What is venous stasis, what are its causes, and how is it treated?

What is Venous Stasis?

Venous stasis is the slowing or pooling of blood in the veins, most commonly in the lower extremities, caused by impaired venous return to the heart. 1 This occurs when the normal mechanisms that propel blood upward against gravity fail, leading to increased venous pressure (venous hypertension) and subsequent tissue damage. 1

Pathophysiology

Venous stasis develops when blood cannot efficiently return from the legs to the heart, resulting in:

• Elevated venous pressure that increases from normal levels (22 mmHg during walking) to 80-90 mmHg when standing motionless, causing blood to pool in the lower extremity veins. 1, 2
• Ambulatory venous hypertension where venous pressure fails to decrease adequately during walking due to impaired calf muscle pump function or valve dysfunction. 1
• Progressive tissue changes including hyperpigmentation (hemosiderin staining), edema, skin thickening (lipodermatosclerosis), and ultimately venous ulceration. 1

The normal calf muscle pump ejects blood proximally during walking while competent venous valves prevent backward flow (reflux). 2 When this system fails, blood accumulates in the veins rather than returning efficiently to the heart. 1

Causes of Venous Stasis

Primary Mechanisms

Venous valvular incompetence (reflux) is the most common cause, where damaged or weakened valves allow blood to flow backward instead of maintaining unidirectional flow toward the heart. 1

• Pathologic reflux is defined as retrograde venous flow lasting ≥500 milliseconds on duplex ultrasound. 1, 2
• Valve damage results from genetic predisposition, loss of vein wall elasticity, or inflammatory processes. 1
• Reflux causes increased downstream venous pressure, leading to vein dilation, tortuosity (varicose veins), and tissue damage. 1

Venous outflow obstruction blocks blood flow from returning to the heart, causing upstream pressure buildup. 1, 3

• Deep vein thrombosis (DVT) is the most common obstructive cause, with incomplete recanalization leaving residual obstruction even after the acute phase. 1, 4
• Post-thrombotic syndrome develops in patients after DVT through a combination of persistent obstruction and secondary valve damage. 1
• Iliac vein compression or stenosis can cause outflow obstruction even without prior thrombosis. 3

Risk Factors

• Prior DVT is strongly associated with venous stasis syndrome, particularly when involving the left leg or iliofemoral veins. 1, 4
• Increasing age correlates with venous outflow obstruction and progressive valve deterioration. 1, 4
• Obesity (increased body mass index) independently increases risk through elevated intra-abdominal pressure and mechanical stress on veins. 1, 4
• Prolonged standing or immobility prevents the calf muscle pump from functioning, allowing blood to pool in dependent veins. 1, 5
• Varicose veins indicate underlying valvular incompetence and are both a manifestation and risk factor for progressive venous stasis. 1, 4
• Pregnancy increases intra-abdominal pressure and venous volume, temporarily impairing venous return. 1
• Female sex is associated with higher prevalence of venous disease, though the mechanism is multifactorial. 1

Treatment of Venous Stasis

Conservative Management (First-Line)

Compression therapy with medical-grade gradient compression stockings (20-30 mmHg minimum pressure) is the cornerstone of treatment for all patients with venous stasis. 1, 6, 7

• Compression increases venous blood flow velocity, reduces blood pooling, improves venous pumping function, and decreases capillary filtration. 2
• A documented 3-month trial of properly fitted compression stockings is required before considering interventional procedures. 1, 6
• Compression must be continued lifelong after ulcer healing to prevent recurrence, as recurrence rates approach 70% without ongoing compression. 7, 8

Lifestyle modifications complement compression therapy:

• Leg elevation above heart level when resting reduces hydrostatic pressure and promotes venous drainage. 1, 7
• Regular walking and calf muscle exercises activate the muscle pump to improve venous return. 1, 2
• Weight loss in overweight patients reduces intra-abdominal pressure and mechanical stress on veins. 1
• Avoidance of prolonged standing or sitting prevents blood pooling. 1

Pharmacologic adjuncts may provide symptomatic relief:

• Horse chestnut seed extract and other phlebotonics may ease symptoms, though long-term safety and effectiveness data are lacking. 1

Interventional Treatment (When Conservative Management Fails)

Referral for interventional treatment should not be delayed when valvular reflux is documented on duplex ultrasound, particularly in patients with lifestyle-limiting symptoms or skin changes. 1, 6

Treatment Algorithm Based on Vein Size and Reflux Pattern

For saphenofemoral or saphenopopliteal junction reflux with vein diameter ≥4.5mm:

• Endovenous thermal ablation (radiofrequency or laser) is first-line interventional treatment, with technical success rates of 91-100% at 1 year. 1, 6
• Thermal ablation has largely replaced surgical stripping due to similar efficacy with fewer complications, faster recovery, and improved early quality of life. 1, 6
• Treating junctional reflux is mandatory before or concurrent with tributary vein treatment to prevent recurrence rates of 20-28% at 5 years. 6

For tributary veins or veins 2.5-4.5mm in diameter:

• Foam sclerotherapy (including Varithena/polidocanol) is appropriate as second-line or adjunctive treatment, with occlusion rates of 72-89% at 1 year. 1, 6
• Sclerotherapy is particularly useful for residual refluxing segments after thermal ablation or for patients where thermal ablation is not feasible. 6
• Vessels <2.5mm have poor outcomes with sclerotherapy (only 16% patency at 3 months) and should generally not be treated. 6

For large bulging tributary varicose veins:

• Ambulatory phlebectomy (stab phlebectomy) is medically necessary as an adjunctive procedure to remove symptomatic varicose tributaries that persist after treating the main saphenous trunk. 6

Special Considerations

For venous ulceration (CEAP C6):

• Definitive treatment with endovenous ablation should not be delayed for compression therapy trials, as ulceration represents severe disease requiring intervention. 6
• Treating underlying reflux improves ulcer healing rates significantly compared to compression alone. 3

For venous outflow obstruction:

• Iliac-femoral venous stenting may be indicated when significant stenosis (≥50% reduction in cross-sectional area) is documented by venography and intravascular ultrasound. 3
• This is particularly relevant for patients with open ulcers who fail conventional treatment, with ulcer healing rates of 58% after stenting. 3

Common Pitfalls to Avoid

• Do not treat tributary veins with sclerotherapy alone without addressing saphenofemoral junction reflux, as untreated junctional reflux causes persistent downstream pressure and high recurrence rates. 6
• Do not attempt sclerotherapy on vessels <2.5mm diameter, as outcomes are poor with only 16% patency at 3 months. 6
• Do not assume all venous stasis is post-thrombotic—most cases occur without prior DVT and are due to primary valvular incompetence. 4, 8
• Ensure duplex ultrasound is performed within 6 months before any interventional procedure to document reflux duration ≥500ms, vein diameter, junction competence, and deep vein patency. 6

Complications and Risks

• Endovenous thermal ablation carries approximately 7% risk of temporary nerve damage from thermal injury, 0.3% risk of deep vein thrombosis, and 0.1% risk of pulmonary embolism. 6
• Foam sclerotherapy has fewer thermal complications but may cause phlebitis, new telangiectasias, residual pigmentation, and rarely deep vein thrombosis. 6
• Even with successful treatment, lifelong compression therapy is necessary as recurrence rates remain 20-28% at 5 years. 6, 8