Author(s): Ady Correa-Mendoza, MD
Originally published: September 20, 2014 Last updated: March 26, 2026
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Disease/Disorder

Definition

Chronic venous disorders (CVDs): this term includes the full spectrum of morphologic and functional abnormalities of the venous system.1

Chronic venous disease: (Any) morphological and functional abnormalities of the venous system of long duration manifested either by symptoms and/or signs indicating the need for investigation and/or care.1

Chronic venous insufficiency (CVI): A term reserved for advanced CVD, which is applied to functional abnormalities of the venous system producing edema, skin changes, or venous ulcers.1

Post-thrombotic syndrome (PTS): Chronic venous symptoms and/or signs secondary to proximal deep vein thrombosis and its sequelae.1 It is the most common sequela of deep vein thrombosis (DVT), affecting approximately 20–50% of patients.2

Epidemiology including risk factors and primary prevention

Chronic Venous Insufficiency

 A systematic review of global epidemiologic studies reported prevalence estimates of approximately 19% for varicose veins and 8% for venous edema in the general population.3 In the United States, it is estimated that more than 25 million adults have a diagnosis of CVI and >20% of them have severe disease. Venous leg ulcers affect approximately 500,000–600,000 individuals each year in the United States and are the most common type of leg ulcer managed in wound care centers.4 Due to their high prevalence, venous leg ulcers impose a substantial economic burden on the healthcare system, with annual costs estimated between $1.5 and $3 billion.4

Risk factors for venous insufficiency include intrinsic venous or valvular defects, family history, older age, female sex, pregnancy, obesity, occupations with prolonged sitting or standing, tobacco use, diet, phlebitis, and previous leg trauma.

Primary prevention of chronic venous insufficiency focuses on mitigating modifiable risk factors, including avoiding prolonged sitting or standing, smoking cessation, and maintaining a healthy weight and balanced diet.

Post-thrombotic Syndrome

The incidence of PTS is about 20-50% in the first two years following a DVT, and 5-10% of patients will develop severe disease, including ulcers.5

Risk factors for PTS include DVT location (proximal > distal), especially involving iliac or common femoral arteries, previous or recurrent ipsilateral DVT, premorbid venous insufficiency, obesity (body mass index higher than 30kg/m2), older age, severity of the symptoms at the onset of DVT, subtherapeutic anticoagulation used to treat acute DVT in the first three months after diagnosis of DVT, persistent venous sign and symptoms at 3 months after acute DVT, residual thrombosis 3 to 6 months after acute DVT, and persistently elevated D-dimer levels. Inflammatory markers including C-reactive protein (CRP), interleukin-6 (IL-6, IL-8, IL-10, and ICAM-1 and higher level of certain metalloproteinases are associated with PTS as well. Overall, the most important risk factor for PTS is the development of recurrent ipsilateral DVT.2,5

Primary prevention of PTS includes the following6

  • Thromboprophylaxis to prevent DVT in high-risk hospitalized patients.
  • Reduce risk of recurrent DVT by appropriate anticoagulation after acute DVT.
  • Thrombolysis of acute DVT followed by standard anticoagulant therapy in patients with extensive thrombosis, and low risk of bleeding.
  • May consider use of elastic compression stockings (ECS) with ankle pressure gradient of 30 to 40 mm Hg for at least 2 years if the patient is symptomatic has a proximal DVT and/or symptoms of PTS; however, supporting data is conflicting.

Patho-anatomy/physiology

The venous circulation of the lower extremities consists of the superficial veins, deep veins, and perforator veins. The superficial veins drain blood from the skin and subcutaneous tissues, whereas the deep veins, located within the muscular compartments, carry the majority of venous return from the lower limbs toward the heart. Perforator veins connect the superficial and deep systems and normally direct blood flow from the superficial to the deep veins. Venous valves maintain unidirectional flow, while contraction of the calf muscles during ambulation compresses the deep veins and propels blood proximally. This mechanism, known as the calf muscle pump, plays a critical role in facilitating venous return and maintaining low venous pressure in the lower extremities.

Chronic venous insufficiency develops when normal mechanisms of venous return are impaired, leading to venous reflux or obstruction. Damage to venous valves and dilation of the veins allow blood to pool in the lower extremities, resulting in venous hypertension. Elevated venous pressure triggers endothelial dysfunction and inflammation, with increased expression of adhesion molecules and inflammatory mediators. Over time, persistent venous hypertension and inflammation lead to structural and skin changes, edema, and venous leg ulcers. Contributing factors such as venous thrombosis, venous stenosis, and weakness of the calf muscle pump may further impair venous return and worsen disease progression.7 The extracellular matrix is further disrupted by transforming growth factor-β1 (TGF- β1) and its stimulation of tissue inhibitors of metalloproteinase production, which may trigger a prothrombotic process.8

Pathophysiology of PTS starts with an obstructive thrombus causing damage to the vein wall, initiating an inflammatory response. A phenotypic change of the vascular smooth muscle cell occurs, which promotes collagen and other matrix accumulation, vein wall fibrosis, leading to functional obstruction and resulting in reflux, and stiffness.9 The combination of obstruction and reflux produces ambulatory venous hypertension, meaning that the venous pressure cannot be reduced with exercise. Prolonged venous hypertension results in dilation of the vessels, increased permeability of proteins and red blood cells, which translates into skin changes that may include hyperpigmentation, edema, fibrosis and ulcers.2

Genetic predisposition and various candidate genes and their polymorphisms and environmental factors (obesity and standing posture) are also important in the development of chronic venous disease.10

Specific secondary or associated conditions and complications 

Chronic Pain

Aching, or cramping pain is present in 15-70% of patients with CVI and can severely impact quality of life.11 It is thought to be due to sensitization of venous nociceptors or due to venous stasis resulting in venous microangiopathy and increased endoneurial pressure. The severity of pain is not associated with the severity of CVI.

Phlebolymphedema

When there is excessive fluid load in the tissues due to CVI, the capillary system does not function properly and places additional load to the lymphatic system, which is also responsible for draining excess fluid and proteins from the tissues back to the bloodstream. When the lymphatic system exceeds its capacity to compensate for excess fluid in CVI, the valves of the lymph vessels may become insufficient (lymphostasis), which may lead to chronic lymphatic insufficiency. The dysfunction of both systems (venous and lymphatic) secondary to CVI results in phebolymphedema.12

Lipodermatosclerosis

It is a chronic inflammatory and fibrosing disorder of the skin and subcutaneous tissue associated with longstanding venous hypertension in chronic venous insufficiency and represents an advanced cutaneous manifestation of chronic venous disease.13

Cellulitis

Bacterial cellulitis is a common complication of CVI and can occur in the presence of dermatitis or open ulcers or in the absence of skin breakdown (spontaneously).18 The most common bacterial organisms include beta-hemolytic streptococci and Staphylococcus bacterial organisms involves include beta hemolytic streptococci and staphylococcus aureus.14 The patient would experience sudden pain, redness and new or increased leg swelling. Fever and leukocytosis are often absent. Differential diagnosis includes superficial thrombophlebitis and DVT.

Venous Ulceration

Progression of venous insufficiency can lead to ulceration over time. Venous leg ulcers affect 3-5% of patients 65 or older.19 The ulcers are typically in the supramalleolar region and vary in size.19,20 The majority of these wounds heal within 12 weeks with lower leg compression; however, depending on vasculature they can persist or never heal. Furthermore, the wounds may recur if CVI is not treated and the same factors persist. The ulcers may be complicated by infection.

Essentials of Assessment

History

Medical history should include the following

  • Current symptoms, their duration, worsening and alleviating factors
    • Pain in the upper or lower extremities, pelvis, flank, back
    • Skin changes in the extremities: discoloration/hyperpigmentation/redness/cold/pallor/numbness/hair loss/ulcers22
    • Edema in the calves or feet
    • Symptoms of intermittent claudication
    • Redness or tenderness
  • Prior treatments/compression therapy23
  • Pregnancies
  • Age
  • Previous DVT/thrombophlebitis
  • Medications/oral contraceptives
  • Smoking
  • Family history

A thorough history should consider other potential causes of edema, including systemic conditions such as heart failure, liver failure, nephrosis, or endocrine dysfunction; medication side effects; lymphedema or lipedema; and local tissue trauma such as ruptured popliteal cyst, hematoma, gastrocnemius tear, or compartment syndrome.  Physical exam findings, as discussed below, may also help to inform the differential diagnosis in patient’s presenting with edema.7

Physical examination

Examine patients in a warm, well-lit room while standing to allow physiologic distention of the veins.

  • Inspection: Note the distribution of abnormal spider veins, telangiectasias, ankle or malleolar flare, size, location, and distribution of varicose veins, skin changes, edema, location of active or healed ulcers, and inflammatory changes, trophic changes on the skin, hair distribution/loss, hyper or hypopigmentation of the skin, auscultation for bruits
  • Palpation: distal pulses to assess for underlying arterial disease, venous cord, calf muscle consistency, assess for tenderness
  • Measure bilateral calf and ankle circumference at a consistent time of day
  • Range of motion: assess upper and lower extremities
  • Neurologic exam

Note that, in contrast to other causes of peripheral edema, the forefoot is often spared of pitting edema which may be seen in the dependent lower leg.  In more chronic cases, skin may become more resilient to pitting.  There are numerous scales available for grading edema, but none is universally agreed-upon.7

Functional assessment

Patients with CVD and venous leg ulcers have poorer quality of life (QOL) in all aspects of daily living compared with the general population. Pain is the main factor that impacts QOL. The presence, size, and duration of ulcers also has a significant and substantial association with decreased QOL, as does decreased mobility. Age has been shown to have a strong negative association with QOL. Other factors, such as social and emotional isolation, socioeconomic status, comorbidities, feeling of uncleanliness, and problems finding appropriate footwear have also been implicated but findings are mixed. Loss of employment has a significant social impact

Imaging

  • Duplex ultrasound [DUS] is recommended as the first diagnostic test for all patients with suspected CVD. Additionally, it has an important role in identifying patients at risk of PTS, as two important parameters for development of PTS are residual vein thrombosis and venous reflux (valve incompetence).
  • Air plethysmography (APG) is used for assessing severity of disease. APG can evaluate calf muscle pump function and quantify global venous reflux and outflow obstruction.
  • Computed Tomographic Venography [CTV] and Magnetic Resonance Venography [MRV] are helpful in more complex disease and preoperatively as it provides more detail than duplex ultrasonography. It is especially useful for the evaluation of more proximal veins and their surrounding structures and may help in the assessment of post-thrombotic obstruction, venous compression or stenosis.4,13 However, evidence of its efficacy for evaluating venous system is mixed, for which these studies are not routinely recommended.2
  • Contrast venography is an invasive test that involves the injection of contrast from either an ascending or descending pathway to delineate venous anatomy prior to surgical intervention or to identify reflux, usually in cases where venous duplex imaging is unable to give sufficient information to guide venous reconstruction.
  • Intravascular ultrasound is an invasive technique that uses a catheter-based ultrasound probe to assess for stenosis or venous obstruction and has been gaining popularity as a tool to help guide interventions, as it seems to give more detailed and curate information regarding the morphology of vessels in comparison to venography.

Photoplethysmography, strain gauge plethysmography, and foot volumetry are additional available techniques; the latter two may better correlate with clinical disease severity than venous duplex imaging but are not routinely used.7

Supplemental assessment tools

The Brodie-Trendelenberg Percussion Test can be performed at the bedside to help differentiate superficial reflux from deep venous disease. To perform the test, place your finger over the distal part of the vein being examined, and tap the proximal part of the vein. The test is positive if the percussion is felt at the distal portion and indicates valvular incompetence. The Brodie- Trendelenburg Tourniquet test is used specifically to identify venous insufficiency at the saphenofemoral junction. The affected leg is raised, and a tourniquet is applied tightly to constrict the saphenous vein, and the subject then stands up for 30 seconds, then the tourniquet is removed. The test is positive if once the tourniquet is removed the internal saphenous vein rapidly fills, indicating that saphenous valves are incompetent. It is doubly positive if the veins rapidly fill on standing and worsen when the tourniquet is removed indicating incompetency of saphenous valves, and those of the communicating veins. For hemodynamic assessment in CVI, ambulatory venous pressure monitoring remains the gold standard. However, for practical reasons it is seldom used in clinical practice.15 In practice, venous duplex imaging is typically a preferred modality for noninvasive testing.15

Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification was established in 1993 and is the international standard for describing chronic venous disease, and takes into account the clinical factors, etiologic factors, anatomic location, and pathophysiologic mechanisms that, together, play a role in CVD. It is used routinely in clinical practice as a standardized tool designed to clearly define a patient’s disease at any given moment in time in a reliable and reproducible fashion, and yet provide the flexibility to change as a patient’s disease changes over time.26 The clinical, etiologic, and anatomic sections were updated in 2020 for more accurate representation of current disease findings.16

Table 1. 2020 CEAP classification (modified from Lurie et al.)16

Venous-Insufficiency-Table-1-2020-CEAP-Classification

The Villalta score was constructed to diagnose and categorize PTS. Points are given to the following symptoms: pain, cramps, heaviness, paresthesia, and pruritus. Clinical signs scored are pretibial edema, skin induration, hyperpigmentation, redness, venous ectasia, and pain on calf compression. Points ranging from 0 to 3 for each of these elements are recorded. PTS is diagnosed if the Villalta score is greater than 4 and the disease is considered severe if the score is greater than 14 or if an ulcer is present.

Table 2. Villalta Score (modified from Villalta et al.)17

Venous-Insufficiency-Table-2-Villalta-Score

The score has also been used on follow-up to assess the effectiveness of treatment.There are several other scoring mechanisms including the Ginsberg, Brandjes, Widmer and Venous Clinical Severity Score; however, only the Villalta score can reliably diagnose PTS, categorize disease severity, and be used to monitor disease progression over time. A key limitation of the Villalta scale, however, is its inability to distinguish PTS from other causes of chronic venous insufficiency. In contrast, the Ginsberg scale is more likely to identify the most severe disease cases.2,5

Environmental

Environmental and behavioral factors associated with CVI include an unhealthy weight and diet, prolonged sitting, and standing at work, and inappropriate skin care.

Social role and social support system

Chronic venous insufficiency has a significant socioeconomic impact, imposing a substantial economic burden on the healthcare system, with total annual treatment costs estimated to exceed $3 billion.18 This results in impaired ability to engage in social and occupational activities, reducing QOL and imposing financial constraints. 0 Disability related to venous ulcers leads to loss of productive work hours (estimated at 2 million workdays per year). Of workers with venous ulcers, 12% will retire prematurely.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Lifestyle Modifications

Weight loss, diet, exercise, leg elevation, ECS are recommended. Compression therapy is the mainstay of management.

Systematic reviews suggest that exercise may provide benefits for patients with post-thrombotic syndrome and after deep vein thrombosis. The review by Jasionowska et al19. found that exercise programs can improve venous hemodynamics, calf muscle pump function, and symptoms in patients with chronic venous disease, although evidence specific to post-thrombotic syndrome remains limited. Similarly, the systematic review by Rook et al.20 reported that exercise following deep vein thrombosis appears safe and may improve functional capacity, quality of life, and venous symptoms without increasing complications. 

Compression Therapy

  • Graduated ECS with higher pressure at the ankle are the cornerstone of CVD management.
  • Knee-length stockings are as effective as thigh-length stockings, easier to apply, more comfortable, have better compliance, and less expensive.
  • Stockings with 30 to 40 mm Hg compression pressure are recommended for C5-6 CVI; 20 to 30 mm Hg are recommended for symptomatic varicose veins and mixed venous and arterial disease.
  • Unna boot (50-60 mm Hg pressure) is used for ambulatory patients unable to tolerate graduated ECS.
  • Multilayer bandages (40 mm Hg pressure) are more effective in healing ulcers.
  • Indications for intermittent pneumatic compression are nonambulatory patients, need for higher compression, patients not responding to stockings/wraps, or patients with very large legs who cannot tolerate stockings/wraps.

Pharmacologic Therapy

  • Venoactive drugs (saponins, flavonoids, pentoxifylline, acetylsalicylic acid): used in the management of pain and swelling at initial stages of CVI. Not recommended for PTS or venous ulcers.
  • Diuretics are not recommended for PTS related edema.
  • Sulodexide: Antithrombotic agent proven to be beneficial for symptoms of CVD including cramps, heaviness and edema.
  • Anticoagulation therapy: Has been shown to be beneficial in the prevention of PTS and venous ulcers after acute DVT. However, prolonged treatments after the recommended length of therapy for DVT is not proven to provide further benefits.
  • Supplements: Horse chestnut seed extract (HCSE), which contains aescin as its active component, has vasoactive properties and has been shown to improve symptoms of chronic venous insufficiency, including leg pain and edema, although larger long-term studies are needed to confirm its effectiveness.

*Data on pharmacologic treatments for CVD is heterogenous and further studies are needed to evaluate its efficacy.

Surgical Treatment

  • Vein stripping: This procedure involves ligation and surgical removal of the affected vein. Due to variable long-term outcomes and risk of recurrence, and with the advent of minimally invasive endovenous ablation techniques, it is now less commonly performed in Western countries and is typically reserved for patients whose symptoms persist despite conservative management.21
  • Sclerotherapy: Includes the use of different chemicals such as polidocanol, glycerin or sodium tetradecyl sulfate, which works as a type of chemical ablation of varicose veins in CVD. Additionally, this procedure may have a role in accelerating venous ulcer healing but it’s considered as a second line of treatment in fragile patients or those who cannot undergo surgical treatments.21Cyanoacrylate adhesive closure is a non-thermal endovenous sclerotherapy technique used to treat symptomatic primary axial reflux associated with varicose veins by sealing the venous lumen with medical adhesive; however, it is generally avoided in patients with a history of significant hypersensitivity reactions.21
  • Endovenous thermal ablation (EVLA): This procedure has been recommended as first line of therapy for patients with CVD and reflux of the great saphenous vein (varicose vein- VV). There are two types of ablation: Endovenous Laser Therapy (EVLT) and Radiofrequency Ablation (RFA). In both techniques, thermal injury is induced to the affected varicose vein, leading to occlusion and eventual fibrosis of the saphenous vein. EVLT has been proven to have higher efficacy versus RFA.
  • Mechanochemical ablation (MOCA): This procedure combines mechanical injury to the vein endothelium with the injection of a sclerosant. Devices such as ClariVein® use a rotating wire to damage the endothelium, while newer systems like Flebogrif use retractable radial hooks to create endothelial disruption followed by foam sclerosant delivery. A major advantage of MOCA is less procedural pain, since it is a non-thermal technique and does not require tumescent anesthesia.22
  • Subfascial endoscopic perforator surgery: Small studies have assessed the efficacy of ligating and clamping perforator veins to disrupt the connection between deep and superficial veins. The goal is to interrupt the venous flow in those veins where there is increased congestion and potentially decrease the risk of developing venous ulcers. However, further studies are needed to better assess the efficacy of these procedures.39
  • Bioprosthetic veno-valve implantation in the femoral vein: bioprosthesis that contains porcine cardiac valve and is implanted in cases of deep venous valvular disease with the goal to improve venous reflux. It has been proven to be efficient at 1-year post-implantation in patients with severe deep CVI.
  • Percutaneous transluminal angioplasty + stenting: utilized in cases where conservative therapy does not provide relief, specifically persistent CVI symptoms in patients with pathology of the iliac veins.

At different disease stages

The clinical, etiology, anatomy, pathophysiology (CEAP) classification is a useful guide for treatment at different stages of the disease. Changes in the 2020 update include adding Corona phlebectatica as the C4c clinical subclass, introducing the modifier “r” for recurrent varicose veins and recurrent venous ulcers, and replacing numeric descriptions of the venous segments by their common abbreviations.16

  • In CEAP class 1, patients display spider veins and telangiectasias.
  • In class 2, patients have varicose veins. They have mild symptoms and no venous insufficiency. No treatment is recommended. For cosmetic concerns, vein stripping, Endovenous thermal ablation (EVLA), or foam sclerotherapy may be prescribed, along with ECS of 20 to 30 mm Hg. Class 2r is recurrent varicose veins.
  • CEAP class 3 displays edema. Treatment is similar to CEAP classes 1 and 2.
  • CEAP class 4 was further subdivided in the 2020 update:
    • CEAP class 4a displays edema and early skin changes (e.g., pigmentation, eczema). This is indicative of venous reflux, which is sufficiently severe to cause venous hypertension. Daily compression and/or correction of venous hypertension by venous ablation or other techniques are recommended.
    • CEAP class 4b has severe skin changes, lipodermatosclerosis, significant tissue inflammation, or induration. These patients are at a higher risk to progress to ulceration. They need a corrective venous procedure.
    • CEAP class 4c is corona phlebectatica, or abnormally dilated veins around the ankle.
  • CEAP classes 5 (healed ulcer) and 6 (active ulcer) should undergo correction of venous hypertension to speed the healing of the ulcer and prevent recurrence. Class 6r is a recurrent active venous ulcer. The preferred procedure for correction of reflux in the perforator veins.

The 2025 SCAI Clinical Practice Guidelines for Chronic Venous Disease recommend a patient-centered, multimodal approach to management, with compression therapy as the first-line treatment for symptomatic disease and venous ulcers. Minimally invasive interventions, including endovenous ablation, sclerotherapy, phlebectomy, and venous stenting for selected patients with obstruction, are emphasized over traditional surgery.21

Lifelong ECS with 30 to 40 mm Hg compression is recommended to prevent recurrence of ulceration.23

Contraindications for compression therapy include Ankle-brachial index <0.6, severe heart failure, allergy to materials used for compression therapy, severe diabetic neuropathy at risk of necrosis.24

Coordination of care

Recent literature emphasizes that management of chronic venous insufficiency, particularly in patients with venous leg ulcers, benefits from a multidisciplinary approach involving vascular specialists, wound-care clinicians, nursing care, and rehabilitation professionals.25 A randomized controlled trial demonstrated that a multidisciplinary patient education program improved adherence to treatment and self-management behaviors in patients with venous leg ulcers. This intervention was associated with improved early wound healing outcomes compared with standard care.25

Patient & family education

Patient education should emphasize lifelong use of elastic compression stockings, leg elevation, smoking cessation, regular exercise, avoidance of leg trauma, weight management, and adequate nutrition. Home-based exercise programs aimed at improving calf muscle pump function are also recommended. Studies suggest that stretching, leg strengthening and flexibility exercises, and walking for 45–60 minutes three times per week for six months may improve overall fitness, disease-specific quality of life, and severity of post-thrombotic syndrome. Additional measures such as leg elevation, use of insoles, cooling therapy, and avoiding heat exposure may help reduce pain and improve quality of life. In terms of diet, a low carb diet, high fiber, vitamins and polyunsaturated acids (PUFA) promotes adequate function of the immune system. Additionally, the Mediterranean diet has anti-inflammatory and cardioprotective effects, which could have a potentially positive effect in decreasing risk of CVD and PTS.26A systematic review found that nutritional deficiencies, particularly in protein, vitamin C, zinc, folate, and vitamin B12, are associated with venous leg ulcers, and that correcting these deficiencies alongside compression therapy may help promote ulcer healing. However, evidence remains limited, and further clinical trials are needed to determine the most effective nutritional strategies and compression treatments.27

Emerging/unique interventions

Commonly used generic QOL measures include the Medical Outcomes Study 36-Item Short-Form Health Survey and visual analog scale. Disease-specific scales include the Venous Insufficiency Epidemiologic and Economic Study of Quality of Life and Charing Cross Venous Ulceration Questionnaire.28

Neuromuscular electrical stimulation appears to improve symptoms and venous hemodynamics in patients with chronic venous disease of the lower limbs, although the overall quality of evidence remains limited.29

Translation into practice: Practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  • Lifestyle modification is important in prevention and management of CVI.
  • Compression therapy is the mainstay of management.

Cutting Edge/Emerging and Unique Concepts and Practice

  • The association of circulating biomarkers with CVI. The neutrophil-to-lymphocyte ratio (NLR) is an emerging prognostic marker in cardiovascular and inflammatory diseases [120], and although it has not been specifically studied in post-thrombotic syndrome, elevated levels have been associated with worse outcomes in venous thrombosis. 6
  • The SAVVE trial demonstrated that implantation of a bioprosthetic venous valve (VenoValve) resulted in clinically meaningful improvement in approximately 84–85% of patients, with an average reduction of 7–8 points in the Revised Venous Clinical Severity Score (rVCSS), along with significant improvements in pain and quality of life. Among patients with venous ulcers, approximately 84–92% showed healing or improvement at 12 months, with sustained benefits over time.30
  • Clinical trial investigating a bioactive debridement agent aimed at promoting granulation tissue formation, reducing bacterial load, and accelerating healing in venous leg ulcers.
  • A Phase III randomized trial is currently evaluating a bioactive debridement agent (EscharEx) for venous leg ulcers (ClinicalTrials.gov identifier: NCT06568627), building on earlier studies demonstrating improved debridement and granulation tissue formation.
  • Artificial intelligence is increasingly being applied in chronic venous insufficiency to assist with diagnosis, imaging interpretation, risk stratification, and treatment planning, although its clinical use remains evolving and requires further validation.31

Gaps in the Evidence-Based Knowledge

The 2025 SCAI guidelines highlight key evidence gaps in chronic venous disease management, particularly the lack of data supporting perforator vein ablation in non-ulcer disease and limited evidence for interventions targeting common femoral vein post-thrombotic disease, underscoring the need for further high-quality studies.21

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Original Version of the Topic

Sikha Guha, MD, Eathar Saad, MD. Venous Insufficiency: Rehabilitation Management of Venous Stasis and Postphlebitic Syndrome. 9/20/2014

Previous Revision(s) of the Topic

Laurentiu Dinescu, MD, Rebecca Sussman, MD, Michael Mosier, MD, Amarin Suriyakhamhaengwongse, MD. Venous Insufficiency: Rehabilitation Management of Venous Stasis and Postphlebitic Syndrome. 12/10/2020

Ady Correa-Mendoza, MD, Rosalynn Conic, MD, PhD. Venous Insufficiency: Rehabilitation Management of Venous Stasis and Postphlebitic Syndrome. 6/14/2023

Author Disclosures

Ady Correa-Mendoza, MD
Nothing to Disclose