Chronic Venous Insufficiency

Etiology

The etiology of the chronic venous disease remains elusive. It appears to have a hereditary component since genetic disorders like Klippel-Trenaunay and Parkes-Weber are known to cause CVD.[4] The risk factors associated with CVD are as follows:

• Age
• Sex
• Overweight
• Use of oral contraceptives
• Tobacco use
• Pregnancy
• Family history of varicose veins
• A history of deep vein thrombosis
• History of thrombophlebitis
• History of the leg injury
• Prolonged standing or sitting

Epidemiology

The risk of chronic venous disease increases with age and has a 3 to 1 female predominance.[5] The Framingham research found an annual incidence of 2.6% in women and 1.9% in males.[6] Varicose veins are more widespread in industrialized and developed nations than underdeveloped ones.

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 to function the venous system 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 facial muscle layer), deep (below the fascial layer), and perforator.[7] 

The superficial venous system consists of the great saphenous vein (GSV) and small saphenous vein, in addition to several accessory veins. Deep veins are made up of axial veins. Perforating veins traverse the fascial layer connecting superficially to deep veins. Throughout the deep and superficial veins are a number of one-way bicuspid valves that allow blood to travel toward the heart while preventing it from returning to the feet.[5] 

Multiple processes contribute to the development of venous disease wherein venous pressure is elevated and blood return is impeded, such as valvular incompetence, thrombotic or non-thrombotic venous blockage, or extrinsic compression of the veins. These variables are worsened by dysfunctional muscular pumps, particularly in the calf muscles. These trajectories result in global or localized venous hypertension, especially when standing or walking. Persistent venous hypertension can result in hyperpigmentation of the skin, lipodermatosclerosis of the subcutaneous tissue, and, eventually, ulceration. 

Preexisting vascular wall weakness, superficial phlebitis, or severe venous distention due to hormonal influences might result in a weakened superficial veins valve. In contrast, deep vein thrombosis or venous stenosis may cause dysfunction of the deep veins valve.[5]

History and Physical

The major clinical manifestations of chronic venous insufficiency (CVI) are dilated veins such as telangiectasias, reticular veins, varicose veins, leg edema, pain/achiness/heaviness, and skin alterations. Varicose veins are dilated superficial veins that get increasingly convoluted and larger over time.

The edema originates in the peri malleolar region, progresses up the leg in a dependent manner, is pitting in nature, and spares the forefoot. Deep venous system occlusion may cause venous claudication, which improves with rest. Cutaneous alterations include skin darkening due to hemosiderin deposition and eczematous dermatitis. Lipodermatosclerosis is a fibrotic process involving the dermis and subcutaneous fat.

Venous ulcers most commonly occur along the medial surface above the malleolus. There is an increased risk of cellulitis and superficial thrombophlebitis. An international consensus conference developed the Clinical, Etiology, Anatomic, and Pathophysiology (CEAP) classification to improve consistency in reporting, diagnosis, and treating CVI.[8] In addition to complementing the CEAP, the revised venous clinical severity score better reflects the CVI severity and has extended clinical utility.[9] It aids in determining the efficacy of CVD treatments. Consequently, it is recommended for routine clinical usage (1B grade).[10][11] 

CEAP Classification and Description

Clinical Classification

• C0-No visible or palpable signs of venous disease 
• C1-Telengiectases 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

Evaluation

Accurately diagnosing chronic venous disease requires a thorough history and physical examination, supplemented by noninvasive testing. Invasive testing is typically reserved for cases where surgery is being considered. In an upright position, the skin should be inspected for conspicuous, dilated veins such as telangiectasia, reticular veins, or varicose veins, and their distribution should also be noted. Additionally, active or healed ulcers, hyperpigmentation, stasis dermatitis, atrophie Blanche, or lipodermatosclerosis should be evaluated. The standard tourniquet test (e.g., the Brodie-Trendelenburg) can be conducted at the bedside to differentiate between deep and superficial reflux. In addition, a handheld continuous-wave Doppler may be used to aid in bedside assessment.[12]

Currently, venous duplex imaging is the most popular and recommended method for assessing the etiology and anatomy and diagnosing CVD. Venous duplex imaging combines B-mode imaging of the deep and superficial veins with pulsed Doppler assessment of flow direction using provocative methods.[5] 

Air plethysmography (APG) can assess all potential pathophysiologic processes of CVI, such as reflux, obstruction, and muscle pump failure.[13] Abnormal venous filling indices correlate with the severity of CVI, provide information on several features of global venous function, and can be utilized for intervention selection and response evaluation.[14][15] 

When a venous duplex fails to provide conclusive evidence on the etiology of CVI, APG may be therapeutically beneficial. 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.[5] 

Photoplethysmography, strain gauge plethysmography, and foot volumetry are other noninvasive diagnostic procedures.

Invasive testing includes a) contrast venography is most beneficial to identify reflux in the common femoral vein and at the saphenofemoral junction and may be used in cases of venous reconstruction; b) intravascular ultrasound is a catheter-based ultrasound probe and is employed to visualize periluminal vascular anatomy to detect venous obstruction or stenosis;  c) Ambulatory venous pressure measurement is the gold standard for determining the hemodynamics of CVI; it requires insertion of a needle into the dorsal foot vein and connecting it to a pressure transducer.[16]

Despite its value in determining CVI's severity and clinical outcomes, it is rarely used because of its invasive nature and alternative diagnostic modalities.

Treatment / Management

Conservative treatments, such as compression stockings, are the cornerstone and initial step of CVI management. Compression treatment aims to provide graduated external compression to the lower extremities and counteract the hydrostatic pressures of venous hypertension. Available compression garments consist of graded elastic compressive stockings, gauze boots, layered bandaging, and adjustable compression garments.[5] 

The tension between 30- and 50-mm Hg is believed to produce considerable improvement in pain, edema, and pigmentation with a compliance of 70 and 80%.[17] It is also helpful in both healing ulcers and preventing their recurrences. Obesity is a well-established risk factor for developing CVI and its associated consequences; thus, maintaining an optimal body weight may improve CVI symptoms. It has been proven that weight loss following bariatric surgery improves CVI symptoms, including edema and ulceration.[18](B2)

Skin and wound care: Advanced CVI may affect skin integrity; therefore, it is crucial to maintain skin health and avoid infection. 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. A range of hydrocolloids and foam dressings can reduce wound fluid drainage and skin maceration.[19] Biologic skin replacements derived from tissue engineering have been used to treat ulcers with some effectiveness, although silver-impregnated dressing has been controversial.(A1)

Sclerotherapy: Sclerotherapy is beneficial in treating telangiectasias, reticular veins, varicose veins (1-4 mm diameter), and veins with reflux. It can be used as a primary or in combination 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. For veins with a lower diameter, the sclerosing agent must often be diluted to prevent tissue irritation and necrosis. Polidocanol is superior to normal saline, eliminating incompetent varicose veins and enhancing venous hemodynamics.[20] (A1)

Darkening of the surrounding skin because of hemosiderin degradation is a common side effect of sclerotherapy, which may be mitigated by microthrombectomy, which involves the expulsion of the thrombus.

Endovenous ablative therapy: Ablation of incompetent veins utilizes thermal energy through radiofrequency or laser. This procedure is often utilized for GSV reflux as an alternative to stripping. The heat produced induces local thermal damage to the vein wall, leading to thrombosis and fibrosis. Radiofrequency ablation of the GSV results in complete obliteration in 85% of patients after two years. Laser therapy with either an 810-nm or 940-nm diode has shown outstanding outcomes, with saphenous vein obliteration in 93% of patients at two years.[21] 

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 such as cross-femoral venous bypass or prosthetic iliac vein reconstructions. Close monitoring is recommended to ensure that stent patency is maintained since in-stent restenosis or occlusion can occur in individuals with thrombotic illness; however, restenosis is uncommon (5%).[5] The efficacy of iliac stenting seems to be lasting, with 85 to 90 percent of patients being free of recurrent ulcers after five years.[22](B2)

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. Specifically for individuals with persistent discomfort and disability, recurrent varicose veins, inability to cooperate with compression treatment, and chronic non-healing venous ulcers.

The prospective method is contingent upon the underlying pathophysiologic processes and afflicted vein area. Ligation and stripping have been shown to enhance venous hemodynamics, alleviate pain and promote ulcer healing. The excision of GSV with high ligation at the saphenofemoral junction is sustainable and applicable to all CEAP classes with GSV reflux. Venous valve reconstruction procedures include valvuloplasty, transposition, transplant, cryopreserved vein valve allografts, and neo-valve construction.

Differential Diagnosis

• Acute deep vein thrombosis 
• Heart failure
• Cirrhosis
• Renal failure
• Endocrine disorders such as hypothyroidism
• Medication side effects, e.g., calcium channel blockers, NSAIDs, oral hypoglycemic agents
• Lymphedema
• Lipedema
• Ruptured popliteal cyst
• Soft tissue hematoma/mass
• Exertional compartment syndrome
• Gastrocnemius tear

Complications

Untreated chronic venous disease imposes the following 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