Continuing Education Activity

Venous insufficiency is a progressive vascular disorder characterized by impaired venous blood flow, often caused by incompetent venous valves, leading to venous hypertension. This condition results in a spectrum of clinical manifestations, including lower extremity edema, varicose veins, skin discoloration, cramping, pruritus, and, in advanced cases, venous ulcers. Chronic venous insufficiency (CVI) is highly prevalent worldwide, contributing to decreased quality of life and significant healthcare costs. This course reviews the diagnostic evaluation of CVI, which relies on thorough clinical assessment, classification using the CEAP system, and confirmatory studies such as venous duplex ultrasound, air plethysmography, and, when necessary, advanced imaging or invasive testing, as well as recommended management strategies that range from conservative measures to pharmacologic and interventional procedures. Early recognition and intervention are essential to prevent progression and complications, such as postphlebitic syndrome, chronic ulceration, and deep vein thrombosis.

This activity reviews the pathophysiology, risk factors, diagnostic tools, and treatment modalities of venous insufficiency. Participants will also gain a deeper understanding of the assessment of disease severity using CEAP and VCSS scoring, interpretation of venous duplex ultrasound, and the integration of conservative, pharmacologic, and procedural interventions into patient-centered care plans. This activity for healthcare professionals is designed to enhance the learner's competence in identifying venous insufficiency, performing the recommended evaluation, and implementing an appropriate interprofessional approach when managing this condition to improve patient outcomes, reduce complications, and optimize long-term management of CVI, thereby promoting patient safety and quality of life.

Objectives:

• Assess the various etiologies for venous insufficiency.
• Identify the clinical features of venous insufficiency.
• Select the appropriate management approach for venous insufficiency.
• Implement interprofessional team strategies to improve care and optimize outcomes for patients affected by venous insufficiency.

Introduction

Venous insufficiency is a condition in which the flow of superficial or deep venous blood is impaired, causing venous hypertension. Chronic venous insufficiency (CVI) encompasses several pathological changes (eg, lower extremity edema, skin trophic changes, cramping, and wounds) that result secondary to venous hypertension.[1][2] CVI is a prevalent disease process worldwide. Disability associated with CVI contributes to diminished quality of life and reduced work productivity. In most cases, the underlying cause of CVI is incompetent venous valves. Each year, approximately 150,000 new patients are diagnosed with CVI, and nearly $500 million is spent on the care of these patients. If left untreated, CVI is usually progressive and leads to postphlebitic syndrome and venous ulcers. Other common symptoms include pain, leg swelling, pruritus, skin discoloration, limb heaviness, and edema that improves with elevation.[3]

The diagnosis of CVI is based on clinical features and confirmatory diagnostic studies. International consensus through the American Venous Forum developed the Clinical, Etiology, Anatomic, and Pathophysiology (CEAP) classification to improve consistency in reporting, diagnosis, and management of CVI.[4][5][6] Venous duplex ultrasound is the primary modality to confirm a CVI diagnosis and is considered the gold standard. In addition to complementing the CEAP, the revised Venous Clinical Severity Score (VCSS) was developed to help assess CVI severity and determine the efficacy of CVD treatments.[7][8][9][10][5] The approach to CVI management involves several different strategies, including conservative therapies (eg, compression, elevation, and exercise), pharmacologic treatments, and more invasive procedures (eg, sclerotherapy, endovenous laser, radiofrequency ablation, or surgical ligation).[5] Delayed treatment can result in a more rapid disease progression, leading to complications including venous ulcers, infection, and deep vein thrombosis.[5][3][1] 

Etiology

Though the exact etiology of venous insufficiency is unclear, the primary underlying mechanism is believed to be valvular reflux. Other CVI etiologies include venous outflow obstruction, arteriovenous malformation, and calf muscle pump failure. There may also be a hereditary component since genetic disorders like Klippel-Trenaunay and Parkes-Weber are known to cause CVI.[11] These etiologic factors can lead to chronic endothelial inflammation and other pathophysiologic changes.[2][3]

Chronic Venous Insufficiency Risk Factors

The following risk factors are associated with the development of venous insufficiency:

• Advanced age (ie, aged 55 or older)
• Family history of varicose veins or venous pathology
• Obesity
• Oral contraceptive use
• Tobacco use
• Pregnancy
• History of deep vein thrombosis or thrombophlebitis
• History of the leg injury
• Prolonged standing or sitting
• Sedentary lifestyle
• Female sex [5][3]

Epidemiology

An estimated 10% to 35% of adults have CVI in the United States, with 4% of adults aged 65 years or older developing venous ulcers.[3] Results across studies suggest that in the general population, between 1% and 17% of men and 1% and 40% of women may experience CVI. Furthermore, the prevalence of varicose veins has been reported to range from under 1% to 70%. The variation in these estimates is likely due to differences in diagnostic criteria and the population surveyed.[1] Globally, the prevalence of CVI is higher in industrialized nations (eg, Western Europe and the US) due to more inactive lifestyles.[5] 

The prevalence of venous ulcers, a common complication of CVI, in the United States ranges from approximately 1% to 3%.[3] Similarly, lower leg ulceration occurs in approximately 1% to 2% of the global adult population and is reported to increase to 3% in patients older than 65.[5] The formation of an ulcer carries a poor prognosis, with 40% of patients experiencing recurrence despite standard treatment. Management of CVI accounts for approximately 2% of the United States' total healthcare costs.[12][13]

Pathophysiology

The peripheral venous system serves as a blood reserve and a channel for returning blood to the heart. The patency of blood veins, valves, and muscle pumps is necessary for the venous system to function properly. To return to the central circulation, blood must travel against gravity and other pressures in the upright position. The veins of the lower extremities are classified as superficial (above the fascial muscle layer), deep (below the fascial layer), and perforator.[14] 

The superficial venous system consists of the great saphenous vein, small saphenous vein, and several accessory veins. Deep veins are made up of axial veins. Perforating veins traverse the fascial layer, connecting superficially to deep veins. A number of 1-way bicuspid valves throughout the deep and superficial veins allow blood to travel toward the heart while preventing it from returning to the feet.[15] CVI pathophysiology is due to either reflux (ie, backward flow) or obstruction of venous blood flow. CVI can develop from the protracted valvular incompetence of superficial, deep, or perforating veins that connect them. In all cases, the result is ultimately the development of venous hypertension of the lower extremities. The resting venous pressure is a summation of the outflow obstruction, capillary inflow, valve function, and muscle pump function.

Superficial incompetence is usually due to weakened or abnormally shaped valves or widened venous diameters, which prevent normal valve congruence. In most cases, the leaky valve is located near the termination of the greater saphenous vein into the common femoral vein. Deep vein dysfunction usually results from a prior deep vein thrombosis (DVT), which leads to inflammation, valve scarring and adhesions, and luminal narrowing. Perforating vein valvular failure allows higher pressure to enter the superficial venous system. The subsequent dilation prevents the proper closure of the valve cusps in the superficial veins. Most patients will also have the disease in the superficial veins. 

Primary CVI is the symptomatic presentation without a precipitating event due to congenital disabilities or changes in venous wall biochemistry. Recent studies suggest that approximately 70% of patients have primary CVI, and 30% have secondary disease. Studies into primary CVI have identified reduced elastin content, increased extracellular matrix remodeling, and inflammatory infiltrate as contributing factors. The culmination alters the vein's integrity, promoting dilation and valvular incompetence. Secondary CVI occurs in response to a DVT, which triggers an inflammatory response, subsequently injuring the vein wall.

Irrespective of the specific etiology, CVI promotes venous hypertension. The most common nonmodifiable risk factors are female gender and nonthrombotic iliac vein obstruction (eg, May-Thurner syndrome). Several studies have also suggested a genetic component contributing to vein wall laxity. Modifiable risk factors include smoking, obesity, pregnancy, prolonged standing, DVT, and venous injury.[16][17] Regardless of the cause, persistently elevated venous hydrostatic pressure may result in lower-extremity pain, edema, and venous microangiopathy. Some patients develop permanent skin hyperpigmentation from hemosiderin deposition as red blood cells extravasate into the surrounding tissue.[5] Many of these patients will also have lipodermatosclerosis, skin thickening from subcutaneous fat fibrosis. As the disease progresses, the perturbed microcirculation and dermal weakening can form ulcers.[18]

History and Physical

Clinical Features

Patients with CVI commonly present initially with a combination of dependent pitting edema, leg discomfort, fatigue, and itching. Although there can be variations in presentation among patients, certain features are more prevalent, including telangiectasias, reticular veins, varicose veins, pain, cramping, itching, prickling, and a throbbing sensation. Patients may describe symptoms that improve with rest and leg elevation and with no association with exercise. This latter feature can be used to distinguish venous from arterial claudication.

As their disease progresses, varicose veins, tenderness, refractory edema, and skin changes can be noted. (see Image. Chronic Venous Insufficiency) Patients with advanced disease will present with a severe blanched skin lesion, dermal atrophy, hyperpigmentation, dilated venous capillaries, and ulcer formation, most commonly overlying the medial malleolus. A thorough history should note any hypercoagulable condition, oral contraceptive use, previous DVT or intervention, level of physical activity, as well as occupation. The patient's presentation should be carefully distinguished from other pathologies with similar symptoms: diabetic ulcers, ischemic ulcers, and dermatologic conditions, including cancer.[4][5][3]

The physical exam should involve a detailed assessment of any ulcers, distal pulses, and neuropathy in the upright and supine positions. The Trendelenburg test may help differentiate between CVI caused by superficial vein valves and that caused by the deep system. The patient's leg is elevated to perform the test, and all the venous blood is emptied. The surgeon then compresses the groin firmly to occlude the greater saphenous vein junction and asks the patient to stand up. If the leg does not fill up with venous blood, this indicates that incompetent valves in the superficial veins cause CVI. If the leg fills with venous blood, the valves connecting the superficial veins to the deep ones are incompetent. The treatment is limited to compression stockings if the deep system valves are involved.[4][5][3]

Clinical, Etiology, Anatomic, and Pathophysiology Classification

An international consensus conference developed the following CEAP classification to improve consistency in reporting, diagnosis, and management of CVI.[4][5] The revised VCSS is a clinical tool developed to help assess CVI severity and determine the efficacy of treatments. The VCSS grades 10 CVI clinical features from absent to severe, including pain, varicose veins, edema, skin pigmentation, inflammation, induration, ulcer characteristics (eg, number, duration and size) and compressive therapy. This scoring system can be used to complement the CEAP during clinical assessment.[7][8][9][10][5] CEAP classification involves the following components:

• Clinical classification

  • C0: No visible or palpable signs of venous disease 
  • C1: Telangiectasias or reticular veins 
  • C2: Varicose veins 
  • C3: Edema 
  • C4a: Pigmentation and eczema 
  • C4b: Lipodermatosclerosis and atrophy (see Image. Chronic Venous Insufficiency and Lipodermatosclerosis).
  • C5: Healed venous ulcer
  • C6: Active venous ulcer 

• Etiologic classification

  • Ec: Congenital 
  • Ep: Primary 
  • Es: Secondary 
  • En: No venous etiology identified 

• Anatomic classification

  • As: Superficial veins 
  • Ap: Perforator veins
  • Ad: Deep veins 
  • An: No venous location identified 

• Pathophysiologic classification

  • Pr: Reflux 
  • P0: Obstruction
  • Pr/o: Reflux and obstruction 
  • Pn: No venous pathophysiology identifiable

Evaluation

The diagnosis of CVI is based on clinical features and confirmatory diagnostic studies. Venous duplex ultrasound is the primary modality for confirming a CVI diagnosis; however, several ancillary studies may also be considered.

Venous Duplex Ultrasound

When evaluating CVI, color duplex ultrasound is considered the gold standard. Guidelines developed by a consensus of the American Venous Forum, the Society for Vascular Surgery, the American Vein and Lymphatic Society, and the Society of Interventional Radiology recommended that patients be in the upright position in individuals with the capability to stand safely when a duplex ultrasound is performed to evaluate venous reflux.

Evaluation in the supine or steep reverse Trendelenburg positions is not preferred. A Doppler waveform reflux duration in the superficial veins of greater than 0.5 seconds and greater than 1 second in the deep veins (eg, femoral and popliteal) was used as the diagnostic threshold for venous reflux of an incompetent valve. To induce venous reflux, distal calf compression may be performed. Doppler ultrasound with color flow may help visualize venous flow patterns.[5]

Air Plethysmography

Air plethysmography can assess all potential pathophysiologic processes of CVI (eg, reflux, obstruction, and muscle pump failure) by measuring the air displaced in a cuff wrapped around the calf while moving the legs through various positions and exercises. The air displaced correlates with the venous volume and refilling time. The Air plethysmography is utilized primarily when the venous duplex ultrasound evaluation is equivocal or inadequate.[19] Abnormal venous filling indices correlate with the severity of CVI, provide information on several aspects of overall venous function, and can be used to guide intervention selection and response evaluation.[20][21] 

Ancillary Diagnostic Studies

Computed tomography and magnetic resonance venography require intravenous contrast material and are particularly useful for evaluating proximal veins and their surrounding structures to assess for intrinsic and extrinsic compression. Before intervention is advised, these procedures may be utilized to characterize complex venous anatomy, such as an iliofemoral venous blockage.[15] Photoplethysmography measures venous filling times by the amount of reflected infrared light of hemoglobin. This modality is typically used for subcutaneous veins. Other noninvasive modalities include strain gauge plethysmography and foot volumetry.

Invasive diagnostic tests that may be considered include contrast venography, which is most beneficial for identifying reflux in the common femoral vein and at the saphenofemoral junction, and, in cases of venous reconstruction, intravascular ultrasound, a catheter-based ultrasound probe used to visualize periluminal vascular anatomy and detect venous obstruction or stenosis. Ambulatory venous pressure measurement is the gold standard for determining the hemodynamics of CVI; it requires inserting a needle into the dorsal foot vein and connecting it to a pressure transducer.[22] Despite its value in assessing CVI severity and clinical outcomes, ambulatory venous pressure is rarely used due to its invasive nature and the availability of alternative diagnostic modalities.

Treatment / Management

Patients with venous insufficiency should be treated based on the severity and nature of the disease. The primary goals of management are to reduce discomfort and edema, stabilize skin appearance, reduce venous reflux and varicose veins, and heal ulcers. The recommended management approach is to utilize conservative treatments (eg, leg elevation, resistance exercises, weight management, and compression therapy) alone or in conjunction with other therapies, including medications and interventional procedures.

Compression Therapy and Other Conservative Strategies

Compression treatment is the main component of the conservative approach, which aims to provide graduated external compression to the lower extremities and counteract the hydrostatic pressures of venous hypertension. Available compression garments comprise graded elastic compressive stockings, gauze boots, layered bandaging, and adjustable compression garments.[15] Compression strengths between 30 and 50 mm Hg are believed to improve venous reflux, pain, edema, pigmentation, ulcer healing, and prevention, with 70% and 80% compliance rates.[23] Compression therapy is long-term and only benefits patients who remain compliant. Ulcers are treated best with compression bandaging systems. Chronic venous ulcerations entail a risk of infection and cancerous transformation (eg, Marjolin ulcer). Compression therapy should be used with caution in patients with coexisting peripheral arterial disease. Severe arterial insufficiency and uncompensated congestive heart failure are contraindications to compression therapy. Patients whose ulcers fail to respond to compression may ultimately need surgical intervention.

Other conservative treatments include leg elevation, weight management, and exercise. Leg elevation above the heart for at least 30 minutes, 3 times a day, helps to reduce venous pressure and edema and prevent recurrent ulcers. Obesity is a well-established risk factor for developing CVI and associated complications; thus, maintaining an optimal body weight may improve CVI symptoms.[24] Resistance exercises help improve the calf muscle pump, which normally aids venous blood return from the lower extremities in healthy individuals and is impaired in those with CVI. Activities that involve ankle dorsiflexion, ankle plantarflexion, and forceful toe flexion (eg, walking and cycling) are the most effective movements for increasing systolic blood velocity.[3][1]

Proper skin and wound care are essential in conjunction with other conservative therapies. Advanced CVI may affect skin integrity; therefore, maintaining skin health and avoiding infection is crucial. Topical moisturizers, commonly containing lanolin, minimize skin fissuring and disintegration. Topical steroids may be used to treat stasis dermatitis. Bacterial overgrowth may occur with venous ulcers; hence, diligent wound care is needed to limit infection. Hydrocolloids and foam dressings can reduce wound fluid drainage and skin maceration.[25] Biologic skin replacements derived from tissue engineering have been used to treat ulcers with some effectiveness, although silver-impregnated dressing has been controversial.

Interventional Procedures

Superficial vein reflux can be managed with foam sclerotherapy, endovenous thermal ablation, or stripping. Deep vein reflux may be treated with valve reconstruction or valve transplant. Perforator reflux can be managed with sclerotherapy, endovenous thermal ablation, or subfascial endoscopic perforator surgery (SEPS). However, adherence to compression therapy regimens is highly effective in treating all forms of venous pathophysiology.[10][26][27]

Sclerotherapy

Sclerotherapy is beneficial in treating telangiectasias, reticular veins, varicose veins 1 to 4 mm in diameter, and venous reflux. This treatment modality can be used alone or with other treatments. Sclerosing agents include the hypertonic solution of sodium chloride (23.4%), polidocanol, sodium iodide, chromated glycerin, sodium tetradecyl sulfate, and sodium morrhuate. The sclerosing agent must often be diluted for veins with a lower diameter to prevent tissue irritation and necrosis. Polidocanol is superior to normal saline, eliminating incompetent varicose veins and enhancing venous hemodynamics. However, sclerosants are used to manage spider veins, not varicose veins, as a large amount of solution would be required to collapse a varicosity, leading to extreme pain, thrombosis, and permanent skin discoloration.[28] Darkening of the surrounding skin due to hemosiderin degradation is a common adverse effect of sclerotherapy, which may be mitigated by microthrombectomy, which involves the removal of the thrombus.

Endovenous ablative therapy

Ablation of incompetent veins utilizes thermal energy through radiofrequency or laser. This procedure is often used for venous reflux as an alternative to stripping. The heat produced induces local thermal damage to the vein wall, leading to thrombosis and fibrosis. Venous radiofrequency ablation results in complete obliteration in 85% of patients after 2 years. Laser therapy with an 810 nm or 940 nm diode has shown outstanding outcomes, with saphenous vein obliteration in 93% of patients at 2 years.[29] Both radiofrequency and laser treatments are administered under tumescent anesthesia to avoid skin burns, minimize discomfort, and facilitate a speedier return to regular activities. Deep venous thrombosis and pulmonary embolism remain, although seldom, the possible complications of ablation.

Endovenous deep system therapy

For iliac vein stenosis and occlusion, endovascular stenting has superseded surgical techniques, eg, cross-femoral venous bypass or prosthetic iliac vein reconstruction. Close monitoring is recommended to maintain stent patency since in-stent restenosis or occlusion can occur in individuals with thrombotic illness; however, restenosis is uncommon.[15] The efficacy of iliac stenting appears durable, with 85% to 90% of patients free of recurrent ulcers after 5 years.[30]

Surgical management

In individuals who do not respond to pharmacological or endovenous therapy, surgical surgery for CVI may be considered in addition to compression stockings. Surgical treatment may be beneficial for individuals with persistent discomfort and disability, recurrent varicose veins, inability to cooperate with compression treatment, and chronic nonhealing venous ulcers. The surgical method depends on the underlying pathophysiologic processes and the affected venous segment. However, the effectiveness of valvular surgical interventions has not been established definitively.[31]

Ligation and stripping have been shown to enhance venous hemodynamics, alleviate pain, and promote ulcer healing. Venous valve reconstruction procedures include valvuloplasty, transposition, transplant, cryopreserved vein valve allografts, and neo-valve construction. Valvuloplasty is performed in some centers, but the procedure is technically demanding and not consistently successful. No matter which surgery is selected, patients should combine it with compression stockings for maximal effectiveness. Complications related to surgery include:

• Infection
• Injury to the arterial system
• Nerve injury (eg, saphenous and or sural nerves)
• Poor cosmesis
• Deep vein thrombosis
• Scarring [3][1]

Differential Diagnosis

Other diagnoses that should also be considered when evaluating patients with suspected venous insufficiency include:

• Lymphedema
• Cellulitis
• Stasis dermatitis
• Ischemic ulcer
• Varicose veins
• Acute deep vein thrombosis 
• Heart failure
• Cirrhosis
• Renal failure
• Endocrine disorders (eg, hypothyroidism)
• Medication adverse effects (eg, calcium channel blockers, NSAIDs, and oral hypoglycemic agents)
• Lipedema
• Ruptured popliteal cyst
• Soft tissue hematoma or mass
• Exertional compartment syndrome
• Gastrocnemius tear

Prognosis

Venous insufficiency is not a benign disorder and carries various morbidities. Without correction, the condition is progressive. Venous ulcers are common and very difficult to treat. Chronic venous ulcers are painful and debilitating. Even with treatment, recurrences are common if venous hypertension persists. Nearly 60% develop phlebitis, which often progresses to deep vein thrombosis in more than 50% of patients. The venous insufficiency can also lead to severe hemorrhage. Surgery for CVI remains unsatisfactory despite the availability of numerous procedures. The financial cost of care to the patient can also be significant.[3]

Complications

CVI is associated with the following complications:

• Chronic venous ulceration 
• Deep vein thrombosis 
• Recurrent cellulitis 
• Lipodermatosclerosis
• Secondary lymphedema 
• Stasis dermatitis 
• Chronic pain
• Superficial thrombophlebitis 
• Secondary hemorrhage 
• Atrophie blanche
• Ankle joint stiffness from chronic scarring

Deterrence and Patient Education

The patient should be instructed on effectively and adequately using compression stockings, emphasizing compliance and using the optimal tension gradient. Compression stockings alone may ease discomfort, edema, and venous distention, aid healing of venous ulcers, and prevent recurrences. In addition, the patient should be instructed to preserve skin integrity by regularly checking the skin for breakdowns or infections and diligently applying moisturizer to prevent fissuring.

Furthermore, patients should be advised to elevate their legs to minimize swelling and to avoid prolonged standing or sitting. Patients should also be encouraged to maintain ideal body weight and identify any obstacles that hamper losing weight, including mental health issues (eg, depression, anxiety, and eating disorders), medications causing weight gain, or mobility issues. An appropriate specialist referral or patient counseling should address these concerns. In addition, patients should be made aware that chronic venous disease is a long-term health concern. Hence, regular follow-up with clinicians and compliance with medical treatment plans are essential for preventing its consequences.

Enhancing Healthcare Team Outcomes

Venous insufficiency represents a progressive disorder of venous blood flow caused primarily by valvular reflux, leading to venous hypertension and a spectrum of clinical manifestations ranging from edema and skin changes to venous ulceration. The condition significantly affects quality of life and work productivity and, when untreated, often progresses to postphlebitic syndrome, infection, and deep vein thrombosis. Diagnosis relies on clinical evaluation supported by standardized tools such as the CEAP classification and VCSS, with venous duplex ultrasound serving as the diagnostic gold standard. Management includes conservative measures such as compression therapy, elevation, exercise, and weight optimization, along with pharmacologic therapy and interventional or surgical procedures when indicated.

Optimal care requires coordinated interprofessional collaboration. Surgeons, primary care practitioners, and nurses are responsible for early recognition, diagnostic evaluation, initiation of evidence-based therapy, and timely referral to specialists. Podiatry and wound care professionals play a central role in ulcer management, skin care, patient education, and monitoring adherence to compression therapy. Pharmacists support medication reconciliation, identify agents that may worsen edema, and assist with alternative treatment plans. Physical and occupational therapists, dieticians, and weight management teams address mobility, calf muscle pump function, and obesity-related risk, while vascular and surgical specialists manage refractory disease. Effective communication and coordinated follow-up enhance patient-centered care, safety, outcomes, and team performance.

Review Questions

• Access free multiple choice questions on this topic.
• Click here for a simplified version.
• Comment on this article.

References

1.

Orhurhu V, Chu R, Xie K, Kamanyi GN, Salisu B, Salisu-Orhurhu M, Urits I, Kaye RJ, Hasoon J, Viswanath O, Kaye AJ, Karri J, Marshall Z, Kaye AD, Anahita D. Management of Lower Extremity Pain from Chronic Venous Insufficiency: A Comprehensive Review. Cardiol Ther. 2021 Jun;10(1):111-140. [PMC free article: PMC8126535] [PubMed: 33704678]

2.

de Moraes Silva MA, Nakano LC, Cisneros LL, Miranda F. Balneotherapy for chronic venous insufficiency. Cochrane Database Syst Rev. 2023 Jan 09;1(1):CD013085. [PMC free article: PMC9828836] [PubMed: 36622745]

3.

Bonkemeyer Millan S, Gan R, Townsend PE. Venous Ulcers: Diagnosis and Treatment. Am Fam Physician. 2019 Sep 01;100(5):298-305. [PubMed: 31478635]

4.

Porter JM, Moneta GL. Reporting standards in venous disease: an update. International Consensus Committee on Chronic Venous Disease. J Vasc Surg. 1995 Apr;21(4):635-45. [PubMed: 7707568]

5.

Azar J, Rao A, Oropallo A. Chronic venous insufficiency: a comprehensive review of management. J Wound Care. 2022 Jun 02;31(6):510-519. [PubMed: 35678787]

6.

Gloviczki P, Lawrence PF, Wasan SM, Meissner MH, Almeida J, Brown KR, Bush RL, Di Iorio M, Fish J, Fukaya E, Gloviczki ML, Hingorani A, Jayaraj A, Kolluri R, Murad MH, Obi AT, Ozsvath KJ, Singh MJ, Vayuvegula S, Welch HJ. The 2023 Society for Vascular Surgery, American Venous Forum, and American Vein and Lymphatic Society clinical practice guidelines for the management of varicose veins of the lower extremities. Part II: Endorsed by the Society of Interventional Radiology and the Society for Vascular Medicine. J Vasc Surg Venous Lymphat Disord. 2024 Jan;12(1):101670. [PMC free article: PMC11523430] [PubMed: 37652254]

7.

Vasquez MA, Rabe E, McLafferty RB, Shortell CK, Marston WA, Gillespie D, Meissner MH, Rutherford RB., American Venous Forum Ad Hoc Outcomes Working Group. Revision of the venous clinical severity score: venous outcomes consensus statement: special communication of the American Venous Forum Ad Hoc Outcomes Working Group. J Vasc Surg. 2010 Nov;52(5):1387-96. [PubMed: 20875713]

8.

Chamanga ET. Understanding venous leg ulcers. Br J Community Nurs. 2018 Sep 01;23(Sup9):S6-S15. [PubMed: 30156878]

9.

Garcia R, Labropoulos N, Gasparis AP, Elias S. Present and future options for treatment of infrainguinal deep vein disease. J Vasc Surg Venous Lymphat Disord. 2018 Sep;6(5):664-671. [PubMed: 30007531]

10.

Schwahn-Schreiber C, Breu FX, Rabe E, Buschmann I, Döller W, Lulay GR, Miller A, Valesky E, Reich-Schupke S. [S1 guideline on intermittent pneumatic compression (IPC)]. Hautarzt. 2018 Aug;69(8):662-673. [PubMed: 29951853]

11.

Noel AA, Gloviczki P, Cherry KJ, Rooke TW, Stanson AW, Driscoll DJ. Surgical treatment of venous malformations in Klippel-Trénaunay syndrome. J Vasc Surg. 2000 Nov;32(5):840-7. [PubMed: 11054214]

12.

DePopas E, Brown M. Varicose Veins and Lower Extremity Venous Insufficiency. Semin Intervent Radiol. 2018 Mar;35(1):56-61. [PMC free article: PMC5886767] [PubMed: 29628617]

13.

Taylor J, Hicks CW, Heller JA. The hemodynamic effects of pregnancy on the lower extremity venous system. J Vasc Surg Venous Lymphat Disord. 2018 Mar;6(2):246-255. [PubMed: 29454441]

14.

Caggiati A, Bergan JJ, Gloviczki P, Jantet G, Wendell-Smith CP, Partsch H., International Interdisciplinary Consensus Committee on Venous Anatomical Terminology. Nomenclature of the veins of the lower limbs: an international interdisciplinary consensus statement. J Vasc Surg. 2002 Aug;36(2):416-22. [PubMed: 12170230]

15.

Eberhardt RT, Raffetto JD. Chronic venous insufficiency. Circulation. 2014 Jul 22;130(4):333-46. [PubMed: 25047584]

16.

Sutzko DC, Obi AT, Kimball AS, Smith ME, Wakefield TW, Osborne NH. Clinical outcomes after varicose vein procedures in octogenarians within the Vascular Quality Initiative Varicose Vein Registry. J Vasc Surg Venous Lymphat Disord. 2018 Jul;6(4):464-470. [PMC free article: PMC6005729] [PubMed: 29752187]

17.

Kavousi Y, Al Adas Z, Karamanos E, Kennedy N, Kabbani LS, Lin JC. Men present with higher clinical class of chronic venous disease before endovenous catheter ablation. J Vasc Surg Venous Lymphat Disord. 2018 Nov;6(6):702-706. [PubMed: 30064962]

18.

Mutlak O, Aslam M, Standfield NJ. Chronic venous insufficiency: a new concept to understand pathophysiology at the microvascular level - a pilot study. Perfusion. 2019 Jan;34(1):84-89. [PubMed: 30067139]

19.

Christopoulos D, Nicolaides AN, Szendro G. Venous reflux: quantification and correlation with the clinical severity of chronic venous disease. Br J Surg. 1988 Apr;75(4):352-6. [PubMed: 3359149]

20.

Gillespie DL, Cordts PR, Hartono C, Woodson J, Obi-Tabot E, LaMorte WW, Menzoian JO. The role of air plethysmography in monitoring results of venous surgery. J Vasc Surg. 1992 Nov;16(5):674-8. [PubMed: 1433653]

21.

Owens LV, Farber MA, Young ML, Carlin RE, Criado-Pallares E, Passman MA, Keagy BA, Marston WA. The value of air plethysmography in predicting clinical outcome after surgical treatment of chronic venous insufficiency. J Vasc Surg. 2000 Nov;32(5):961-8. [PubMed: 11054228]

22.

Nicolaides AN, Zukowski AJ. The value of dynamic venous pressure measurements. World J Surg. 1986 Dec;10(6):919-24. [PubMed: 3798938]

23.

Motykie GD, Caprini JA, Arcelus JI, Reyna JJ, Overom E, Mokhtee D. Evaluation of therapeutic compression stockings in the treatment of chronic venous insufficiency. Dermatol Surg. 1999 Feb;25(2):116-20. [PubMed: 10037516]

24.

Sugerman HJ, Sugerman EL, Wolfe L, Kellum JM, Schweitzer MA, DeMaria EJ. Risks and benefits of gastric bypass in morbidly obese patients with severe venous stasis disease. Ann Surg. 2001 Jul;234(1):41-6. [PMC free article: PMC1421946] [PubMed: 11460821]

25.

Karlsmark T, Agerslev RH, Bendz SH, Larsen JR, Roed-Petersen J, Andersen KE. Clinical performance of a new silver dressing, Contreet Foam, for chronic exuding venous leg ulcers. J Wound Care. 2003 Oct;12(9):351-4. [PubMed: 14601228]

26.

Update on Current Care Guideline: Venous insufficiency of the lower limb. Duodecim. 2017;133(6):571-2. [PubMed: 29243470]

27.

Appelen D, van Loo E, Prins MH, Neumann MH, Kolbach DN. Compression therapy for prevention of post-thrombotic syndrome. Cochrane Database Syst Rev. 2017 Sep 26;9(9):CD004174. [PMC free article: PMC6483721] [PubMed: 28950030]

28.

Kahle B, Leng K. Efficacy of sclerotherapy in varicose veins-- prospective, blinded, placebo-controlled study. Dermatol Surg. 2004 May;30(5):723-8; discussion 728. [PubMed: 15099314]

29.

Min RJ, Khilnani N, Zimmet SE. Endovenous laser treatment of saphenous vein reflux: long-term results. J Vasc Interv Radiol. 2003 Aug;14(8):991-6. [PubMed: 12902556]

30.

Raju S, Darcey R, Neglén P. Unexpected major role for venous stenting in deep reflux disease. J Vasc Surg. 2010 Feb;51(2):401-8; discussion 408. [PubMed: 20006920]

31.

Goel RR, Hardy SC, Brown T. Surgery for deep venous insufficiency. Cochrane Database Syst Rev. 2021 Sep 30;9(9):CD001097. [PMC free article: PMC8483065] [PubMed: 34591328]

Disclosure: Shivik Patel declares no relevant financial relationships with ineligible companies.

Disclosure: Calin Manea declares no relevant financial relationships with ineligible companies.

Disclosure: Scott Surowiec declares no relevant financial relationships with ineligible companies.