REVIEW ARTICLE: Current Concepts in Chronic Venous Ulceration

REVIEW ARTICLE: Current Concepts in Chronic Venous Ulceration

Eur J Vasc Endovasc Surg 20, 227–232 (2000) doi:10.1053/ejvs.2000.1157, available online at http://www.idealibrary.com on REVIEW ARTICLE Current Con...

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Eur J Vasc Endovasc Surg 20, 227–232 (2000) doi:10.1053/ejvs.2000.1157, available online at http://www.idealibrary.com on

REVIEW ARTICLE

Current Concepts in Chronic Venous Ulceration A. K. Tassiopoulos, E. Golts, D. S. Oh and N. Labropoulos∗ Department of Surgery, Loyola University Medical Center, Maywood, Illinois, U.S.A. Objectives: despite numerous reports on the distribution of reflux in patients with venous ulceration, there is no consensus on the contribution of each venous system. This study was performed to evaluate the distribution of reflux in this group of patients. Methods: a literature search from 1980 to 1998 was performed. Because duplex scanning is the best method for detecting venous reflux, we only included reports that used this diagnostic modality. All studies with less than 30 ulcerated limbs were excluded. Since most reports did not give detailed data on perforator veins, reflux in these veins was combined with the superficial and deep veins. Documented episodes of superficial or deep vein thrombosis were noted. Results: thirteen studies that included 1249 ulcerated limbs fulfilled the inclusion criteria. The mean age of patients was 59 years (95% CI: 54–63, range: 14–93). Reflux was detected in 1153 (92%) of limbs. Reflux confined to the superficial veins alone was seen in 45% of limbs, in the deep veins alone in 12% and in both the superficial and deep veins in 43% of limbs. The overall involvement of the superficial veins was 88% and of the deep veins 56% (p<0.0001). A documented episode of deep vein thrombosis was reported in only six of the 13 studies and the incidence was found to be 32%. Conclusions: reflux in the superficial veins is seen in 88% of limbs with venous ulcers (CEAP classes 5 and 6). Isolated superficial vein incompetence is detected in 45%, while reflux in the deep venous system alone is seen in only 12%. These data have significant clinical implications, since reflux in the superficial system can be easily eliminated by excision of the affected veins. Key Words: Venous ulcers; Reflux; Obstruction; Duplex scanning.

Introduction The prevalence of lower extremity ulceration secondary to chronic venous disease (CVD) in European and Western populations is estimated to be 0.5%– 1%.1,2 Approximately 12%–14% of patients with CVD in recent series3,4 have venous ulcers (clinical classes C5 and C6). It was recently reported that 1.3% of the total health care budget in the United Kingdom is used for the treatment of venous ulcers,5 indicating the significant financial burden this disease imposes on the community. Duplex ultrasound examination of the lower extremity veins, which was introduced in the 1980s, has significantly improved our understanding of the aetiology of CVD and has allowed precise identification of the malfunctioning vein segments. ∗ Please address all correspondence to: N. Labropoulos, Assistant Professor of Surgery, Department of Surgery, Loyola University Medical Center, 2160 South First Avenue, Maywood, Illinois 601533304, U.S.A. 1078–5884/00/090227+06 $35.00/0  2000 Harcourt Publishers Ltd.

Despite numerous reports that have suggested the importance of the distribution of reflux in the development of venous ulceration, there is no consensus in the contribution of each venous system. Many of the recent studies on the distribution and extent of reflux have a relatively small sample size; therefore they are unable to describe adequately the entire spectrum of venous disease. Even when the study focused on a specific category of patients with CVD, such as those with venous ulcers, the diversity of the disease (active vs healed ulcers, history of previous thrombosis, the presence or absence of deep venous insufficiency, duration and progression of disease, the contribution of each venous system in the development or healing of the ulcer, etc.) made the sample size small for meaningful analysis. In this study we analysed data from recent large reports in an attempt to describe the involvement of the different venous systems in patients presenting with the most severe form of CVD: venous ulcers.

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Table 1. Prevalence of reflux and previous deep venous thrombosis in limbs with chronic venous ulceration. Study/Year Hanrahan, 1991 Weingarten, 1993 Neglen, 1993 Shami, 1993 Van Rij, 1994 Myers, 1995 Labropoulos, 1995 Labropoulos, 1995 Welch, 1996 Grabs, 1996 Labropoulos, 1997 Scriven, 1997 Ghauri, 1998 Total

No. of limbs 95 192 31 79 12 96 112 34 30 111 54 95 200

CEAP class 6 5–6 5–6 6 5–6 5 5–6 5–6 5–6 5–6 5–6 5–6 6

1249

No. of limbs with reflux 89 (93.7%) 148 (77.1%) 31 (100%) 79 (100%) 119 (99.2%) 90 (93.7%) 108 (96.4%) 34 (100%) 25 (83.3%) 105 (94.6%) 54 (100%) 95 (100%) 176 (88%) 1153/1249 (92.3%)

No. of limbs with previous DVT Not reported (∗) Not reported (∗) 26 (84%) 5 (6.3%) Not reported Not reported 44 (39.3%) 17 (50%) Not reported Not reported 11 (34.4%) 22 (23%) Not reported 129/405 (31.9%)

∗ In these studies deep and superficial vein thrombosis were reported together.

Methods We performed a literature search for reports on venous ulcers from 1980 to 1998. Duplex scanning is the best method for detecting venous reflux, therefore only reports that used this diagnostic modality were included in our study. All studies with less than 30 ulcerated limbs were excluded. The CEAP classification system was used for analysis of the combined data; therefore all reports based on the older classification system were converted to the equivalent categories of CEAP. The prevalence of superficial and/or deep venous reflux and obstruction in patients belonging to clinical classes 5 and 6 from all reports was the main subject of our analysis. Since most of the reports included did not give detailed data on perforator veins, reflux in these veins was combined with the superficial and deep veins. A separate analysis of the subgroup of studies that provided detailed analysis on the status of the perforator veins was also performed and the results were compared to those of the entire study. Documented episodes of superficial or deep vein thrombosis (DVT) were also noted. Statistical comparisons were performed using 95% confidence interval analysis and Chi-squared test.

Results Thirteen studies6,18 that included 1249 ulcerated limbs fulfilled the inclusion criteria (Tables 1 and 2). The mean age of patients was 59 years (95% CI 54–63, range 14–93). Reflux was seen in 1153 limbs (92%, 95% CI 91–94). When reflux in the perforating veins was combined with that in the superficial and deep veins, reflux confined to the superficial veins alone was seen Eur J Vasc Endovasc Surg Vol 20, September 2000

in 45% of limbs (95% CI 42–47), in the deep veins alone in 12% (95% CI 10–14) and in both the superficial and deep veins in 43% (95% CI 40–46). The overall involvement of the superficial veins was 88% and of the deep veins 56% (p<0.0001). Five studies6,12,13,16,17 with a total of 380 limbs provided detailed data on the status of the perforator veins (Table 3). Based on these reports, reflux in the superficial veins alone is seen in 28% of limbs (95% CI 24–33), in the deep veins alone in 6.6% (95% CI 4.3–9.6), and in the perforator veins only in 3.3% (95% CI 1.8–5.8). Reflux in the superficial and perforator veins was found in 16% of limbs (95% CI 12–19), in the deep and perforators in 3.2% (95% CI 1.6-5.5), and in both the superficial and deep veins in 19% (95% CI 15–23). Reflux in all three systems was seen in 24% of limbs (95% CI 20–29). A previous documented episode of DVT was reported only in six of the 13 studies (405 limbs total)7,8,12,13,16,17 and the incidence was found to be 32% (95% CI 27–36).

Discussion Venous ulceration is a debilitating problem associated with significant financial cost due to loss of work hours and cost of medical care for the patients. Venous hypertension resulting from reflux and/or obstruction in the venous system is the underlying pathophysiological mechanism. The optimal management of this problem requires precise identification of the aetiology and anatomic distribution of venous malfunction, and subsequent interventions targeting the affected vessels in each individual patient. The treatment of these patients was revolutionised in recent

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Table 2. Distribution of reflux in limbs with chronic venous ulceration. Study/Year

Limbs with reflux

Hanrahan, 1991 Weingarten, 1993 Neglen, 1993 Shami, 1993 Van Rij, 1994 Myers, 1995 Labropoulos, 1995 Labropoulos, 1995 Welch, 1996 Grabs, 1996 Labropoulos, 1997 Scriven, 1997 Ghauri, 1998 Total

89 148 31 79 119 90 108 34 25 105 54 95 176

Reflux in the superficial and/or perforator veins 42 25 2 42 86 36 52 10 7 57 22 54 78

1153

(47.2%) (16.9%) (6.5%) (53.2%) (72.3%) (40.0%) (48.1%) (29.4%) (28.0%) (54.3%) (40.7%) (56.8%) (44.3%)

513/1153 (44.5%)

Reflux in the deep and/or Reflux in the superficial perforator veins and deep and/or perforator veins 6 (6.7%) 42 (28.4%) 9 (29.0%) 12 (15.2%) 9 (7.6%) 8 (8.9%) 12 (11.1%) 3 (8.8%) 7 (28.0%) 6 (5.7%) 3 (5.6%) 13 (13.7%) 11 (6.3%)

41 (46.1%) 81 (54.7%) 20 (64.5%) 25 (31.6%) 24 (20.1%) 46 (51.1%) 44 (40.7%) 21 (61.8%) 11 (44.0%) 42 (40.0%) 29 (53.7%) 28 (29.5%) 87 (49.4%)

141/1153 (12.2%)

499/1153 (43.3%)

Table 3. Distribution of reflux in the studies describing reflux in perforators separately. Hanrahan, 1991

Labropoulos, 1995

Labropoulos, 1995

Labropoulos, 1997

Scriven, 1997

Total

%

S only D only P only S+P S+D D+P S+D+P

16 2 8 18 11 4 30

26 7 3 23 13 5 31

8 2 0 2 9 1 12

10 3 0 12 10 0 19

48 11 2 4 28 2 0

108 25 13 59 71 12 92

28.4% 6.6% 3.4% 15.5% 18.7% 3.2% 24.2%

Total

89

108

34

54

95

380

100%

years by the widespread use of duplex ultrasound. This method has provided accurate anatomic and functional data regarding the distribution of both reflux and obstruction in all venous systems, and has contributed to a better understanding of the pathogenesis of CVD. For many years it was a common belief that venous ulcers resulted from reflux and/or obstruction of the deep venous system secondary to an episode of DVT. The main mechanisms responsible for venous ulcers are reflux, venous outflow obstruction, or a combination of the two. Calf muscle pump dysfunction has also been associated with ulceration.19,20 In a recent study it was reported that conditions associated with calf muscle pump dysfunction significantly impaired ulcer healing.21 Out of 122 ulcerated limbs with superficial vein insufficiency that was surgically corrected, 18 limbs failed to heal. Two of these limbs had recurrent venous reflux, eight had a fixed, rigid ankle joint and four were chronically immobilised due to sever hip osteoarthritis. Reflux is the most common mechanism and was detected in 92% of the limbs. There were two reports that indicated this prevalence to be significantly lower (77% and 83%, respectively).9,14 It must be pointed out

that in both studies only selected sites of the superficial and deep venous systems were examined and the perforator veins were not imaged at all. In the rest of the reports the prevalence of reflux exceeded 90%. Only six studies provided data on the presence of venous obstruction.7,9,11,15–17 In five of them, the prevalence of venous obstruction ranged between 1 and 6%. One study7 reported a significantly higher prevalence (32%) but in this patient population the incidence of previous DVT was extremely high as well (84%). Although in all these reports chronic thrombus was detected by venography or ultrasound, there was no documentation of venous pressure measurements or plethysmographic tests to evaluate the haemodynamic significance of obstruction. In a small percentage of limbs with apparent venous ulcers, no abnormality in any venous system can be detected. In these patients, other possible aetiologies include lymphedema, arterial insufficiency, collagen disease, vasculitis, diabetes and skin malignancies.17,18 Occasionally, no apparent aetiology for ulceration can be found.18 The results of our analysis clearly show that a significant number of limbs (45%) had reflux confined to the superficial veins alone or in combination with the Eur J Vasc Endovasc Surg Vol 20, September 2000

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perforator veins. The deep venous system in these limbs was normal. This is a significant finding, because it has been shown that when venous ulceration is due to superficial and perforator incompetence only, surgical treatment may heal up to 90% of the ulcers with very good medium to long-term results.21–23 In one of the most recent reports, the median time for ulcer healing after superficial vein surgery was 18 weeks and the healing rates at 6, 12 and 18 months were 57%, 74% and 82%, respectively.21 Perhaps even more gratifying than the overall healing rate is the fact that ulcer recurrence is significantly smaller after superficial venous surgery when compared to compression therapy alone and as low as 4% in 2 years.18 The overall involvement of the superficial venous system in the limbs studied was 88%. The prevalence of deep vein reflux has been reported to be higher in patients with venous ulcers when compared to patients with less severe forms of CVD.3,4,16 Our analysis showed that deep vein insufficiency alone or in combination with the perforator veins was responsible for 12% of venous ulcers, but the overall involvement of the deep venous system was significantly higher (56%). There was significant variability in the prevalence of deep vein reflux in the reports used for this analysis that ranged between 28% and 94%. This variability can be explained by the diversity of the patient population in each study (duration of disease, previous surgery, etc.) and the differences in the venous sites examined in each study. The study with the highest reported prevalence of deep vein insufficiency comes from a centre that specialises in deep venous reconstruction.7 Another study with very high prevalence of deep vein reflux included a large number of limbs with extensive superficial vein stripping.14 Ulcerated limbs that have already undergone superficial vein stripping are very likely to have their deep veins involved. The lowest prevalence of isolated deep venous reflux reported was 2.1%.6 In that study only the common femoral, superficial femoral and popliteal veins were examined. Therefore, reflux in the deep veins might have been underestimated. A significant number of limbs (43%) had reflux in both the superficial and the deep venous systems. This is also a very important observation, since superficial vein ligation and/or stripping has worst results, with very high recurrence rates at 5 years, when there is reflux in the deep venous system.23 In these patients additional procedures that are designed to improve the underlying abnormality may be required, and several studies have shown encouraging results.24–27 The haemodynamic significance of incompetent perforating veins remains a controversial issue. Some Eur J Vasc Endovasc Surg Vol 20, September 2000

investigators reported that incompetent perforators do not contribute to venous hypertension,28–30 whereas others suggest that they are important.6,31–34 In recent studies, reflux in the perforator veins only was seen in less than 3% of patients with CVD.3,4,12,13 Although the role of these veins in the development of signs and symptoms remains unclear, their number and size increases with worsening of CVD.6,35–39 Furthermore, it was recently shown that the duration of outward flow in these veins was longer in patients with ulcers compared to the milder classes of CVD.39 Unfortunately, most of the studies included in this analysis did not report on the status of the perforator veins. Therefore, no conclusions can be drawn as regards the contribution of these vessels to the development of ulceration. In the studies that examined the perforator veins,6,12,13,16,17 reflux in these veins only was reported to be present in 3.3% of ulcerated limbs. There was one study, however, which reported that 8.4% of all venous ulcers were associated with perforator reflux only.6 Isolated reflux was identified in 10 perforating veins of eight limbs. Neither the location of these veins in relation to the ulcer nor the effect of intervention was described. Therefore, such isolated reflux might have been an incidental finding rather than the cause of the ulcer. In limbs with venous ulceration and superficial vein reflux, when the deep venous system was competent, correction of reflux in the superficial system results in a significant reduction in the number and diameter of incompetent perforating veins.40 In contrast, when the deep venous system was incompetent, correction of reflux in the superficial system did not correct outward perforator flow in the majority f cases. This may explain the high rate of ulcer healing reported in limbs with reflux limited to the superficial and perforating veins after resection of the incompetent superficial veins.21 It also suggests that in the presence of deep vein reflux, superficial vein surgery may not significantly reduce venous hypertension to allow for ulcer healing. The effect of perforator disconnection on ulcer healing has not been adequately defined yet. Several studies have reported very good early and mid-term results on ulcer healing and recurrence after superficial vein surgery and SEPS.32,33,37,41 This was clearly evident when the deep veins were normal. The presence of deep venous insufficiency, seems to be associated with both lower ulcer healing and higher recurrence rates.32,42 A detailed analysis in a large prospective non-randomised study indicated that this usually occurs in postthrombotic limbs compared to those with primary deep venous insufficiency.32 In one of the reports,13 examination of the local veins

Current Concepts in Chronic Venous Ulceration

(veins passing through the ulcer or within 2 cm of its periphery) revealed reflux in 86% of ulcerated areas. Reflux in the superficial veins was detected in 63% of ulcers and deep venous reflux in 40%. Reflux in the perforating veins at the ulcerated area was seen in only 28% of ulcers, contrary to the old belief that under every ulcer there is a perforator vein feeding it. Furthermore, perforator reflux at that level was always associated with superficial and/or deep vein incompetence. Interestingly, 14% of the ulcers had no local venous abnormality. This demonstrates that some ulcers can exist in the presence of axial vein pathology alone A documented episode of previous DVT was reported in 32% of limbs. This prevalence is probably underestimated because many thrombi remain undetected and may resolve without leaving any evidence of luminal damage other than reflux due to destruction of the valves. Several recent reports6,13,16,43–45 have shown that in limbs with ulcers, the incidence of previous DVT is higher compared to limbs with clinically less severe CVD. If one considers that more than 50% of ulcerated limbs have deep venous insufficiency and that deep venous reflux is frequently the consequence of a previous episode of deep vein thrombosis (symptomatic or asymptomatic), it is logical to assume that the prevalence of previous DVT in these patients is higher than reported. However, it must be pointed out that primary deep venous insufficiency has been well documented24 and may account for an unknown percentage of reflux in the deep venous system. We believe that, despite the diversity of the methods in the reports used, the cumulative analysis of the data provides interesting information on the distribution of venous reflux in ulcerated limbs. Such an analysis, however, has a lot of inherent weaknesses that result from the large variability in the patient population and the inadequate description of their status at the time the examination was performed. Therefore, a large prospective study that will take into consideration the above variables and utilise a uniform examination and report protocol is necessary to obtain a more accurate description of the anatomic and pathophysiological parameters of chronic venous ulceration.

References 1 Cornwall JV, Lewis JD. Leg ulcer revisited. Br J Surg 1983; 70: 681. 2 Callam MJ, Ruckley CV, Harper DR, Dale JJ. Chronic ulceration of the leg: extent of the problem and provision of care. Br Med J 1985; 290: 1855–1856. 3 Kistner RL, Eklof B, Masuda EM. Diagnosis of chronic venous

4 5 6 7 8 9

10 11 12 13

14 15 16 17 18 19 20

21 22 23

24 25 26 27

231

disease of the lower extremities: The ‘‘CEAP’’ classification. Mayo Clin Proc 1996; 71: 338–345. Labropoulos N. CEAP in clinical practice. Vasc Surg 1997; 31: 224–225. Office of Health Economics. Chronic Venous Disease of the Leg. Report 108. London: Office of Health Economics, 1992: 24–33. Hanrahan LM, Araki CT, Rodriguez AA et al. Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg 1991; 3: 805–812. Neglen P, Raju S. A rational approach to detection of significant reflux with duplex Doppler scanning and air plethysmography. J Vasc Surg 1993; 17: 590–595. Shami SK, Sarin S, Cheatle TR, Scurr JH, Coleridge Smith PD. Venous ulcers and the superficial venous system. J Vasc Surg 1993; 17: 487–490. Weingarten MS, Branas CC, Czeredarczuk M, Schmidt JD, Wolferth CC. Distribution and quantification of venous reflux in lower extremity chronic venous stasis disease with duplex scanning. J Vasc Surg 1993; 18: 753–759. Van Rij AM, Solomon C, Christie R. Anatomic and physiologic characteristics of venous ulceration. J Vasc Surg 1994; 20: 759–764. Myers KA, Ziegenbein RW, Zeng GH, Matthews PG. Duplex ultrasonography scanning for chronic venous disease: patterns of venous reflux. J Vasc Surg 1995; 21: 605–612. Labropoulos N, Leon M, Geroulakos G et al. Venous hemodynamic abnormalities in patients with leg ulceration. Am J Surg 1995; 169: 572–574. Labropoulos N, Giannnoukas AD, Nicolaides AN et al. New insights into the pathophysiologic condition of venous lceration with color-flow duplex imaging: implications for treatment? J Vasc Surg 1995; 22: 45–50. Welch HJ, Young CM, Semegran AB et al. Duplex assessment of venous reflux and chronic venous insufficiency: the significance of deep venous reflux. J Vasc Surg 1996; 24: 755–762. Grabs AJ, Wakely MC, Nyamekye I, Ghauri ASK, Poskitt KR. Colour duplex ultrasonography in the rational management of chronic venous leg ulcers. B J Surg 1996; 83: 1380–1382. Labropoulos N. Clinical correlation to various patterns of reflux. Vasc Surg 1997; 31: 242–248. Scriven JM, Hartshorne T, Bell PR, Naylor AR, London NJ. Single-visit venous ulcer assessment clinic: the first year. Br J Surg 1997; 84: 334–336. Ghauri ASK, Nyamekye I, Grabs AJ et al. Influence of a specialised leg ulcer service and venous surgery on the outcome of venous leg ulcers. Eur J Vasc Endovasc Surg 1998; 16: 238–244. Christopoulos D, Nicolaides AN, Cook A et al. Pathogenesis of venous ulceration in relation to the calf muscle pump function. Surgery 1989; 106: 829–835. Labropoulos N, Giannnoukas AD, Nicolaides AN et al. The role of venous reflux and calf muscle pump function in nonthrombotic chronic venous insufficiency. Correlation with severity of signs and symptoms. Arch Surg 1996; 131: 403–406. Bello M, Scriven M, Hartshorne T et al. Role of superficial venous surgery in the treatment of venous ulceration. Br J Surg 1999; 86: 755–759. Darke SG, Penfold CAD. Venous ulceration and saphenous ligation. Eur J Vasc Surg 1992; 6: 4–9. Burnand KG, Thomas ML, O’Donnell TF Jr, Browse NL. Relation between postphlebitic changes in the deep veins and results of surgical treatment of venous ulcers. Lancet 1976; 1: 936–938. Masuda EM, Kistner RL. Long-term results of venous valve reconstruction: a four- to twenty-one-year follow-up. J Vasc Surg 1994; 19: 391–403. Kistner RL, Eklof B, Masuda EM. Deep venous valve reconstruction. Cardiovasc Surg 1995; 3: 129–140. Raju S, Neglen P, Doolittle J, Meydrech EF. Axillary vein transfer in trabeculated postthrombotic veins. J Vasc Surg 1999; 29: 1050–1064. Juhan CM, Alimi YS, Barthelemy PJ, Fabre DF, Riviere CS. Eur J Vasc Endovasc Surg Vol 20, September 2000

232

28

29 30

31 32

33

34

35 36

A. K. Tassiopoulos et al.

Late results of iliofemoral venous thrombectomy. J Vasc Surg 1997; 25: 417–422. Burnand KG, O’Donnell TF Jr, Thomas ML, Browse NL. The relative importance of incompetent communicating veins in the production of varicose veins and venous ulcers. Surgery 1977; 82: 9–14. Bjordal R. Flow and pressure studies in venous insufficiency. Acta Chir Scand Suppl 1988; 544: 30–33. Stacey MC, Burnand KG, Layer GT, Pattison M. Calf pump function in patients with healed venous ulcers is not improved by surgery to the communicating veins or by elastic stockings. Br J Surg 1988; 75: 436–439. Zukowski AJ, Nicolaides AN, Szendro G et al. Haemodynamic significance of incompetent calf perforating veins. Br J Surg 1991; 78: 625–629. Gloviczki P, Bergan JJ, Rhodes JM et al. Mid-term results of endoscopic perforator vein interruption for chronic venous insufficiency: lessons learned from the North American subfascial endoscopic perforator surgery registry. The North American Study Group. J Vasc Surg 1999; 29: 489–502. Pierik EG, van Urk H, Wittens CH. Efficacy of subfascial endoscopy in eradicating perforating veins of the lower leg and its relation with venous ulcer healing. J Vasc Surg 1997; 26: 255–259. Labropoulos N, Delis K, Nicolaides AN et al. The role of the distribution and anatomic extent of reflux in the development of signs and symptoms in chronic venous insufficiency. J Vasc Surg 1996; 23: 504–510. Nicolaides AN, Sumner DS, eds. Investigation of patients with deep vein thrombosis and chronic venous insufficiency. London: Med-Orion, 1991: 39–43. Lees TA, Lambert D. Patterns of venous reflux in limbs with

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37 38 39 40 41 42

43

44 45

skin changes associated with chronic venous insufficiency. Br J Surg 1993; 80: 725–728. Pierik EG, Wittens CH, van Urk H. Subfascial endoscopic ligation in the treatment of incompetent perforating veins. Eur J Vasc Endovasc Surg 1995; 9: 38–41. Cockett FB, Elgan-Jones DE. The ankle blow-out syndrome. Lancet 1953; 1: 17–23. Labropoulos N, Mansour MA, Kang SS, Gloviczki P, Baker WH. New insights into perforator vein incompetence. Eur J Vasc Endovasc Surg 1999; 18: 228–234. Stuart WP, Adam DJ, Allan PL, Ruckley CV, Bradbury AW. Saphenous surgery does not correct perforator incompetence in the presence of deep venous reflux. J Vasc Surg 1998; 28: 834–838. Nelze` n O. Prospective study of safety, patient satisfaction and leg ulcer healing following saphenous and subfascial endoscopic perforator surgery. Br J Surg 2000; 87: 86–91. Scriven JM, Bianchi V, Hartshorne T et al. A clinical and hemodynamic investigation into the role of calf perforating vein surgery in patients with venous ulceration and deep venous incompetence. Eur J Vasc Endovasc Surg 1998; 16: 148–152. Browse NL, Clemenson G, Lea Thomas M. Is the postphlebitic leg always postphlebitic? Relation between phlebographic appearances of deep-vein thrombosis and late sequelae. Br J Med 1980; 281: 1167–1170. Train JS, Schanzer H, Peirce EC, Dan SJ, Mitty HA. Radiological evaluation of the chronic venous stasis syndrome. JAMA 1987; 258: 941–944. Raju S, Fredericks R. Valve reconstruction procedures for nonobstructive venous insufficiency: rationale, techniques, and results in 107 procedures with two- to eight-year follow-up. J Vasc Surg 1988; 7: 301–310.

Accepted 18 April 2000