Chronic venous disorders

Epidemiology

• Prevalence 2-56% in men and 1-60% in women
• Varicose veins in 40% of men and 16% of women
• Ankle oedema 7% of men and 16% of women
• Venous ulcers 1% of people
• 57.8% of patients in Edinburgh Vein Study progressed over 13 years, with superficial vein reflux a predictor for increased likelihood of progression

Aetiology

• Varicose veins
• Incompetent perforator
• Deep venous reflux
  • Pelvic congestion syndrome
    • Pelvic pain, perineal heaviness, urgency of micturition and post-coital pain, caused by ovarian and/or pelvic vein reflux and/or obstruction
    • May be associated with vulvar, perineal or lower extremity varices
    • Type 1: reflux secondary to pelvic and ovarian vein incompetence
    • Type 2: secondary to obstruction of outflow
    • Type 3: secondary to a local compression phenomenon
    • Condition often disappears after menopause
    • Diagnose based on a 6mm-diameter ovarian vein on DUS
    • CT venogram can be useful - look for pelvic varices, exclude other lesions
    • Management:
      • Medroxyprogesterone acetate 30mg daily for 6 months has been shown to be effective in the short term, but not curative
      • Different surgical techniques have been described, including vein ligation
      • Embolisation of refluxing veins is first-line treatment now for refluxing veins
      • PCS secondary to obstruction should be treated with stents
• Deep venous obstruction
  • Thrombotic
  • Trauma
  • Radiation
  • External compression
    • Retroperitoneal fibrosis
    • May-Thurner syndrome (compression of left CIV by right CIA)
    • Tumours
    • Aneurysms
    • Abnormal muscle bands (popliteal vein entrapment)
    • Fibrous bands or ligaments (soleal arch syndrome or femoral vein compression by the inguinal ligament)
• Inadequate muscle pump function

Presentation

• See 'clinical evaluation'
• Telangiectasias
• Enlarged reticular veins
• Varicose veins
• Lipodermatosclerosis
• Lower extremity pain and swelling
  • Oedema from chronic venous disease usually occurs at the ankle. Oedema from lymphoedema involves the foot.
• Venous ulcers
  • Venous hypertension causes protein extravasation, impeding oxygen diffusion, and activating the inflammatory response
  • Inflammatory cascade - mast cell degranulation, leucocyte recruitment, prostacyclins, fibroblast differentiation into myofibroblasts
  • Chronic inflammation and venous stasis favours thrombus formation, causing further fibrosis
  • Red blood cell degradation causes local iron overload, which keeps macrophages in an M1 phenotype, leading to tissue destruction instead of dermal repair
  • Inflammatory cascade also impairs wound healing, resulting in ulcer formation upon wounding

Management

• Non-operative:
  • Lifestyle
    • Exercise - may be beneficial for ulcer healing, as an adjunct to compression
    • Leg elevation - aids venous drainage and reduces ankle oedema, and probably helps ulcer healing. Elevate legs 30cm above heart several times per day.
    • Weight loss - obesity is an important factor in development and progression of chronic venous disease.
  • Compression
    • Essential for patients with C2-C6 CVD
    • Opposes venous hypertension
    • Gradient compression stockings:
      • Class I: 10-15mmHg (OTC)
        • Symptom control in C1s
        • Varicose veins in pregnancy
        • Prevention of leg oedema relating to prolonged sitting/standing
        • Prevention of VTE
      • Class II: 20-30mmHg (prescription)
        • Symptom relief in uncomplicated VV
        • Possibly prevent PTS after DVT
      • Class III: 30-40mmHg (high compression - prescription)
        • C4-C6 disease
      • Should be replaced every 6-9 months
    • Layered compression bandages
      • Can achieve up to 60-70mmHg
      • Includes Coban bandages
      • Four-layer bandages have been shown to heal venous ulcers faster than single-layer
• Medication
  • Diuretics - only useful in the presence of CCF
  • Zinc - no known benefit
  • MPFF - appears to help, in conjunction with compression (500mg BD)
• Surgery
  • Treat underlying cause

CEAP classification for chronic venous disorders

Clinical classification
C0	No visible or palpable signs of venous disease
C1	Telangiectasias, reticular veins
C2	Varicose veins
C2r	Recurrent varicose veins
C3	Edema
C4	Changes in skin and subcutaneous tissue secondary to chronic venous disease
C4a	Pigmentation or eczema
C4b	Lipodermatosclerosis or atrophie blanche
C4c	Corona phlebectatica
C5	Healed
C6	Active venous ulcer
C6r	Recurrent active venous ulcer
S	With symptoms attributable to venous disease
A	Absence of symptoms attributable to venous disease
Etiology classification
Ep	Primary
Es	Secondary
Esi	Secondary (intravenous)
Ese	Secondary (extravenous)
Ec	Congenital
En	No cause identified
Anatomy classification*
As	Superficial veins (Tel, Ret, GSVa, GSVb, SSV, AASV, NSV)
Ad	Deep veins (IVC, CIV, IIV, EIV, PELV, CFV, DFV, FV, POPV, TIBV, PRV, ATV, PTV, MUSV, GAV, SOV)
Ap	Perforator veins (TPV, CPV)
An	No venous anatomic location identified
Pathophysiology classification*
Pr	Reflux
Po	Obstruction
Pr,o	Reflux and obstruction
Pn	No venous pathophysiology identifiable