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Classification of lower extremity chronic venous disorders

Classification of lower extremity chronic venous disorders
Literature review current through: Jan 2024.
This topic last updated: May 08, 2023.

INTRODUCTION — Lower extremity chronic venous disorders encompass a large spectrum of morphologic and functional abnormalities of the venous system. They can present in childhood as congenital lesions or acquired disorders that by adulthood are quite common. Vein-related anatomic and physiologic abnormalities may or may not be symptomatic and include and/or result in a wide range of clinical signs varying from minimal dilation of superficial veins to massive varicosities, edema, chronic skin changes including discoloration or ulceration, or bleeding from varicosities or high pressure telangiectasias. Patient symptoms can also be highly variable, including pain, itching, burning, positional discomfort, and even "venous claudication." Together, the physical manifestations and symptoms of chronic venous disease have major impacts on patient quality of life [1].

The Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification, which is an internationally recognized and the most widely used classification system for chronic venous disease, is reviewed. An overview of the clinical evaluation and management of lower extremity chronic venous disease is presented elsewhere. (See "Overview of lower extremity chronic venous disease".)

TERMINOLOGY — Standard definitions for venous diagnosis have been adopted by international consensus [2].

Chronic venous disorders — This term includes the full spectrum of morphological and functional abnormalities of the venous system.

Chronic venous disease — The term chronic venous disease is used when morphological or functional abnormalities (venous valvular incompetence and/or venous obstruction) are present of long duration and manifested as symptoms and/or signs indicating the need for treatment and/or further investigation. Overall adverse physiologic effects of venous valvular incompetence and/or obstruction may be identified by air plethysmography, photoplethysmography, or ambulatory venous pressure measurements. However, specific sites of venous valvular incompetence are most commonly identified by duplex ultrasound as retrograde venous flow of abnormal duration. Duplex ultrasound; computed tomographic, magnetic resonance, or catheter-based contrast venography; or intravascular ultrasound are used to identify specific sites of venous obstruction. (See "Diagnostic evaluation of lower extremity chronic venous disease" and "Overview of iliocaval venous obstruction", section on 'Diagnosis'.)

Symptoms may include but are not limited to lower extremity tingling, burning, aching, pain, tightness, skin irritation, itching, heaviness, swelling, fatigue, or muscle cramps.

Venous signs include dilated veins (eg, telangiectasia, varicose veins), leg/ankle edema, skin changes, or ulceration.

The severity of both symptoms and signs of venous disease tends to correlate with the degree of underlying venous valvular dysfunction or venous obstruction. However, minimal visible evidence of venous disease may be associated with venous valvular incompetence. Symptoms of limb aching, heaviness, and swelling can all be of venous origin even when not associated with visible or palpable varicose veins (picture 2B) [3]. (See "Pathophysiology of chronic venous disease".)

Chronic venous insufficiency — The term chronic venous insufficiency is generally used to describe patients with chronic venous disease who display more advanced clinical signs, such as significant edema, skin changes, or ulceration (picture 1A-B). (See "Diagnostic evaluation of lower extremity chronic venous disease".)

CEAP CLASSIFICATION — An international consensus conference initiated the Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification to categorize chronic venous disorders to facilitate communication between practitioners and serve as a basis for standardized reporting during scientific analysis of management alternatives (table 1). The CEAP classification was developed in 1993 and widely adopted. It was updated in 1996, revised in 2004, and updated and refined again in 2020 by an ad hoc committee of the American Venous Forum to better reflect evolving understanding of the natural history of venous disease and evolving methods of diagnosis and treatment of venous disease [2,4-8].

It is very important to remember that CEAP is a classification system, not a measure of disease severity. CEAP should not be used as a measure of the clinical severity of venous disease and is not meant to be used to measure the response to therapy. As categorical variables, components of CEAP cannot be reported as means or medians; rather, changes in CEAP in a study group or in individual limbs over time or following therapy are best reported as the distribution of CEAP classes over time for study groups or as pre- and post-therapy values for individual limbs. Measures of clinical severity are described below. (See 'Measures of clinical severity' below.)

Clinical signs (The "C" component of CEAP) — The clinical spectrum of chronic venous disorders is wide. Some individuals with minimally dilated veins (picture 2A) or even varicosities do not have significant complaints and may not find the appearance of their veins concerning (picture 3A). Others find even the smallest dilated veins cosmetically troublesome even in the absence of symptoms. (See "Clinical manifestations of lower extremity chronic venous disease".)

The visible signs of chronic venous disorders are categorized as C0 to C6 depending on appearance. Additionally, patients are classified as asymptomatic (a) or symptomatic (s) depending on the presence of lower extremity symptoms such as aching, pain, tightness, skin irritation, heaviness, or muscle cramps. (See "Clinical manifestations of lower extremity chronic venous disease".)

No visible or palpable signs of venous disease (C0) — In the absence of symptoms, patients without significant visible evidence of venous disease are unlikely to have venous pathology [3]. However, C0 patients may be symptomatic; venous obstruction and/or reflux may be identified with venous diagnostic testing.

Telangiectasias/reticular veins (C1) — Telangiectasias are a confluence of dilated intradermal venules <1 mm in diameter (picture 2A-B). Synonyms include spider veins, hyphen webs, and thread veins. Telangiectatic matting consists of typically fine, red vessels (<0.2 mm) that can develop following any venous treatment (eg, laser therapy, surgical stripping, sclerotherapy).

Reticular veins are dilated bluish subdermal veins 1 to 3 mm in diameter (picture 2A-B). They are usually tortuous. Excluded are normal visible veins in persons with thin, transparent skin. Synonyms include blue veins and subdermal varices.

Varicose veins (C2, C2r) — Varicose veins are subcutaneous dilated veins 3 mm or greater in size (picture 3A-B). They may involve the great or small saphenous veins, saphenous vein tributaries, or nonsaphenous superficial leg veins. Synonyms include varix, varices, and varicosities. Recurrent varicose veins (C2r) are those that occur following intervention and were not present preintervention.

Edema (C3) — The edema associated with chronic venous disease is due to an increase in the volume of fluid in the skin and subcutaneous tissues and will indent when pressure is applied (picture 2B). Lower extremity swelling due to lymphedema is often confused with that due to venous origin. Edema only related to the presence of venous disease usually occurs at the ankle and may extend to the leg but less commonly extends to the foot and toes, distinguishing it from lymphedema. In addition, edema due to venous disease alone generally resolves or greatly improves overnight when the patient sleeps (elevated legs), while lymphedema is more recalcitrant and generally persists and is still present in the morning. Phlebolymphedema is perhaps the most common form of lymphedema in Western societies and results from anatomic and physiologic changes in the lymphatic system arising secondary to advanced forms of chronic venous disease that lead to lymphatic overload [9]. The evaluation and management of lymphedema is discussed separately. (See "Lower extremity lymphedema" and "Clinical features and diagnosis of peripheral lymphedema", section on 'Clinical features' and "Clinical staging and conservative management of peripheral lymphedema".)

Pigmentation or eczema (C4a) — Pigmentation related to venous disease is a characteristic brownish darkening of the skin due to hemosiderin deposition as a consequence of extravasated red blood cells (picture 1A). It usually occurs in the ankle region but may extend to the more proximal leg or to the foot.

Eczema is an erythematous dermatitis, which may progress to blistering, weeping, or scaling eruption of skin of the leg (picture 4). It is often located near varicose veins, but the presence of varicosities is not required for eczema of venous origin, and venous eczema may be located anywhere on the leg below the knee.

Lipodermatosclerosis (C4b) — Lipodermatosclerosis is localized chronic inflammation and fibrosis of the skin and subcutaneous tissues of the lower leg (picture 5), sometimes associated with scarring or contracture of the Achilles tendon (picture 6). It is sometimes preceded by diffuse inflammatory edema of the skin, which may be painful and which is often referred to as hypodermatitis. The differential diagnosis includes lymphangitis, erysipelas, or cellulitis.

Atrophie blanche (white atrophy) is a localized, circular, or stellate ivory-colored depressed region of abnormal skin surrounded by dilated capillaries and sometimes hyperpigmentation (picture 7). It is prone to ulceration and a sign of severe chronic venous disease that arises spontaneously and must not be confused with a healed ulcer scar (patient history of ulceration is often lacking).

Corona phlebectatica (C4c) — Corona phlebectatica is described as a circular or fan-shaped collection, a "crown," of nonpalpable, small intradermal veins in the regions of the medial or lateral ankles, sometimes extending distally onto the foot (picture 8). It is considered by many to be an early sign of more advanced underlying venous disease and is associated with an increased risk of venous ulcer [10]. Synonyms include ankle flare or malleolar flare.

Healed venous ulcer (C5) — Healed venous ulcerations may also exhibit atrophic skin with pigmentary changes (picture 1A). Healed venous ulcers are distinguishable by appearance and history of ulceration from atrophie blanche.

Active or recurrent venous ulcer (C6, C6r) — Active venous ulcers (C6) are full-thickness defects of the skin, most frequently in the ankle region, but they can extend more proximally, and even circumferentially around the distal to mid-calf. They generally will not heal spontaneously, but they can usually be healed with proper therapy and wound care (picture 1B). Recurrent venous ulcer (C6r) is an ulcer that occurs after a period of complete ulcer healing.

Etiology (The "E" component of CEAP) — From an etiologic viewpoint, venous disorders are considered to be one of the following:

Primary (Ep) — Primary venous disorders develop independently of other diseases. They account for the majority of cases of chronic venous insufficiency and are usually due to degeneration of venous valves or the vein wall leading to valvular reflux involving the great or small saphenous veins or their branches.

Secondary (Es, Esi, Ese) — Secondary venous disorders develop as a consequence of another pathology, such as following venous thrombosis or trauma. (See "Post-thrombotic (postphlebitic) syndrome".)

Intravenous causes of venous disease (Esi) include venous wall and/or vein valve damage resulting from conditions that include deep vein thrombosis (DVT; especially recurrent DVT), traumatic arteriovenous fistulas, and primary intravenous sarcoma.

Extravenous causes of venous disease (Ese), have no venous wall or valve damage. Symptoms are present owing to alterations in venous hemodynamics either locally or systemically, including conditions such as central venous hypertension (eg, heart failure, obesity, nutcracker syndrome, pelvic venous congestion), extrinsic compression, or muscle pump dysfunction from chronic motor disorders (eg, paraplegia, arthritis, chronic immobility). Chronic external compression of an iliac vein, most commonly the left common iliac vein by the right common iliac artery (ie, May Thurner syndrome), is also recognized as a source of chronic venous insufficiency [11].

Congenital (Ec) — Congenital venous disorders present at birth or noted to develop in childhood (eg, Klippel-Trenaunay syndrome). (See "Vascular lesions in the newborn" and "Venous malformations" and "Arteriovenous malformations of the extremities" and "Overview of vascular intervention and surgery for vascular anomalies".)

No cause identified (En) — In clinical studies, if an origin of venous disease is not identified, En is assigned.

Combined etiologies — Both primary and secondary etiologies can be present. As an example, a limb may have primary varicose veins and then develop more varicosities or edema after a deep venous thrombosis and thus be classified as Epsi.

Anatomy (The "A" component of CEAP) — The axial veins of the venous system of the lower extremity are divided into the superficial and deep systems. Veins that traverse between the same system (superficial to superficial or deep to deep) are termed communicating veins, whereas veins that connect the superficial to the deep system are called perforating veins. The nomenclature of the venous anatomy of the lower extremity is standardized to eliminate confusing terminology [5,6]. Eighteen named venous segments are used as locators of pathology and classified anatomically as superficial veins (As), deep veins (Ad), perforating veins (Ap), or venous location not specified (An) (table 2).

Superficial venous system (As) — The superficial veins are contained in the subcutaneous tissue of the lower extremity within a superficial space that is bounded deeply by the muscular fascia and superficially by the dermis. The major axial superficial veins of the lower extremity include the great and small saphenous veins. Other lower extremity superficial veins with more variant anatomy include the anterior, posterior, and superficial accessories of the great saphenous vein (GSV); the superficial accessory of the small saphenous vein (SSV); intersaphenous veins (communicating veins between the great and small saphenous veins); and the lateral venous system.

The GSV is one of the axial superficial veins in the lower extremity (figure 1A-B). It is the longest vein in the body, originating from the dorsal venous network of the foot and crossing anterior to the medial malleolus and coursing cephalad and medially in the lower leg and thigh to the saphenofemoral junction in the groin (figure 1A). It can vary in diameter along its course, and is generally, but not always, contained within a fascial layer. Just below the inguinal ligament, it enters the fossa ovalis and terminates in the common femoral vein at the confluence of the superficial inguinal veins at the saphenofemoral junction, the anatomy of which can be quite variable (figure 2) [12]. The GSV also drains into the deep venous system through both calf and thigh perforating veins.

The SSV is another of the axial superficial veins, and it originates laterally from the dorsal venous arch of the foot, crosses posterior to the lateral malleolus, and ascends posteriorly along the midline of the calf overlying the fascia between the heads of the gastrocnemius muscle (figure 1B). In the upper calf, the SSV passes through the deep muscle fascia and terminates in the popliteal vein at the saphenopopliteal junction, which also has highly variable anatomy (figure 3) [13-16]. The SSV can join a superficial cephalad extension in the posterior thigh (vein of Giacomini), connect to both the popliteal vein and the posterior thigh vein, or join the popliteal vein with no major tributaries near the junction. Anatomic variations in the SSV have implications for SSV ablation [16].

The accessory saphenous veins (ASVs) are any of several venous segments that ascend parallel to the GSV. Anterior ASVs are located anteriorly and can be found anteriorly on the lower extremity (figure 1A-B) [5]. The ASVs can become more prominent after saphenous ablation procedures and are a potential source of recurrent and primary varicose veins.

Deep venous system (Ad) — The deep veins of the lower extremity are contained within the deep muscle compartments bounded by the muscle fascia (figure 4). The deep veins of the lower extremity are classified as intramuscular (within the muscle) or intermuscular (between muscle groups). The intermuscular veins are more important in the development of chronic venous disease [7].

Leg – The intermuscular veins of the leg include the popliteal veins and crural veins (paired anterior tibial, posterior tibial, and peroneal veins) (figure 4). The intramuscular veins include the gastrocnemius and soleal sinus veins.

The three paired crural veins are named after the artery they accompany. The posterior tibial veins originate from the medial foot at the medial malleolus, the anterior tibial veins from the dorsum of the foot, and the peroneal veins from venous collaterals originating between the distal tibia and fibula. The popliteal vein originates in the popliteal space as the confluence of the crural veins. The popliteal vein transitions to be renamed the femoral vein at the level of the adductor canal in the thigh. Duplication of the femoral vein in the thigh is a well-recognized anatomic variant. The popliteal vein may also be duplicated.

Thigh – The intermuscular veins of the thigh include the femoral vein, deep femoral vein, and common femoral vein. The femoral vein is joined just below the saphenofemoral junction by the deep femoral vein to form the common femoral vein (figure 4).

Pelvis – The pelvic veins draining blood away from the lower extremities can, when narrowed or thrombosed, contribute significantly to the development of chronic venous disease. The main collecting veins of the pelvis include the external iliac veins, internal iliac veins, and common iliac veins.

After passing beneath the inguinal ligament, the common femoral vein becomes the external iliac vein, which is joined by the internal iliac vein to form the common iliac vein. The right and left common iliac veins merge at the level of the umbilicus to form the inferior vena cava. Because the inferior vena cava is usually located to the right of the spine, the left common iliac vein is longer with a less vertical path to the vena cava (figure 4). The left common iliac vein is crossed anteriorly by the right common iliac artery, and this results in variable degrees of compression of the left common iliac vein by the right common iliac artery. When associated with left lower extremity edema or iliac vein thrombosis, this is referred to as May-Thurner syndrome.

Perforator veins (Ap) — Perforating veins are those veins that traverse the muscular fascia to connect superficial veins with deep veins. They are located anteriorly, posteriorly, laterally, and medially in both the thigh and calf.

The normal flow in the perforating veins is from superficial to deep; however, many perforators demonstrate bidirectional flow. When the perforating veins are incompetent, flow is from deep to superficial. The most clinically significant perforating veins connect the posterior arch vein to the posterior tibial vein and are termed posterior tibial perforators (formerly known as Cockett perforators).

When needed, the specific region of anatomic involvement of the superficial or deep veins can be localized. Specific anatomic involvement is shown under the pathophysiologic class (P) that corresponds with the identified vein segment [4].

No venous anatomic location identified — In clinical studies, if an anatomic location is not identified, An is assigned.

Pathophysiology (The "P" component of CEAP) — The pathophysiologic element of the CEAP classification designates the presence or absence of venous reflux and/or obstruction.

In the upright position, the effects of gravity must be overcome for blood from the lower extremities to return to the heart. The venous valves and "venous pump" (effect of leg muscle contraction on venous flow) are the two major determinants of lower extremity venous flow when subjects are upright [8]. Blood is directed from the superficial system (draining the skin and subcutaneous tissues) to the deep venous system by muscular contractions and prevented from flowing retrograde, refluxing, by passive closure of one-way venous valves.

Specific anatomic location(s) are to be reported under each pathophysiologic (P) class to identify anatomic location(s) corresponding to the P class.

Venous reflux (Pr) — Congenital valvular abnormalities or damage to the vein valves from trauma or prior venous thrombosis may result in varying degrees of retrograde flow (abnormal is defined as >0.5 seconds of reverse flow detected by duplex scanning) in the venous system and is termed reflux. Reflux may be present in isolated segments or throughout the entire course of the superficial and/or deep venous systems. Deep venous reflux is generally associated with the most severe clinical symptoms and signs, but ulceration is also possible with superficial venous reflux alone. Superficial venous reflux is associated with more chronic venous ulcers compared with deep venous reflux [3]. (See "Pathophysiology of chronic venous disease" and "Diagnostic evaluation of lower extremity chronic venous disease".)

Venous obstruction (Po) — Superficial or deep venous thrombosis causes obstruction and impedes flow in the venous system. Superficial veins become more prominent as venous return is rerouted around a venous obstruction. Over time, an acute thrombus within a vein may degrade and be totally or partially resorbed; however, the vein segment and its valves may become permanently damaged, resulting in a combination of obstruction and reflux. (See "Post-thrombotic (postphlebitic) syndrome" and "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)

Venous reflux and obstruction (Pr,o) — When both reflux and obstruction are identified, (Pr,o) is designated.

No venous pathophysiology identifiable — When neither reflux nor obstruction is identified, or in clinical studies, if the presence of reflux or obstruction is not identified, Pn is assigned.

MEASURES OF CLINICAL SEVERITY — Measures of clinical severity are important tools that help to objectively follow patient response to clinical management. These measures are also useful for clinical research to define patient populations, quantify outcomes, and compare different management strategies [17]. Both disease-specific measures (see below) of venous disease clinical severity and generic quality-of-life (QoL) instruments, such as the Short Form 36 (SF-36), Nottingham Health Profile, or Euro QoL, are useful in describing the impact of venous disease on the individual patient. It is recognized that higher levels of physical activity help improve clinical symptoms (eg, fatigue) and QoL associated with chronic venous disease [18].

Venous clinical severity score — The venous clinical severity score (VCSS) is a disease-specific instrument that is complementary to the CEAP classification [19,20]. It has both physician-determined and patient-reported elements. Ten clinical parameters (pain, varicose veins, venous edema, pigmentation, inflammation, induration, number of active ulcers, duration of active ulcers, size of active ulcers, and compliance with compression therapy) are graded from zero to three depending upon severity (None = 0, Mild = 1, Moderate = 2, Severe = 3) (calculator 1).

Venous disability score — The venous disability score (VDS) quantifies physical limitations due to chronic venous disease. Patients are considered [20]:

Score = 0; asymptomatic

Score = 1; symptomatic, but able to carry out usual activities without compression therapy

Score = 2; symptomatic, able to carry out usual activities only with compression therapy or limb elevation

Score = 3; symptomatic, but unable to carry out usual activities even with compression therapy or limb elevation

Venous segmental disease score (VSDS) — VSDS combines the anatomic and physiologic components of CEAP [20]. Major venous segments are evaluated for the presence of reflux and/or obstruction. The relative importance of each anatomic segment is weighted, with a maximum score of 20, 10 for reflux (calculator 2) and 10 for obstruction (calculator 3).

Villalta scale — The Villalta scale is a validated clinical measure for post-thrombotic syndrome (PTS) that includes both patient symptoms and physician-observed signs of chronic venous disease.

Points are awarded for six physician-observed clinical signs (skin induration, pretibial edema, redness, hyperpigmentation, pain with calf compression, and venous ectasia) and five patient symptoms (itching, paresthesia, pain, cramps, and heaviness) with each valued from 0 (not present) to 3 (severe). A patient is considered to have PTS if a venous ulcer is present or the score is >5 (calculator 4). Mild PTS is signified by scores of 5 to 9 and moderate disease by a score of 10 to 14, with a score >15 indicating severe PTS. The Villalta score may help in identifying and treating patients earlier in the course of developing the syndrome [21,22]. While the Villalta score has been used as an outcome measure in major clinical trials of venous disease [23], the ability of the Villalta scale to detect meaningful differences between groups, as well as its ability to distinguish chronic underlying primary venous disease from post-thrombotic syndrome, has been questioned [24].

The symptoms and signs associated with PTS are the same as in other chronic venous diseases; however, following acute deep venous thrombosis, these symptoms and signs develop over a shorter interval [25]. (See "Post-thrombotic (postphlebitic) syndrome".)

DISEASE-SPECIFIC QUALITY-OF-LIFE MEASURES

Aberdeen varicose vein questionnaire — The Aberdeen varicose vein questionnaire (AVVQ) is a validated scoring system for patients with varicose veins as their primary manifestation of chronic venous disease [26]. It is used as a disease-specific quality of life (QoL) outcome measure in trials of therapy for varicose veins. The patient is asked to draw their varicose veins on a manikin diagram and is also asked 12 questions that include appearance, life impact, skin changes, pain, and use of compression stockings. AVVQ scores may range from 0 (no impact on QoL) to 100 (worst possible QoL), with the manikin diagram contributing up to 22 points of the total AVVQ score. It reflects primarily clinical disease severity, as its focus is clinical symptoms and signs. Difficulty with the manikin diagram and the need for a paper questionnaire rather than an electronic format have led to proposals to modify the AVVQ [27].

Chronic Venous Insufficiency Quality of Life Questionnaire — The Chronic Venous Insufficiency Quality of Life Questionnaire (CIVIQ-20) is another disease-specific, health-related, QoL tool. It differs from the AVVQ in that it focuses more on the psychosocial, everyday impact of lower extremity venous disease. There are 20 questions in four domains (physical, psychological, social impairment and pain level). Each question has a five-point response range, with higher values indicating more impairment. Individual, dimensional, and global scores can be reported with a lower QoL due to varicose veins or chronic venous disease reflected in higher scores [28].

Other less commonly used, condition-specific instruments for assessing QoL in patients with chronic venous disease include the Widmer score, Ginsberg score, Brandjes score, the health questionnaire for leg ulcers, and the Charing Cross venous ulcer questionnaire, among others [29,30].

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".)

SUMMARY AND RECOMMENDATIONS

Classification of venous disease – Lower extremity chronic venous disorders encompass a spectrum of morphologic and functional abnormalities of the venous system. Several classification systems are used to categorize chronic venous disease with the Clinical-Etiology-Anatomy-Pathophysiology (CEAP) system (table 1), developed by international consensus, the most widely used to classify lower extremity venous disease based upon clinical signs, etiology, anatomic location, and pathophysiologic abnormality (table 1). (See 'CEAP classification' above.)

Severity of venous disease – Different instruments are available to determine disease severity and the impact of venous disease on health-related quality of life (QoL) for the purpose of providing an accurate record of the patient's disease status, facilitating communication between practitioners, and serving as a basis for standardized reporting. Both generic and disease-specific QoL instruments can be used to quantify effects of chronic venous disease on QoL.

Measures of lower extremity venous clinical severity and QoL should be used to augment the CEAP criteria by assigning point values to various clinical, anatomic, activity, and lifestyle-related parameters. Higher scores indicate more severe debilitation due to chronic venous disease. (See 'Measures of clinical severity' above and 'Disease-specific quality-of-life measures' above.)

The Villalta scale is a clinical scale used to help identify patients who have developed post-thrombotic syndrome following lower extremity deep vein thrombosis and to grade the severity of the post-thrombotic syndrome. (See 'Villalta scale' above.)

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Topic 8177 Version 30.0

References

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