This consensus document provides an updated overview of diagnostic methods for chronic venous insufficiency (CVI) of the lower limbs. CVI is characterized by symptoms or signs caused by venous hypertension due to structural or functional abnormalities in veins. Common causes include primary vein wall and valve abnormalities and secondary changes from previous venous thrombosis leading to reflux or obstruction. Since clinical history and examination may not fully reveal the nature of the abnormality, various diagnostic tests have been developed to assess calf muscle pump function and the extent of venous obstruction or reflux. The document aims to outline these tests, their usefulness, limitations, and indications for patients. The consensus was developed by experts from multiple organizations, including the American Venous Forum, European Society of Vascular Surgery, and others, following a meeting in 1997. Subsequent revisions in 1998 and 1999 ensured the document reflects current diagnostic methods. CVI has significant socioeconomic impact due to its high prevalence, cost of treatment, and loss of working days. Varicose veins affect 25% to 33% of women and 10% to 20% of men. Venous ulcers occur in approximately 0.3% of the adult population in Western countries, with a combined prevalence of active and healed ulcers around 1%. The prognosis for venous leg ulcers is poor, with only 50% healing at 4 months and 20% remaining open at 2 years. CVI symptoms include aching, heaviness, cramps, and skin changes. The pathophysiology of CVI is due to ambulatory venous hypertension from obstruction, reflux, or both. Varicose veins are the most common manifestation, often due to abnormal vein wall distensibility. Reflux in deep veins can result from past thrombosis or idiopathic causes. Outflow obstruction can result from DVT without adequate recanalization. Venous recanalization occurs in 50% to 80% of patients several months after DVT. The chronic sequelae of DVT are often due to reflux rather than obstruction. Microcirculation changes in CVI include impaired capillary circulation, leading to skin changes, eczema, and ulceration. Microangiopathy in lymphatics plays a role in skin changes and venous ulcers. Hematological changes include increased fibrinogen levels and impaired fibrinolysis, which may contribute to venous ulcers. Diagnostic challenges include determining the nature and extent of venous abnormalities. Various diagnostic methods, including phlebiography, duplex scanning, and thermography, are used to assess venous anatomy and function. Duplex scanning is a noninvasive method that can detect reflux and determine its anatomic extent. Ambulatory venous pressure measurements provide hemodynamic information on venous hypertension. Femoral vein pressure measurements assess the severity of iliocavalThis consensus document provides an updated overview of diagnostic methods for chronic venous insufficiency (CVI) of the lower limbs. CVI is characterized by symptoms or signs caused by venous hypertension due to structural or functional abnormalities in veins. Common causes include primary vein wall and valve abnormalities and secondary changes from previous venous thrombosis leading to reflux or obstruction. Since clinical history and examination may not fully reveal the nature of the abnormality, various diagnostic tests have been developed to assess calf muscle pump function and the extent of venous obstruction or reflux. The document aims to outline these tests, their usefulness, limitations, and indications for patients. The consensus was developed by experts from multiple organizations, including the American Venous Forum, European Society of Vascular Surgery, and others, following a meeting in 1997. Subsequent revisions in 1998 and 1999 ensured the document reflects current diagnostic methods. CVI has significant socioeconomic impact due to its high prevalence, cost of treatment, and loss of working days. Varicose veins affect 25% to 33% of women and 10% to 20% of men. Venous ulcers occur in approximately 0.3% of the adult population in Western countries, with a combined prevalence of active and healed ulcers around 1%. The prognosis for venous leg ulcers is poor, with only 50% healing at 4 months and 20% remaining open at 2 years. CVI symptoms include aching, heaviness, cramps, and skin changes. The pathophysiology of CVI is due to ambulatory venous hypertension from obstruction, reflux, or both. Varicose veins are the most common manifestation, often due to abnormal vein wall distensibility. Reflux in deep veins can result from past thrombosis or idiopathic causes. Outflow obstruction can result from DVT without adequate recanalization. Venous recanalization occurs in 50% to 80% of patients several months after DVT. The chronic sequelae of DVT are often due to reflux rather than obstruction. Microcirculation changes in CVI include impaired capillary circulation, leading to skin changes, eczema, and ulceration. Microangiopathy in lymphatics plays a role in skin changes and venous ulcers. Hematological changes include increased fibrinogen levels and impaired fibrinolysis, which may contribute to venous ulcers. Diagnostic challenges include determining the nature and extent of venous abnormalities. Various diagnostic methods, including phlebiography, duplex scanning, and thermography, are used to assess venous anatomy and function. Duplex scanning is a noninvasive method that can detect reflux and determine its anatomic extent. Ambulatory venous pressure measurements provide hemodynamic information on venous hypertension. Femoral vein pressure measurements assess the severity of iliocaval