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J Chest Surg 2024; 57(2): 109-119
Published online March 5, 2024 https://doi.org/10.5090/jcs.23.110
Copyright © Journal of Chest Surgery.
Jae Ho Chung , M.D., Ph.D., Seonyeong Heo , M.D.
Department of Thoracic and Cardiovascular Surgery, Korea University College of Medicine, Seoul, Korea
Correspondence to:Jae Ho Chung
Tel 82-2-920-5369
Fax 82-2-928-8793
E-mail bozof@hanmail.net
ORCID
https://orcid.org/0000-0002-4203-4933
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Varicose veins usually present in the superficial veins of the lower extremities and are one of the main clinical presentations of chronic venous disease (CVD). Patients’ symptoms may vary according to the pathophysiology, location, and severity of CVD. The prevalence of CVD in Korea has been increasing gradually. However, due to its broad clinical spectrum and the subjective nature of its diagnosis using ultrasound, discrepancies in diagnostic and treatment quality may exist among treating physicians. There have been recent efforts to improve the quality of the diagnosis and treatment of varicose veins in Korea by standardizing the diagnostic criteria and the indications for treatment. This study is a comprehensive review of the clinical manifestations and diagnostic criteria of CVD based on the most recent international and domestic guidelines and reports.
Keywords: Chronic venous disease, Varicose veins, Lower extremity, Diagnosis, Ultrasonography
Varicose veins are dilated, palpable, tortuous veins, that are generally larger than 3 mm and usually present in the superficial veins of the lower extremities [1]. They are one of the main clinical presentations of chronic venous disease (CVD), which has a broad clinical spectrum ranging from reticular veins, telangiectasias, varicose veins, edema, skin pigmentation, lipodermatosclerosis, and atrophie blanche, to venous ulceration [2,3]. Patients’ symptoms may vary, from asymptomatic cosmetic problems to severely painful symptoms with complications. Severe symptoms such as venous ulceration may negatively impact a patient’s capacity to participate in occupational and social activities, resulting in poor quality of life and economic deterioration [3].
The global prevalence of varicose veins varies widely, with reports ranging from 1% to 73% of women and 2% to 56% of men [4]. The number of patients who receive medical treatment for varicose veins in Korea has increased 5.4% every year according to recent reports from the National Health Insurance Corporation. The prevalence of CVD may differ according to risk factors such as geographic location, advanced age, female sex, obesity, family history, hypertension, a standing occupation, lifestyle, and smoking [4]. According to previous population-based studies, the prevalence of varicose veins increases with age. Aging usually contributes to the deterioration of vessel walls and venous valves, as well as the weakening of calf muscles, which are known to affect prolonged venous hypertension. Female sex is also a known risk factor, although it is unclear whether this is related to other factors such as pregnancy, hormones, or environment. Ethnicity is also related to the prevalence of CVD, with a lower prevalence among Asians than among non-Hispanic whites [5].
When combined, the complex pathophysiology of multifactorial CVD, the subjectivity of ultrasonography in the diagnostic process, and the wide variety of treatment modalities may result in diagnostic and treatment variations among physicians. Furthermore, a variety of guidelines have been provided by related academic groups.
As noted above, the prevalence of CVD in Korea has been increasing gradually, and recent efforts have been made to improve the quality of the diagnosis and treatment of varicose veins in Korea by standardizing the diagnostic criteria and indications for treatment.
In November 2021 the Korean Society for Phlebology created an ethics declaration to celebrate the 20th anniversary of its founding. They also updated their clinical practice guidelines for varicose veins, based on evidence they had accumulated over 8 years. This year, in collaboration with 5 other academic societies including the Korean Society for Vascular Surgery, the Korean Society for Thoracic and Cardiovascular Surgery, the Korean Surgical Society, the Korean Surgical Ultrasound Society, and the Korean Society of Interventional Radiology, they presented “Evidence-based guideline for the use of ultrasonography in the diagnosis and assessment of Varicose veins,” a guideline for the use of ultrasonography to diagnose and assess varicose veins.
This study is a comprehensive review of the clinical manifestations and diagnostic criteria of CVD, based on the most recent international and domestic guidelines and reported studies.
Patients with CVD of the lower extremities may present with many different clinical features. Depending on location and severity, patients may complain of leg discomfort such as heaviness, tired legs, swelling, itching of the skin, nocturnal cramps, throbbing, burning pain, and aching. In many circumstances, these symptoms may be nonspecific and difficult to differentiate from other non-venous etiologies. The symptoms do not always correlate with the presence or degree of venous hypertension. The heterogeneity of symptoms, even between the same clinical, etiological, anatomical, and pathophysiological (CEAP) classes, also makes the diagnosis difficult. Visible varicose veins, which are dilated, bulging, tortuous, superficial veins with a diameter larger than 3 mm, are not always the reason for the patient’s symptoms. Approximately 75% of the adult population has visible veins (spider veins or tributary veins) without any sign of chronic venous insufficiency [6]. Therefore, care must be taken when diagnosing CVD, and the possibility of other non-venous etiologies must be considered.
Leg discomfort or pain, one of the most common symptoms of CVD, is absent in approximately 20% of CVD patients, whereas it is the only clinical feature in approximately 10% of patients [2]. Specifically, venous leg discomfort is frequently related to prolonged standing and is relieved by elevation of the leg, walking, or compression stockings.
The differential diagnosis for leg pain includes neurologic or orthopedic pain, arterial pain, lipedema, arthrogenic pain, and muscular pain. Neurologic or orthopedic pain is primarily related to the lumbar spine or sacroiliac joints and is usually associated with radiation down the leg, tingling or paresthesia, and numbness. It may be aggravated when lying down or sitting in a comfortable chair. Arterial pain is mostly caused by peripheral arterial occlusive disease and is exacerbated by activity and improved with rest. Arthrogenic pain is usually localized to the joint and may be related to a ruptured Baker’s cyst. Muscular pain usually presents with tenderness or pain on moving the affected muscle. In contrast, venous leg pain may be the result of superficial vein thrombosis (phlebitis), deep vein thrombosis, tension pain due to edema, inflammatory changes in hyperpigmentation, venous ulcers, and enlargement of varicose veins [7].
Leg edema is another common feature of CVD. Patients may complain of heaviness, tired legs, or a sensation of swelling. Leg edema related to varicose veins represents stage C3 and is most pronounced in the leg with the varicose veins. In the CEAP classification, the C3 category is broad and does not explain subcategories of edema. It does not quantify the degree or extent of the edema or recognize other causes of leg edema. For example, transitory ankle edema at the end of the day likely has a different pathophysiology and natural history than severe permanent edema. Venous edema may be unilateral or bilateral, may show an acute or a gradual onset over the years, and may be accompanied by tension pain. Venous leg edema is usually relieved by the application of compression stockings, and is aggravated by prolonged standing. However, like other symptoms, leg edema may often be due to other problems. Deep vein thrombosis, another vein related disease, usually occurs abruptly with unilateral swelling accompanied by pain, a feeling of tension, and bluish discoloration. The Wells score and D-dimer levels can be used to determine the possibility of deep vein thrombosis and the necessity for further diagnostic imaging such as ultrasonography or computed tomography (CT) venography. Drugs, such as Parkinson’s medications and hypertensive agents may also cause leg edema. Lymphedema, lipedema, infection, and many general medical conditions such as heart failure, liver failure, and acute kidney injury should also be differentiated. Therefore, to diagnose venous edema (i.e., clinical C3 status), physicians should not only check the presence of lower leg edema on physical examination but should also take a complete patient history to facilitate accurate, efficient, and cost-effective diagnostic testing and management. The site of swelling and any associated manifestations should be assessed, including whether it is unilateral, bilateral and equal, or bilateral but asymmetric, along with any changes in severity related to position and time of day.
Chronic skin inflammation can also result from CVD. The skin becomes indurated, with brownish discoloration, and may be surrounded by varicose veins. This usually develops gradually, often ignored in the beginning, and represents stages C4a and C4b. Treatment with compression only may be unsuccessful, and in such cases, ultrasound scanning is required.
Patients at the more advanced C5–6 stages of CVD may present with venous leg ulcers. Venous ulcers are normally located on the lower leg above the ankle level. They are shallow ulcers with uneven edges and may be accompanied by necrotic tissue, serous or serosanguinous drainage, and dark hemosiderin staining of the surrounding skin. Although they are usually painless, acute pain may occur if complicated by secondary infection. Therefore, wound management is also important at these stages. Venous ulcers must be differentiated from arterial or neuropathic ulcers. Unlike venous ulcers, arterial ulcers are caused by poor perfusion of the lower leg and usually present with pain, which is aggravated by walking and exercise. The skin with arterial ulcers presents with the “punched out” appearance of deep ulcers with well-defined edges. The ankle-brachial index is useful in differentiating arterial from venous ulcers, and additional ultrasound duplex scans may be used for further examination.
Many of the clinical features in the leg that patients present with may or may not be related to CVD. In fact, non-venous origins exceed venous origins. Therefore, thorough history-taking and physical examination of the legs are essential before moving on to examinations such as ultrasonography.
To understand the pathophysiology of CVD or varicose veins and to localize the exact site for correction, it is essential to be deeply familiar with the anatomy of veins in the lower extremity as well as possible variations. The venous network in the lower extremity consists of superficial and deep veins connected by perforators, and each vein contains intraluminal valves that direct the venous blood flow unidirectionally upwards toward the heart.
The main superficial truncal veins of the lower extremities include the great saphenous vein (GSV) and the small saphenous vein (SSV). The GSV lies between the superficial and deep compartments, which are separated by the saphenous fascia. Its cross-sectional view on ultrasound resembles the so-called “Egyptian eye.” The distal GSV originates from the medial side of the foot, ascends in front of the medial malleolus of the foot, and courses up the medial side of the calf and thigh. It finally joins the common femoral vein at the saphenofemoral junction. The anatomy of the GSV has many variations and does not always course within the saphenous compartment throughout the leg. Furthermore, when it is outside the saphenous compartment, it is not referred to as the GSV, but as the superficial tributary vein or superficial accessory saphenous vein.
The Union Internationale de Phlébologie (UIP) consensus reported the most common variations in lower limb venous anatomy to help identify veins correctly and diagnose disease using ultrasound imaging [8]. The relationship of the fascial compartments to the GSV and anatomical variations in the thigh are described below:
(1) A single GSV lying within the saphenous compartment with no large parallel tributary.
(2) The GSV in the thigh comprising 2 parallel veins, both lying within the saphenous compartment for 3–25 cm (true GSV duplication). This is present in fewer than 1% of cases.
(3) A single GSV lying within the saphenous compartment as well as a large subcutaneous tributary that pierces the superficial fascia to join the GSV at a variable level in the thigh.
(4) Two veins, the GSV and the anterior accessory saphenous vein (AASV), both present in the thigh, are located distally in 2 separate ‘saphenous eyes’ and come together in a single compartment just before entering the saphenofemoral junction (SFJ). In many cases, the AASV is incompetent, filling varicosities over the anterior and lateral aspects of the thigh.
(5) A single GSV lying within the proximal saphenous compartment and a large subcutaneous tributary more distally, with no substantial vein visible in the saphenous compartment. The distal subcutaneous vein pierces the saphenous fascia at a variable level in the thigh to become the GSV within the fascial compartment.
When utilizing ultrasound, it may be difficult and confusing to recognize the GSV and its fascia as they form the “saphenous eye” near the knee, since the GSV relates to a number of subcutaneous tributaries and perforating veins confined within a small space in the region. The GSV in this area can be identified in transverse ultrasound images by the tibio–gastrocnemius angle sign between the distal third of the thigh and the proximal third of the calf. The 5 common patterns (1–5) reported by the UIP are listed below [8].
(1) The GSV is visible, and no large tributary is seen.
(2) The GSV is visible, but there are 1 or more tributaries below the knee, the most typical being the posterior arch or “Leonardo” vein.
(3) The GSV is visible, but there is also a large tributary that begins above the knee, which (whether normal or varicose) is sometimes so large that it may be erroneously assumed to be the GSV itself. The GSV is always present in the knee area in the 3 patterns described above (1–3), though it is sometimes smaller than its normal or varicose tributaries. In contrast, the middle portion of the GSV is barely visible or not visible at all (hypoplastic or absent) for a variable length in about 30% of cases with the “missing” portion bypassed by a subcutaneous tributary. Two patterns are observed and are described below in (4) and (5).
(4) The GSV cannot be demonstrated for some distance above and below the knee. The GSV pierces the saphenous fascia at about the mid-calf to become a subcutaneous tributary that crosses the knee and again pierces the saphenous fascia in the distal thigh to become the GSV in its saphenous compartment.
(5) This is like (4), but the absent portion of the GSV is very short and just below rather than across the knee.
The GSVs in the legs are often accompanied by parallel veins that may be confused with the GSV itself or considered as double saphenous veins. The UIP consensus has defined these veins, not as duplications of the GSV, but as tributaries lying subcutaneously, which may then pierce the superficial fascia to enter the saphenous compartment. The relationship between the GSV and these subcutaneous tributaries have been classified below in 3 anatomical patterns [8].
(1) Type I: The saphenous trunk is present with a normal diameter throughout the length of the saphenous compartment and there are no large parallel tributaries.
(2) Type h: The saphenous trunk is present throughout the saphenous compartment, and there is also a tributary vein that may be even larger than the GSV.
(3) Type S: A superficial tributary ascends and pierces the superficial fascia, continuing as the GSV within its compartment, while distal to this point the GSV is absent or only barely visible on ultrasound imaging (absent or hypoplastic).
The SSV is located in the posterior calf between the 2 heads of the gastrocnemius muscle. It courses upward through the popliteal fossa and finally joins the popliteal vein at the saphenopopliteal junction (SPJ). The SSV lies in the saphenous compartment, which is bordered by the superficial and muscular fascia. In some variations, it may continue upwards and directly join the femoral vein or the GSV more proximally. The 3 most common anatomical variations at the SSV termination are described below.
(1) The SSV joins the popliteal vein at the SPJ and joins the deep veins at a higher level through its thigh extension (TE) or joins the GSV via the Giacomini vein (GV).
(2) The SSV continues upwards as the TE or GV, but it also connects with the popliteal vein through a tiny anastomotic vein.
(3) There may be no connection to the deep veins, so that the SSV continues proximally as the TE or GV.
Other axial veins coursing parallel to the GSV include the AASV and the posterior accessory saphenous vein (PASV). The AASV is noted in approximately half of patients and can be a source of recurrent varicose veins. The PASV should be carefully examined in patients with venous ulcers because, in some circumstances, the posterior tibial (Cockett) perforators may connect to posterior tibial veins and the PASV instead of connecting to the distal GSV.
The deep veins of the lower extremities are responsible for approximately 90% of the venous blood flow in the lower extremities. They usually have a thinner wall than superficial veins and are supported by the muscle and/or fascia. The deep veins of the deep plantar venous arch at the foot level becomes the posterior tibial vein at the medial malleolus, whereas the dorsalis pedis vein on the dorsum of the foot becomes the anterior tibial vein at the ankle. The tibioperoneal trunk and the anterior tibial veins join and become the popliteal vein, which courses upwards passing through the adductor canal and becomes the femoral vein. The femoral vein finally joins the deep femoral vein to become the common femoral vein [9].
Perforator veins are veins that obliquely penetrate the deep fascia to connect the superficial and deep veins. They are usually located in the medial thigh and calf. They are numerous and highly variable in arrangement, connection, and size. The perforator veins usually connect the saphenous vein and the deep veins. However, they may also become superficial nonaxial tributary veins. The 4 clinically important perforator groups are usually found at the upper thigh (Hunterian), lower thigh (Dodd’s), knee level (Boyd’s), and calf region (Cockett’s) [10]. Valve incompetence in these perforator veins is frequently associated with chronic venous insufficiency, and therefore, their status should always be examined. However, it is not always necessary to treat these perforating veins in patients with C2 CVD [11]. According to Gloviczki et al. [12], routine concomitant treatment of incompetent perforating veins with initial ablation of the superficial truncal veins is not recommended in class C2 varicose veins. However, pathologic perforating veins with an outward flow of >500 ms and size >3.5 mm, located beneath a healed or open venous ulcer (C4–6) may need to be treated [12]. Vein anatomy of the lower extremity is summarized in Fig. 1 [12].
At their initial presentation, patients suspected of having CVD should be asked about their symptoms, aggravating and alleviating factors, family history, occupation, exercise habits, changes in weight, thromboembolic history, allergies, medications, pregnancy history, and any cardiac, renal, or other comorbidities [13]. Physical examination of the legs should then be performed while the patient is standing, checking for varicose veins, swelling, skin pigmentation, induration, inflammation, and ulcers. Filling of the varicose veins can be checked by applying a tourniquet or manual compression over the superficial veins and then asking the patient to stand up. This test is called the Brodie-Trendelenburg test and, if vein filling exceeds 20 seconds, it may suggest that the varicose veins are caused by superficial venous insufficiency [10].
If venous insufficiency is suspected, further examination with lower-extremity duplex ultrasound scanning (DUS) should be considered. DUS is currently the most used and recommended diagnostic technique for evaluation of CVD. Etiological and anatomical information can be obtained through DUS. The size, reflux, obstruction, and venous flow patterns of the superficial and deep veins can be examined using the combination of grayscale B-mode imaging and spectral Doppler [12]. Specifically, 2-dimensional images of the blood vessels can be achieved with the grayscale B-mode (brightness mode), and blood flow or reflux can be evaluated by the Doppler mode [9].
To maintain the most accurate, reproducible, and credible diagnostic and treatment results, many international and domestic vascular societies have developed clinical ultrasound guidelines, which they reevaluate and update based on newly gathered accredited evidence [14-17].
It is recommended that the lower extremity DUS should be performed with the patient standing whenever possible, and evaluated by an accredited ultrasonographer. A reverse Trendelenburg position can also be used if the patient has difficulty standing [12].
To achieve the most accurate and standardized ultrasound images, it is recommended that high-frequency (5–16 MHz) linear probes be used [12-17]. A complete DUS examination of the lower extremity for CVD starts just proximal to the SFJ at the common femoral vein and includes images of the superficial truncal veins (SFJ, GSV, SPJ, SSV, AAGSV, and PASV), the deep truncal veins (common femoral, femoral, and popliteal veins), and the perforating veins.
To achieve a complete DUS examination for venous reflux in the lower extremities, Gloviczki et al. [12] recommended including examinations of the common femoral vein; proximal, mid, and distal femoral veins; popliteal veins; the SFJ and the GSV at the proximal thigh and knee; and the AASV, and SSV at the SPJ or proximal calf.
For a complete report, the exact name of the examined vein, the location, diameter (from anterior to posterior wall), and pathologic findings such as reflux must be documented with the images [12,17]. Images of both normal and abnormal findings should be documented in the patient’s record.
Multiple reliable references, including the UIP consensus document and the most recently reported Korean Society for Phlebology Society guidelines, recommend including both the transverse and longitudinal sections when performing an ultrasound examination of the lower extremities to obtain thorough and accurate information. Information on the surrounding anatomy of the vein, the diameter of the vein, and the presence or absence of thrombus are well visualized in the transverse section. To exam for reflux, however, the longitudinal section is recommended to provide clearer objective information, as appropriate given the principle of spectral Doppler examination.
Venous reflux is an uninterrupted retrograde venous flow from the groin to the calf and is mainly caused by venous hypertension, venous valve damage, and venous flow obstruction [10]. An evaluation for reflux is necessary to check the vein patency and valvular functions.
Pathologic venous reflux in the superficial truncal veins (GSV, SSV, AASV, PASV) and in the tibial, deep femoral, and perforating veins is defined as a reversed flow with a minimum value of >500 ms. Pathologic reflux in the common femoral, femoral, and popliteal veins is defined as a reversed flow with a minimum value of >1 second. Junctional reflux is limited to the SFJ or SPJ. Segmental reflux occurs only in a portion of a superficial or deep truncal vein. A “pathologic” perforating vein in patients with varicose veins includes those with an outward flow duration of ≥500 ms together with a vein diameter exceeding 3.5 mm on DUS [12].
To evaluate for reflux, use of the Valsalva maneuver or distal augmentation is recommended to assess the common femoral vein and SFJ, and distal augmentation with either manual compression or cuff inflation/deflation for evaluation of the more distal segments [10,12]. If abnormal retrograde flow suggesting venous reflux is confirmed under color Doppler imaging, measurement of the spectral Doppler waveform using calipers is recommended. In this imaging modality, both the augmentation waveform (reflux in response to a Valsalva maneuver or distal compression of calf muscles) and the reflux waveform (wave created by the pathologic retrograde venous reflux) should appear on opposite sides of the baseline (Fig. 2). Documentation of the name of the vein with reflux, location of the reflux, and the exact reflux time measured in seconds or milliseconds on the ultrasound image is recommended to enhance the quantification and accuracy of image interpretation.
To fully understand the pathophysiology and choose the correct treatment plan, it is also essential to examine for the presence of venous obstruction in the deep veins. Venous obstruction can be suspected if there is an absence of flow, blunted augmentation, presence of an echogenic thrombus within the vein, or failure of the vein to collapse with a compression maneuver. More caution is necessary if a patient presents with combined superficial venous insufficiency and deep venous thrombosis.
Venous disease can also be evaluated using CT and magnetic resonance venography. These techniques do not provide functional information, and therefore are not considered first-line diagnostic tools for CVD. However, they may be useful in evaluating focal or complex lesions that may be equivocal on ultrasound images, evaluating surrounding structures, and assessing for intrinsic or extrinsic obstruction [13].
If CVD has been confirmed with history-taking, a clinical examination, and ultrasonography, the next step is a precise description of the disease status.
The CEAP classification, an internationally accepted standard for describing patients with chronic venous disorders, was developed in 1993 and most recently updated in 2020. It is a classification system based on the clinical manifestations of chronic venous disorders, the current understanding of its etiology, the involved anatomy, and the underlying venous pathology [18]. It has been revised and updated by the American Venous Forum in order to improve the reproducibility of clinical findings between physicians, clarify the differences between older and new versions of the CEAP classification, add new evidence-based knowledge into the CEAP classification, and finally to balance the simple practical use of the classification with the highly specific and detailed descriptions of patients with CVD.
This classification uses a range of symptoms and signs of CVD to describe the severity (C: clinical); categorizes the etiology as congenital, primary, or secondary (E: etiology); localizes the affected veins as superficial, deep, or perforating (A: anatomy); and finally, characterizes the pathophysiology as reflux, obstruction, both, or neither (P: pathophysiology). Tables 1 and 2 briefly summarizes the CEAP classification.
Table 1. Updated CEAP classification of chronic venous disease
CEAP | Description |
---|---|
Clinical classification (C) | |
C0 | No visible or palpable signs of venous disease |
C1 | Telangiectasias or reticular veins |
C2 | Varicose veins |
C2r | Recurrent varicose veins |
C3 | Edema |
C4 | Changes in skin and subcutaneous tissue secondary to chronic venous disease |
C4a | Pigmentation or eczema |
C4b | Lipodermatosclerosis or atrophie blanche |
C4c | Corona phlebectatica |
C5 | Healed ulcer |
C6 | Active venous ulcer |
C6r | Recurrent active venous ulcer |
Etiologic classification (E) | |
Ep | Primary |
Es | Secondary |
Esi | Secondary–intravenous |
Ese | Secondary–extravenous |
Ec | Congenital |
En | No cause identified |
Anatomic classification (A) | |
As | Superficial |
Ad | Deep |
Ap | Perforator |
An | No venous anatomic location identified |
Pathophysiologic classification (P) | |
Pr | Reflux |
Po | Obstruction |
Pr,o | Reflux and obstruction |
Pn | No pathophysiology identified |
CEAP, clinical, etiological, anatomical, and pathophysiological.
Table 2. Updated anatomic classification of chronic venous disease
Anatomic classification | Old | New | Description |
---|---|---|---|
As (superficial) | 1. | Tel | Telangiectasia |
1. | Ret | Reticular veins | |
2. | GSVa | Great saphenous vein above knee | |
3. | GSVb | Great saphenous vein below knee | |
4. | SSV | Small saphenous vein | |
AASV | Anterior accessory saphenous vein | ||
5. | NSV | Nonsaphenous vein | |
Ad (deep) | 6. | IVC | Inferior vena cava |
7. | CIV | Common iliac vein | |
8. | IIV | Internal iliac vein | |
9. | EIV | External iliac vein | |
10. | PELV | Pelvic veins | |
11. | CFV | Common femoral vein | |
12. | DFV | Deep femoral vein | |
13. | FV | Femoral vein | |
14. | POPV | Popliteal vein | |
15. | TIBV | Crural (tibial) vein | |
15. | PRV | Peroneal vein | |
15. | ATV | Anterior tibial vein | |
15. | PTV | Posterior tibial vein | |
16. | MUSV | Muscular veins | |
16. | GAV | Gastrocnemius vein | |
16. | SOV | Soleal vein | |
Ap (perforator) | 17. | TPV | Thigh perforator vein |
18. | CPV | Calf perforator vein | |
An | No venous anatomic location identified |
As mentioned above, the CEAP classification was updated in 2020. The clinical classification (C), which is the most widely used component of CEAP, is currently arranged so that more severe manifestations of venous disease are assigned a higher class. However, its weakness is that the clinical classification is not a quantitative severity scale and does not reflect changes over time.
Unfortunately, recurrence of varicose veins (C2) and venous ulcers (C6) after intervention to correct reflux is common. Therefore, as shown in Tables 1 and 2, the tendency of varicose veins and venous ulcers to recur is reflected in the 2020 update of the CEAP classification, with the addition of the modifier “r” to the C2 and C6 clinical classes. Although the clinical definition of recurrence is identical to that of the previously suggested “recurrent varices after surgery” [19], the previous treatments were not limited to surgical treatments.
Another change in the C classification includes corona phlebectatica, which is a fan-shaped pattern of numerous small intradermal veins on the medial or lateral aspects of the ankle and foot. To differentiate corona phlebectatica from C1 lesions and reduce the risk of misclassification, it is important to recognize the essential elements of corona phlebectatica: telangiectasia, more than 5 nonconfluent intradermal veins, venous cups, stasis spots (clusters of dilated papillary capillaries), extension equal to or greater than half the length of the foot, and tiny areas of perivenous pigmentation. Many phlebologists consider corona phlebectatica an early sign of advanced venous disease that therefore warrants inclusion in more advanced C categories. The risk of developing ulcers in corona phlebectatica has been reported to be 5.3 times higher, like with eczema (C4a) and lipodermatosclerosis (C4b). Furthermore, the relative risk of finding incompetent leg or calf perforators by duplex ultrasound is 4.4 times greater. These results suggest that corona phlebectatica should not be compared to telangiectasias and reticular veins in other locations. Therefore, because of the association of corona phlebectatica with more advanced venous disease, corona phlebectatica was placed in the C4 class as a separate subclass (C4c) in the 2020 CEAP update [20].
The etiology (E) classification of venous disease, is categorized as congenital (Ec), primary (Ep), or secondary (post-thrombotic) (Es). Besides small refinements in the definitions of E subclasses, no major changes were made in the 2020 update [18].
The anatomic (A) classification of venous disease is categorized as superficial (As), deep (Ad), or perforating (Ap) veins. Changes were made in 2020 replacing the previous numeric descriptions of the venous segments with their common abbreviations. This allowed a more intuitive identification of these anatomic segments (Table 2).
The pathophysiologic (P) classification includes reflux (r), obstruction (o), reflux and obstruction (r,o), and no venous pathophysiology (n). The advanced designations did not change.
Because of the CEAP classification’s descriptive nature and static categorical classification scheme, the Venous Clinical Severity Score (VCSS) was also developed and widely used as an evaluation tool to reflect the changes in disease severity over time and in response to treatment. The VCSS includes 9 parameters of venous disease with a symptom severity scale from 0 to 3 (0–1=mild; 2=moderate; and 3=severe). The scored parameters include pain, varicose veins, edema, skin pigmentation, inflammation, induration, ulcers (number, size, and duration), and compressive therapy [9,10]. The VCSS is shown in Table 3.
Table 3. Venous Clinical Severity Score
Absent=0 | Mild=1 | Moderate=2 | Severe=3 | |
---|---|---|---|---|
Pain | None | Occasional, not restricting daily activity | Daily, interfering but not preventing daily activity | Daily, limits most daily activity |
Varicose veins | None | Few isolated branch varices or clusters; includes ankle flare | Confined to calf or thigh | Involves calf and thigh |
Venous edema | None | Limited to foot and ankle | Extends above the ankle but below the knee | Extends to knee and above |
Skin pigmentation | None or focal | Limited to the peri-malleolar area | Diffuse, over lower third of calf | Wider distribution above lower third of calf |
Inflammation | None | Mild cellulitis, ulcer margin limited to the peri-malleolar area | Diffuse over lower third of calf | Wider distribution above lower third of calf |
Induration | None | Limited to the peri-malleolar area | Diffuse over lower third of calf | Wider distribution above lower third of calf |
Ulcer number | 0 | 1 | 2 | ≥3 |
Ulcer duration | NA | <3 mo | >3 mo, <1 yr | Not healed >1 yr |
Ulcer size | NA | Diameter <2 cm | Diameter 2–6 cm | Diameter >6 cm |
Compressive therapy | Not used | Intermittent | Most days | Full compliance |
NA, not applicable.
Lower-extremity CVD is a common disease with an increasing global and national prevalence. It is a disease with a very broad clinical spectrum and diverse symptoms, which may not exactly correlate with the severity of the CVD. Therefore, a thorough understanding of venous anatomy and the pathophysiology of CVD, as well as the correct use of duplex ultrasound in the diagnosis of CVD are essential to achieving an accurate diagnosis and optimal treatment results. Unfortunately, with the increasing prevalence of CVD in Korea, there have also been some ethical concerns regarding the diagnosis and management of varicose veins in Korea. However, multiple Korean academic societies have collaborated to improve the quality of diagnosis and treatment by standardizing the diagnostic criteria and indications for treatment of varicose veins. Hopefully these evidence-based clinical guidelines on CVD and DUS will help to optimize the diagnostic and treatment results of CVD and ultimately benefit Korean patients.
Authors contributions
Conceptualization: JHC. Investigation: JHC, SH. Data curation: JHC, SH. Visualization: JHC. Writing–original draft: JHC. Writing–review and editing: JHC, SH. Final approval of the manuscript: all authors.
Conflict of interest
Jae Ho Chung is an editorial board member of the journal but was not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflict of interest relevant to this article was reported.
Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
J Chest Surg 2024; 57(2): 109-119
Published online March 5, 2024 https://doi.org/10.5090/jcs.23.110
Copyright © Journal of Chest Surgery.
Jae Ho Chung , M.D., Ph.D., Seonyeong Heo , M.D.
Department of Thoracic and Cardiovascular Surgery, Korea University College of Medicine, Seoul, Korea
Correspondence to:Jae Ho Chung
Tel 82-2-920-5369
Fax 82-2-928-8793
E-mail bozof@hanmail.net
ORCID
https://orcid.org/0000-0002-4203-4933
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Varicose veins usually present in the superficial veins of the lower extremities and are one of the main clinical presentations of chronic venous disease (CVD). Patients’ symptoms may vary according to the pathophysiology, location, and severity of CVD. The prevalence of CVD in Korea has been increasing gradually. However, due to its broad clinical spectrum and the subjective nature of its diagnosis using ultrasound, discrepancies in diagnostic and treatment quality may exist among treating physicians. There have been recent efforts to improve the quality of the diagnosis and treatment of varicose veins in Korea by standardizing the diagnostic criteria and the indications for treatment. This study is a comprehensive review of the clinical manifestations and diagnostic criteria of CVD based on the most recent international and domestic guidelines and reports.
Keywords: Chronic venous disease, Varicose veins, Lower extremity, Diagnosis, Ultrasonography
Varicose veins are dilated, palpable, tortuous veins, that are generally larger than 3 mm and usually present in the superficial veins of the lower extremities [1]. They are one of the main clinical presentations of chronic venous disease (CVD), which has a broad clinical spectrum ranging from reticular veins, telangiectasias, varicose veins, edema, skin pigmentation, lipodermatosclerosis, and atrophie blanche, to venous ulceration [2,3]. Patients’ symptoms may vary, from asymptomatic cosmetic problems to severely painful symptoms with complications. Severe symptoms such as venous ulceration may negatively impact a patient’s capacity to participate in occupational and social activities, resulting in poor quality of life and economic deterioration [3].
The global prevalence of varicose veins varies widely, with reports ranging from 1% to 73% of women and 2% to 56% of men [4]. The number of patients who receive medical treatment for varicose veins in Korea has increased 5.4% every year according to recent reports from the National Health Insurance Corporation. The prevalence of CVD may differ according to risk factors such as geographic location, advanced age, female sex, obesity, family history, hypertension, a standing occupation, lifestyle, and smoking [4]. According to previous population-based studies, the prevalence of varicose veins increases with age. Aging usually contributes to the deterioration of vessel walls and venous valves, as well as the weakening of calf muscles, which are known to affect prolonged venous hypertension. Female sex is also a known risk factor, although it is unclear whether this is related to other factors such as pregnancy, hormones, or environment. Ethnicity is also related to the prevalence of CVD, with a lower prevalence among Asians than among non-Hispanic whites [5].
When combined, the complex pathophysiology of multifactorial CVD, the subjectivity of ultrasonography in the diagnostic process, and the wide variety of treatment modalities may result in diagnostic and treatment variations among physicians. Furthermore, a variety of guidelines have been provided by related academic groups.
As noted above, the prevalence of CVD in Korea has been increasing gradually, and recent efforts have been made to improve the quality of the diagnosis and treatment of varicose veins in Korea by standardizing the diagnostic criteria and indications for treatment.
In November 2021 the Korean Society for Phlebology created an ethics declaration to celebrate the 20th anniversary of its founding. They also updated their clinical practice guidelines for varicose veins, based on evidence they had accumulated over 8 years. This year, in collaboration with 5 other academic societies including the Korean Society for Vascular Surgery, the Korean Society for Thoracic and Cardiovascular Surgery, the Korean Surgical Society, the Korean Surgical Ultrasound Society, and the Korean Society of Interventional Radiology, they presented “Evidence-based guideline for the use of ultrasonography in the diagnosis and assessment of Varicose veins,” a guideline for the use of ultrasonography to diagnose and assess varicose veins.
This study is a comprehensive review of the clinical manifestations and diagnostic criteria of CVD, based on the most recent international and domestic guidelines and reported studies.
Patients with CVD of the lower extremities may present with many different clinical features. Depending on location and severity, patients may complain of leg discomfort such as heaviness, tired legs, swelling, itching of the skin, nocturnal cramps, throbbing, burning pain, and aching. In many circumstances, these symptoms may be nonspecific and difficult to differentiate from other non-venous etiologies. The symptoms do not always correlate with the presence or degree of venous hypertension. The heterogeneity of symptoms, even between the same clinical, etiological, anatomical, and pathophysiological (CEAP) classes, also makes the diagnosis difficult. Visible varicose veins, which are dilated, bulging, tortuous, superficial veins with a diameter larger than 3 mm, are not always the reason for the patient’s symptoms. Approximately 75% of the adult population has visible veins (spider veins or tributary veins) without any sign of chronic venous insufficiency [6]. Therefore, care must be taken when diagnosing CVD, and the possibility of other non-venous etiologies must be considered.
Leg discomfort or pain, one of the most common symptoms of CVD, is absent in approximately 20% of CVD patients, whereas it is the only clinical feature in approximately 10% of patients [2]. Specifically, venous leg discomfort is frequently related to prolonged standing and is relieved by elevation of the leg, walking, or compression stockings.
The differential diagnosis for leg pain includes neurologic or orthopedic pain, arterial pain, lipedema, arthrogenic pain, and muscular pain. Neurologic or orthopedic pain is primarily related to the lumbar spine or sacroiliac joints and is usually associated with radiation down the leg, tingling or paresthesia, and numbness. It may be aggravated when lying down or sitting in a comfortable chair. Arterial pain is mostly caused by peripheral arterial occlusive disease and is exacerbated by activity and improved with rest. Arthrogenic pain is usually localized to the joint and may be related to a ruptured Baker’s cyst. Muscular pain usually presents with tenderness or pain on moving the affected muscle. In contrast, venous leg pain may be the result of superficial vein thrombosis (phlebitis), deep vein thrombosis, tension pain due to edema, inflammatory changes in hyperpigmentation, venous ulcers, and enlargement of varicose veins [7].
Leg edema is another common feature of CVD. Patients may complain of heaviness, tired legs, or a sensation of swelling. Leg edema related to varicose veins represents stage C3 and is most pronounced in the leg with the varicose veins. In the CEAP classification, the C3 category is broad and does not explain subcategories of edema. It does not quantify the degree or extent of the edema or recognize other causes of leg edema. For example, transitory ankle edema at the end of the day likely has a different pathophysiology and natural history than severe permanent edema. Venous edema may be unilateral or bilateral, may show an acute or a gradual onset over the years, and may be accompanied by tension pain. Venous leg edema is usually relieved by the application of compression stockings, and is aggravated by prolonged standing. However, like other symptoms, leg edema may often be due to other problems. Deep vein thrombosis, another vein related disease, usually occurs abruptly with unilateral swelling accompanied by pain, a feeling of tension, and bluish discoloration. The Wells score and D-dimer levels can be used to determine the possibility of deep vein thrombosis and the necessity for further diagnostic imaging such as ultrasonography or computed tomography (CT) venography. Drugs, such as Parkinson’s medications and hypertensive agents may also cause leg edema. Lymphedema, lipedema, infection, and many general medical conditions such as heart failure, liver failure, and acute kidney injury should also be differentiated. Therefore, to diagnose venous edema (i.e., clinical C3 status), physicians should not only check the presence of lower leg edema on physical examination but should also take a complete patient history to facilitate accurate, efficient, and cost-effective diagnostic testing and management. The site of swelling and any associated manifestations should be assessed, including whether it is unilateral, bilateral and equal, or bilateral but asymmetric, along with any changes in severity related to position and time of day.
Chronic skin inflammation can also result from CVD. The skin becomes indurated, with brownish discoloration, and may be surrounded by varicose veins. This usually develops gradually, often ignored in the beginning, and represents stages C4a and C4b. Treatment with compression only may be unsuccessful, and in such cases, ultrasound scanning is required.
Patients at the more advanced C5–6 stages of CVD may present with venous leg ulcers. Venous ulcers are normally located on the lower leg above the ankle level. They are shallow ulcers with uneven edges and may be accompanied by necrotic tissue, serous or serosanguinous drainage, and dark hemosiderin staining of the surrounding skin. Although they are usually painless, acute pain may occur if complicated by secondary infection. Therefore, wound management is also important at these stages. Venous ulcers must be differentiated from arterial or neuropathic ulcers. Unlike venous ulcers, arterial ulcers are caused by poor perfusion of the lower leg and usually present with pain, which is aggravated by walking and exercise. The skin with arterial ulcers presents with the “punched out” appearance of deep ulcers with well-defined edges. The ankle-brachial index is useful in differentiating arterial from venous ulcers, and additional ultrasound duplex scans may be used for further examination.
Many of the clinical features in the leg that patients present with may or may not be related to CVD. In fact, non-venous origins exceed venous origins. Therefore, thorough history-taking and physical examination of the legs are essential before moving on to examinations such as ultrasonography.
To understand the pathophysiology of CVD or varicose veins and to localize the exact site for correction, it is essential to be deeply familiar with the anatomy of veins in the lower extremity as well as possible variations. The venous network in the lower extremity consists of superficial and deep veins connected by perforators, and each vein contains intraluminal valves that direct the venous blood flow unidirectionally upwards toward the heart.
The main superficial truncal veins of the lower extremities include the great saphenous vein (GSV) and the small saphenous vein (SSV). The GSV lies between the superficial and deep compartments, which are separated by the saphenous fascia. Its cross-sectional view on ultrasound resembles the so-called “Egyptian eye.” The distal GSV originates from the medial side of the foot, ascends in front of the medial malleolus of the foot, and courses up the medial side of the calf and thigh. It finally joins the common femoral vein at the saphenofemoral junction. The anatomy of the GSV has many variations and does not always course within the saphenous compartment throughout the leg. Furthermore, when it is outside the saphenous compartment, it is not referred to as the GSV, but as the superficial tributary vein or superficial accessory saphenous vein.
The Union Internationale de Phlébologie (UIP) consensus reported the most common variations in lower limb venous anatomy to help identify veins correctly and diagnose disease using ultrasound imaging [8]. The relationship of the fascial compartments to the GSV and anatomical variations in the thigh are described below:
(1) A single GSV lying within the saphenous compartment with no large parallel tributary.
(2) The GSV in the thigh comprising 2 parallel veins, both lying within the saphenous compartment for 3–25 cm (true GSV duplication). This is present in fewer than 1% of cases.
(3) A single GSV lying within the saphenous compartment as well as a large subcutaneous tributary that pierces the superficial fascia to join the GSV at a variable level in the thigh.
(4) Two veins, the GSV and the anterior accessory saphenous vein (AASV), both present in the thigh, are located distally in 2 separate ‘saphenous eyes’ and come together in a single compartment just before entering the saphenofemoral junction (SFJ). In many cases, the AASV is incompetent, filling varicosities over the anterior and lateral aspects of the thigh.
(5) A single GSV lying within the proximal saphenous compartment and a large subcutaneous tributary more distally, with no substantial vein visible in the saphenous compartment. The distal subcutaneous vein pierces the saphenous fascia at a variable level in the thigh to become the GSV within the fascial compartment.
When utilizing ultrasound, it may be difficult and confusing to recognize the GSV and its fascia as they form the “saphenous eye” near the knee, since the GSV relates to a number of subcutaneous tributaries and perforating veins confined within a small space in the region. The GSV in this area can be identified in transverse ultrasound images by the tibio–gastrocnemius angle sign between the distal third of the thigh and the proximal third of the calf. The 5 common patterns (1–5) reported by the UIP are listed below [8].
(1) The GSV is visible, and no large tributary is seen.
(2) The GSV is visible, but there are 1 or more tributaries below the knee, the most typical being the posterior arch or “Leonardo” vein.
(3) The GSV is visible, but there is also a large tributary that begins above the knee, which (whether normal or varicose) is sometimes so large that it may be erroneously assumed to be the GSV itself. The GSV is always present in the knee area in the 3 patterns described above (1–3), though it is sometimes smaller than its normal or varicose tributaries. In contrast, the middle portion of the GSV is barely visible or not visible at all (hypoplastic or absent) for a variable length in about 30% of cases with the “missing” portion bypassed by a subcutaneous tributary. Two patterns are observed and are described below in (4) and (5).
(4) The GSV cannot be demonstrated for some distance above and below the knee. The GSV pierces the saphenous fascia at about the mid-calf to become a subcutaneous tributary that crosses the knee and again pierces the saphenous fascia in the distal thigh to become the GSV in its saphenous compartment.
(5) This is like (4), but the absent portion of the GSV is very short and just below rather than across the knee.
The GSVs in the legs are often accompanied by parallel veins that may be confused with the GSV itself or considered as double saphenous veins. The UIP consensus has defined these veins, not as duplications of the GSV, but as tributaries lying subcutaneously, which may then pierce the superficial fascia to enter the saphenous compartment. The relationship between the GSV and these subcutaneous tributaries have been classified below in 3 anatomical patterns [8].
(1) Type I: The saphenous trunk is present with a normal diameter throughout the length of the saphenous compartment and there are no large parallel tributaries.
(2) Type h: The saphenous trunk is present throughout the saphenous compartment, and there is also a tributary vein that may be even larger than the GSV.
(3) Type S: A superficial tributary ascends and pierces the superficial fascia, continuing as the GSV within its compartment, while distal to this point the GSV is absent or only barely visible on ultrasound imaging (absent or hypoplastic).
The SSV is located in the posterior calf between the 2 heads of the gastrocnemius muscle. It courses upward through the popliteal fossa and finally joins the popliteal vein at the saphenopopliteal junction (SPJ). The SSV lies in the saphenous compartment, which is bordered by the superficial and muscular fascia. In some variations, it may continue upwards and directly join the femoral vein or the GSV more proximally. The 3 most common anatomical variations at the SSV termination are described below.
(1) The SSV joins the popliteal vein at the SPJ and joins the deep veins at a higher level through its thigh extension (TE) or joins the GSV via the Giacomini vein (GV).
(2) The SSV continues upwards as the TE or GV, but it also connects with the popliteal vein through a tiny anastomotic vein.
(3) There may be no connection to the deep veins, so that the SSV continues proximally as the TE or GV.
Other axial veins coursing parallel to the GSV include the AASV and the posterior accessory saphenous vein (PASV). The AASV is noted in approximately half of patients and can be a source of recurrent varicose veins. The PASV should be carefully examined in patients with venous ulcers because, in some circumstances, the posterior tibial (Cockett) perforators may connect to posterior tibial veins and the PASV instead of connecting to the distal GSV.
The deep veins of the lower extremities are responsible for approximately 90% of the venous blood flow in the lower extremities. They usually have a thinner wall than superficial veins and are supported by the muscle and/or fascia. The deep veins of the deep plantar venous arch at the foot level becomes the posterior tibial vein at the medial malleolus, whereas the dorsalis pedis vein on the dorsum of the foot becomes the anterior tibial vein at the ankle. The tibioperoneal trunk and the anterior tibial veins join and become the popliteal vein, which courses upwards passing through the adductor canal and becomes the femoral vein. The femoral vein finally joins the deep femoral vein to become the common femoral vein [9].
Perforator veins are veins that obliquely penetrate the deep fascia to connect the superficial and deep veins. They are usually located in the medial thigh and calf. They are numerous and highly variable in arrangement, connection, and size. The perforator veins usually connect the saphenous vein and the deep veins. However, they may also become superficial nonaxial tributary veins. The 4 clinically important perforator groups are usually found at the upper thigh (Hunterian), lower thigh (Dodd’s), knee level (Boyd’s), and calf region (Cockett’s) [10]. Valve incompetence in these perforator veins is frequently associated with chronic venous insufficiency, and therefore, their status should always be examined. However, it is not always necessary to treat these perforating veins in patients with C2 CVD [11]. According to Gloviczki et al. [12], routine concomitant treatment of incompetent perforating veins with initial ablation of the superficial truncal veins is not recommended in class C2 varicose veins. However, pathologic perforating veins with an outward flow of >500 ms and size >3.5 mm, located beneath a healed or open venous ulcer (C4–6) may need to be treated [12]. Vein anatomy of the lower extremity is summarized in Fig. 1 [12].
At their initial presentation, patients suspected of having CVD should be asked about their symptoms, aggravating and alleviating factors, family history, occupation, exercise habits, changes in weight, thromboembolic history, allergies, medications, pregnancy history, and any cardiac, renal, or other comorbidities [13]. Physical examination of the legs should then be performed while the patient is standing, checking for varicose veins, swelling, skin pigmentation, induration, inflammation, and ulcers. Filling of the varicose veins can be checked by applying a tourniquet or manual compression over the superficial veins and then asking the patient to stand up. This test is called the Brodie-Trendelenburg test and, if vein filling exceeds 20 seconds, it may suggest that the varicose veins are caused by superficial venous insufficiency [10].
If venous insufficiency is suspected, further examination with lower-extremity duplex ultrasound scanning (DUS) should be considered. DUS is currently the most used and recommended diagnostic technique for evaluation of CVD. Etiological and anatomical information can be obtained through DUS. The size, reflux, obstruction, and venous flow patterns of the superficial and deep veins can be examined using the combination of grayscale B-mode imaging and spectral Doppler [12]. Specifically, 2-dimensional images of the blood vessels can be achieved with the grayscale B-mode (brightness mode), and blood flow or reflux can be evaluated by the Doppler mode [9].
To maintain the most accurate, reproducible, and credible diagnostic and treatment results, many international and domestic vascular societies have developed clinical ultrasound guidelines, which they reevaluate and update based on newly gathered accredited evidence [14-17].
It is recommended that the lower extremity DUS should be performed with the patient standing whenever possible, and evaluated by an accredited ultrasonographer. A reverse Trendelenburg position can also be used if the patient has difficulty standing [12].
To achieve the most accurate and standardized ultrasound images, it is recommended that high-frequency (5–16 MHz) linear probes be used [12-17]. A complete DUS examination of the lower extremity for CVD starts just proximal to the SFJ at the common femoral vein and includes images of the superficial truncal veins (SFJ, GSV, SPJ, SSV, AAGSV, and PASV), the deep truncal veins (common femoral, femoral, and popliteal veins), and the perforating veins.
To achieve a complete DUS examination for venous reflux in the lower extremities, Gloviczki et al. [12] recommended including examinations of the common femoral vein; proximal, mid, and distal femoral veins; popliteal veins; the SFJ and the GSV at the proximal thigh and knee; and the AASV, and SSV at the SPJ or proximal calf.
For a complete report, the exact name of the examined vein, the location, diameter (from anterior to posterior wall), and pathologic findings such as reflux must be documented with the images [12,17]. Images of both normal and abnormal findings should be documented in the patient’s record.
Multiple reliable references, including the UIP consensus document and the most recently reported Korean Society for Phlebology Society guidelines, recommend including both the transverse and longitudinal sections when performing an ultrasound examination of the lower extremities to obtain thorough and accurate information. Information on the surrounding anatomy of the vein, the diameter of the vein, and the presence or absence of thrombus are well visualized in the transverse section. To exam for reflux, however, the longitudinal section is recommended to provide clearer objective information, as appropriate given the principle of spectral Doppler examination.
Venous reflux is an uninterrupted retrograde venous flow from the groin to the calf and is mainly caused by venous hypertension, venous valve damage, and venous flow obstruction [10]. An evaluation for reflux is necessary to check the vein patency and valvular functions.
Pathologic venous reflux in the superficial truncal veins (GSV, SSV, AASV, PASV) and in the tibial, deep femoral, and perforating veins is defined as a reversed flow with a minimum value of >500 ms. Pathologic reflux in the common femoral, femoral, and popliteal veins is defined as a reversed flow with a minimum value of >1 second. Junctional reflux is limited to the SFJ or SPJ. Segmental reflux occurs only in a portion of a superficial or deep truncal vein. A “pathologic” perforating vein in patients with varicose veins includes those with an outward flow duration of ≥500 ms together with a vein diameter exceeding 3.5 mm on DUS [12].
To evaluate for reflux, use of the Valsalva maneuver or distal augmentation is recommended to assess the common femoral vein and SFJ, and distal augmentation with either manual compression or cuff inflation/deflation for evaluation of the more distal segments [10,12]. If abnormal retrograde flow suggesting venous reflux is confirmed under color Doppler imaging, measurement of the spectral Doppler waveform using calipers is recommended. In this imaging modality, both the augmentation waveform (reflux in response to a Valsalva maneuver or distal compression of calf muscles) and the reflux waveform (wave created by the pathologic retrograde venous reflux) should appear on opposite sides of the baseline (Fig. 2). Documentation of the name of the vein with reflux, location of the reflux, and the exact reflux time measured in seconds or milliseconds on the ultrasound image is recommended to enhance the quantification and accuracy of image interpretation.
To fully understand the pathophysiology and choose the correct treatment plan, it is also essential to examine for the presence of venous obstruction in the deep veins. Venous obstruction can be suspected if there is an absence of flow, blunted augmentation, presence of an echogenic thrombus within the vein, or failure of the vein to collapse with a compression maneuver. More caution is necessary if a patient presents with combined superficial venous insufficiency and deep venous thrombosis.
Venous disease can also be evaluated using CT and magnetic resonance venography. These techniques do not provide functional information, and therefore are not considered first-line diagnostic tools for CVD. However, they may be useful in evaluating focal or complex lesions that may be equivocal on ultrasound images, evaluating surrounding structures, and assessing for intrinsic or extrinsic obstruction [13].
If CVD has been confirmed with history-taking, a clinical examination, and ultrasonography, the next step is a precise description of the disease status.
The CEAP classification, an internationally accepted standard for describing patients with chronic venous disorders, was developed in 1993 and most recently updated in 2020. It is a classification system based on the clinical manifestations of chronic venous disorders, the current understanding of its etiology, the involved anatomy, and the underlying venous pathology [18]. It has been revised and updated by the American Venous Forum in order to improve the reproducibility of clinical findings between physicians, clarify the differences between older and new versions of the CEAP classification, add new evidence-based knowledge into the CEAP classification, and finally to balance the simple practical use of the classification with the highly specific and detailed descriptions of patients with CVD.
This classification uses a range of symptoms and signs of CVD to describe the severity (C: clinical); categorizes the etiology as congenital, primary, or secondary (E: etiology); localizes the affected veins as superficial, deep, or perforating (A: anatomy); and finally, characterizes the pathophysiology as reflux, obstruction, both, or neither (P: pathophysiology). Tables 1 and 2 briefly summarizes the CEAP classification.
Table 1 . Updated CEAP classification of chronic venous disease.
CEAP | Description |
---|---|
Clinical classification (C) | |
C0 | No visible or palpable signs of venous disease |
C1 | Telangiectasias or reticular veins |
C2 | Varicose veins |
C2r | Recurrent varicose veins |
C3 | Edema |
C4 | Changes in skin and subcutaneous tissue secondary to chronic venous disease |
C4a | Pigmentation or eczema |
C4b | Lipodermatosclerosis or atrophie blanche |
C4c | Corona phlebectatica |
C5 | Healed ulcer |
C6 | Active venous ulcer |
C6r | Recurrent active venous ulcer |
Etiologic classification (E) | |
Ep | Primary |
Es | Secondary |
Esi | Secondary–intravenous |
Ese | Secondary–extravenous |
Ec | Congenital |
En | No cause identified |
Anatomic classification (A) | |
As | Superficial |
Ad | Deep |
Ap | Perforator |
An | No venous anatomic location identified |
Pathophysiologic classification (P) | |
Pr | Reflux |
Po | Obstruction |
Pr,o | Reflux and obstruction |
Pn | No pathophysiology identified |
CEAP, clinical, etiological, anatomical, and pathophysiological..
Table 2 . Updated anatomic classification of chronic venous disease.
Anatomic classification | Old | New | Description |
---|---|---|---|
As (superficial) | 1. | Tel | Telangiectasia |
1. | Ret | Reticular veins | |
2. | GSVa | Great saphenous vein above knee | |
3. | GSVb | Great saphenous vein below knee | |
4. | SSV | Small saphenous vein | |
AASV | Anterior accessory saphenous vein | ||
5. | NSV | Nonsaphenous vein | |
Ad (deep) | 6. | IVC | Inferior vena cava |
7. | CIV | Common iliac vein | |
8. | IIV | Internal iliac vein | |
9. | EIV | External iliac vein | |
10. | PELV | Pelvic veins | |
11. | CFV | Common femoral vein | |
12. | DFV | Deep femoral vein | |
13. | FV | Femoral vein | |
14. | POPV | Popliteal vein | |
15. | TIBV | Crural (tibial) vein | |
15. | PRV | Peroneal vein | |
15. | ATV | Anterior tibial vein | |
15. | PTV | Posterior tibial vein | |
16. | MUSV | Muscular veins | |
16. | GAV | Gastrocnemius vein | |
16. | SOV | Soleal vein | |
Ap (perforator) | 17. | TPV | Thigh perforator vein |
18. | CPV | Calf perforator vein | |
An | No venous anatomic location identified |
As mentioned above, the CEAP classification was updated in 2020. The clinical classification (C), which is the most widely used component of CEAP, is currently arranged so that more severe manifestations of venous disease are assigned a higher class. However, its weakness is that the clinical classification is not a quantitative severity scale and does not reflect changes over time.
Unfortunately, recurrence of varicose veins (C2) and venous ulcers (C6) after intervention to correct reflux is common. Therefore, as shown in Tables 1 and 2, the tendency of varicose veins and venous ulcers to recur is reflected in the 2020 update of the CEAP classification, with the addition of the modifier “r” to the C2 and C6 clinical classes. Although the clinical definition of recurrence is identical to that of the previously suggested “recurrent varices after surgery” [19], the previous treatments were not limited to surgical treatments.
Another change in the C classification includes corona phlebectatica, which is a fan-shaped pattern of numerous small intradermal veins on the medial or lateral aspects of the ankle and foot. To differentiate corona phlebectatica from C1 lesions and reduce the risk of misclassification, it is important to recognize the essential elements of corona phlebectatica: telangiectasia, more than 5 nonconfluent intradermal veins, venous cups, stasis spots (clusters of dilated papillary capillaries), extension equal to or greater than half the length of the foot, and tiny areas of perivenous pigmentation. Many phlebologists consider corona phlebectatica an early sign of advanced venous disease that therefore warrants inclusion in more advanced C categories. The risk of developing ulcers in corona phlebectatica has been reported to be 5.3 times higher, like with eczema (C4a) and lipodermatosclerosis (C4b). Furthermore, the relative risk of finding incompetent leg or calf perforators by duplex ultrasound is 4.4 times greater. These results suggest that corona phlebectatica should not be compared to telangiectasias and reticular veins in other locations. Therefore, because of the association of corona phlebectatica with more advanced venous disease, corona phlebectatica was placed in the C4 class as a separate subclass (C4c) in the 2020 CEAP update [20].
The etiology (E) classification of venous disease, is categorized as congenital (Ec), primary (Ep), or secondary (post-thrombotic) (Es). Besides small refinements in the definitions of E subclasses, no major changes were made in the 2020 update [18].
The anatomic (A) classification of venous disease is categorized as superficial (As), deep (Ad), or perforating (Ap) veins. Changes were made in 2020 replacing the previous numeric descriptions of the venous segments with their common abbreviations. This allowed a more intuitive identification of these anatomic segments (Table 2).
The pathophysiologic (P) classification includes reflux (r), obstruction (o), reflux and obstruction (r,o), and no venous pathophysiology (n). The advanced designations did not change.
Because of the CEAP classification’s descriptive nature and static categorical classification scheme, the Venous Clinical Severity Score (VCSS) was also developed and widely used as an evaluation tool to reflect the changes in disease severity over time and in response to treatment. The VCSS includes 9 parameters of venous disease with a symptom severity scale from 0 to 3 (0–1=mild; 2=moderate; and 3=severe). The scored parameters include pain, varicose veins, edema, skin pigmentation, inflammation, induration, ulcers (number, size, and duration), and compressive therapy [9,10]. The VCSS is shown in Table 3.
Table 3 . Venous Clinical Severity Score.
Absent=0 | Mild=1 | Moderate=2 | Severe=3 | |
---|---|---|---|---|
Pain | None | Occasional, not restricting daily activity | Daily, interfering but not preventing daily activity | Daily, limits most daily activity |
Varicose veins | None | Few isolated branch varices or clusters; includes ankle flare | Confined to calf or thigh | Involves calf and thigh |
Venous edema | None | Limited to foot and ankle | Extends above the ankle but below the knee | Extends to knee and above |
Skin pigmentation | None or focal | Limited to the peri-malleolar area | Diffuse, over lower third of calf | Wider distribution above lower third of calf |
Inflammation | None | Mild cellulitis, ulcer margin limited to the peri-malleolar area | Diffuse over lower third of calf | Wider distribution above lower third of calf |
Induration | None | Limited to the peri-malleolar area | Diffuse over lower third of calf | Wider distribution above lower third of calf |
Ulcer number | 0 | 1 | 2 | ≥3 |
Ulcer duration | NA | <3 mo | >3 mo, <1 yr | Not healed >1 yr |
Ulcer size | NA | Diameter <2 cm | Diameter 2–6 cm | Diameter >6 cm |
Compressive therapy | Not used | Intermittent | Most days | Full compliance |
NA, not applicable..
Lower-extremity CVD is a common disease with an increasing global and national prevalence. It is a disease with a very broad clinical spectrum and diverse symptoms, which may not exactly correlate with the severity of the CVD. Therefore, a thorough understanding of venous anatomy and the pathophysiology of CVD, as well as the correct use of duplex ultrasound in the diagnosis of CVD are essential to achieving an accurate diagnosis and optimal treatment results. Unfortunately, with the increasing prevalence of CVD in Korea, there have also been some ethical concerns regarding the diagnosis and management of varicose veins in Korea. However, multiple Korean academic societies have collaborated to improve the quality of diagnosis and treatment by standardizing the diagnostic criteria and indications for treatment of varicose veins. Hopefully these evidence-based clinical guidelines on CVD and DUS will help to optimize the diagnostic and treatment results of CVD and ultimately benefit Korean patients.
Authors contributions
Conceptualization: JHC. Investigation: JHC, SH. Data curation: JHC, SH. Visualization: JHC. Writing–original draft: JHC. Writing–review and editing: JHC, SH. Final approval of the manuscript: all authors.
Conflict of interest
Jae Ho Chung is an editorial board member of the journal but was not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflict of interest relevant to this article was reported.
Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Table 1 . Updated CEAP classification of chronic venous disease.
CEAP | Description |
---|---|
Clinical classification (C) | |
C0 | No visible or palpable signs of venous disease |
C1 | Telangiectasias or reticular veins |
C2 | Varicose veins |
C2r | Recurrent varicose veins |
C3 | Edema |
C4 | Changes in skin and subcutaneous tissue secondary to chronic venous disease |
C4a | Pigmentation or eczema |
C4b | Lipodermatosclerosis or atrophie blanche |
C4c | Corona phlebectatica |
C5 | Healed ulcer |
C6 | Active venous ulcer |
C6r | Recurrent active venous ulcer |
Etiologic classification (E) | |
Ep | Primary |
Es | Secondary |
Esi | Secondary–intravenous |
Ese | Secondary–extravenous |
Ec | Congenital |
En | No cause identified |
Anatomic classification (A) | |
As | Superficial |
Ad | Deep |
Ap | Perforator |
An | No venous anatomic location identified |
Pathophysiologic classification (P) | |
Pr | Reflux |
Po | Obstruction |
Pr,o | Reflux and obstruction |
Pn | No pathophysiology identified |
CEAP, clinical, etiological, anatomical, and pathophysiological..
Table 2 . Updated anatomic classification of chronic venous disease.
Anatomic classification | Old | New | Description |
---|---|---|---|
As (superficial) | 1. | Tel | Telangiectasia |
1. | Ret | Reticular veins | |
2. | GSVa | Great saphenous vein above knee | |
3. | GSVb | Great saphenous vein below knee | |
4. | SSV | Small saphenous vein | |
AASV | Anterior accessory saphenous vein | ||
5. | NSV | Nonsaphenous vein | |
Ad (deep) | 6. | IVC | Inferior vena cava |
7. | CIV | Common iliac vein | |
8. | IIV | Internal iliac vein | |
9. | EIV | External iliac vein | |
10. | PELV | Pelvic veins | |
11. | CFV | Common femoral vein | |
12. | DFV | Deep femoral vein | |
13. | FV | Femoral vein | |
14. | POPV | Popliteal vein | |
15. | TIBV | Crural (tibial) vein | |
15. | PRV | Peroneal vein | |
15. | ATV | Anterior tibial vein | |
15. | PTV | Posterior tibial vein | |
16. | MUSV | Muscular veins | |
16. | GAV | Gastrocnemius vein | |
16. | SOV | Soleal vein | |
Ap (perforator) | 17. | TPV | Thigh perforator vein |
18. | CPV | Calf perforator vein | |
An | No venous anatomic location identified |
Table 3 . Venous Clinical Severity Score.
Absent=0 | Mild=1 | Moderate=2 | Severe=3 | |
---|---|---|---|---|
Pain | None | Occasional, not restricting daily activity | Daily, interfering but not preventing daily activity | Daily, limits most daily activity |
Varicose veins | None | Few isolated branch varices or clusters; includes ankle flare | Confined to calf or thigh | Involves calf and thigh |
Venous edema | None | Limited to foot and ankle | Extends above the ankle but below the knee | Extends to knee and above |
Skin pigmentation | None or focal | Limited to the peri-malleolar area | Diffuse, over lower third of calf | Wider distribution above lower third of calf |
Inflammation | None | Mild cellulitis, ulcer margin limited to the peri-malleolar area | Diffuse over lower third of calf | Wider distribution above lower third of calf |
Induration | None | Limited to the peri-malleolar area | Diffuse over lower third of calf | Wider distribution above lower third of calf |
Ulcer number | 0 | 1 | 2 | ≥3 |
Ulcer duration | NA | <3 mo | >3 mo, <1 yr | Not healed >1 yr |
Ulcer size | NA | Diameter <2 cm | Diameter 2–6 cm | Diameter >6 cm |
Compressive therapy | Not used | Intermittent | Most days | Full compliance |
NA, not applicable..