Chronic Venous Insufficiency: A Comprehensive Guide to Differential Diagnosis

Chronic venous disease (CVD) is a widespread condition characterized by impaired venous return in the legs, often underestimated and overlooked by healthcare professionals. Varicose veins are a common manifestation, affecting over 25 million people in the US, with more than 6 million experiencing severe venous disease. Telangiectases, reticular veins, varicose veins, and venous ulcers are typical signs of CVD. Chronic venous insufficiency (CVI) arises from persistent venous hypertension, frequently due to ineffective muscle pumping, faulty venous valves (reflux), and venous obstruction. This condition triggers a series of morphological, physiological, and histological abnormalities. Understanding CVI and its differential diagnosis is crucial for accurate diagnosis and management. This article will explore the etiology, risk factors, pathophysiology, clinical presentations, and importantly, the differential diagnosis of CVI, aiming to provide a comprehensive overview for healthcare professionals.

Introduction to Chronic Venous Insufficiency and Diagnostic Challenges

Chronic venous insufficiency (CVI) is defined by structural and functional abnormalities of the venous system, primarily affecting the lower limbs. Patients often present with symptoms such as leg heaviness, aching, edema, telangiectasia, and varicose veins. The underlying cause is persistent ambulatory venous hypertension and subsequent inflammation. In the United States, over 2.5 million individuals are estimated to suffer from CVD, with about 20% progressing to venous ulcers.

CVD and chronic venous ulcers significantly impact patients’ quality of life, hindering occupational and social participation and creating financial burdens. Venous ulcer-related disability leads to approximately 2 million lost workdays annually, and over 12% of workers with venous ulcers retire prematurely.

The economic impact of venous ulcers on healthcare systems is substantial, with annual costs in the US estimated at $1 billion for chronic wound treatment and $3 billion for venous ulcer care specifically. Accurate diagnosis is paramount, but CVI shares symptoms with various other conditions, making differential diagnosis critical. This article emphasizes the importance of considering other potential diagnoses when evaluating patients presenting with signs and symptoms suggestive of CVI.

Etiology and Risk Factors Contributing to CVI

The precise cause of chronic venous disease is still not fully understood. However, a hereditary component is evident, as genetic conditions like Klippel-Trenaunay and Parkes-Weber syndromes are known to predispose individuals to CVD. Several risk factors are associated with the development of CVI:

• Age: The risk increases with advancing age.
• Sex: Females are more prone to CVI, with a female to male ratio of approximately 3:1.
• Obesity: Excess weight is a significant risk factor.
• Oral Contraceptives: Use is associated with increased risk.
• Tobacco Use: Smoking contributes to venous disease.
• Pregnancy: Pregnancy increases venous pressure and risk.
• Family History: A family history of varicose veins elevates individual risk.
• Deep Vein Thrombosis (DVT) History: Previous DVT can damage venous valves.
• Thrombophlebitis History: Superficial thrombophlebitis can also contribute.
• Leg Injury History: Trauma can damage veins.
• Prolonged Standing or Sitting: Occupations requiring prolonged static postures increase risk.

Understanding these risk factors is essential in identifying individuals at higher risk of developing CVI and considering preventative strategies. Furthermore, when evaluating patients with symptoms, these risk factors can help guide the diagnostic process and broaden the differential diagnosis.

Epidemiology of Chronic Venous Disease

The prevalence of chronic venous disease rises with age and shows a notable female predominance (3:1). The Framingham study reported annual incidence rates of 2.6% in women and 1.9% in men. Varicose veins are more prevalent in industrialized and developed nations compared to less developed countries, possibly due to lifestyle factors and occupational demands involving prolonged standing or sitting. These epidemiological trends highlight the widespread nature of CVI and the importance of considering it in the differential diagnosis of leg symptoms, particularly in at-risk populations.

Pathophysiology of Chronic Venous Insufficiency: A Foundation for Differential Diagnosis

The venous system in the legs functions as a blood reservoir and a pathway for returning blood to the heart. Proper venous function relies on patent blood vessels, competent valves, and effective muscle pumps. Returning blood to the central circulation against gravity in an upright position requires these mechanisms to work efficiently. The lower extremity veins are categorized into superficial, deep, and perforator veins.

The superficial system includes the great saphenous vein (GSV) and small saphenous vein, along with accessory veins. Deep veins consist of axial veins. Perforating veins connect the superficial and deep systems, traversing the fascial layer. Both deep and superficial veins contain one-way bicuspid valves that ensure unidirectional blood flow towards the heart, preventing backflow towards the feet.

CVI develops when venous pressure increases and blood return is compromised. This can result from valvular incompetence, venous blockage (thrombotic or non-thrombotic), or external compression of veins. Dysfunctional muscle pumps, especially in the calf, exacerbate these issues. These factors lead to localized or generalized venous hypertension, particularly during standing or walking. Persistent venous hypertension can cause skin hyperpigmentation, lipodermatosclerosis, and ultimately, ulceration.

Valve weakness in superficial veins may arise from pre-existing vascular wall weakness, superficial phlebitis, or hormonal influences leading to venous distention. Deep vein valve dysfunction can be a consequence of deep vein thrombosis or venous stenosis. Understanding this pathophysiology is crucial for differentiating CVI from other conditions with similar symptoms. For example, lymphedema, heart failure, and renal failure can also cause leg edema, but their underlying mechanisms differ significantly from venous hypertension in CVI.

History and Physical Examination: Clues for Differential Diagnosis

Clinical manifestations of chronic venous insufficiency (CVI) include dilated veins (telangiectasias, reticular veins, varicose veins), leg edema, pain, aching, heaviness, and skin changes. Varicose veins are enlarged, tortuous superficial veins that worsen over time.

Edema typically starts around the malleolar region, progressing upwards in a dependent manner, is pitting, and spares the forefoot. Venous claudication, which improves with rest, may occur with deep venous system occlusion. Skin changes include hyperpigmentation due to hemosiderin deposition and eczematous dermatitis. Lipodermatosclerosis involves fibrosis of the dermis and subcutaneous fat. Venous ulcers are most commonly located on the medial aspect above the malleolus. Cellulitis and superficial thrombophlebitis risks are elevated in CVI patients.

The CEAP (Clinical, Etiology, Anatomic, and Pathophysiology) classification system is used to standardize reporting, diagnosis, and treatment of CVI. The revised venous clinical severity score complements CEAP and better reflects CVI severity, aiding in assessing treatment effectiveness.

CEAP Classification and Description

Clinical Classification

• C0: No visible or palpable signs of venous disease
• C1: Telangiectases or reticular veins
• C2: Varicose veins
• C3: Edema
• C4a: Pigmentation and/or eczema
• C4b: Lipodermatosclerosis and/or atrophy
• 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

When taking patient history and performing a physical exam, it is critical to consider conditions that mimic CVI. For instance, bilateral edema could point towards systemic conditions like heart failure or renal disease rather than solely CVI. Unilateral edema raises suspicion for DVT or lymphatic obstruction. Skin changes like hyperpigmentation, while common in CVI, can also be seen in other dermatological conditions or drug reactions. Therefore, a comprehensive history and physical exam are crucial first steps in the differential diagnosis process.

Evaluation and Diagnostic Modalities for CVI

Accurate diagnosis of chronic venous disease relies on a detailed history and physical examination, supplemented by noninvasive testing. Invasive tests are typically reserved for surgical planning. Examination in an upright position helps visualize dilated veins (telangiectasia, reticular veins, varicose veins) and assess their distribution. Evaluation should also include assessment for ulcers (active or healed), hyperpigmentation, stasis dermatitis, atrophie blanche, and lipodermatosclerosis. The Brodie-Trendelenburg tourniquet test can be used at the bedside to differentiate deep and superficial reflux. Handheld Doppler can also assist in bedside assessment.

Venous duplex imaging is the preferred and most commonly used method for evaluating CVI etiology and anatomy. It combines B-mode imaging of veins with pulsed Doppler assessment of flow direction using provocative maneuvers.

Air plethysmography (APG) can assess CVI pathophysiology, including reflux, obstruction, and muscle pump failure. Abnormal venous filling indices correlate with CVI severity and can inform treatment decisions and response evaluation. APG can be particularly useful when venous duplex imaging is inconclusive.

Computed tomography (CT) and magnetic resonance venography (MRV) with contrast are useful for evaluating proximal veins and surrounding structures for intrinsic or extrinsic compression, especially when assessing for iliofemoral venous blockage before intervention.

Other noninvasive diagnostic procedures include photoplethysmography, strain gauge plethysmography, and foot volumetry.

Invasive testing includes:
a) Contrast venography: Best for identifying reflux in the common femoral vein and saphenofemoral junction, and useful in venous reconstruction cases.
b) Intravascular ultrasound (IVUS): Catheter-based ultrasound to visualize periluminal vascular anatomy and detect venous obstruction or stenosis.
c) Ambulatory venous pressure measurement: The gold standard for CVI hemodynamics assessment, but rarely used due to its invasive nature.

In the context of differential diagnosis, these evaluation methods help rule out other conditions. For example, duplex ultrasound can distinguish venous reflux from deep vein thrombosis or venous obstruction. APG can help quantify the severity of venous dysfunction, aiding in differentiating CVI from conditions causing similar symptoms but without significant venous hemodynamic abnormalities. When edema is present, evaluation may need to include cardiac and renal function tests to exclude heart failure and renal failure as primary causes, especially if venous studies are not conclusive for CVI.

Differential Diagnosis of Chronic Venous Insufficiency: Key Considerations

The differential diagnosis of chronic venous insufficiency is broad and includes conditions that share similar signs and symptoms, particularly leg edema, pain, and skin changes. A thorough consideration of these alternatives is crucial to avoid misdiagnosis and ensure appropriate management. Key conditions to consider in the differential diagnosis include:

• Acute Deep Vein Thrombosis (DVT): DVT presents with acute onset of leg swelling, pain, and warmth. While CVI is chronic, acute DVT can be a complication of or mimic early CVI symptoms. Duplex ultrasound is essential to differentiate. DVT requires immediate anticoagulation, while CVI management is different.

• Heart Failure: Heart failure can cause bilateral leg edema, often pitting, and may be associated with shortness of breath, fatigue, and jugular venous distention. Unlike CVI edema which is often worse at the end of the day and improves with elevation, heart failure edema may be more persistent. Cardiac evaluation (ECG, echocardiogram, BNP) helps differentiate.

• Cirrhosis: Liver cirrhosis can also lead to generalized edema including legs and abdomen (ascites). Liver disease markers (LFTs, bilirubin, albumin) and clinical signs (jaundice, spider angiomata) are crucial for differentiation.

• Renal Failure: Renal failure can cause generalized edema due to fluid retention and hypoalbuminemia. Renal function tests (serum creatinine, BUN, urinalysis) are essential to rule out renal causes of edema.

• Endocrine Disorders such as Hypothyroidism: Hypothyroidism can cause non-pitting edema (myxedema), fatigue, and other systemic symptoms. Thyroid function tests (TSH, free T4) are necessary if hypothyroidism is suspected.

• Medication Side Effects: Certain medications, such as calcium channel blockers, NSAIDs, and oral hypoglycemic agents (thiazolidinediones), can cause peripheral edema. Medication review is important, and edema typically resolves upon discontinuation of the offending drug.

• Lymphedema: Lymphedema results from lymphatic system dysfunction, causing non-pitting edema, often affecting the dorsum of the foot and toes (unlike CVI). Skin changes in lymphedema can include hyperkeratosis and papillomatosis. Lymphoscintigraphy or clinical assessment may be needed for differentiation.

• Lipedema: Lipedema is characterized by symmetrical, bilateral swelling of the legs and thighs due to abnormal fat deposition, typically sparing the feet. It is often painful to palpation and more common in women. Clinical presentation and distribution of swelling help differentiate from CVI.

• Ruptured Popliteal Cyst (Baker’s Cyst): Rupture can cause acute calf pain and swelling, mimicking DVT or thrombophlebitis. Ultrasound can identify the cyst and rule out DVT.

• Soft Tissue Hematoma/Mass: Trauma or soft tissue tumors can cause localized swelling and pain. History of injury and physical examination, potentially with imaging (ultrasound, MRI), are helpful for diagnosis.

• Exertional Compartment Syndrome: This condition causes pain, tightness, and sometimes swelling in the leg muscles after exercise. Symptoms are activity-related and resolve with rest, unlike CVI symptoms which are often worsened by prolonged standing. Compartment pressure measurement can confirm the diagnosis.

• Gastrocnemius Tear: A calf muscle tear can cause acute calf pain and swelling, mimicking DVT or thrombophlebitis. Physical exam, focusing on muscle tenderness and range of motion, and ultrasound can differentiate.

A systematic approach, combining history, physical examination, and appropriate investigations, is crucial to effectively differentiate CVI from these conditions and ensure targeted and effective management.

Treatment and Management Strategies for CVI

Conservative treatments are the foundation of CVI management, with compression stockings being the initial step. Compression therapy provides graduated external compression to the lower extremities, counteracting venous hypertension. Options include graded elastic compression stockings, gauze boots, layered bandaging, and adjustable compression garments.

Compression of 30-50 mm Hg is generally effective in improving pain, edema, and pigmentation, with compliance rates of 70-80%. Compression is also vital for venous ulcer healing and preventing recurrence. Obesity is a risk factor for CVI; thus, maintaining optimal body weight can alleviate symptoms. Weight loss, including after bariatric surgery, has been shown to improve CVI symptoms like edema and ulceration.

Skin and wound care: Maintaining skin health and preventing infection is crucial in advanced CVI. Topical moisturizers (e.g., lanolin-based) minimize skin fissuring. Topical steroids can treat stasis dermatitis. Venous ulcers require diligent wound care to prevent bacterial overgrowth. Hydrocolloids and foam dressings can manage wound exudate and prevent maceration. Biologic skin replacements have shown some effectiveness for ulcers, although silver-impregnated dressings remain controversial.

Sclerotherapy: Effective for telangiectasias, reticular veins, small varicose veins (1-4 mm), and veins with reflux. It can be used alone or with other treatments. Sclerosing agents include hypertonic saline (23.4%), polidocanol, sodium iodide, chromated glycerin, sodium tetradecyl sulfate, and sodium morrhuate. Dilution is often needed for smaller veins to prevent tissue damage. Polidocanol is superior to saline in treating incompetent varicose veins and improving venous hemodynamics. A common side effect is skin darkening due to hemosiderin, which can be mitigated by microthrombectomy.

Endovenous ablative therapy: Radiofrequency or laser ablation uses thermal energy to treat incompetent veins, often for GSV reflux as an alternative to stripping. Heat-induced vein wall damage leads to thrombosis and fibrosis. Radiofrequency ablation of GSV achieves complete obliteration in about 85% of patients after two years. Laser therapy shows similar success rates (around 93% obliteration at two years). These procedures are performed under tumescent anesthesia to prevent burns, reduce discomfort, and allow quicker recovery. Deep vein thrombosis and pulmonary embolism are rare but potential complications.

Endovenous deep system therapy: Endovascular stenting has replaced surgical bypass for iliac vein stenosis and occlusion. Stent patency monitoring is crucial due to potential in-stent restenosis or occlusion, though restenosis is uncommon (around 5%). Iliac stenting shows lasting efficacy, with 85-90% of patients ulcer-free after five years.

Surgical management: Surgical intervention may be considered for CVI patients who do not respond to conservative or endovenous therapy, in addition to compression. Indications include persistent symptoms, recurrent varicose veins, compression intolerance, and chronic non-healing ulcers. Procedures depend on the underlying pathophysiology and affected vein area. Ligation and stripping can improve venous hemodynamics and promote ulcer healing. GSV excision with high ligation is effective for GSV reflux across CEAP classes. Venous valve reconstruction (valvuloplasty, transposition, transplant, allografts, neo-valve construction) are also options.

While these treatments are effective for CVI, it is important to remember the differential diagnosis. For example, edema due to heart failure will not respond to varicose vein treatments. Lymphedema management differs significantly from CVI management, focusing on lymphatic drainage and compression. Therefore, accurate diagnosis, excluding differential diagnoses, is paramount before initiating CVI-specific treatments.

Complications of Untreated Chronic Venous Disease

Untreated chronic venous disease can lead to several complications:

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

These complications highlight the importance of timely diagnosis and management of CVI. Furthermore, some complications, like DVT and cellulitis, can also be part of the differential diagnosis when evaluating leg pain and swelling, emphasizing the interconnectedness of diagnosis and understanding potential disease progression.

Deterrence and Patient Education for CVI

Patient education is crucial for managing CVI and preventing disease progression. Key aspects include:

• Compression Stocking Education: Proper and consistent use of compression stockings with optimal tension gradient is vital. Emphasize compliance and benefits in symptom relief, ulcer healing, and recurrence prevention.
• Skin Care: Educate on maintaining skin integrity through regular skin checks for breakdown or infection and consistent moisturizer application to prevent fissuring.
• Leg Elevation: Advise patients to elevate legs to minimize swelling, especially during rest.
• Avoid Prolonged Static Postures: Recommend avoiding extended periods of standing or sitting.
• Weight Management: Encourage maintaining ideal body weight and address barriers to weight loss (psychiatric conditions, medications, mobility issues) with appropriate referrals or education.
• Long-Term Management: Educate patients that CVI is a chronic condition requiring ongoing follow-up and adherence to treatment plans to prevent complications.

Patient education should also include information about conditions in the differential diagnosis. Patients need to understand that leg swelling can have various causes and should promptly report any new or worsening symptoms to their healthcare provider for accurate diagnosis and management.

Enhancing Healthcare Team Outcomes in CVI Management

Optimal management of chronic venous disease requires an interprofessional healthcare team, including:

• Primary care physician
• Vascular and general surgeons
• Wound care nurses
• Physical and occupational therapists
• Dietitians
• Weight management team
• Bariatric surgeon
• Pharmacist

Early diagnosis, a comprehensive treatment plan, and timely specialist referral are crucial. Primary care providers should perform initial diagnostic tests to rule out other causes of lower limb edema and avoid medications that can exacerbate CVI. Pharmacists can review medications and suggest alternatives to prevent worsening of the condition. Wound care nurses and occupational therapists are essential in venous ulcer management.

Referral to vascular and general surgeons is necessary for non-healing ulcers or disease recurrence. Close patient follow-up is essential to prevent progression and recurrence. Patients who fail conservative weight loss approaches should be considered for referral to a bariatric surgeon.

Effective interprofessional collaboration ensures comprehensive patient care, accurate differential diagnosis, and optimized outcomes for individuals with chronic venous insufficiency. Recognizing the broad differential and working as a team is the best approach to managing this complex condition.

References

1.Rhodes JM, Gloviczki P, Canton LG, Rooke T, Lewis BD, Lindsey JR. Factors affecting clinical outcome following endoscopic perforator vein ablation. Am J Surg. 1998 Aug;176(2):162-7. [PubMed: 9737624]
2.Da Silva A, Navarro MF, Batalheiro J. [The importance of chronic venous insufficiency. Various preliminary data on its medico-social consequences]. Phlebologie. 1992 Nov-Dec;45(4):439-43. [PubMed: 1302319]
3.Pierce GF, Mustoe TA. Pharmacologic enhancement of wound healing. Annu Rev Med. 1995;46:467-81. [PubMed: 7598479]
4.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]
5.Eberhardt RT, Raffetto JD. Chronic venous insufficiency. Circulation. 2014 Jul 22;130(4):333-46. [PubMed: 25047584]
6.Brand FN, Dannenberg AL, Abbott RD, Kannel WB. The epidemiology of varicose veins: the Framingham Study. Am J Prev Med. 1988 Mar-Apr;4(2):96-101. [PubMed: 3395496]
7.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]
8.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]
9.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]
10.Gloviczki P, Comerota AJ, Dalsing MC, Eklof BG, Gillespie DL, Gloviczki ML, Lohr JM, McLafferty RB, Meissner MH, Murad MH, Padberg FT, Pappas PJ, Passman MA, Raffetto JD, Vasquez MA, Wakefield TW., Society for Vascular Surgery. American Venous Forum. The care of patients with varicose veins and associated chronic venous diseases: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg. 2011 May;53(5 Suppl):2S-48S. [PubMed: 21536172]
11.Kakkos SK, Rivera MA, Matsagas MI, Lazarides MK, Robless P, Belcaro G, Geroulakos G. Validation of the new venous severity scoring system in varicose vein surgery. J Vasc Surg. 2003 Aug;38(2):224-8. [PubMed: 12891101]
12.Folse R, Alexander RH. Directional flow detection for localizing venous valvular incompetency. Surgery. 1970 Jan;67(1):114-21. [PubMed: 5409849]
13.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]
14.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]
15.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]
16.Nicolaides AN, Zukowski AJ. The value of dynamic venous pressure measurements. World J Surg. 1986 Dec;10(6):919-24. [PubMed: 3798938]
17.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]
18.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]
19.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]
20.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]
21.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]
22.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]