Version May 2024
INTRODUCTION — Chronic venous disease refers to a wide spectrum of longstanding abnormalities. These morphologic abnormalities may result from venous hypertension; one of the etiologies of venous hypertension is reflux (superficial, deep) [1-3]. Vein-related problems may or may not be symptomatic and, when symptomatic, include a wide range of clinical signs that vary from minimal superficial venous dilation to chronic skin changes with ulceration.
An overview of chronic venous disease is provided. Additional detail is provided in the topic reviews that are linked throughout.
PATHOPHYSIOLOGY — Inadequate muscle pump function, incompetent venous valves (reflux), venous thrombosis, or nonthrombotic venous obstruction are causes of elevated venous pressure (venous hypertension), which initiates a sequence of anatomic, physiologic, and histologic changes leading to vein dilation, skin changes, and/or skin ulceration. The factors that determine whether a given patient will progress from mild to more severe disease are largely unknown. (See 'Clinical progression' below and "Pathophysiology of chronic venous disease" and "Post-thrombotic (postphlebitic) syndrome", section on 'Pathophysiology'.)
EPIDEMIOLOGY AND RISK FACTORS — Chronic vein abnormalities are present in up to 50 percent of individuals [4-7]. However, estimates of prevalence rates of chronic venous disease vary depending upon the population studied [8].
Epidemiologic studies typically focus on defined population subsets based upon the visible manifestations of venous disease. Study populations are generally limited to either those with mild abnormalities (telangiectasias, reticular veins), uncomplicated varicose veins with or without truncal reflux (eg, great saphenous), or chronic venous insufficiency (ie, chronic edema, skin changes, venous ulceration). While it is convenient to stratify the study of venous abnormalities in this manner, it is important to remember that these subsets represent varying levels of disease severity in a spectrum of a single pathology; risk factors for development are the same.
Telangiectasias and reticular veins are the most frequent manifestation (50 to 66 percent of individuals depending upon the population studied) and frequently occur in the absence of more severe signs of chronic venous disease (eg, varicose veins, skin changes) [8,9]. However, corona phlebectatica may be a sign of more advanced disease.
Varicose veins are present in 10 to 30 percent of the general population, with increasing rates in older individuals [6,7]. The incidence of chronic venous insufficiency with and without ulceration also increases with age [10-17]. In the United States, prevalence estimates vary from 15 to 80 percent of the population depending on study population [18]. In an international review, the pooled estimate of prevalence by CEAP classification (table 1) was 9 percent for C0, 26 percent for C1, 19 percent for C2, 8 percent for C3, 4 percent for C5 and 0.46 percent for C6 [19]. Point prevalence estimates of venous ulceration in Western nations range from 0.02 to 1 percent [15,16,20,21], while the period prevalence is higher, between 1 and 5 percent [20,22]. Since venous ulceration can be recurrent as well as chronic, studies of point prevalence tend to underestimate the number of cases.
Chronic venous disease appears to affect females more commonly than males. Telangiectasias affect 56 to 71 percent of females versus 36 to 44 percent of males [8,9]. Varicose veins are generally thought to be more common in females; however, depending upon the population evaluated, males may have a higher rate [5-7,23-25]. Chronic venous insufficiency may also be more common in females; however, estimates may be influenced by female longevity [15,16,20,26-28]. In one population sample, the rate of moderate disease was twice as high among females, but the rate of severe disease was higher in males [29]. Males who worked as laborers had higher rates of severe disease compared with non-laborers. There were no ethnic differences for prevalence of moderate disease.
Risk factors — The risk factors for developing chronic venous disease include advancing age, female sex, family history of venous disease, ligamentous laxity (eg, hernia, flat feet), prolonged standing, increased body mass index, smoking, lower extremity trauma, prior venous thrombosis (ie, post-thrombotic), some hereditary conditions (eg, Klippel-Trenaunay syndrome), high estrogen states, and higher parity [5,6,9,19,30-44]. The proportion of the population with obesity and chronic venous insufficiency is increasing, and patients with obesity are more likely to be symptomatic as a result of their venous disease [45].
Prevalence rates appear to be lower in non-Western populations and lower in the Middle East and African populations [19,46]. Based upon these observations, it is widely thought that factors related to Western lifestyle such as prolonged standing and sitting increase the likelihood of developing chronic venous disease. However, a large population-based study in Scotland that examined multiple potential risk factors found no consistent relationship between varicose veins and these lifestyle risk factors [24].
In spite of the well-known association, a history of deep venous thrombosis is obtained in fewer than one-third of patients with severe clinical manifestations of chronic venous disease (ie, skin changes, ulcer) [20,47,48]. Duplex ultrasound in these patients may identify valvular insufficiency, chronic vein wall thickening, or chronic thrombosis indicative of post-thrombotic syndrome [49-51]. (See "Post-thrombotic (postphlebitic) syndrome".)
Many studies have suggested a strong familial component [9,24,29]. In a case control study of 67 patients and their parents, the risk for varicose veins was 90 percent when both parents were affected, 25 percent for men and 62 percent for women when one parent was affected, and 20 percent if neither parent had varicose veins [52].
Other venous conditions can contribute to the development of dilated veins and skin changes and include venous wall degeneration (ie, venous aneurysm), arteriovenous (AV) shunt (eg, traumatic AV fistula, AV malformation), and non-thrombotic iliac vein obstruction (eg, May-Thurner syndrome) [37,38]. Telangiectasias associated with cutaneous pigmentation and atrophy can also result from radiation treatments or sequelae. (See "Acquired arteriovenous fistula of the lower extremity" and "Arteriovenous malformations of the extremities" and "May-Thurner syndrome".)
CLINICAL FEATURES — Lower extremity chronic venous disorders encompass an entire spectrum of morphologic and functional abnormalities of the venous system.
Symptoms and signs — Symptoms or findings include pain, leg heaviness, aching, swelling, skin dryness, tightness, itching, irritation, and muscle cramps. The clinical evaluation of the patient with lower extremity chronic venous disease is discussed in detail elsewhere. (See "Clinical manifestations of lower extremity chronic venous disease", section on 'Symptoms'.)
Venous claudication, which is a severe deep pain and tightness typically in the thigh muscles with vigorous exercise, can occur in the setting of acute, severe venous obstruction or longstanding venous obstruction. (See "Overview of iliocaval venous obstruction", section on 'Clinical features'.)
Visible clinical signs of chronic venous disorders in increasing severity include dilated veins (eg, telangiectasia, varicose veins), leg edema, skin changes, and skin ulceration. The prevalence of symptoms and clinical signs of venous disease correlates with the presence of venous reflux (superficial, deep venous obstruction) identified on duplex ultrasound [9,53].
●Telangiectasias, reticular veins, small varicose veins – Telangiectasias and reticular veins are dilated intradermal and subdermal veins, respectively (picture 1). (See "Clinical manifestations of lower extremity chronic venous disease", section on 'Telangiectasia/reticular veins (C1)'.)
●Varicose veins – Varicose veins are dilated, elongated, tortuous, subcutaneous veins ≥3 mm in diameter (picture 2A-B). (See "Clinical manifestations of lower extremity chronic venous disease", section on 'Varicose veins (C2)'.)
●Edema – Dependent edema at the ankle is associated with venous reflux (picture 3), which may progress over time to include the calf region. In the early stages of chronic venous insufficiency, edema may be present only at the end of the day; however, with time it can become persistent throughout the day. (See "Clinical manifestations of lower extremity chronic venous disease", section on 'Symptoms'.)
●Skin changes, venous ulceration – Patients with severe edema, skin changes (pigmentation, dermatitis, lipodermatosclerosis) (picture 4), or ulceration (picture 5) are regarded as having chronic venous insufficiency (advanced venous disease) [54], which is associated with superficial and/or deep venous reflux and/or obstruction [22]. (See "Clinical manifestations of lower extremity chronic venous disease", section on 'Chronic venous insufficiency'.)
Clinical and anatomic classification — Patients are classified as asymptomatic or symptomatic. The visible signs of chronic venous disease are categorized as C0 to C6 (CEAP [Clinical, Etiologic, Anatomic, Pathophysiology] classification) (table 1). Veins are described anatomically as axial (traversing caudal to cranial) versus nonaxial veins, superficial versus deep, and communicating (between named segments) or perforator (between superficial and deep) (figure 1A-B). The classification of lower extremity chronic venous disorders, including measures of clinical severity (eg, venous clinical severity scale), is discussed in detail elsewhere. (See "Classification of lower extremity chronic venous disorders", section on 'CEAP classification' and "Classification of lower extremity chronic venous disorders", section on 'Measures of clinical severity'.)
Clinical progression — The factors responsible for a transition from mild to more severe clinical manifestations, and whether there necessarily is a sequential progression, are not well known. Disease progression and increasing severity of symptoms appear to be related to the extent of venous valvular incompetence [9,23,28,55-58]. Varicose veins tend to remain more stable in the absence of superficial or deep venous reflux. In an observational study that followed 73 patients, the asymptomatic limb contralateral to the limb undergoing treatments for varicose veins developed varicose veins in approximately one half of the patients over a five-year follow-up period [59].
The Framingham Study examined participants for the presence of varicose veins every two years over a 16-year period. Over this time, 396 of 1720 men (23 percent) and 629 of 2102 women (30 percent) who were initially free from the condition developed varicose veins. However, the presence or absence of venous reflux was not evaluated. The two-year incidence of varicose veins was, on average, 39.4 per 1000 for men and 51.9 per 1000 for women. The incidence was highest in women 40 to 49 years of age [5].
Selected markers of inflammation may predict disease severity and progression. In a study of 80 patients, the serum fibrinogen-to-albumin ratio was a sensitive and specific marker (75 and 87.5 percent, respectively) for determining increasing CEAP classification [60]. The fibrinogen-to-albumin ratio was also a predictor of disease progression but is not commonly used in practice.
DIAGNOSIS — The diagnosis of chronic venous disease is suggested by the presence of typical symptoms (leg pain, fatigue, heaviness) and physical examination findings. (See 'Symptoms and signs' above.)
Venous duplex ultrasound examination confirms the diagnosis demonstrating the presence of venous reflux (table 2) [1,61-63]. Most symptomatic patients should undergo venous duplex ultrasonography to evaluate the nature and extent of venous reflux, which impacts the choice of treatment. Any combination of superficial, perforator or deep venous reflux, or deep venous obstruction can be present. (See "Diagnostic evaluation of lower extremity chronic venous disease" and 'Approach by presence and location of reflux' below.)
DIFFERENTIAL DIAGNOSIS — Visibly dilated superficial veins, in conjunction with typical symptoms, suggest chronic venous disease. The differential diagnosis of chronic venous disease includes many entities that can cause lower extremity pain, edema (table 3), skin changes, or nonhealing wounds. (See "Clinical manifestations and evaluation of edema in adults" and "Approach to the differential diagnosis of leg ulcers" and "Clinical assessment of chronic wounds", section on 'Differentiation of chronic ulcers'.)
Conditions other than chronic venous disease that are associated with telangiectasias include systemic sclerosis, cirrhosis, hereditary hemorrhagic telangiectasia, and ataxia telangiectasia; however, these do not typically involve the lower extremities [64]. (See "Clinical manifestations and diagnosis of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)" and "Ataxia-telangiectasia".)
MANAGEMENT
Approach by clinical severity — Patients with chronic venous disorders are managed according to clinical severity and the nature and level of underlying venous reflux.
Asymptomatic — Some individuals with large, dilated veins (ie, varicosities) do not have significant complaints and may not find the appearance of their veins at all concerning. Others find even the smallest veins cosmetically troublesome, even in the absence of symptoms.
In the absence of symptoms, telangiectasias, reticular veins, and small varicose veins can generally be treated as desired to improve cosmetic appearance without further diagnostic studies as these patients are not as likely as patients with symptoms to have underlying venous reflux [8,28] However, such treatment generally requires being paid for out-of-pocket in the US. (See 'No axial vein reflux' below.)
Sclerotherapy and surface laser therapy of telangiectasias and reticular veins are generally considered cosmetic treatments and are not typically covered by insurance, though occasionally sclerotherapy will be reimbursed for treating veins that have bled [65]. Typically, several treatment sessions are required. It is important to note that such treatment does not prevent the future development of venous reflux and the occurrence of chronic venous disease.
Symptomatic — Initial nonoperative management is recommended for most symptomatic patients and may include skin care, leg elevation, exercise, and compression therapy [1,3]. Patients who have refractory symptom management should undergo comprehensive lower extremity duplex examination to confirm the diagnosis of chronic venous disease with the demonstration of venous reflux (table 2) [1]. For patients with symptomatic varicose veins and axial venous reflux who are candidates, we suggest intervention.(See "Compression therapy for the treatment of chronic venous insufficiency" and "Approach to treating symptomatic superficial venous insufficiency", section on 'Response to initial measures'.)
Chronic symptoms — Whether to offer additional treatment for symptomatic venous disease depends upon the response to nonoperative management, ongoing symptoms, extent of disease, presence of reflux (superficial, deep, perforator), patient expectations, and likelihood that treatment would provide a durable benefit with respect to appearance or improvement in symptoms [1]. The majority of patients with chronic symptoms will exhibit some degree of venous reflux (superficial, deep), and some patients with skin changes or venous ulceration may have isolated saphenous incompetence and may be candidates for superficial venous ablation [66,67]. When offered, venous ablation for treatment of superficial venous reflux can be performed before or simultaneous with the management of visibly dilated veins. Treatment of large varicose veins prior to superficial venous ablation is appropriate when specific ablation techniques are used, such as ambulatory selective varicose vein ablation under local anesthesia (ASVLA) or Conservatrice et Hémodynamique de l'Insuffisance Veineuse en Ambulatoire (CHIVA). [3]. (See 'With superficial venous reflux' below.)
For patients with lipodermatosclerosis (C4b), healed ulcer (C5), or active ulcer (C6) following superficial venous ablation, treatment of refluxing perforator veins (table 2) may offer a benefit [68]. However, not all patients with lipodermatosclerosis need perforator ablation. Appropriate candidates may include lipodermatosclerosis with impending skin breakdown when the incompetent perforating vein is directly under the affected area of skin.
Many clinicians approach venous obstruction first in patients with active ulceration (C6), before or at the same time as superficial truncal reflux. Options for treating deep venous reflux are few but treatment of deep venous obstruction may include endovenous intervention for proximal lesions (eg, iliac vein stenosis), or surgery to improve venous outflow. (See 'With deep venous reflux' below and 'With perforator reflux' below.)
Bleeding — Telangiectasias, reticular veins, or varicose veins that are superficial or located near bony prominences are easily traumatized and prone to bleeding. Bleeding from dilated superficial veins can generally be managed with direct pressure and elevation of the limb. If bleeding persists despite these measures, the bleeding point can be suture ligated, but fortunately the need for this is rare.
For patients with stigmata of recent venous bleeding or recurrent bleeding, sclerotherapy or vein excision can be used as a temporizing measure, depending upon the location and size of the vein [69,70]. Even in the presence of venous insufficiency, sclerotherapy reduces the risk of future bleeding at the treated site; however, reducing venous hypertension by eliminating the truncal reflux is the more optimal strategy [8]. Larger varicose veins are best treated with excision (phlebectomy). (See "Approach to treating symptomatic superficial venous insufficiency", section on 'Ambulatory phlebectomy'.)
Once bleeding has been controlled, duplex examination should be performed to identify any underlying venous pathology (eg, reflux, obstruction), which can be treated to reduce the risk of recurrence. Additional treatments may be warranted to manage superficial venous or perforator reflux. (See 'With superficial venous reflux' below.)
Approach by presence and location of reflux
No axial vein reflux — Patients with isolated varicose veins without axial vein (eg, great saphenous) reflux are typically treated with sclerotherapy or excision (phlebectomy), depending on vein size, location, and number of veins involved [71]. (See "Injection sclerotherapy techniques for the treatment of telangiectasias, reticular veins, and small varicose veins" and "Approach to treating symptomatic superficial venous insufficiency", section on 'Ambulatory phlebectomy'.)
For the treatment of most patients with lower extremity telangiectasias, reticular veins, and varicose veins , liquid sclerotherapy is often the preferred initial approach depending on the skills of the clinician. The results of sclerotherapy are generally thought to be superior to those of laser therapy. Thus, laser therapy is generally reserved for patients with a fear of needles, those who are allergic to sclerosing agents, have post-sclerotherapy matting, or have failed sclerotherapy. A combination therapy (cryolaser and cryosclerotherapy [ClaCS]) is becoming popularized for reticular veins and telangiectasia [72]. Outcomes depend upon the diameter of the vein being treated and the presence or absence of underlying reticular veins and skin type. (See "Laser and light therapy of lower extremity telangiectasias, reticular veins, and small varicose veins", section on 'Laser versus sclerotherapy'.)
With superficial venous reflux — Patients with persistent symptoms and signs of chronic venous disease after a period of nonoperative management and documented superficial venous reflux as a source of their symptoms are candidates for superficial venous ablation. A decision to offer ablation therapy depends upon symptom severity, response to medical therapy, extent of disease, patient expectations, and likelihood of providing a durable benefit with respect to appearance or improvement in symptoms or ulcer healing. (See "Approach to treating symptomatic superficial venous insufficiency", section on 'Candidates for venous intervention' and "Approach to treating symptomatic superficial venous insufficiency" and "Approach to treating symptomatic superficial venous insufficiency", section on 'Endovenous versus surgical ablation'.)
Treatment of superficial venous reflux is typically accomplished in the office setting using one of several venous ablation techniques, which are classified by the nature and method of vein destruction, including non-thermal and thermal methods. Combination treatments have also been described [73,74]. Superficial venous ablation is thought to produce beneficial effects by reducing the venous volume in the limb and thereby the effects of venous hypertension on skin [75]. (See "Comparison of methods for endovenous ablation for chronic venous disease".)
The timing of treatment of significant symptomatic telangiectasias, reticular veins, and varicose veins can be immediate with microphlebectomy or sclerotherapy at the same time as venous ablation, or as deferred treatment [76,77]. Delaying treatment may minimize the number of veins that need further treatment. Following successful ablation, residual telangiectasias, reticular veins, and small varicosities can become more prominent, but usually stabilize. Management of larger varicosities can also be delayed; however, it is equally appropriate to perform phlebectomy concurrently with ablation [78]. (See "Approach to treating symptomatic superficial venous insufficiency", section on 'Treatment timing'.)
With deep venous reflux — For selected patients, endovenous treatment of central venous obstruction (eg, angioplasty/stenting) improves venous outflow and reduces symptoms. For post-thrombotic iliofemoral obstructive disease combined with superficial venous reflux, hemodynamics determines the course of treatment. Most interventionalists will initially relieve the deep venous obstruction and then consider superficial (saphenous) venous ablation, or ablation of a refluxing perforator. Management of iliocaval venous obstruction including compressive lesions (eg, May-Thurner) is reviewed separately. (See "May-Thurner syndrome" and "Overview of iliocaval venous obstruction" and "Endovenous intervention for iliocaval venous obstruction".)
For those with severe deep venous reflux, venous reconstruction is another option that is moderately successful with acceptable morbidity [79]. Options include internal or external approaches to valve repair, as well as translocation of vein segments, transplantation of vein segments, and substitution. Other techniques under investigation include implantation of mechanical valves or endovenous creation of deep vein valves [80]. (See "Techniques used for open iliocaval venous reconstruction".)
●Patients with primary deep vein valvular incompetence can usually be treated with vein valve repair. It is worth noting that common femoral venous reflux is abolished in most patients who undergo great saphenous venous ablation.
●Patients with secondary deep vein valvular incompetence (ie, following prior deep venous thrombosis) require more extensive transplantation or transposition procedures.
In general, better outcomes are achieved in patients with primary valvular incompetence compared with secondary incompetence with 10 year cumulative clinical success rates of 73 and 43 percent, respectively [81,82]. Such procedures are performed at a small number of academic centers by individuals who have dedicated their practice to the improvement of this difficult problem.
With perforator reflux — Symptomatic patients whose physical examination and duplex study are consistent with perforator reflux (table 2) as a source of impending skin breakdown, or venous ulceration, may be candidates for perforator ablation with ultrasound-guided sclerotherapy or endovenous methods. Incompetent perforators can contribute significantly to increased local venous pressure, reducing skin perfusion and inhibiting ulcer healing [83]. For patients with venous ulceration, incompetent perforator veins are less likely to be identified in isolation (incidence of 14 percent). When combined saphenous and perforator reflux are identified, saphenous venous reflux is treated first; perforator reflux often resolves following saphenous ablation [83]. Minimally invasive techniques for managing perforators are preferred rather than open surgical techniques [84-87].
Isolated perforator reflux (ie, no saphenous or deep venous reflux), as a source of clusters of varicose veins, will often resolve when associated varicose veins are ablated or removed. Persistent or new perforators identified by duplex ultrasound following saphenous ablation can be managed concurrently with treatment of residual veins or later.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic venous disorders".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Varicose veins and other vein disease in the legs (The Basics)" and "Patient education: Vein ablation (The Basics)")
●Beyond the Basics topic (see "Patient education: Lower extremity chronic venous disease (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Chronic venous disease – Visibly dilated lower extremity veins (ie, telangiectasias, reticular veins, varicose veins) can occur in the absence of symptoms or venous reflux but are often a source of significant distress to the patient. Significant symptoms (aching, swelling, heaviness) may be indicative of underlying venous insufficiency. Patients with skin changes or venous ulceration have chronic venous insufficiency, which may be due to superficial venous reflux, deep venous reflux, or a combination of these. (See 'Clinical features' above and 'Pathophysiology' above.)
●Venous duplex – Symptomatic patients with lower extremity telangiectasias, reticular veins, varicose veins, skin changes, or venous ulceration should undergo further evaluation with venous duplex to identify the presence of superficial, perforator, or deep venous reflux, which alters treatment options. (See 'Diagnosis' above.)
●Management – Initial treatment for most patients is nonoperative and includes limb elevation, exercise, and compression therapy. Patients with persistent symptoms and signs of venous disease after a period of nonoperative management and documented superficial venous reflux as a source of their symptoms are candidates for superficial venous ablation. The primary goal of treatment is improvement in symptoms, but for some patients improved cosmetic appearance is also an important goal. (See 'Management' above.)
•Axial vein ablation – For the elimination of superficial venous insufficiency due to axial venous reflux, endovenous ablation techniques are preferred to surgical vein stripping. Endovenous techniques are typically performed using local anesthesia in the office setting and are very successful in achieving vein closure and contributing to high rates of patient satisfaction. (See 'With superficial venous reflux' above and "Approach to treating symptomatic superficial venous insufficiency", section on 'Technique selection by axial vein'.)
•Perforator vein ablation – For the elimination of perforator reflux that remains following superficial venous ablation that is associated with an area of lipodermatosclerosis (C4b), or ulceration (C5,C6), ultrasound-guided sclerotherapy or endovenous method can be used. On occasion, surgical methods may be required for patients with recurrent or refractory venous ulceration. (See 'With perforator reflux' above.)
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