ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Clinical manifestations of lower extremity chronic venous disease

Clinical manifestations of lower extremity chronic venous disease
Literature review current through: Sep 2023.
This topic last updated: Nov 15, 2022.

INTRODUCTION — Chronic lower extremity venous disease is the most common vascular disorder [1]. Chronic venous disease refers to the presence of morphological (ie, venous dilation) or functional (eg, venous reflux) abnormalities of long duration and manifested by symptoms and/or signs indicating the need for further investigation or treatment [2,3].

Chronic venous disease encompasses the full spectrum of signs and symptoms associated with classes C0 to C6 of the Clinical-Etiology-Anatomy-Pathophysiology classification (table 1), whereas classes C4 to C6 comprise "chronic venous insufficiency" or "advanced venous disease" [4].

Initial clinical presentation is highly variable with the most common symptoms consisting of lower extremity heaviness, aching, swelling, itching, discomfort, and pain. Physical findings include abnormal venous dilation (ie, telangiectasias-corona phlebectatica, reticular veins, varicose veins), edema, inflammation, dermatitis, skin changes, and ulceration. Chronic venous insufficiency is associated with chronic disability, diminished quality of life, and high health care costs [5-9].

The clinical evaluation of chronic venous disease is reviewed here. The classification, diagnostic evaluation, and management of chronic venous disease are discussed elsewhere. (See "Classification of lower extremity chronic venous disorders" and "Overview of lower extremity chronic venous disease".)

APPROACH TO THE PATIENT — The diagnosis of chronic lower extremity venous disease is predominantly clinical. Initial evaluation consists of a thorough history and physical examination, with clinical classification of disease according to the Clinical-Etiology-Anatomy-Pathophysiology (CEAP) criteria (table 1) [2]. The CEAP classification is helpful in documenting venous disease both at initial presentation as well as in during follow-up examinations. The CEAP clinical classification is discussed in detail elsewhere. (See "Classification of lower extremity chronic venous disorders" and 'Clinical signs by CEAP category' below.)

Because the presence of dilated veins is a common incidental finding on routine physical examination, many individuals are already aware that they have a vein problem. Up to one half of patients, even some with very large varicosities, have no specific symptoms [10]. Symptomatic patients may or may not correlate certain lower extremity symptoms with the presence of abnormal veins; alternatively, the patient may erroneously attribute symptoms that are more consistent with orthopedic or arterial vascular disease to their visible veins.

The major goal in the clinical evaluation of lower extremity chronic venous disease is a full clinical assessment of the lower extremities with correct interpretation of the patient's symptoms and correlation with physical signs [3]. Commonly, venous symptoms commonly occur later in the day rather than in the beginning and progress throughout the day. Sometimes venous symptoms can be confusing and overlap with other medical problems. Inconsistencies between symptoms and clinical signs may require additional diagnostic evaluation. (See "Overview of lower extremity chronic venous disease", section on 'Differential diagnosis'.)

Risk factors for venous disease — The patient is often very interested in knowing why they have developed a vein problem. To help the patient better understand their disorder, the patient should be questioned specifically for risk factors known to contribute to the development of chronic venous disease. The most common risk factors include advancing age, family history of venous disease, increased body mass index, smoking, a history of lower extremity trauma, prior venous thrombosis, and, in women, pregnancy. A more complete review of risk factors is discussed elsewhere. (See "Overview of lower extremity chronic venous disease", section on 'Risk factors'.)

Particular attention should be paid to identifying risk factors that can be modified (eg, obesity, lifestyle).

The patient who has no identifiable risk factors may have suffered a remote lower extremity trauma that they do not recall, or an undiagnosed deep vein thrombosis (DVT). Duplex ultrasound in these patients may identify valvular insufficiency, chronic vein wall thickening, or chronic thrombosis indicative of post-thrombotic syndrome [11-13]. (See "Post-thrombotic (postphlebitic) syndrome".)

Medical history — A complete medical history should be obtained with particular attention to cardiovascular and other risk factors.

Patients with more severe clinical manifestations (ie, edema, inflammation, ulcer) are typically older and may have significant associated medical conditions (eg, peripheral artery disease [PAD], heart failure, diabetes, arthritis, obesity).

Chronic venous disease and arterial vascular disease have some common risk factors (eg, smoking, obesity) and pathophysiologic processes [14]. The presence of varicose veins was associated with arterial disease in two studies [15,16]. One of these, a cross-sectional study, documented a 36 percent increase in the risk of developing coronary artery disease for men with varicose veins [15].

Quality of life — Health-related quality of life outcome measures are increasingly being considered in the evaluation of the outcomes of treatment for chronic venous disease [17-20]. Patients should be specifically questioned regarding the impact of symptoms on their daily activities, especially with respect to employment. The venous clinical severity score (VCSS) (calculator 1) and venous disability score (VDS) may aid with initial and follow-up assessment and, in the United States, are required by Medicare. (See "Classification of lower extremity chronic venous disorders", section on 'Measures of clinical severity'.)

Individuals with varicose veins may have a lower perception of their general health compared to individuals without varicose veins, especially if clinical manifestations are more significant (eg, edema, skin changes) [17]. Quality of life measures improve with management of their superficial venous disease [21]. (See "Overview of lower extremity chronic venous disease", section on 'Management'.)

Patients with severe skin changes or venous ulceration also have reductions in quality of life measures that are further reduced coincident with the need for chronic wound management [18,19,22]. Ulcer healing, however, may not always result in perceived improvements in quality of life [23]. (See "Evaluation and management of chronic venous insufficiency including venous leg ulcer", section on 'Ulcer care'.)

SYMPTOMS — The clinical presentation of symptoms varies widely. The onset of these symptoms relative to the appearance of visibly dilated veins, skin changes, edema, or ulceration should be ascertained and correlated with any positive risk factors. (See 'Risk factors for venous disease' above.)

The most common symptoms reported by patients with chronic venous disease are limb discomfort including leg heaviness or aching, throbbing or burning pain, itching, and limb swelling [24]. Pain and limb discomfort were reported as a significant symptom for each of the six Clinical-Etiology-Anatomy-Pathophysiology (CEAP) clinical categories in at least 50 percent of individuals surveyed in one large cross-sectional study [10]. Pain may be generalized (ie, aching, burning) or localized to specific veins, areas of skin discoloration (hemosiderin deposition; alone or coupled with inflammation), or areas of lipodermatosclerosis or ulceration. When pain accompanies more severe clinical manifestations, ambulation may become difficult or even impossible.

Pain associated with venous disease is typically worse when standing, or when seated with the feet dependent for prolonged periods of time, and improves with limb elevation and walking [25]. These features distinguish chronic venous disease from typical symptoms associated with lower extremity occlusive peripheral artery disease. Patients with mild-to-moderate lower extremity PAD (ie, claudication) complain of pain with walking that is relieved by rest while those with more severe PAD may complain of more pain when the limb is elevated. (See "Clinical features and diagnosis of lower extremity peripheral artery disease".)

The pain associated with venous disease is typically directly associated with the affected veins, skin changes, or ulceration; it does not radiate as with radiculopathies and is not exacerbated by joint movement as in arthritis. (See "Acute lumbosacral radiculopathy: Pathophysiology, clinical features, and diagnosis".)

With venous disease, extremity swelling is quite common, whether related to venous insufficiency or obstruction, Extremity swelling is reported by 25 to 75 percent of patients and correlates with increasing clinical severity (ie, increasing CEAP category). With isolated superficial venous insufficiency, ankle swelling is common, whereas ankle, calf, and/or thigh is more common with deep venous insufficiency and/or deep venous obstruction. Swelling is generally worse with prolonged standing and improves with leg elevation and walking. In females, exacerbation of symptoms may occur with the menses or pregnancy, due to increased fluid volume and/or higher circulating levels of estrogen.

Other symptoms include limb aching or generalized fatigue, skin discoloration or redness, muscle cramping, restless legs, numbness, tingling, or itching. Numbness and tingling due to chronic venous disease can become chronic and may be difficult to distinguish from other causes of peripheral neuropathy that affect the lower extremity [26-28]. (See "Approach to the patient with sensory loss", section on 'Distal sensory polyneuropathy'.)

Some patients with chronic venous disease may seek medical attention for the first time due to chronic ulcers, or bleeding that can be spontaneous (varicose vein hemorrhage) or related to a wound. The prevalence of nonhealing venous ulcers for more than a year has been reported in 55 to 60 percent of patients with inadequately treated chronic venous disease [29-32].

Patients should be asked about the number and location of prior ulcerations, as well as the nature of any treatments used to aid in wound care. A history of a previous venous ulcer is the strongest predictor of recurrent ulceration [29].

PHYSICAL ASSESSMENT — The patient should undergo a complete physical examination with a detailed lower extremity examination that includes assessment of clinical signs of venous disease (see 'Clinical signs by CEAP category' below), pulse examination, and neurologic assessment [3,33]. The goal of physical assessment is to correlate the patient's symptoms with the clinical signs of venous disease, and ultimately, with diagnostic vascular laboratory findings (eg, duplex ultrasound). (See "Diagnostic evaluation of lower extremity chronic venous disease".)

It is important to keep in mind that a subset of patients with chronic venous disease may have typical symptoms but no visible clinical signs. Clinicians may occasionally report their patients having tenderness to palpation; however, this finding in not typical in chronic venous disease (in the absence of active phlebitis). (See "Superficial vein thrombosis and phlebitis of the lower extremity veins".)

The femoral and pedal pulses (ie, dorsalis pedis and posterior tibial pulses) are usually palpable. For those in whom the clinician is unable to palpate the pedal pulses, a handheld Doppler ultrasound may be necessary to assess arterial flow. If there are any indications of arterial ischemia (ie, cool extremity, pulselessness, forefoot or digital ulceration), further noninvasive arterial evaluation should be undertaken.

CLINICAL SIGNS BY CEAP CATEGORY — The Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification is a method to categorize chronic venous disorders to serve as a basis for standardized reporting. The visible signs of chronic venous disorders are categorized as C0 to C6 depending on appearance (table 1) [34]. CEAP is a classification system and should not be used as a measure of the clinical severity of venous disease. (See "Classification of lower extremity chronic venous disorders", section on 'CEAP classification'.)

No clinical signs (C0) — Approximately 20 percent of patients with clinical symptoms consistent with a chronic venous disorder have no visible clinical signs [10]. Duplex examination identifies functional disease (ie, venous reflux) in approximately 20 percent of these patients. (See "Overview of lower extremity chronic venous disease", section on 'Management'.)

Telangiectasia/reticular veins (C1) — The most frequently encountered manifestation of venous disease is mild venous dilation.

Telangiectasias are a confluence of dilated intradermal venules/capillaries less than 1 millimeter in diameter (picture 1).

Reticular veins are dilated, bluish subdermal veins, 1 to 3 millimeters in diameter, and are usually tortuous.

Varicose veins (C2) — Varicose veins are subcutaneous dilated, tortuous veins greater than three millimeters in diameter (picture 2). They may involve the saphenous veins, saphenous tributaries, or nonsaphenous superficial leg veins (figure 1A-B). (See "Classification of lower extremity chronic venous disorders", section on 'Anatomy (The "A" component of CEAP)'.)

The appearance of visible varicose veins is often the most common concern. However, it is important to note that varicose veins are often associated with superficial axial venous reflux (eg, great saphenous vein, small saphenous vein). (See "Approach to treating symptomatic superficial venous insufficiency".)

Edema (C3) — Longstanding venous disease associated with venous reflux is characterized by the development of dependent ankle edema (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.

The presence of edema is not a specific finding. It occurs when the hydrostatic pressure gradient is substantially increased (eg, heart failure, renal failure, or locally with venous thrombosis or insufficiency), the oncotic pressure gradient is substantially reduced (marked hypoalbuminemia), vascular (capillary) permeability is increased, or lymphatic flow is obstructed (table 2). Other etiologies may also lead to lower extremity edema. (See "Pathophysiology and etiology of edema in adults" and "Clinical features and diagnosis of peripheral lymphedema" and "Popliteal (Baker's) cyst".)

The following clues point to venous insufficiency as the cause of lower extremity edema:

The edema is limited to the lower extremities and is often unilateral (particularly early) and is accompanied by venous abnormalities (telangiectasias, reticular veins, varicose veins), hyperpigmentation, or other signs of venous disease. By contrast, the edema in generalized edematous states is usually bilateral and is often not limited to the legs.

The edema typically subsides with recumbency. While many other edematous states also improve in this setting, this finding distinguishes venous insufficiency from chronic lymphatic obstruction, which is often unilateral and may not subside with recumbency. (See "Clinical features and diagnosis of peripheral lymphedema".)

The central venous pressure is normal, a finding that excludes heart failure as a cause for the edema. This distinction is more difficult when both heart failure and venous disease are present.

Patients who have been given diuretics will have a poor response and can develop signs of hypoperfusion.

Chronic venous insufficiency — Chronic severe edema (see 'Edema (C3)' above), skin changes (pigmentation, dermatitis, lipodermatosclerosis), and venous ulceration are signs of advanced venous disease (ie, chronic venous insufficiency) [35], which is associated with superficial and/or deep venous reflux and/or obstruction [36]. (See "Evaluation and management of chronic venous insufficiency including venous leg ulcer".)

Skin pigmentation/dermatitis (C4a) — Pigmentation changes are initially most prominent at the medial ankle but subsequently may encroach upon the foot and lower leg (picture 4). Brown and blue-grey hyperpigmentation on the anterior lower leg is a common finding. The pigmentation is due to hemosiderin deposition, which derives from the breakdown of red blood cells that have extravasated through damaged capillaries into the dermis because of venous hypertension.

Individuals with functional venous disease due to venous reflux are prone to develop stasis dermatitis, which is a common and possibly early dermatologic sign of chronic venous insufficiency. Stasis dermatitis is an inflammatory process that presents as an eczematous rash characterized by itching, erythema, scaling, weeping, erosions, and crusting (picture 5).

The pruritus associated with the dry, scaly skin can be difficult to relieve; excoriations are often present secondary to scratching and can be a source of skin infection. Rashes mimicking the dermatitis on the legs can appear as eczematous patches on other body sites or can present as a generalized body rash, an auto eczematous or "id" reaction (picture 6).

Atrophie blanche manifests as atrophic, hypopigmented patches with focal red punctate dots or telangiectasias, surrounded by hyperpigmentation. These are most often seen on the medial distal leg near the malleolus, or can occur within lipodermatosclerotic skin, where they correspond to points of avascular fibrosis (picture 7). These areas do not represent healed venous ulcers, but they are vulnerable to future ulceration because of poor perfusion. (See "Livedoid vasculopathy" and 'Venous ulceration (C5, C6, C6r)' below.)

Lipodermatosclerosis (C4b) — Chronic venous insufficiency of sufficient severity (eg, following severe cases of deep venous thrombosis or that associated with lymphatic compromise) may lead to the development of lipodermatosclerosis, a fibrosing panniculitis of the subcutaneous tissue. This disorder is characterized by a firm area of induration, which is initially located at the medial ankle (picture 8) and in the acute phase can be exquisitely tender to touch [37]. As the process progresses, the entire leg can become circumferentially involved with extension up to the mid leg in more advanced cases (picture 9).

The skin overlying the panniculitis is typically heavily pigmented and bound down to the subcutaneous tissues. The fibrosis may be so extensive and constrictive as to girdle and strangle the lower leg, further impeding lymphatic and venous flow. Brawny edema above the fibrotic area and on the foot below is seen in advanced cased of lipodermatosclerosis. The limb now resembles an inverted champagne bottle; the bulbous cork represents the lymphedematous foot, the fibrosed area the neck of the bottle, and edematous leg the body of the bottle (picture 10).

Characteristic histologic findings are almost exclusively in the subcutaneous tissue and include adipose changes such as micropseudocyst and macropseudocyst formation, necrotic adipocytes, lipomembranous change, and lipogranulomas with xanthomatous macrophages. In a pathologic study of 25 cases, the lesions were largely devoid of dermal, septal, or lobular neutrophilic or lymphocytic inflammation [38]. Medium vessel calcification was seen in 13 cases. The accumulation of basophilic elastic fibers located deep in the septa was present in all the cases.

Patients with lipodermatosclerosis are particularly prone to repeated bouts of cellulitis, usually caused by Staphylococcal or Streptococcal organisms (picture 11). (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

Corona phlebectatica (C4c) — The presence of corona phlebectatica, which is a crown of numerous small intradermal veins on the medial or lateral aspects of the ankle and foot (picture 12) [34], is often a clinical indicator of venous hypertension secondary to saphenous or perforator venous insufficiency [34]. One series review reported that patients with the physical examination finding of corona phlebectatica had a fourfold increased risk of an incompetent superficial axial vein or an incompetent perforating vein [39]. There was no correlation between deep venous insufficiency and corona phlebectatica in this study.

Venous ulceration (C5, C6, C6r) — Chronic venous disease is a common cause of lower extremity ulcers [29-32,40]. Patients commonly have superficial reflux, deep venous reflux/obstruction, or perforator reflux, alone or in combination. Risk factors associated with venous ulcer formation include older age, low physical activity, arterial hypertension, lipodermatosclerosis, obesity, and family history of venous ulceration [41-43].

Venous ulcers (C5: healed; C6: active; C6r: recurrent) are usually located low on the medial ankle over a perforating vein or sometimes near on the lateral malleolus, or along the course of the great or small saphenous veins (figure 1A-B); they can occur more proximally on the leg if precipitated by trauma, but never in the forefoot or above the level of the knee. The ulcers may be multiple or single and are exquisitely tender when infected, shallow, exudative, and have a granulation base (picture 13). The ulcer borders are usually irregular but not undermined. They can extend circumferentially around the leg if left untreated [4].

These characteristic findings often allow distinction between venous ulcers and the following types of ulcers that also appear on the lower extremities (table 3):

Arterial ulcers are typically painful and punched out or stellate in appearance. The surrounding skin is red and taut. Some arterial ulcers are pale; others may have a black or yellow eschar. On the leg, they are more often associated with trauma and commonly occur on the foot over pressure points. In addition, the leg and/or foot may display other signs of arterial insufficiency, including thin atrophic and hairless skin, poor or absent pedal pulses, diminished capillary refill, or hypertrophic deformed nails. (See "Clinical features and diagnosis of lower extremity peripheral artery disease", section on 'Nonhealing wound/ulcer'.)

Neuropathic foot ulcers, including diabetic ulcers, most commonly occur at areas of increased pressure at sites of bony prominences, such as over the metatarsal heads. They typically are surrounded by a thick hyperkeratosis, and the ulcer often has undermined borders (picture 14). The extremity and the ulcer are usually insensitive. (See "Evaluation of the diabetic foot".)

Other possible causes of ulcers include rheumatoid arthritis and other connective tissue diseases with associated vasculitis, hemoglobinopathies (eg, sickle cell disease), pyoderma gangrenosum, and tumors, especially squamous cell carcinoma and basal cell carcinoma. It may be necessary to have the ulcer biopsied in order to rule out these uncommon causes of lower extremity ulcers. (See "Approach to the differential diagnosis of leg ulcers".)

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)")

Beyond the Basics topics (see "Patient education: Lower extremity chronic venous disease (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Chronic venous disease – Chronic lower extremity venous disease is the most common vascular disorder encompassing the full spectrum of signs and symptoms as classified by the Clinical-Etiology-Anatomy-Pathophysiology (CEAP) system (C0 to C6) (table 1). Advanced levels of chronic venous disease (ie, C4 to C6) are associated with chronic disability, diminished quality of life, and high health care costs. (See 'Introduction' above.)

Symptoms – Initial clinical presentation is highly variable. The most common symptoms of chronic venous disease are lower extremity heaviness, aching, swelling, itching, discomfort, and pain. Physical findings include abnormal venous dilation (ie, telangiectasias-corona phlebectatica, reticular veins, varicose veins), edema, inflammation, dermatitis, skin changes, and ulceration. Pain associated with venous disease is typically worse at the end of the day than the beginning of the day and when standing or when seated with the feet dependent for prolonged periods of time and improves with limb elevation and walking. (See 'Symptoms' above.)

Clinical signs – The most common clinical sign of lower extremity chronic venous disease is abnormal venous dilation (ie, telangiectasias, reticular veins, varicose veins). The signs of advanced venous disease (CEAP 4 to 6) include lower extremity edema, skin pigmentation, dermatitis/eczema, lipodermatosclerosis, and ulceration.

No clinical signs – Approximately 20 percent of patients with symptoms consistent with venous disease have no visible clinical signs. (See 'No clinical signs (C0)' above.)

Telangiectasias/reticular veins – Telangiectasias are a confluence of dilated intradermal venules/capillaries less than 1 millimeter in diameter and are the most frequently encountered manifestation of venous disease. Reticular veins are dilated, bluish subdermal veins, 1 to 3 millimeters in diameter, and are usually tortuous. (See 'Telangiectasia/reticular veins (C1)' above.)

Varicose veins – Varicose veins are subcutaneous dilated, tortuous veins greater than 3 millimeters in diameter. (See 'Varicose veins (C2)' above.)

Edema – Lower extremity swelling is generally worse with prolonged standing and improves with leg elevation and walking. 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 'Edema (C3)' above.)

Advanced venous disease – Chronic severe edema, skin changes (ie, pigmentation, dermatitis, lipodermatosclerosis), and venous ulceration are signs of advanced venous disease (ie, chronic venous insufficiency), which is associated with superficial and/or deep venous reflux and/or obstruction.

-Skin pigmentation – Pigmentation associated with chronic venous insufficiency is derived from the breakdown of red blood cells that have extravasated through damaged capillaries into the dermis. (See 'Skin pigmentation/dermatitis (C4a)' above.)

-Stasis dermatitis – Stasis dermatitis is an inflammatory process that presents as an eczematous rash. The associated pruritus can be difficult to relieve. The resulting excoriations from scratching can be a source of skin infection, and areas of skin breakdown can develop into ulcers. (See 'Skin pigmentation/dermatitis (C4a)' above.)

-Lipodermatosclerosis – Lipodermatosclerosis is a fibrosing panniculitis of the subcutaneous tissue. Patients with lipodermatosclerosis are particularly prone to repeated bouts of cellulitis. (See 'Lipodermatosclerosis (C4b)' above.)

-Venous ulcers – Venous ulcers are usually located low on the medial or lateral malleolus in the anatomic distribution of the refluxing saphenous veins. Venous ulcers are tender, shallow, exudative, and have a base of granulation tissue; these features usually distinguish venous ulcers from other types of ulcers that occur in the lower extremities. (See 'Venous ulceration (C5, C6, C6r)' above.)

  1. Criqui MH, Jamosmos M, Fronek A, et al. Chronic venous disease in an ethnically diverse population: the San Diego Population Study. Am J Epidemiol 2003; 158:448.
  2. Porter JM, Moneta GL. Reporting standards in venous disease: an update. International Consensus Committee on Chronic Venous Disease. J Vasc Surg 1995; 21:635.
  3. Gloviczki P, Comerota AJ, Dalsing MC, et al. 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; 53:2S.
  4. Bergan JJ, Schmid-Schönbein GW, Smith PD, et al. Chronic venous disease. N Engl J Med 2006; 355:488.
  5. Chiesa R, Marone EM, Limoni C, et al. Effect of chronic venous insufficiency on activities of daily living and quality of life: correlation of demographic factors with duplex ultrasonography findings. Angiology 2007; 58:440.
  6. Tsai S, Dubovoy A, Wainess R, et al. Severe chronic venous insufficiency: magnitude of the problem and consequences. Ann Vasc Surg 2005; 19:705.
  7. Kaplan RM, Criqui MH, Denenberg JO, et al. Quality of life in patients with chronic venous disease: San Diego population study. J Vasc Surg 2003; 37:1047.
  8. Duque MI, Yosipovitch G, Chan YH, et al. Itch, pain, and burning sensation are common symptoms in mild to moderate chronic venous insufficiency with an impact on quality of life. J Am Acad Dermatol 2005; 53:504.
  9. Langer RD, Ho E, Denenberg JO, et al. Relationships between symptoms and venous disease: the San Diego population study. Arch Intern Med 2005; 165:1420.
  10. Chiesa R, Marone EM, Limoni C, et al. Chronic venous disorders: correlation between visible signs, symptoms, and presence of functional disease. J Vasc Surg 2007; 46:322.
  11. Asbeutah AM, Asfar SK, Shawa NJ, et al. Is venous reflux a common disease in post-thrombotic patients with unilateral deep vein thrombosis episode? Phlebology 2007; 22:8.
  12. Yamaki T, Nozaki M. Patterns of venous insufficiency after an acute deep vein thrombosis. J Am Coll Surg 2005; 201:231.
  13. Labropoulos N, Waggoner T, Sammis W, et al. The effect of venous thrombus location and extent on the development of post-thrombotic signs and symptoms. J Vasc Surg 2008; 48:407.
  14. Sprague AH, Khalil RA. Inflammatory cytokines in vascular dysfunction and vascular disease. Biochem Pharmacol 2009; 78:539.
  15. Scott TE, Mendez MV, LaMorte WW, et al. Are varicose veins a marker for susceptibility to coronary heart disease in men? Results from the Normative Aging Study. Ann Vasc Surg 2004; 18:459.
  16. Mäkivaara LA, Ahti TM, Luukkaala T, et al. Persons with varicose veins have a high subsequent incidence of arterial disease: a population-based study in Tampere, Finland. Angiology 2007; 58:704.
  17. Kurz X, Lamping DL, Kahn SR, et al. Do varicose veins affect quality of life? Results of an international population-based study. J Vasc Surg 2001; 34:641.
  18. Palfreyman S. Assessing the impact of venous ulceration on quality of life. Nurs Times 2008; 104:34.
  19. Hareendran A, Bradbury A, Budd J, et al. Measuring the impact of venous leg ulcers on quality of life. J Wound Care 2005; 14:53.
  20. van Korlaar I, Vossen C, Rosendaal F, et al. Quality of life in venous disease. Thromb Haemost 2003; 90:27.
  21. Almeida JI, Kaufman J, Göckeritz O, et al. Radiofrequency endovenous ClosureFAST versus laser ablation for the treatment of great saphenous reflux: a multicenter, single-blinded, randomized study (RECOVERY study). J Vasc Interv Radiol 2009; 20:752.
  22. Kahn SR, Hirsch A, Shrier I. Effect of postthrombotic syndrome on health-related quality of life after deep venous thrombosis. Arch Intern Med 2002; 162:1144.
  23. Renner R, Gebhardt C, Simon JC, Seikowski K. Changes in quality of life for patients with chronic venous insufficiency, present or healed leg ulcers. J Dtsch Dermatol Ges 2009; 7:953.
  24. Wrona M, Jöckel KH, Pannier F, et al. Association of Venous Disorders with Leg Symptoms: Results from the Bonn Vein Study 1. Eur J Vasc Endovasc Surg 2015; 50:360.
  25. Van der Velden SK, Shadid NH, Nelemans PJ, Sommer A. How specific are venous symptoms for diagnosis of chronic venous disease? Phlebology 2014; 29:580.
  26. Newland MR, Patel AR, Prieto L, et al. Neuropathy and gait disturbances in patients with venous disease: a pilot study. Arch Dermatol 2009; 145:485.
  27. Padberg FT Jr, Maniker AH, Carmel G, et al. Sensory impairment: a feature of chronic venous insufficiency. J Vasc Surg 1999; 30:836.
  28. Shiman MI, Pieper B, Templin TN, et al. Venous ulcers: A reappraisal analyzing the effects of neuropathy, muscle involvement, and range of motion upon gait and calf muscle function. Wound Repair Regen 2009; 17:147.
  29. Abbade LP, Lastória S, Rollo Hde A. Venous ulcer: clinical characteristics and risk factors. Int J Dermatol 2011; 50:405.
  30. Moffatt CJ, Franks PJ, Doherty DC, et al. Prevalence of leg ulceration in a London population. QJM 2004; 97:431.
  31. Margolis DJ, Bilker W, Santanna J, Baumgarten M. Venous leg ulcer: incidence and prevalence in the elderly. J Am Acad Dermatol 2002; 46:381.
  32. O'Brien JF, Grace PA, Perry IJ, Burke PE. Prevalence and aetiology of leg ulcers in Ireland. Ir J Med Sci 2000; 169:110.
  33. Wittens C, Davies AH, Bækgaard N, et al. Editor's Choice - Management of Chronic Venous Disease: Clinical Practice Guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg 2015; 49:678.
  34. Lurie F, Passman M, Meisner M, et al. The 2020 update of the CEAP classification system and reporting standards. J Vasc Surg Venous Lymphat Disord 2020; 8:342.
  35. Zenilman J, Valle MF, Malas MB, et al. Chronic Venous Ulcers: A Comparative Effectiveness Review of Treatment Modalities. Report No: 13(14)-EHC121-EF, Agency for Healthcare Research and Quality (US); Rockland, MD 2013.
  36. Coon WW, Willis PW 3rd, Keller JB. Venous thromboembolism and other venous disease in the Tecumseh community health study. Circulation 1973; 48:839.
  37. Miteva M, Romanelli P, Kirsner RS. Lipodermatosclerosis. Dermatol Ther 2010; 23:375.
  38. Walsh SN, Santa Cruz DJ. Lipodermatosclerosis: a clinicopathological study of 25 cases. J Am Acad Dermatol 2010; 62:1005.
  39. Uhl JF, Cornu-Thénard A, Carpentier PH, et al. Clinical and hemodynamic significance of corona phlebectatica in chronic venous disorders. J Vasc Surg 2005; 42:1163.
  40. Forssgren A, Nelzén O. Changes in the aetiological spectrum of leg ulcers after a broad-scale intervention in a defined geographical population in Sweden. Eur J Vasc Endovasc Surg 2012; 44:498.
  41. Meulendijks AM, de Vries FMC, van Dooren AA, et al. A systematic review on risk factors in developing a first-time Venous Leg Ulcer. J Eur Acad Dermatol Venereol 2019; 33:1241.
  42. Vivas A, Lev-Tov H, Kirsner RS. Venous Leg Ulcers. Ann Intern Med 2016; 165:ITC17.
  43. Mervis JS, Kirsner RS, Lev-Tov H. Protocol for a longitudinal cohort study: determination of risk factors for the development of first venous leg ulcer in people with chronic venous insufficiency, the VEINS (venous insufficiency in South Florida) cohort. BMJ Open 2019; 9:e023313.
Topic 8198 Version 23.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟