: 30-50% (Bailey & Love); ~15% in men and ~30% in women in the United States (Harrison's).
  • Chronic venous insufficiency with edema affects ~7.5% of men and 5% of women.
  • ~20% of patients with chronic venous insufficiency develop venous ulcers.
Risk factors:
FactorDetail
SexHigher prevalence in women
AgePrevalence rises sharply with age; from 11.5% (18-24 yr) to 55.7% (55-64 yr) in the Edinburgh Vein Study
PregnancyIncreases risk
Family historyStrong familial susceptibility
Obesity / tall statureHigher BMI and height associated
OccupationProlonged standing (evidence inconclusive)
  • Bailey and Love's Short Practice of Surgery 28th Ed., p. 1052

Anatomy and Pathophysiology

Relevant anatomy:
  • Superficial veins: great saphenous vein (GSV) - longest vein in the body, medial side from foot to common femoral vein; small saphenous vein (SSV) - posterolateral calf to popliteal vein.
  • Deep veins accompany arteries (tibial, popliteal, femoral, iliac).
  • Perforating veins connect the two systems; normally allow flow from superficial to deep only.
Mechanism:
  1. Venous valves in perforating and axial veins become incompetent.
  2. This allows retrograde (reflux) blood flow under raised hydrostatic pressure.
  3. The increased volume and pressure cause progressive dilation and tortuosity of the superficial veins.
  4. Continued venous hypertension leads to capillary leak, edema, inflammatory cell infiltration, and eventual skin changes (lipodermatosclerosis, pigmentation, ulceration).
Valve incompetence commonly starts at the saphenofemoral junction (SFJ) or saphenopopliteal junction (SPJ), leading to axial reflux down the GSV or SSV respectively.
  • Harrison's, p. 2223-2224
  • Gray's Anatomy for Students, p. 44

Clinical Features

Symptoms

  • Aching, heaviness, throbbing, burning, or bursting sensation in the legs
  • Symptoms worsen throughout the day and with prolonged standing
  • Relieved by leg elevation and compression hosiery
  • Itching (especially with complications)
  • Ankle swelling

Signs (on examination - patient standing)

  • Visible, distended, tortuous surface veins along the GSV or SSV territory
  • Ankle edema (pitting in early stages, later indurated)
  • Skin changes:
    • Hyperpigmentation (hemosiderin deposition)
    • Lipodermatosclerosis - induration + inflammation, just above the ankle
    • Atrophie blanche - white scar patches near the medial malleolus
    • Stasis eczema/dermatitis
    • Phlebectasia corona - fan-shaped intradermal veins near ankle
    • Venous ulcer - shallow, irregular border, near medial/lateral malleolus

Complications

  • Chronic: skin changes, venous ulceration
  • Acute: superficial vein thrombosis (thrombophlebitis), bleeding
  • Bailey and Love, p. 1052
  • Harrison's, p. 2224

CEAP Classification

The internationally accepted classification of CVD:
ClassDescription
C0No visible/palpable signs
C1Telangiectasias or reticular veins
C2Varicose veins
C2rRecurrent varicose veins
C3Edema
C4aPigmentation or eczema
C4bLipodermatosclerosis or atrophie blanche
C4cCorona phlebectatica
C5Healed venous ulcer
C6Active venous ulcer
C6rRecurrent active venous ulcer
Etiologic (E): Primary, Secondary, Congenital
Anatomic (A): Superficial, Perforator, Deep
Pathophysiologic (P): Reflux, Obstruction, Both, None
  • Harrison's Table 293-1

Investigations

Duplex Ultrasound (Gold Standard)

  • Combines B-mode imaging with spectral/color Doppler
  • Identifies reflux (retrograde flow >0.5 sec in superficial/crural veins; >1 sec in proximal deep veins) and obstruction
  • Performed with patient standing
  • Maps the SFJ/SPJ, full length of GSV/SSV, and perforators
  • The "Mickey Mouse" sign on transverse groin scan: GSV and common femoral vein (CFV) medial to common femoral artery (CFA)

Bedside Tests (largely replaced by ultrasound)

  • Brodie-Trendelenburg test: tourniquet applied to thigh after elevating leg; fast refilling after tourniquet release = SFJ incompetence; rapid filling before release = deep vein incompetence.
  • Perthes test: tourniquet at mid-thigh, patient walks; collapse of below-knee varices indicates competent deep system; distension indicates deep vein obstruction.

Other imaging (rarely needed)

  • MR/CT/conventional venography for IVC/iliofemoral disease, May-Thurner syndrome, post-DVT obstruction.
  • Bailey and Love, p. 1053
  • Harrison's, p. 2224

Treatment

1. Conservative (Supportive) Measures

  • Leg elevation periodically, avoid prolonged standing
  • Compression hosiery:
    • British Class 1: 14-17 mmHg; Class 2: 18-24 mmHg; Class 3: 25-35 mmHg
    • 20-30 mmHg suitable for simple varicose veins; 30-40 mmHg for venous ulcers
    • Relieves symptoms but does not prevent progression or cure varicose veins
    • Poor long-term patient compliance
  • Exercise, weight loss, skin care

2. Endothermal Ablation (Current Gold Standard for axial reflux)

Replaced surgical ligation/stripping as first-line treatment. Performed outpatient under local anaesthetic (tumescent anaesthesia). Tumescent anaesthesia compresses the vein onto the device, displaces heat away from nerves, and acts as a heat sink.
TechniqueMechanismNotes
Endovenous Laser Ablation (EVLA)Laser fibre (1470 nm wavelength) inserted into vein; heat destroys vein wall~60-80 J/cm energy delivery; high technical efficacy
Radiofrequency Ablation (RFA)Electromagnetic current heats catheter coil to 120°C for 20-sec cycles (ClosureFast device)Most evidence-supported RFA device; 3 cm and 7 cm coils available
Both techniques have equivalent outcomes; RFA may have slightly less postoperative pain/bruising. A 2024 meta-analysis (PMID 38316290) comparing EVLA vs RFA found comparable safety and efficacy profiles.

3. Foam Sclerotherapy

  • Sclerosant foam (e.g., sodium tetradecyl sulfate or polidocanol) injected under ultrasound guidance
  • Destroys vein endothelium and causes fibrosis
  • Used for axial veins, tributaries, residual/recurrent veins, and as an alternative to ablation
  • Higher recurrence rates than endothermal ablation

4. Mechanochemical Ablation (MOCA) and Cyanoacrylate Glue

  • Newer non-thermal, non-tumescent techniques
  • Avoid tumescent injection and thus reduce procedure time/discomfort
  • MOCA combines mechanical abrasion with sclerosant

5. Surgical Treatment (where endovenous techniques not suitable)

  • High ligation and stripping (Trendelenburg operation):
    • SFJ flush ligation at groin + stripping of GSV to knee
    • Stripping below the knee increases sural nerve injury risk
    • SPJ ligation + SSV stripping/resection for small saphenous disease
  • Phlebectomy (avulsions):
    • Removal of varicose tributaries via multiple small stab incisions using mosquito forceps/phlebectomy hooks
    • Can be performed alone under local anaesthetic or combined with axial vein treatment
  • Complication rates: wound infection, haematoma, nerve injury (sural nerve with SSV surgery), DVT, popliteal vein injury
  • Bailey and Love, pp. 1054-1060
  • Harrison's, pp. 2224-2225
  • Schwartz's Principles of Surgery 11th Ed.

Venous Ulcer Management

  • Compression bandaging (multilayer) is standard of care
  • Wound dressings: low-adherent absorptive (first-line); hydrocolloid, hydrogel, foam, or alginate as alternatives
  • Debridement of necrotic tissue
  • Antibiotics only if ulcer is infected
  • Treat underlying reflux once ulcer healed (reduces recurrence)

Key Points Summary

AspectKey Fact
DefinitionTortuous superficial veins ≥3 mm
Commonest siteLower limb GSV territory
Primary causeValvular incompetence + reflux
Gold standard investigationDuplex ultrasound
Gold standard treatmentEndothermal ablation (EVLA or RFA)
ClassificationCEAP C0-C6
Most serious complicationVenous ulceration
Acute complicationsThrombophlebitis, bleeding

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