9
Chronic Venous Insufficiency

This chapter recommends revisions of the chronic venous insufficiency (CVI) listing (4.11) in the following areas: documentation of the presence of CVI, criteria for establishing the severity of CVI, and appropriate therapy and duration of therapy for CVI. The listing should require documentation that the visible leg abnormalities assumed to be CVI are caused by underlying venous disease. The listing should require documentation of venous reflux or obstruction using the current diagnostic standard—that is, duplex ultrasound. The terminology for skin changes in the lower leg secondary to CVI should be updated. The trial period of therapy in attempting to heal a venous ulcer should be longer. Three hospitalizations within a year for CVI should meet the functional limitation criterion, consistent with other listings.

DESCRIPTION

Chronic venous insufficiency (CVI) is a common disease and cause of debility in the United States. It can be defined as a pathological condition of the skin and subcutaneous tissue secondary to prolonged stasis of venous blood flow (Fowkes, 1996). CVI often may be associated with changes in skin pigmentation due to venous hypertension, and venous ulceration of the skin can occur. Physical manifestations include trophic changes, such as hyperpigmentation, induration, lipodermatosclerosis, and venous ulcers (Criqui et al., 2003). Leg symptoms associated with CVI include aching, itching, heaviness, fatigue, and swelling (Langer et al., 2005).



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9 Chronic Venous Insufficiency this chapter recommends revisions of the chronic venous insuf- ficiency (CVI) listing (4.) in the following areas: documentation of the presence of CVI, criteria for establishing the severity of CVI, and appropriate therapy and duration of therapy for CVI. the listing should require documentation that the visible leg ab- normalities assumed to be CVI are caused by underlying venous disease. the listing should require documentation of venous reflux or obstruction using the current diagnostic standard—that is, du- plex ultrasound. the terminology for skin changes in the lower leg secondary to CVI should be updated. the trial period of therapy in attempting to heal a venous ulcer should be longer. three hospital- izations within a year for CVI should meet the functional limitation criterion, consistent with other listings. DESCRIPTION Chronic venous insufficiency (CVI) is a common disease and cause of debility in the United States. It can be defined as a pathological condition of the skin and subcutaneous tissue secondary to prolonged stasis of venous blood flow (Fowkes, 1996). CVI often may be associated with changes in skin pigmentation due to venous hypertension, and venous ulceration of the skin can occur. Physical manifestations include trophic changes, such as hyperpigmentation, induration, lipodermatosclerosis, and venous ulcers (Criqui et al., 2003). Leg symptoms associated with CVI include aching, itching, heaviness, fatigue, and swelling (Langer et al., 2005). 

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  CaRdIoVaSCUlaR dISabIlIty EPIDEMIOLOGY In the United States, 3 to 4 percent of the population suffer from CVI (Coon et al., 1973). Approximately 1.5 percent of adults will be affected by venous ulceration. In 2007, more than 500,000 individuals in the United States had venous stasis ulcers. Risk factors for CVI include older age, family history, multiple preg- nancies, standing occupation, obesity in females, history of leg trauma, and prior deep venous thrombosis (Adhikari et al., 2000; Criqui et al., 2007). The annual incidence of varicose veins in the Framingham study was 2.6 percent in women and 1.9 percent in men. The prevalence of changes in skin pigmentation varied between 3 and 13 percent in the population. The presence of active or healed ulcers varied between 1.0 and 2.7 percent. DIAGNOSTIC CRITERIA AND METHODS CVI is often diagnosed by a visual inspection of the lower limbs to identify the presence of characteristic trophic changes of the skin, such as hyperpigmentation, edema, and ulcers (Criqui et al., 2003). Duplex ultra- sound has become the standard for diagnosing the underlying venous reflux or obstruction, and is a procedure that is noninvasive and highly accurate (Neglen and Raju, 1992). The duplex ultrasound examination can detect reflux, or reverse flow of venous blood through a valve, and the probe can detect incompressibility of a vein, indicating obstruction from a prior blood clot. Other diagnostic techniques include contrast venography and plethysmography (Meissner et al., 2007). Visible changes in the lower extremity consistent with CVI should not be assumed to be caused by CVI without documentation of venous reflux or obstruction (Criqui et al., 2003). Other conditions, such as right heart failure, can produce leg edema. In addition, distal leg swelling can reflect impaired lymphatic rather than venous drainage, a condition known as lymphedema. Lymphedema can be congenital, postinfectious, or posttrau- matic, or can result from cancer or other surgery (Rockson, 2010). It is as- sociated with functional limitations and reduced quality of life comparable to that reported by patients with venous leg ulcers (Augustin et al., 2005). There is no listing for lymphedema but the current introductory section of the cardiovascular system stipulates that it can medically equal the CVI listing in severity. Nevertheless, the committee believes that an accurate diagnosis should be made before granting disability for lymphedema. Seven clinical categories have been developed to help clinicians under- stand and categorize the nature of chronic peripheral venous disease (see Table 9-1). The etiology of these disorders may be described as congenital, primary (i.e., not associated with an identifiable mechanism of venous dys-

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 ChRonIC VEnoUS InSUffICIEnCy TABLE 9-1 Clinical Classification of Chronic Venous Disease (CVD) Class No signs of venous disease C0 Telangiectasias or reticular veins C1 Varicose veins C2 Edema C3 Skin changes secondary to CVD without ulceration C4 C4a—Pigmentation or eczema C4b—Lipodermatosclerosis or atrophie blanche Healed venous ulcer C5 Active venous ulcer C6 NOTE: The 0–6 clinical classification in this table is part of the CEAP (Clinical-Etiologic- Anatomic-Pathophysiologic) classification system developed by an international ad hoc com- mittee of the American Venous Forum and is widely used in clinical research on CVD. In this classification system, chronic venous insufficiency indicates more severe disease. “The term ‘chronic venous insufficiency’ implies a functional abnormality of the venous system, and is usually reserved for more advanced disease, including edema (C3), skin changes (C4), or venous ulcers (C5–C6)” (Eklöf et al., 2004:1249). SOURCE: Eklöf et al., 2004. function), or secondary (i.e., the result of an antecedent event, usually an episode of acute deep venous thrombosis). TREATMENT Effective preventive and curative treatments for CVI are currently lim- ited. The recurrent nature of the disease places the cost of care at more than $1 billion annually. The main treatment for CVI and venous ulceration is compression stockings, leg elevation, and intensive skin care (Korn et al., 2002). An ex- tensive review of clinical trials indicates that compression stocking therapy increases healing of ulcers; multicomponent systems are more effective than single component systems; and multicomponent systems containing elastic are more effective than those with largely inelastic components (O’Meara et al., 2009). Some drugs have shown efficacy in helping ulcer healing, including pentoxifylline (Jull et al., 2007). Various surgical interventions have also shown efficacy in many patients (White and Ryjewski, 2005). DISABILITY CVI is associated with pain, physical function and mobility limitations, and depression and social isolation. Assessments of quality of life correlate

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0 0 CaRdIoVaSCUlaR dISabIlIty directly with the severity of disease (Comerota, 2009; Kaplan et al., 2003). In addition to the discomfort caused by CVI, patients require leg elevation and avoidance of prolonged sitting or standing, which can impair participa- tion in activities of daily living and instrumental activities of daily living. CURRENT LISTING Currently, the listing is for CVI of a lower extremity, with incompe- tency or obstruction of the deep venous system and either extensive brawny edema or superficial varicosities, stasis dermatitis, and recurrent or persis- tent ulceration that has not healed despite 3 or more months of treatment (Box 9-1). CONCLUSIONS AND RECOMMENDATION CVI results from either venous reflux or obstruction. The committee suggests replacing the outmoded term incompetency with reflux. The listing should also require the presence of symptoms as well as evidence, ideally by duplex ultrasound examination, of venous reflux or obstruction. The requirement that reflux or obstruction should be in the deep ve- nous system should be revised to refer to the venous system more gener- ally, including the superficial, perforating, and deep veins, because research BOX 9-1 Current Listing for Chronic Venous Insufficiency 4.11 Chronic venous insufficiency of a lower extremity with incompetency or ob- struction of the deep venous system and one of the following:   A.    xtensive brawny edema (see 4.00G3) involving at least two-thirds of the  E leg between the ankle and knee or the distal one-third of the lower extrem- ity between the ankle and hip.   OR   B.  Superficial  varicosities,  stasis  dermatitis,  and  either  recurrent  ulceration    or persistent ulceration that has not healed following at least 3 months of  prescribed treatment. SOURCE: SSA, 2008.

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 ChRonIC VEnoUS InSUffICIEnCy shows that disease of the superficial and perforator veins can also cause CVI and associated disability (Shami et al., 1993). The listing should require documentation of reflux or obstruction with duplex or equivalent diagnostic techniques. The committee recommends that the current (A) criterion, “extensive brawny edema,” should be changed to trophic skin changes below the knee consistent with severe CVI, such as brawny edema, hyperpigmentation, or lipodermatosclerosis, that is not responsive to compression therapy. The current (B) criteria should be limited to recurrent or persistent venous ul- cers. “Superficial varicosities” should be deleted because alone they are not indicative of CVI. “Stasis dermatitis” should also be deleted because this is a generic term referring to the trophic changes suggested for the new (A) listing above. Requiring a minimum of 6 months or more of unsuccessful prescribed therapy in attempting to heal a venous ulcer is a more definitive criterion than a 3-month trial. Finally, a third criterion (C) should be added: three hospitalizations for CVI within a year. RECOMMENDATION 9-1. Listing 4.11 should be revised to require symptoms attributed to chronic venous insufficiency (CVI) as well as reflux or obstruction in the venous system, documented by duplex ultrasound or comparable technique. The documented symptomatic venous reflux or obstruction should be coupled with a requirement of the following: Trophic changes of skin below the knee consistent with severe • chronic venous insufficiency (e.g., hyperpigmentation, lipoder- matosclerosis, brawny edema) and unresponsive to compres- sion therapy; OR Recurrent or persistent venous ulceration that has not been • responsive to prescribed treatment for at least 6 months; OR Three hospitalizations for CVI during a 12-month period. • Also, if the committee’s recommendations are adopted, the current introductory text to the cardiovascular system relevant to the current list- ing 4.11 would need to be revised. For example, the discussion of tro- phic changes required in the listing, which currently includes only brawny edema, should also include hyperpigmentation and lipodermatosclerosis.

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  CaRdIoVaSCUlaR dISabIlIty REFERENCES Adhikari, A., M. H. Criqui, V. Wooll, J. O. Deneberg, A. Fronek, R. D. Langer, and M. Klauber. 2000. The epidemiology of venous diseases. Phlebology 15(1):2–18. Augustin, M., F. Bross, E. Foldi, W. Vanscheidt, and I. Zschocke. 2005. Development, valida- tion and clinical use of the FLQA-I, a disease-specific quality of life questionnaire for patients with lymphedema. Vasa 34(1):31–35. Comerota, A. J. 2009. Treatment of chronic venous disease of the lower extremities: What’s new in guidelines? Phlebolymphology 16(4):313–320. http://www.phlebolymphology. org/2009/11/treatment-of-chronic-venous-disease-of-the-lower-extremities (accessed June 14, 2010). Coon, W. W., P. W. Willis III, and J. B. Keller. 1973. Venous thromboembolism and other venous disease in the Tecumseh Community Health Study. Circulation 48(4):839–846. http://circ.ahajournals.org/cgi/reprint/48/4/839 (accessed June 14, 2010). Criqui, M. H., M. Jamosmos, A. Fronek, J. O. Denenberg, R. D. Langer, J. Bergan, and B. A. Golomb. 2003. Chronic venous disease in an ethnically diverse population: The San Diego Population Study. american Journal of Epidemiology 158(5):448–456. http://aje. oxfordjournals.org/cgi/reprint/158/5/448 (accessed July 2, 2010). Criqui, M. H., J. O. Denenberg, J. Bergan, R. D. Langer, and A. Fronek. 2007. Risk fac- tors for chronic venous disease: The San Diego Population Study. Journal of Vascular Surgery 46(2):331–337. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2023874/pdf/ nihms28091.pdf (accessed July 2, 2010). Eklöf, B., R. B. Rutherford, J. J. Bergan, P. H. Carpentier, P. Gloviczki, R. L. Kistner, M. H. Meissner, G. L. Moneta, K. Myers, F. T. Padberg, M. Perrin, C. V. Ruckley, P. C. Smith, and T. W. Wakefield. 2004. Revision of the CEAP classification for chronic venous disorders: Consensus statement. Journal of Vascular Surgery 40(6):1248–1252. http:// download.journals.elsevierhealth.com/pdfs/journals/0741-5214/PIIS0741521404012777. pdf (accessed June 14, 2010). Fowkes, F. G. R. 1996. Epidemiology of chronic venous insufficiency. Phlebology 11(1):2–5. Jull, A., B. Arroll, V. Parag, and J. Waters. 2007. Pentoxifylline for treating venous leg ulcer. Cochrane database of Systematic Reviews 3(CD001733). Kaplan, R. M., M. H. Criqui, J. O. Denenberg, J. Bergan, and F. Fronek. 2003. Quality of life in patients with chronic venous disease: San Diego Population Study. Journal of Vascular Surgery 37(5):1047–1053. http://download.journals.elsevierhealth.com/pdfs/ journals/0741-5214/PIIS0741521402753093.pdf (accessed July 2, 2010). Korn, P., S. T. Patel, J. A. Heller, J. S. Deitch, K. V. Krishnasastry, H. L. Bush, and K. C. Kent. 2002. Why insurers should reimburse for compression stockings in patients with chronic venous stasis. Journal of Vascular Surgery 35(5):950–957. http://download.journals. elsevierhealth.com/pdfs/journals/0741-5214/PIIS0741521402801021.pdf (accessed July 2, 2010). Langer, R. D., E. Ho, J. O. Denenberg, A. Fronek, M. Allison, and M. H. Criqui. 2005. Relationships between symptoms and venous disease: The San Diego Population Study. archives of Internal medicine 165(12):1420–1424. http://archinte.ama-assn.org/cgi/ content/full/165/12/1420 (accessed June 30, 2010). Meissner, M. H., G. Moneta, K. Burnand, P. Gloviczki, J. M. Lohr, F. Lurie, M. A. Mattos, R. B. McLafferty, G. Mozes, R. B. Rutherford, F. Padberg, and D. S. Sumner. 2007. The hemodynamics and diagnosis of venous disease. Journal of Vascular Sur- gery 46(Suppl S):4S–24S. http://download.journals.elsevierhealth.com/pdfs/journals/ 0741-5214/PIIS0741521407015297.pdf (accessed June 14, 2010). Neglen, P., and S. Raju. 1992. A comparison between descending phlebography and du- plex Doppler investigation in the evaluation of reflux in chronic venous insufficiency:

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 ChRonIC VEnoUS InSUffICIEnCy A challenge to phlebography as the “gold standard.” Journal of Vascular Surgery 16(5):687–693. http://download.journals.elsevierhealth.com/pdfs/journals/0741-5214/ PII074152149290222T.pdf (accessed July 2, 2010). O’Meara, S., N. A. Cullum, and E. A. Nelson. 2009. Compression for venous leg ulcers. Cochrane database of Systematic Reviews 1(CD000265). Rockson, S. G. 2010. Current concepts and future directions in the diagnosis and management of lymphatic vascular disease. Vascular medicine 15(3):223–231. Shami, S. K., S. Sarin, T. R. Cheatle, J. H. Scurr, and P. D. Smith. 1993. Venous ulcers and the superficial venous system. Journal of Vascular Surgery 17(3):487–490. SSA (Social Security Administration). 2008. listing of impairments—adult listings (Part a). disability evaluation under Social Security (blue book). http://www.socialsecurity.gov/ disability/professionals/bluebook/AdultListings.htm (accessed July 22, 2010). White, J. V., and C. Ryjewski. 2005. Chronic venous insufficiency. Perspectives in Vascular Surgery and Endovascular therapy 17(4):319–327.

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