Clinical Imaging xxx (2016) xxx–xxx

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Screening for lower extremity venous disease Benjamin L. Yam ⁎, Ronald S. Winokur, Neil M. Khilnani Department of Vascular and Interventional Radiology, NewYork-Presbyterian/Weill Cornell Medical Center, New York, NY 10065, USA

a r t i c l e

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Article history: Received 8 November 2015 Accepted 21 December 2015 Available online xxxx Keywords: Vein screening Chronic venous disease Chronic venous insufficiency Venous leg ulcers Venous thromboembolic disease

a b s t r a c t Chronic venous disease (CVD) is frequently found in the general population. However, CVD is often overlooked by both healthcare providers and patients due to an underappreciation of the magnitude and impact of this condition. The importance of CVD relates to its prevalence, the natural history of the disease, and the socioeconomic impact of its manifestations. The aim of this article is to improve awareness of lower extremity venous disease and encourage screening to identify undiagnosed CVD and to identify patients at earlier stages of disease to prevent progression to more advanced states at the time of initial diagnosis. © 2016 Elsevier Inc. All rights reserved.

1. Introduction Chronic venous disease (CVD) of the lower extremities is frequently found in the general population [1–6]. However, CVD is often overlooked by both healthcare providers and patients due to an underappreciation of the magnitude and impact of this condition. The importance of CVD relates to its prevalence, the natural history of the disease, and the socioeconomic impact of its manifestations. The aim of this article is to improve awareness of lower extremity venous disease and encourage screening to identify undiagnosed CVD and to identify patients at earlier stages of disease to prevent progression to more advanced states at the time of initial diagnosis. CVD of the lower extremities most commonly results from primary superficial venous incompetence and less often from deep venous reflux, residual obstruction and reflux following prior deep venous thrombosis (DVT), neuromuscular conditions affecting the calf muscle pump, and congenital disorders. Prolonged functional valvular failure and reflux leads to chronic venous hypertension, which in turn triggers the chronic inflammatory changes and vessel wall injury associated CVD. CVD constitutes a spectrum of chronic morphologic and functional venous abnormalities manifested by clinical signs and/or symptoms and can be classified according to CEAP (Clinical, Etiological, Anatomical, and Pathophysiological) classification. Under the CEAP system, groupings (C0–C6) are based on clinical findings including the presence of telangiectasias or reticular veins, varicose veins, venous edema, skin pigmentation changes, or ulceration. Higher C-classification corresponds to more advanced CVD as shown in Table 1 [7–9]. The term CVD is used to summarize findings classified under the full range of

⁎ Corresponding author. Tel.: +1 646 481 5554. E-mail address: [email protected] (B.L. Yam).

CEAP groupings. Chronic venous insufficiency (CVI) refers to venous abnormalities classified as C3 through C6 [8]. The revised Venous Clinical Scoring System (VCSS) is another venous assessment tool utilized to categorize the overall severity of venous disease [10]. Unlike CEAP, VCSS scale is a dynamic tool that provides descriptions of the signs and symptoms of CVD and should be used to assess treatment outcome.

1.1. Epidemiology Approximately 22–29% of the adult Western population carries a diagnosis of varicose veins and 5% have more advanced CVD findings such as skin changes or ulcerations [5,11–14]. In the United States, over 11 million males and 22 million females aged 40–80 years have varicose veins [15]. Over 2 million adults have advanced CVD and at least 20,556 individuals will have newly diagnosed venous ulcers each year [15,16]. Results from the Bonn Vein Study, a German population-based cross-sectional study of 3072 participants (43.9% male, 56.1% female) aged 18–79 years, revealed that nearly half of all men and over half of all women had signs or symptoms of CVD. These included varicose veins without edema or skin changes in 14.3% (12.4% men, 15.8% women), edema in 13.4% (11.6% men, 14.9% women), skin changes in 2.9% (3.1% men, 2.7% women), and healed or active ulceration in 0.6% or 0.1%, respectively [17,18]. In the United States, the American Venous Forum administered the multicenter National Venous Screening Program (NVSP), which screened 2234 adults (23% male, 77% female; 80% Caucasian) aged 17–93 years (mean 60 years) for venous disease. Findings from this program showed CEAP classifications from C0 to C6 to be 29%, 29%, 23%, 10%, 9%, 1.5%, and 0.5%, respectively (Fig. 1). Venous reflux was observed in 37% and obstruction in 5% of participants [19].

http://dx.doi.org/10.1016/j.clinimag.2015.12.018 0899-7071/© 2016 Elsevier Inc. All rights reserved.

Please cite this article as: Yam BL, et al, Screening for lower extremity venous disease, Clin Imaging (2016), http://dx.doi.org/10.1016/ j.clinimag.2015.12.018

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B.L. Yam et al. / Clinical Imaging xxx (2016) xxx–xxx

1.2. Risk factors

Table 1 Summary of basic CEAP classification

Assessment of the severity of CVD is important for risk stratification, patient counseling, and potential therapy. Increased age, female gender, parity, family history of varicose veins, and standing occupation have all been shown to be risk factors for venous insufficiency/hypertension [1,35]. A variety of genetic, environmental, and hemodynamic factors likely influence the development and natural history of CVD, and research to determine associations with specific genes is ongoing [36,37]. Some studies have shown associations between obesity and postmenopausal status with CVD and CVI [11,38,39]. Overweight patients with varicose veins appear to be at higher risk for disease progression to CVI [40,41]. Occupational orthostatism, noncompliance with elastic stocking usage, and arterial hypertension may also serve as independent risk factors for progression of venous disease [42–45]. Risk factors for DVT are generally related to one or more components of Virchow's triad, and many thromboembolic risk factors are associated with a component of hypercoagulability on a genetic, acquired, or situational basis (Table 2). The most important risk factors for acute DVT include age, major surgery, trauma, hypercoagulable state, malignancy, hospital/nursing home care, individual or family history of VTE, immobilization, central venous catheters, pregnancy, estrogen replacement, oral contraceptives, hormonal treatment, and long-distance travel [46,47]. Several tools have been developed to evaluate risk for VTE, including the Caprini risk assessment model, which utilizes population data to calculate an individual's postoperative VTE risk score [48].

Clinical classification C0: no visible or palpable signs of venous disease C1: telangiectasias or reticular veins C2: varicose veins C3: edema C4a: pigmentation and eczema C4b: lipodermatosclerosis and atrophie blanche C5: healed venous ulcer C6: active venous ulcer S: symptoms including ache, pain, tightness, skin irritation, heaviness, muscle cramps, as well as other complaints attributable to venous dysfunction A: asymptomatic Etiologic classification Ec: congenital Ep: primary Es: secondary (postthrombotic) Anatomic classification s: superficial veins p: perforator veins d: deep veins Pathophysiologic classification Pr: reflux Po: obstruction Pr,o: reflux and obstruction Pn: no venous pathophysiology identifiable

There are an estimated 2,000,000 new cases of DVT each year in the United States [20]. DVT is an important manifestation of lower extremity venous disease because it can lead to potentially fatal pulmonary embolism (PE) or postthrombotic syndrome (PTS) [21]. Acute PE is the third most common cause of United States hospital deaths [22,23]. DVT, superficial thrombophlebitis, and PE are described collectively as venous thromboembolism (VTE). The sex- and age-adjusted incidence of first-time symptomatic VTE in the United States is between 71 and 117 cases per 100,000 individuals [24]. These account for over 600,000 hospital admissions each year [25–27]. PTS develops as a frequent chronic complication of DVT, occurring in 20–40% of patients within 1–2 years following symptomatic DVT, and a severe form of PTS is seen in 4–11% of patients [28–31]. Patients with PTS experience deteriorated disease-specific quality of life (QOL) when compared to those without the condition [28,32,33]. Additionally, the management and treatment of PTS contributes a significant portion to the overall economic burden of DVT sequelae [34].

1.3. Vein screening Currently, no universal screening guidelines for lower extremity venous disease exist. However, given the prevalence of CVD and incidence of VTE within the general population, venous screening programs may serve to identify individuals at risk for VTE, detect CVD, and potentially prevent consequences of CVD such as recurrent cellulitis or venous leg ulcers (VLUs). The NVSP enrolled 476 individuals into a pilot study that aimed to educate, identify, and empower individuals with knowledge about common venous diseases affecting themselves and the community at large. The majority of participants (77%) were categorized as high or very high risk of developing VTE, if put in a high-risk situation. Additionally, 40% showed evidence of venous reflux, 6% showed signs of venous obstruction, and 20% had a clinical CEAP classification of CVI (≥C3). Analysis of the screening results demonstrated a correlation between risk stratification, duplex ultrasound (US) findings, and severity of CVD by clinical inspection [49]. In this study, increasing DVT risk scores demonstrated a

70 60

Percentage

50 40 30 20 10 0 C0

C1

C2

C3

C4

C5

C6

C-classification Bonn Vein Study

NVSP

Fig. 1. Prevalence of C-classifications from the Bonn Vein Study and the NVSP [11,19].

Please cite this article as: Yam BL, et al, Screening for lower extremity venous disease, Clin Imaging (2016), http://dx.doi.org/10.1016/ j.clinimag.2015.12.018

B.L. Yam et al. / Clinical Imaging xxx (2016) xxx–xxx Table 2 Thromboembolic risk factors (adapted from Meissner MH et al. [46]) Risk factor

Risk

Age

Relative risk 1.9 per 10-year increase

Surgery • General • Neurosurgery • Hip/knee Trauma Malignancy History of VTE Primary hypercoagulable states • Antithrombin, protein C, or protein S deficiency • Factor V Leiden, homozygous • Factor V Leiden, heterozygous • Prothrombin 20210A • Increased factor VIII • Hyperhomocysteinemia Family history Oral contraceptives Estrogen replacement Immobilization (preoperative) Pregnancy Postpartum Femoral catheters (trauma patients) Antiphospholipid antibodies • Lupus anticoagulant • Anticardiolipin antibody Inflammatory bowel disease Obesity Varicose veins Myocardial infarction/congestive heart failure

19% 24% 48–61% 58% of patients 15% of patients 2–9% 10× 80× 8× 4× 6× 2.5× to 4× 2.9× 2.9× 2× to 4× 2× 0.075% of pregnancies 2.3–6.1 per 1000 deliveries 12% 6× 2× 1.2–7.1% of patients Variable Variable Variable

positive correlation with increasing C-classification of CEAP. In addition, participants who showed reflux in one or more venous segments were more likely to have higher C-classifications when compared to those without reflux. Follow-up studies are needed to determine how participants utilized the screening results and the subsequent course of disease management. Although the natural history of CVD progression is less well studied, progression of primary venous valvular incompetence has been demonstrated. For instance, varicose veins can progress to a more advanced form of chronic venous dysfunction such as CVI [42,50,51]. In CVI, increased ambulatory venous hypertension initiates a series of changes in the subcutaneous tissue and skin that may lead to tissue edema and chronic inflammatory changes. These signs are most frequently noted at and above the ankles and may progress to limb swelling, pigmentation, corona phlebectatica (visible network of dilated intradermal venules and epidermal capillaries at the ankle), lipodermatosclerosis (skin and subcutaneous tissue cicatrization related to inflammation of subcutaneous fat), eczema, or venous ulcerations [8,52]. One study found that individuals with advanced CVI were more likely to have had primary venous valvular incompetence than PTS (70% vs. 30%) [53]. Kostas studied the progression of CVD in the contralateral untreated limbs of patients who underwent unilateral varicose vein surgery and found that over half (52%) of patients developed CVD in the contralateral limb within 5 years despite the fact that they were initially asymptomatic on that side [42]. Findings from a meta-analysis of 390 patients with primary CVD and venous ulcers who were evaluated with duplex US revealed superficial incompetence alone in 44% and superficial incompetence in combination with deep reflux in 43% of ulcerated limbs [54–56]. In what has frequently been referred to as the Bonn 2 study, an average 6.6-year follow-up of the original Bonn Vein Study cohort revealed a nearly 2% per year progression from CEAP class C2 to CVI (Classes C3– C6) and progression from C2 disease to C3–C4 disease in up to 31.8% of individuals [44]. It should be noted that almost none of those with C2 disease progressed to ulceration over this 6.6-year follow-up

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interval, and screening those with C2 disease with the idea of treating all C2 patients to prevent VLU would likely result in a very small population benefit and not be cost effective. Epidemiologic analysis of the Edinburgh Vein Study showed that 58% of all CVD patients demonstrated progression of disease over a 13.4-year follow-up period (4.3% per year) and 32% of those with only varicose veins at baseline had progressed to CVI [40,43]. Reflux becomes more prevalent with time. Follow-up of the Edinburgh Vein Study showed an incidence of venous reflux of 12.7% over the 13-year period or 0.9% per year [57]. A study on patients awaiting interventional treatment for varicose veins showed a 11.2% progression of clinical stage as demonstrated by duplex US at a median follow-up interval of 19 months (range 1–43 months) [58]. Similarly, a mean 4year sonographic follow-up of patients with varicose veins who had refused superficial vein treatment showed progression of venous reflux in 94% [59]. Labropoulos showed that CVD progresses more rapidly when it follows an inciting venous event like PTS [60]. The study demonstrated a fourfold increase in progression to C4–C6 disease in individuals with secondary venous disease in comparison to those with primary venous reflux disease, and 6.5% had progressed to VLU after 5 years. VLU is an underrecognized and undertreated disease within the community for several reasons that include inadequate provider training, the varied nature of the disease presentation, and the lack of understanding of preventability and treatment. For these reasons, the Pacific Vascular Symposium 6 has issued a Call to Action to develop a plan to reduce the incidence of VLU in the United States by 50% in 10 years [61]. Robertson showed that progression from C4 to VLU is more likely than progression of C2–C3 disease to VLU [62]. In this study, risk factors for VLU development included skin changes due to venous disease (corona phlebectatica, hyperpigmentation, eczema, lipodermatosclerosis), history of DVT, higher body mass index, smoking history, deep venous reflux, low pumping function during photoplethysmography, and limited range of ankle motion. Screening for such patients with C4 disease could help reduce the incidence of VLU by allowing for careful followup and appropriate intervention prior to VLU development. In a 4-year follow-up study of 304 patients on a waiting list for varicose vein surgery, 64% reported progression of disease and 12% developed VLU [63]. Hemodynamic factors including plethysmography and duplex US alone do not predict which individuals with venous reflux and/or obstruction progress to ulceration. Several genetic polymorphisms such as HFE and MMP12 appear to play a role in predicting progression to VLU [37]. Further studies are needed to clarify the role of such nonanatomic and hemodynamic factors influencing patients with C4 disease who are at risk for developing VLU. In addition to causing discomfort and chronic pain, complications from varicose veins are frequently associated with lost working days, disability, early retirement, and deterioration of health-related QOL [15,16,64,65]. Severe CVD is associated with significant morbidity and may lead to limb loss in rare cases [66]. Treatment of CVD can be a substantial financial burden on patients and society. In the United States, an estimated US$150 million to US$1 billion is spent on direct medical management of CVD annually [16,66]. Similarly, in the United Kingdom, 2% of the national healthcare budget (US$1 billion) is spent on VLU management yearly [15]. Further investigation to determine the financial impact and potential health benefits of venous screening programs is warranted. 1.4. Screening process A comprehensive vein screening program would ideally include a thorough assessment of patients' risk factors for CVD and VTE. A standardized questionnaire may be administered to obtain information regarding demographics, gender, age, body mass index, medical history, lifestyle, type and degree of physical activity, and QOL along with known risk factors for CVD and VTE including family history, job

Please cite this article as: Yam BL, et al, Screening for lower extremity venous disease, Clin Imaging (2016), http://dx.doi.org/10.1016/ j.clinimag.2015.12.018

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occupation, parity, and history of varicose veins, VLUs, and thromboembolic disease. Lower extremity symptoms like aching, pain, tightness, skin irritation, heaviness, and muscle cramps that may be attributed to CVD should be assessed [8,67]. There is a significant correlation between development of lower limb symptoms and increasing CEAP classes [2]. In patients with varicose veins, development of lower limb symptoms has been shown to have a negative impact on health-related QOL [64]. Patient-reported QOL has become an increasingly important component of disease evaluation, particularly with regard to changes in disease severity over time, and should be used as part of a screening program. For chronic disease states such as CVD and PTS, assessment of health-related QOL provides relevant information regarding the impact of illness-related impairment that may not be adequately assessed utilizing physician-based measures of morbidity or mortality [33,68]. Instruments used to measure health-related QOL are typically in the form of administered questionnaires. In addition to generalized health-related QOL instruments, such as the Short-Form 36 Health Survey, which has been effectively utilized in patients with CVD, venousdisease-specific questionnaires have been developed to obtain more specific information about the impact of CVD [15,69]. The two commonly used disease-specific QOL instruments for CVD are the Aberdeen Varicose Vein Questionnaire (AVVQ) and the Chronic Venous Insufficiency Quality of Life Questionnaire (CIVIQ) [16,70,71]. The AVVQ tends to reflect clinical disease severity by emphasizing the presence of signs and symptoms, while the CIVIQ underscores the psychosocial impact of CVD [70,72,73]. When screening for CVD, a trained professional should conduct a brief physical exam by placing the participant in the standing position and carefully examining the skin around the medial ankle. Note should be made of sequelae of chronic venous hypertension and CEAP classification should be designated. The screening process should also incorporate an abbreviated duplex US examination of the bilateral lower extremities to evaluate for venous reflux and/or obstruction. At minimum, the common femoral vein, saphenofemoral junction, and the above-knee popliteal vein should be interrogated. Ideally, the midthigh greater saphenous vein and small saphenous vein should also be studied. The US examination should be performed with the participant in a standing or reverse Trendelenburg position. Identification of valvular closure and/or flow reversal may be aided by asking the participant to perform the Valsalva maneuver when evaluating the common femoral vein, as well as implementation of a manual calf compression augmentation maneuver during the study. A reflux time of N0.5 s is generally used as the threshold for defining pathologic reflux in the superficial venous system and N1 s in the deep venous system [74]. The sonographer should also evaluate for thrombotic obstruction by performing manual venous compression with the US probe every 3–5 cm and by evaluating flow with Doppler. Monophasic waveforms in the common femoral vein can be indicative of a more central venous obstruction or compression [75]. Duplex US allows for identification of the distribution and extent of venous reflux, which correlates with the severity of CVI [41,76]. A trained professional should discuss screening findings with and provide written copy of these findings to participants. Participants should be encouraged to share the results with their primary care providers. Educational brochures explaining common lower extremity venous diseases should be provided to participants in order to allow them to gain a better understanding of their results and determine appropriate follow-up and management with their physician. 2. Conclusion CVD and VTE are common conditions that have a significant impact on affected individuals and the healthcare system. These conditions have potential for progression to more advanced disease. Venous screening can help identify undiagnosed CVD and VTE, as well as

distinguish those in earlier stages of disease to prevent progression to more advanced disease such as VLU. A successful screening program should include a focused questionnaire to assess pertinent risk factors for disease and current related signs and symptoms of disease, as well as a brief physical and ideally, a focused duplex US examination. In particular, we propose the use of screening to identify patients with C2 disease so as to provide education to them about disease progression and the need for conservative care and periodic evaluation with a healthcare provider. We also propose screening to be able to identify patients with C4 and C5 disease, especially those with a history of DVT, or high body mass index, in whom progression to VLU is higher. These patients should be made aware of the high incidence of progression to VLUs and the warning signs for imminent ulceration. They should be instructed to wear compression stockings and to have frequent evaluations with a healthcare provider with expertise in venous care. Implementation of venous screening programs may be justified to reduce the burden to national healthcare costs associated with treatment of morbid sequelae of CVD and to improve at-risk individuals' overall health-related QOL, although this has yet to be established.

References [1] Beebe-Dimmer JL, Pfeifer JR, Engle JS, Schottenfeld D. The epidemiology of chronic venous insufficiency and varicose veins. Ann Epidemiol 2005;15(3):175–84. http://dx.doi.org/10.1016/j.annepidem.2004.05.015. [2] Rabe E, Guex JJ, Puskas A, Scuderi A, Fernandez Quesada F. Epidemiology of chronic venous disorders in geographically diverse populations: results from the vein consult program. Int Angiol 2012;31(2):105–15. [3] Evans CJ, Fowkes FG, Ruckley CV, Lee AJ. Prevalence of varicose veins and chronic venous insufficiency in men and women in the general population: Edinburgh Vein Study. J Epidemiol Community Health 1999;53(3):149–53. [4] Pannier-Fischer F, Rabe E. Epidemiology of chronic venous diseases. Hautarzt 2003; 54(11):1037–44. http://dx.doi.org/10.1007/s00105-003-0616-0. [5] Criqui MH, Jamosmos M, Fronek A, et al. Chronic venous disease in an ethnically diverse population: the San Diego population study. Am J Epidemiol 2003;158(5): 448–56. [6] Khan AFA, Chaudhri R, Ashraf MA, Mazaffar MS, Zawar-ul-Imam S, Tanveer M. Prevalence and presentation of chronic venous disease in Pakistan: a multicentre study. Phlebology 2013;28(2):74–9. http://dx.doi.org/10.1258/phleb.2012.011122. [7] Eklof B, Perrin M, Delis KT, Rutherford RB, Gloviczki P. Updated terminology of chronic venous disorders: the VEIN-TERM transatlantic interdisciplinary consensus document. J Vasc Surg 2009;49(2):498–501. http://dx.doi.org/10.1016/j.jvs.2008. 09.014. [8] Eklöf B, Rutherford RB, Bergan JJ, et al. Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg 2004;40(6):1248–52. http://dx. doi.org/10.1016/j.jvs.2004.09.027. [9] Caggiati A, Bergan JJ, Gloviczki P, Jantet G, Wendell-Smith CP, Partsch H. Nomenclature of the veins of the lower limbs: an international interdisciplinary consensus statement. J Vasc Surg 2002;36(2):416–22. [10] Vasquez MA, Rabe E, McLafferty RB, et al. Revision of the venous clinical severity score: venous outcomes consensus statement: special communication of the American Venous Forum Ad Hoc Outcomes Working Group. J Vasc Surg 2010; 52(5):1387–96. http://dx.doi.org/10.1016/j.jvs.2010.06.161. [11] Maurins U, Hoffmann BH, Lösch C, Jöckel KH, Rabe E, Pannier F. Distribution and prevalence of reflux in the superficial and deep venous system in the general population—results from the Bonn Vein Study, Germany. J Vasc Surg 2008;48(3): 680–7. http://dx.doi.org/10.1016/j.jvs.2008.04.029. [12] Carpentier PH, Maricq HR, Biro C, Ponçot-Makinen CO, Franco A. Prevalence, risk factors, and clinical patterns of chronic venous disorders of lower limbs: a populationbased study in France. J Vasc Surg 2004;40(4):650–9. http://dx.doi.org/10.1016/j.jvs. 2004.07.025. [13] Chiesa R, Marone EM, Limoni C, Volonté M, Schaefer E, Petrini O. Chronic venous insufficiency in Italy: the 24-cities cohort study. Eur J Vasc Endovasc Surg 2005;30(4): 422–9. http://dx.doi.org/10.1016/j.ejvs.2005.06.005. [14] Jawien A. The influence of environmental factors in chronic venous insufficiency. Angiology 2003;54(Suppl 1):S19–31. [15] Kaplan RM, Criqui MH, Denenberg JO, Bergan J, Fronek A. Quality of life in patients with chronic venous disease: San Diego population study. J Vasc Surg 2003;37(5): 1047–53. http://dx.doi.org/10.1067/mva.2003.168. [16] Smith JJ, Garratt AM, Guest M, Greenhalgh RM, Davies AH. Evaluating and improving health-related quality of life in patients with varicose veins. J Vasc Surg 1999;30(4): 710–9. [17] Wrona M, Jöckel K-H, Pannier F, Bock E, Hoffmann B, Rabe E. Association of venous disorders with leg symptoms: results from the Bonn Vein Study 1. Eur J Vasc Endovasc Surg 2015;50(3):360–7. http://dx.doi.org/10.1016/j.ejvs.2015.05.013. [18] Rabe E, Hertel S, Bock E, Hoffmann B, Jöckel K-H, Pannier F. Therapy with compression stockings in Germany—results from the Bonn Vein studies. J Dtsch Dermatol Ges 2013;11(March 2002):257–61. http://dx.doi.org/10.1111/j.1610-0387.2012. 08048.x.

Please cite this article as: Yam BL, et al, Screening for lower extremity venous disease, Clin Imaging (2016), http://dx.doi.org/10.1016/ j.clinimag.2015.12.018

B.L. Yam et al. / Clinical Imaging xxx (2016) xxx–xxx [19] McLafferty RB, Passman M a, Caprini J a, et al. Increasing awareness about venous disease: the American Venous Forum expands the National Venous Screening Program. J Vasc Surg 2008;48(2):394–9. http://dx.doi.org/10.1016/j.jvs.2008.03.041. [20] Gerotziafas GT, Samama MM. Prophylaxis of venous thromboembolism in medical patients. Curr Opin Pulm Med 2004;10(5):356–65. [21] Kearon C. Natural history of venous thromboembolism. Circulation 2003;107(23 Suppl 1):I22–30. http://dx.doi.org/10.1161/01.CIR.0000078464.82671.78. [22] Lindblad B, Eriksson A, Bergqvist D. Autopsy-verified pulmonary embolism in a surgical department: analysis of the period from 1951 to 1988. Br J Surg 1991;78(7): 849–52. [23] Sandler DA, Martin JF. Autopsy proven pulmonary embolism in hospital patients: are we detecting enough deep vein thrombosis? J R Soc Med 1989;82(4):203–5. [24] White RH. The epidemiology of venous thromboembolism. Circulation 2003;107(23 Suppl 1):I4–8. http://dx.doi.org/10.1161/01.CIR.0000078468.11849.66. [25] Hirsch DR, Ingenito EP, Goldhaber SZ. Prevalence of deep venous thrombosis among patients in medical intensive care. JAMA 1995;274(4):335–7. [26] Christiansen SC. Thrombophilia, clinical factors, and recurrent venous thrombotic events. JAMA 2005;293(19):2352. http://dx.doi.org/10.1001/jama.293.19.2352. [27] López JA, Kearon C, Lee AYY. Deep venous thrombosis. Hematology Am Soc Hematol Educ Program 2004:439–56. http://dx.doi.org/10.1182/asheducation-2004.1.439. [28] Kahn SR, Kearon C, Julian JA, et al. Predictors of the post-thrombotic syndrome during long-term treatment of proximal deep vein thrombosis. J Thromb Haemost 2005;3(4):718–23. http://dx.doi.org/10.1111/j.1538-7836.2005.01216.x. [29] Prandoni P, Lensing AWA, Prins MH, et al. Below-knee elastic compression stockings to prevent the post-thrombotic syndrome: a randomized, controlled trial. Ann Intern Med 2004;141(4):249–56. [30] Prandoni P, Lensing AW, Cogo A, et al. The long-term clinical course of acute deep venous thrombosis. Ann Intern Med 1996;125(1):1–7. [31] Brandjes DP, Büller HR, Heijboer H, et al. Randomised trial of effect of compression stockings in patients with symptomatic proximal-vein thrombosis. Lancet 1997; 349(9054):759–62. http://dx.doi.org/10.1016/S0140-6736(96)12215-7. [32] Kahn SR, Hirsch A, Shrier I. Effect of postthrombotic syndrome on health-related quality of life after deep venous thrombosis. Arch Intern Med 2002;162(10):1144–8. [33] Lamping DL, Schroter S, Kurz X, Kahn SR, Abenhaim L. Evaluation of outcomes in chronic venous disorders of the leg: development of a scientifically rigorous, patient-reported measure of symptoms and quality of life. J Vasc Surg 2003;37(2): 410–9. http://dx.doi.org/10.1067/mva.2003.152. [34] Bergqvist D, Jendteg S, Johansen L, Persson U, Odegaard K. Cost of long-term complications of deep venous thrombosis of the lower extremities: an analysis of a defined patient population in Sweden. Ann Intern Med 1997;126(6):454–7. [35] Criqui MH, Denenberg JO, Bergan J, Langer RD, Fronek A. Risk factors for chronic venous disease: the San Diego population study. J Vasc Surg 2007;46(2):331–7. http:// dx.doi.org/10.1016/j.jvs.2007.03.052. [36] Bharath V, Kahn SR, Lazo-Langner A. Genetic polymorphisms of vein wall remodeling in chronic venous disease: a narrative and systematic review. Blood 2014; 124(8):1242–50. http://dx.doi.org/10.1182/blood-2014-03-558478. [37] Gemmati D, Federici F, Catozzi L, et al. DNA-array of gene variants in venous leg ulcers: detection of prognostic indicators. J Vasc Surg 2009;50(6):1444–51. http://dx. doi.org/10.1016/j.jvs.2009.07.103. [38] Jawien A, Grzela T, Ochwat A. Prevalence of chronic venous insufficiency in men and women in Poland: multicentre cross-sectional study in 40,095 patients. Phlebology 2003;18(3):110–22. http://dx.doi.org/10.1258/026835503322381315. [39] Iannuzzi A, Panico S, Ciardullo AV, et al. Varicose veins of the lower limbs and venous capacitance in postmenopausal women: relationship with obesity. J Vasc Surg 2002; 36(5):965–8. [40] Lee AJ, Robertson LA, Boghossian SM, et al. Progression of varicose veins and chronic venous insufficiency in the general population in the Edinburgh Vein Study. J Vasc Surg Venous Lymphat Disord 2015;3(1):18–26. http://dx.doi.org/10.1016/j.jvsv. 2014.09.008. [41] García-Gimeno M, Rodríguez-Camarero S, Tagarro-Villalba S, et al. Reflux patterns and risk factors of primary varicose veins' clinical severity. Phlebology 2013;28(3): 153–61. http://dx.doi.org/10.1258/phleb.2011.011114. [42] Kostas TI, Ioannou CV, Drygiannakis I, et al. Chronic venous disease progression and modification of predisposing factors. J Vasc Surg 2010;51(4):900–7. http://dx.doi. org/10.1016/j.jvs.2009.10.119. [43] Pannier F, Rabe E. Progression in venous pathology. Phlebology 2015;30(1 Suppl): 95–7. http://dx.doi.org/10.1177/0268355514568847. [44] Rabe E, Pannier F, Ko A, Berboth G, Hoffmann B, Hertel S. Incidence of varicose veins, chronic venous insufficiency, and progression of the disease in the Bonn Vein Study II. J Vasc Surg 2010;51(3):791. http://dx.doi.org/10.1016/j.jvs.2009.11.014. [45] Brand FN, Dannenberg AL, Abbott RD, Kannel WB. The epidemiology of varicose veins: the Framingham Study. Am J Prev Med 1988;4(2):96–101. [46] Meissner MH, Wakefield TW, Ascher E, et al. Acute venous disease: venous thrombosis and venous trauma. J Vasc Surg 2007;46(Suppl S(6)):25S–53S. http://dx.doi. org/10.1016/j.jvs.2007.08.037. [47] Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet (London, England) 1999;353(9159):1167–73. [48] Bahl V, Hu HM, Henke PK, Wakefield TW, Campbell DA, Caprini JA. A validation study of a retrospective venous thromboembolism risk scoring method. Ann Surg 2010;251(2):344–50. http://dx.doi.org/10.1097/SLA.0b013e3181b7fca6.

5

[49] McLafferty RB, Lohr JM, Caprini J a, et al. Results of the National Pilot Screening Program for Venous Disease by the American Venous Forum. J Vasc Surg 2007:45(1). http://dx.doi.org/10.1016/j.jvs.2006.08.079. [50] Raju S, Neglén P. Clinical practice. Chronic venous insufficiency and varicose veins. N Engl J Med 2009;360(22):2319–27. http://dx.doi.org/10.1056/NEJMcp0802444. [51] Eberhardt RT, Raffetto JD. Chronic venous insufficiency. Circulation 2005;111(18): 2398–409. http://dx.doi.org/10.1161/01.CIR.0000164199.72440.08. [52] O'Meara S, Cullum NA, Nelson EA. Compression for venous leg ulcers. Cochrane Database Syst Rev 2009;1:CD000265. http://dx.doi.org/10.1002/14651858.CD000265. pub2. [53] Gloviczki P, Bergan JJ, Menawat SS, et al. Safety, feasibility, and early efficacy of subfascial endoscopic perforator surgery: a preliminary report from the North American Registry. J Vasc Surg 1997;25(1):94–105. [54] Neglen P, Eklöf B, Kulwicki A, et al. Prevention and treatment of venous ulcers in primary chronic venous insufficiency. J Vasc Surg 2010;52(5 Suppl):15S–20S. http://dx. doi.org/10.1016/j.jvs.2010.05.069. [55] Labropoulos N. Hemodynamic changes according to the CEAP classification. Phlebolymphology 2003;40:103–6. [56] Perrin M. Rationale for surgery in the treatment of venous ulcer of the leg. Phlebolymphology 2004;45:276–80. [57] Robertson LA, Evans CJ, Lee AJ, Allan PL, Ruckley CV, Fowkes FGR. Incidence and risk factors for venous reflux in the general population: Edinburgh Vein Study. Eur J Vasc Endovasc Surg 2014;48(2):208–14. http://dx.doi.org/10.1016/j.ejvs.2014.05.017. [58] Labropoulos N, Leon L, Kwon S, et al. Study of the venous reflux progression. J Vasc Surg 2005;41(2):291–5. http://dx.doi.org/10.1016/j.jvs.2004.11.014. [59] Bernardini E, De Rango P, Piccioli R, et al. Development of primary superficial venous insufficiency: the ascending theory. Observational and hemodynamic data from a 9year experience. Ann Vasc Surg 2010;24(6):709–20. http://dx.doi.org/10.1016/j. avsg.2010.01.011. [60] Labropoulos N, Gasparis AP, Pefanis D, Leon LR, Tassiopoulos AK. Secondary chronic venous disease progresses faster than primary. J Vasc Surg 2009;49(3):704–10. http://dx.doi.org/10.1016/j.jvs.2008.10.014. [61] Henke P, Vascular P, Arbor A. The Pacific Vascular Symposium 6: the Venous Ulcer Summit in perspective. YMVA 2010;52(5):1S–2S. http://dx.doi.org/10.1016/j.jvs. 2010.05.066. [62] Robertson L, Lee AJ, Gallagher K, et al. Risk factors for chronic ulceration in patients with varicose veins: a case control study. J Vasc Surg 2009;49(6):1490–8. http://dx. doi.org/10.1016/j.jvs.2009.02.237. [63] Brewster SF, Nicholson S, Farndon JR. The varicose vein waiting list: results of a validation exercise. Ann R Coll Surg Engl 1991;73(4):223–6. [64] Darvall KAL, Bate GR, Adam DJ, Bradbury AW. Generic health-related quality of life is significantly worse in varicose vein patients with lower limb symptoms independent of CEAP clinical grade. Eur J Vasc Endovasc Surg 2012;44(3):341–4. http://dx. doi.org/10.1016/j.ejvs.2012.06.022. [65] Smith JJ, Guest MG, Greenhalgh RM, Davies AH. Measuring the quality of life in patients with venous ulcers. J Vasc Surg 2000;31(4):642–9. http://dx.doi.org/10.1067/ mva.2000.104103. [66] Korn P, Patel ST, Heller JA, et al. Why insurers should reimburse for compression stockings in patients with chronic venous stasis. J Vasc Surg 2002;35(5):1–8. http://dx.doi.org/10.1067/mva.2002.121984. [67] Chiesa R, Marone EM, Limoni C, Volontè M, Petrini O. Chronic venous disorders: correlation between visible signs, symptoms, and presence of functional disease. J Vasc Surg 2007;46(2):322–30. http://dx.doi.org/10.1016/j.jvs.2007.04.030. [68] Kahn SR, M'lan CE, Lamping DL, Kurz X, Bérard A, Abenhaim LA. Relationship between clinical classification of chronic venous disease and patient-reported quality of life: results from an international cohort study. J Vasc Surg 2004;39(4):823–8. http://dx.doi.org/10.1016/j.jvs.2003.12.007. [69] Baker DM, Turnbull NB, Pearson JC, Makin GS. How successful is varicose vein surgery? A patient outcome study following varicose vein surgery using the SF-36 Health Assessment Questionnaire. Eur J Vasc Endovasc Surg 1995;9(3):299–304. [70] Launois R, Reboul-Marty J, Henry B. Construction and validation of a quality of life questionnaire in chronic lower limb venous insufficiency (CIVIQ). Qual Life Res 1996;5(6):539–54. [71] Garratt AM, Macdonald LM, Ruta DA, Russell IT, Buckingham JK, Krukowski ZH. Towards measurement of outcome for patients with varicose veins. Qual Health Care 1993;2(1):5–10. [72] Klem TMAL, Sybrandy JEM, Wittens CHA. Measurement of health-related quality of life with the Dutch translated Aberdeen Varicose Vein Questionnaire before and after treatment. Eur J Vasc Endovasc Surg 2009;37(4):470–6. http://dx.doi.org/10. 1016/j.ejvs.2008.11.036. [73] Klem TMAL, Sybrandy JEM, Wittens CHA, Essink Bot ML. Reliability and validity of the Dutch translated Aberdeen Varicose Vein Questionnaire. Eur J Vasc Endovasc Surg 2009;37(2):232–8. http://dx.doi.org/10.1016/j.ejvs.2008.08.025. [74] van Bemmelen PS, Bedford G, Beach K, Strandness DE. Quantitative segmental evaluation of venous valvular reflux with duplex ultrasound scanning. J Vasc Surg 1989; 10(4):425–31. [75] Needleman L. Update on the lower extremity venous ultrasonography examination. Radiol Clin North Am 2014;52(6):1359–74. http://dx.doi.org/10.1016/j.rcl.2014.08.001. [76] Chastanet S, Pittaluga P. Patterns of reflux in the great saphenous vein system. Phlebology 2013;28(Suppl. 1):39–46. http://dx.doi.org/10.1177/0268355513477021.

Please cite this article as: Yam BL, et al, Screening for lower extremity venous disease, Clin Imaging (2016), http://dx.doi.org/10.1016/ j.clinimag.2015.12.018

Screening for lower extremity venous disease.

Chronic venous disease (CVD) is frequently found in the general population. However, CVD is often overlooked by both healthcare providers and patients...
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