Causes of Chronic Venous Insufficiency (CVI)
Chronic venous insufficiency is primarily caused by valvular incompetence in the veins, which leads to venous hypertension, reflux, and impaired blood return from the lower extremities. 1
Primary Mechanisms of CVI Development
Valvular Dysfunction
- Primary valvular incompetence - The most common cause of CVI 1
- Results from loss of elasticity in vein walls
- Failure of valve leaflets to properly close
- Allows blood to flow in reverse direction (reflux)
- Leads to increased venous pressure and vein dilation
Secondary Causes
- Deep venous thrombosis (DVT) - Second most common cause 1
- Damages valves during thrombosis and recanalization
- Results in post-thrombotic syndrome
- Extrinsic venous obstruction - Less common cause 1
- Compression from tumors, pregnancy, or other structures
- Restricts normal venous return
Pathophysiologic Mechanisms
- Venous hypertension - The fundamental problem in CVI 1, 2
- Causes elongation and tortuosity of veins
- Leads to blood pooling and reduced venous return
- Muscle pump dysfunction 3, 4
- Inefficiency of calf and foot veno-muscular pumps
- Contributes to reduced venous emptying
- Can be worsened by foot dysmorphisms (flatfoot, pes cavus)
Risk Factors for CVI Development
- Genetic predisposition - Family history of venous disease 1
- Female sex - Women are more affected than men 1
- Advancing age - Prevalence increases with age 1
- Chronically increased intra-abdominal pressure 1
- Obesity
- Pregnancy
- Chronic constipation
- Abdominal tumors
- Prolonged standing - Occupational risk factor 1
- Arteriovenous shunting - Disrupts normal flow patterns 1
Cellular and Molecular Mechanisms
- Inflammatory processes 2, 5
- Venous hypertension triggers inflammatory cascade
- Leads to endothelial activation and dysfunction
- Microparticle release 5
- Elevated levels of endothelial microparticles (EMPs) and platelet microparticles (PMPs)
- Contribute to venous wall dysfunction
- Associated with increased tissue factor and P-selectin expression
- Structural changes in venous walls 5
- Activation of endothelial and smooth muscle cells
- Hyperplasic-multilayered basal lamina formation
- Impaired contractile responses
Progression of Disease
Early manifestations
- Telangiectasias and reticular veins
- Varicose veins (dilated, tortuous veins ≥3mm)
- Leg heaviness, aching, cramping, especially at day's end
Advanced manifestations
- Edema worsened by standing, relieved by elevation
- Skin changes (hyperpigmentation, eczema)
- Lipodermatosclerosis (fibrosis and contraction of skin/subcutaneous tissues)
- Venous ulceration - most severe complication 1
Clinical Pearls and Pitfalls
- Important clinical caveat: CVI is often misdiagnosed as other conditions like lymphedema or cellulitis, delaying proper treatment
- Diagnostic pitfall: Not all leg pain and swelling is due to CVI - duplex ultrasonography is essential for confirming diagnosis when intervention is being considered 1
- Treatment consideration: While compression therapy is the mainstay of conservative management, addressing the underlying valvular dysfunction is necessary for long-term improvement 6
Understanding the pathophysiologic mechanisms of CVI is crucial for appropriate management, which should target the specific underlying causes rather than just symptom relief.