Venous Insufficiency

Basics

Description

  • Inability of veins, primarily in the lower extremities, to effectively return blood to the heart
  • Classified as chronic when it progresses to persistent venous hypertension with clinical manifestations such as edema, skin changes, or venous ulcers
  • CEAP (Clinical, Etiologic, Anatomic, Pathophysiologic) classification:
    • C0: No visible or palpable signs of venous disease
    • C1: Telangiectasias or reticular veins (spider veins)
    • C2: Varicose veins (>3 mm in diameter)
    • C3: Varicose veins with edema
    • C4: Skin changes (pigmentation, eczema, lipodermatosclerosis):
      • C4a: Pigmentation, eczema
      • C4b: Lipodermatosclerosis, atrophie blanche
    • C5: Healed venous ulcer
    • C6: Active venous ulcer
  • Types of venous insufficiency:
    • Isolated superficial venous reflux:
      • Often presents as varicose veins but without significant edema or skin changes
    • Superficial and deep venous reflux:
      • Risk of edema, and skin changes associated with chronic venous insufficiency
    • Chronic deep venous obstruction:
      • Blockage in deep veins (often postthrombotic)
    • Combined deep venous reflux and obstruction:
      • The most severe form, typically postthrombotic, involving both venous reflux and obstruction, leading to severe edema, lipodermatosclerosis, and venous ulcers
  • Normal venous flow relies on competent valves and the calf muscle pump to propel blood centrally​
  • Valvular insufficiency causes retrograde flow, venous hypertension, and progressive vein dilation
  • Thrombosis (postthrombotic syndrome) leads to obstruction, impaired venous return, and deep venous hypertension
  • Chronic venous hypertension causes capillary leakage, inflammation, and dermal fibrosis (lipodermatosclerosis)
  • Microvascular dysfunction and tissue hypoxia lead to hemosiderin deposition, ulceration, and poor wound healing
  • Risk factors:
    • Advanced age (estimated prevalence of 5–30% of adult population)
    • Sex (female:male predominance of 3:1)
    • Family history of venous varicosity
    • DVT or phlebitis
    • Leg edema
    • Obesity
    • Pregnancy
    • Prior lower-extremity injury
    • Prolonged immobility
    • Smoking
    • Diabetes
    • Chronic vascular disease

Etiology

  • Valvular dysfunction:
    • Congenital or acquired failure of venous valves
  • Weak vein walls:
    • Inherited connective tissue abnormalities
  • Aging:
    • Progressive loss of vein elasticity and valve degeneration
  • Deep vein thrombosis
  • Postthrombotic syndrome
  • Pelvic venous compression:
    • May–Thurner syndrome (iliac vein compression)
    • Nutcracker syndrome:
      • The left renal vein is compressed between the SMA and aorta, causing venous hypertension, reflux, and secondary venous insufficiency
  • Direct injury to veins or postsurgical changes
  • Chronic external pressure:
    • Tumors
    • Pregnancy
    • Abdominal obesity

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