Leg Veins



Leg Veins





3.4.i SPIDER VEINS

Neil S. Sadick


BACKGROUND

Spider veins are the most frequently encountered manifestation of venous disease and most commonly treated cosmetic leg vein condition. In the United States, approximately 23% of adults suffer from a spectrum of chronic venous disease that includes spider telangiectasias, reticular veins, and true varicosities.1 Latest figures depict over 22 million woman and 11 million men between ages 40 and 80 years to have varicose veins, and when the definition of varicose veins is expanded to include cosmetic telangiectasias, they are present in 79% of men and 88% of women.2,3,4,5 Generally, they are more common in women and older adults, although studies have shown that, as opposed to being a mostly cosmetic concern in women, they are associated with a functional disorder twice as frequently in men than in women.6,7


PRESENTATION

Spider veins present as small, thin, pink-red to purple-blue arborizing or curvilinear threadlike structures close to the surface of the skin.







FIGURE 3.4.I.1 Facial spider vein.



PATHOGENESIS


Causative Factors

Telangiectasias arise from a number of causes, alone or more likely in combination with other etiologic factors, broadly categorized as genetic/congenital, acquired, and iatrogenic. The current body of research indicates that venous hypertension is a secondary event to the etiologic factors that render the vein wall pliable to dilation and affect the valves leading to the appearance of telangiectasia. Some of the congenital/genetic causes of telangiectasias include nevus flammeus (port-wine stains), nevus araneus (spider telangiectasia), hereditary hemorrhagic telangiectasia, and ataxia-telangiectasia. Genetic inheritance with variable penetrance may induce inherited weakness of the venous wall, predisposing vein valves and venous walls to incompetence.11,12 Acquired causes of telangiectasias can arise from a primary cutaneous disorder, such as varicose veins, or factors leading to venous abnormalities such as advanced age, gender, pregnancy, and lifestyle10 (Table 3.4.i.2). Pregnancy and the associated hormonal changes play a key role contributing to the formation of varicose and spider veins. In addition to circulating hormones that weaken vein walls, there is also a significant increase in the blood volume, which tends to distend veins, causing valve dysfunction and blood pooling in the veins. Among other acquired causative factors not related to other venous abnormalities, is acne, rosacea, environmental damage such as that caused by sun or cold exposure, or limited systemic sclerosis/scleroderma. Topical steroids, particularly at high doses, have also been identified as a possible causative factor.








TABLE 3.4.I.2 Causes of Spider Veins









Congenital




  • Nevus flammeus (port-wine stain)



  • Klippel-Trenaunay syndrome



  • Maffucci syndrome (multiple endochondromas and hemangiomas)



  • Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)



  • Ataxia-telangiectasia



  • Sturge-Weber syndrome


Acquired




  • Cushing syndrome



  • Venous hypertension




    • Age



    • Gender



    • Pregnancy



    • Occupation/lifestyle



  • Acne rosacea



  • Blepharitis



  • Photodamage



  • Trauma



  • Radiation



  • Chemotherapy



  • Limited systemic sclerosis



  • Medications (corticosteroids)



  • Tempi syndrome



Molecular and Structural Mechanisms

The pathogenesis of each type of telangiectasia is somewhat different given the breadth of causative factors that may play a role in the development of new blood vessels or the dilation of existing blood vessels. Primary structural changes in the valves may make them “leaky,”
with progressive reflux causing secondary changes in the vein wall. Alternatively, or concurrently, the valves may become incompetent secondary to structural abnormalities and focal dilation in vein wall segments near the valve junctions, and the reflux ensues as a secondary event. Acquired telangiectasias are a consequence of the release or activation of vasoactive substances, such as hormones and other chemicals. Insights from histological evaluations have shown dilation of the valvular annulus, bulging valve leaflets, commissural dilation, leaflet stretching, shortening, tearing and perforation, and, ultimately, complete destruction of the valve, whereas the venous wall presents varied areas of either thickening or deterioration.13 Key ultrastructural findings include the infiltration of leukocytes and monocytes, suggesting activation of inflammatory cascades.14,15 The increase in venous pressure causes structural and functional changes in the vein wall that leads to further venous dilation and increases in vein wall tension that trigger the expression/activity of matrix metalloproteinases (MMPs). Engagement of this biochemical cascade induces degradation of the extracellular matrix proteins, thus affecting the structural integrity of the vein wall and engaging inflammatory pathways to scavenge the cellular debris. Recent evidence also suggests an effect of MMPs on the endothelium and smooth muscle components of the vein wall and thereby causing changes in the venous constriction/relaxation properties.16 Endothelial cell injury also triggers further leukocyte infiltration, activation, and inflammation, which leads to additional vein wall damage and release of several growth factors such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF). Thus, in the underlying general pathogenesis, vein wall dilation and valve dysfunction, via MMP activation and superimposed inflammation and fibrosis, leads to the appearance of telangiectasias.17





REFERENCES

1. Eklof B, Rutherford RB, Bergan JJ, et al. Revision of the CEAP classification for chronic venous disorders: consensus statement. J Vasc Surg. 2004;40(6):1248-1252.

2. Ruckley CV, Evans CJ, Allan PL, Lee AJ, Fowkes FG. Telangiectasia in the Edinburgh Vein Study: epidemiology and association with trunk varices and symptoms. Eur J Vasc Endovasc Surg. 2008;36(6):719-724.

3. Callam MJ. Epidemiology of varicose veins. Br J Surg. 1994;81(2):167-173.

4. Beebe-Dimmer JL, Pfeifer JR, Engle JS, Schottenfeld D. The epidemiology of chronic venous insufficiency and varicose veins. Ann Epidemiol. 2005;15(3):175-184.

5. Piazza G. Varicose veins. Circulation. 2014;130(7):582-587.

6. Chiesa R, Marone EM, Limoni C, Volonte M, Petrini O. Chronic venous disorders: correlation between visible signs, symptoms, and presence of functional disease. J Vasc Surg. 2007;46(2):322-330.

7. Spendel S, Prandl EC, Schintler MV, et al. Treatment of spider leg veins with the KTP (532 nm) laser-a prospective study. Lasers Surg Med. 2002;31(3):194-201.

8. Requena L, Sangueza OP, Cutaneous vascular anomalies. Part I. Hamartomas, malformations, and dilation of preexisting vessels. J Am Acad Dermatol. 1997;37(4):523-549; quiz 549-52.

9. Braverman IM. The cutaneous microcirculation. J Investig Dermatol Symp Proc. 2000;5(1):3-9.

10. Goldman MP. Sclerotherapy: Treatment of Varicose and Telangiectatic Leg Veins. 2nd ed. St. Louis: Mosby; 1995.

11. Rose SS, Ahmed A. Some thoughts on the aetiology of varicose veins. J Cardiovasc Surg (Torino). 1986;27(5):534-543.

12. Pascarella L, Schmid Schonbein GW. Causes of telengiectasias, reticular veins, and varicose veins. Semin Vasc Surg. 2005;18(1):2-4.

13. Leu AJ, Leu HJ, Franzeck UK, Bollinger A. Microvascular changes in chronic venous insufficiency-a review. Cardiovasc Surg. 1995;3(3):237-245.

14. Ono T, Bergan JJ, Schmid-Schonbein GW, Takase S. Monocyte infiltration into venous valves. J Vasc Surg. 1998;27(1):158-166.

15. Takase S, Schmid-Schonbein G, Bergan JJ. Leukocyte activation in patients with venous insufficiency. J Vasc Surg. 1999;30(1):148-156.

16. Michiels C, Bouaziz N, Remacle J. Role of the endothelium and blood stasis in the development of varicose veins. Int Angiol. 2002;21(2 suppl 1):18-25.

17. Raffetto JD, Khalil RA. Mechanisms of varicose vein formation: valve dysfunction and wall dilation. Phlebology. 2008;23(2):85-98.

18. Sadick N, Li C. Small-vessel sclerotherapy. Dermatol Clin. 2001;19(3):475-481; viii.

19. Goldman MP, Sadick NS, Weiss RA. Cutaneous necrosis, telangiectatic matting, and hyperpigmentation following sclerotherapy. Etiology, prevention, and treatment. Dermatol Surg. 1995;21(1):19-29; quiz 31-2.

20. Gupta R, Gautam RK, Bhardwaj M, Chauhan A. A clinical approach to diagnose patients with localized telangiectasia. Int J Dermatol. 2015;54(8):e294-e301.

21. Weiss MA, Hsu JT, Neuhaus I, Sadick NS, Duffy DM. Consensus for sclerotherapy. Dermatol Surg. 2014;40(12):1309-1318.

22. Sadick NS. Choosing the appropriate sclerosing concentration for vessel diameter. Dermatol Surg. 2010;36(suppl 2):976-981.

23. Duffy DM. Sclerosants: a comparative review. Dermatol Surg. 2010;36(suppl 2):1010-1025.

24. Erkin A, Kosemehmetoglu K, Diler MS, Koksal C. Evaluation of the minimum effective concentration of foam sclerosant in an ex-vivo study. Eur J Vasc Endovasc Surg. 2012;44(6):593-597.

25. AlJasser MI, Lui H. Dermoscopy-assisted sclerotherapy for spider leg veins. Dermatol Surg. 2014;40(2):217-218.

26. Thomson L. Sclerotherapy of telangiectasias or spider veins in the lower limb: a review. J Vasc Nurs. 2016;34(2):61-62.

27. Bowes LE, Goldman MP. Sclerotherapy of reticular and telangiectatic veins of the face, hands, and chest. Dermatol Surg. 2002;28(1):46-51.

28. Peterson JD, Goldman MP, Weiss RA, et al. Treatment of reticular and telangiectatic leg veins: double-blind, prospective comparative trial of polidocanol and hypertonic saline. Dermatol Surg. 2012;38(8):1322-1330.

29. Rabe E, Schliephake D, Otto J, Breu FX, Pannier F. Sclerotherapy of telangiectases and reticular veins: a double-blind, randomized, comparative clinical trial of polidocanol, sodium tetradecyl sulphate and isotonic saline (EASI study). Phlebology. 2010;25(3):124-131.

30. Wollina U, Schmidt WD, Hercogova J, Fassler D. Laser therapy of spider leg veins. J Cosmet Dermatol. 2003;2(3-4):166-174.

31. McDaniel DH, Ash K, Lord J, Newman J, Adrian RM, Zukowski M. Laser therapy of spider leg veins: clinical evaluation of a new long pulsed alexandrite laser. Dermatol Surg. 1999;25(1):52-58.

32. Alora MB, Stern RS, Arndt KA, Dover JS. Comparison of the 595 nm long-pulse (1.5 msec) and ultralong-pulse (4 msec) lasers in the treatment of leg veins. Dermatol Surg. 1999;25(6):445-449.

33. Eremia S, Li C, Umar SH. A side-by-side comparative study of 1064 nm Nd:YAG, 810 nm diode and 755 nm alexandrite lasers for treatment of 0.3-3 mm leg veins. Dermatol Surg. 2002;28(3):224-230.

34. Sadick NS. Long-term results with a multiple synchronized-pulse 1064 nm Nd:YAG laser for the treatment of leg venulectasias and reticular veins. Dermatol Surg. 2001;27(4):365-369.

35. Liu J, Zhou BR, Wu D, Xu Y, Luo D. Sequential delivery of intense pulsed light and long-pulse 1,064-nm neodymium-doped yttrium aluminum garnet laser shows better effect on facial telangiectasias than using them separately. G Ital Dermatol Venereol. 2017;152(1):1-7.

36. Varughese N, Keller L, Goldberg DJ. Split face comparison between single band and dual band pulsed light technology for treatment of photodamage. J Cosmet Laser Ther. 2016:1-20.

37. Bernstein EF, Noyaner-Turley A, Renton B. Treatment of spider veins of the lower extremity with a novel 532 nm KTP laser. Lasers Surg Med. 2014;46(2):81-88.

38. Goldman MP, Weiss RA, Brody HJ, Coleman WP III, Fitzpatrick RE. Treatment of facial telangiectasia with sclerotherapy, laser surgery, and/or electrodessication: a review. J Dermatol Surg Oncol. 1993;19:899-906.

39. Ray M, Gold M. A retrospective study of patient satisfaction following a trial of nano-fractional RF treatment. J Drugs Dermatol. 2015;14(11):1268-1271.

40. Kearney C, Brew D. Single-session combination treatment with intense pulsed light and nonablative fractional photothermolysis: a split-face study. Dermatol Surg. 2012;38(7 Pt 1):1002-1009.

41. Mujadzic M, Ritter EF, Given KS. A novel approach for the treatment of spider veins. Aesthet Surg J. 2015;35(7):NP221-NP229.



3.4.ii RETICULAR VEINS

NEIL S. SADICK

CHRISTIAN R. HALVORSON

ROBERT A. WEISS


BACKGROUND

Reticular veins are dilated blue veins, typically found in the legs, that are a subtype of leg varicosity. According to the clinical, etiological, anatomical, and pathological classification (CEAP) definition, reticular veins are included in the C1 class and affect almost 25% of the adult population in the Western world. Treatment is sought mainly for aesthetic reasons, although reticulate eruptions of vascular origin may represent an underlying arterial, venous, microvascular, or combined pathology.

If a reticular vein permits both antegrade and retrograde blood flow depending on vein position in relation to gravitational force, it is termed an “incompetent reticular vein” and is associated with nonfunctioning valves and a more serious venous condition.1


PRESENTATION

Patients present with visible narrow blue veins in a reticulated pattern, usually on the legs. Translucent skin may allow normal veins to be visible as bluish subdermal reticular pattern, but reticular blue veins due to venous dilatation are more prominent, darker blue, and wider.

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Jun 29, 2020 | Posted by in Dermatology | Comments Off on Leg Veins
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