Chronic Venous Insufficiency: Pathophysiology, Diagnosis, and Contemporary Management

Chronic venous insufficiency (CVI) represents a progressive medical condition affecting approximately 25-40% of adults worldwide, with prevalence increasing dramatically with age. This complex vascular disorder extends beyond simple varicose veins, encompassing a spectrum of clinical manifestations resulting from long-standing venous hypertension. This comprehensive guide explores the pathophysiology, diagnostic approaches, and modern management strategies for CVI, providing valuable insights for both healthcare professionals and patients navigating this common but often undertreated condition.

Pathophysiology of Chronic Venous Insufficiency

CVI develops through a cascade of pathophysiological events centered around venous hypertension:

Primary Mechanisms of Venous Hypertension

1. Valvular Incompetence: Failure of one-way venous valves, allowing retrograde blood flow (reflux)
2. Primary valvular dysfunction (genetic/structural abnormalities)
3. Secondary valve damage (post-thrombotic, inflammatory)

4. Progressive valve deterioration with sustained pressure

5. Venous Obstruction: Impedance to normal venous outflow

6. Acute or chronic thrombosis
7. Extrinsic compression (tumors, anatomical anomalies)

8. Post-thrombotic recanalization with residual obstruction

9. Calf Muscle Pump Dysfunction: Impaired “second heart” mechanism

10. Reduced ankle mobility
11. Muscle atrophy or weakness
12. Altered gait mechanics
13. Neurological conditions affecting muscle activation

Microcirculatory Changes

Sustained venous hypertension triggers a cascade of microcirculatory alterations:

• Increased Capillary Pressure: Forces fluid into interstitial spaces
• Endothelial Activation: Upregulation of adhesion molecules
• Leukocyte Adhesion and Migration: White blood cells attach to vessel walls and migrate into tissues
• Inflammatory Mediator Release: Cytokines, growth factors, and proteolytic enzymes damage surrounding tissues
• Capillary Proliferation: Abnormal microvascular networks develop
• Fibrin Cuff Formation: Pericapillary fibrin deposits impair oxygen diffusion
• Tissue Hypoxia: Reduced oxygen availability to skin and subcutaneous tissues

Tissue Remodeling and Progression

Chronic inflammation and hypoxia lead to progressive tissue changes:

• Lipodermatosclerosis: Fibrosis and hardening of subcutaneous tissues
• Hemosiderin Deposition: Iron-containing pigment from extravasated red blood cells
• Dermal Fibrosis: Skin thickening and decreased elasticity
• Impaired Wound Healing: Reduced fibroblast function and angiogenesis
• Ulcer Formation: Breakdown of skin integrity in advanced disease

Clinical Presentation and Classification

CVI presents with a spectrum of signs and symptoms that typically progress over time:

Common Symptoms

• Leg heaviness and fatigue (reported by 85% of patients)
• Aching or throbbing pain, especially after prolonged standing
• Night cramps and restless legs
• Pruritus (itching) around affected areas
• Sensation of swelling, often worse by day’s end
• Discomfort relieved by elevation or compression

Clinical Signs

• Edema (initially pitting, may become non-pitting with chronicity)
• Varicose veins and reticular veins
• Telangiectasias (spider veins)
• Skin changes:
• Hyperpigmentation (brownish discoloration)
• Eczema (stasis dermatitis)
• Atrophie blanche (white atrophic skin with telangiectasias)
• Lipodermatosclerosis (hardened, contracted skin)
• Venous ulceration (typically at medial ankle)

CEAP Classification System

The CEAP (Clinical-Etiology-Anatomy-Pathophysiology) classification provides standardized assessment:

Clinical Classification (C):
– C0: No visible or palpable signs of venous disease
– C1: Telangiectasias or reticular veins
– C2: Varicose veins
– C3: Edema
– C4a: Pigmentation or eczema
– C4b: Lipodermatosclerosis or atrophie blanche
– C5: Healed venous ulcer
– C6: Active venous ulcer

Etiology (E):
– Ec: Congenital
– Ep: Primary
– Es: Secondary (post-thrombotic, post-traumatic)
– En: No venous cause identified

Anatomy (A):
– As: Superficial veins
– Ap: Perforator veins
– Ad: Deep veins
– An: No venous location identified

Pathophysiology (P):
– Pr: Reflux
– Po: Obstruction
– Pr,o: Reflux and obstruction
– Pn: No venous pathophysiology identified

Diagnostic Approaches

Accurate diagnosis requires comprehensive assessment:

临床评估

• Detailed history focusing on risk factors and symptom progression
• Physical examination in standing position
• Assessment of mobility and gait
• Documentation using CEAP classification
• Venous Clinical Severity Score (VCSS) for quantifying disease severity

Non-Invasive Vascular Testing

Duplex Ultrasound:
– Gold standard for initial evaluation (sensitivity/specificity >95%)
– Provides both anatomical and functional information
– Assesses reflux duration and velocity
– Identifies obstruction and post-thrombotic changes
– Maps perforator veins and deep system status

Plethysmography:
– Air plethysmography measures volume changes
– Photoplethysmography assesses refilling times
– Quantifies overall venous function and calf pump efficiency

Advanced Imaging (for selected cases)

• Computed Tomography Venography (CTV): Excellent for iliocaval assessment
• Magnetic Resonance Venography (MRV): Provides detailed anatomical information without radiation
• Intravascular Ultrasound (IVUS): Precise evaluation of venous stenosis and compression
• Contrast Venography: Reserved for complex cases or interventional planning

Contemporary Management Strategies

Management follows a progressive approach based on disease severity:

Conservative Management

Compression Therapy:
– Cornerstone of CVI management (70-80% symptom improvement)
– Graduated compression (highest pressure at ankle, decreasing proximally)
– Pressure classes:
– Class I (15-20 mmHg): Mild CVI, prevention
– Class II (20-30 mmHg): Moderate CVI, most varicose veins
– Class III (30-40 mmHg): Severe CVI, post-ulcer states
– Class IV (40+ mmHg): Lymphedema, severe post-thrombotic syndrome

Compression options:
– Graduated compression stockings
– Adjustable compression wraps
– Multi-component bandaging systems
– Intermittent pneumatic compression devices

Lifestyle Modifications:
– Regular exercise focusing on calf muscle activation
– Weight management (each BMI point above 30 increases CVI risk by ~5%)
– Leg elevation (20-30 minutes, 3-4 times daily)
– Avoiding prolonged standing/sitting
– Proper footwear supporting ankle mobility

Pharmacological Therapy:
– Venoactive drugs:
– Micronized purified flavonoid fraction (MPFF)
– Horse chestnut seed extract (aescin)
– Rutosides
– Pentoxifylline (particularly for venous ulcers)
– Mechanism: Reduce capillary permeability, improve lymphatic drainage, and reduce inflammation
– Evidence: Moderate quality evidence supports symptom improvement and edema reduction

Interventional Management

Endovenous Thermal Ablation:
– First-line intervention for saphenous reflux
– Techniques:
– Endovenous laser ablation (EVLA)
– Radiofrequency ablation (RFA)
– Outcomes: 90-95% technical success with 85-90% five-year durability
– Advantages: Outpatient procedure, minimal recovery time

Non-Thermal, Non-Tumescent Techniques:
– Mechanochemical ablation (MOCA)
– Cyanoacrylate adhesive closure
– Endovenous foam sclerotherapy
– Advantages: No tumescent anesthesia required, reduced post-procedure pain

Sclerotherapy:
– Liquid sclerotherapy for smaller vessels
– Ultrasound-guided foam sclerotherapy for larger veins
– Applications: Primary treatment for smaller veins, adjunctive therapy after other interventions

Surgical Options:
– High ligation and stripping (less commonly performed)
– Ambulatory phlebectomy for varicosity clusters
– CHIVA method (hemodynamic correction)
– Indications: Complex anatomy, recurrent disease, or patient preference

Advanced Interventions for Severe CVI

Deep Venous Reconstruction:
– Balloon angioplasty and stenting for iliocaval obstruction
– Venous bypass procedures for extensive occlusions
– Outcomes: 70-85% patency rates at 3-5 years with significant symptom improvement

Valve Reconstruction Techniques:
– External valvuloplasty
– Internal valvuloplasty
– Valve transposition or transplantation
– Indications: Severe deep venous reflux with advanced symptoms

Management of Venous Ulcers

Comprehensive approach:
– Compression therapy (cornerstone of treatment)
– Wound bed preparation and debridement
– Advanced wound dressings appropriate for exudate level
– Infection control when indicated
– Adjunctive therapies:
– Negative pressure wound therapy
– Cellular and tissue-based products
– Growth factors
– Healing rates: 70-80% within 6 months with optimal therapy

医疗免责声明

重要通知: This information is provided for educational purposes only and does not constitute medical advice. Chronic venous insufficiency can be associated with serious underlying vascular conditions that require proper medical evaluation. The management strategies discussed should only be implemented under the guidance of qualified healthcare professionals after appropriate diagnostic assessment. Individual results may vary, and all interventions carry potential risks and benefits that should be thoroughly discussed with your healthcare provider. If you are experiencing symptoms of chronic venous insufficiency, please consult with a vascular specialist for personalized evaluation and treatment recommendations.

结论

Chronic venous insufficiency represents a progressive condition with significant impact on quality of life and potential for serious complications if left untreated. Modern understanding of the pathophysiology has led to remarkable advances in both diagnostic approaches and management strategies. A comprehensive approach combining appropriate conservative measures with timely interventional treatments offers the best outcomes for patients across the spectrum of disease severity. With continued research and technological innovation, management options continue to evolve, providing increasingly effective solutions for this common vascular condition.