2CVIOccurs when the vein valves become dysfunctional and impairs venous blood return.Affects up to 20% of adults.By age 50 ~40% of women and 20% of men have significant vein problems.More people lose work time from vein disorders then from artery disease. 1.
3RISK FACTORS Advancing age Family history of venous disease Ligamentous laxity (eg, hernia, flat fleet)Prolonged standingIncreased body mass indexSmokingSedentary lifestyleLower extremity traumaPrior venous thrombosis (superficial or deep)Arteriovenous shuntHereditary conditionsHigh estrogen statesPregnancy 2.
4PROGRESSION OF VEIN DISEASE ASYMPTOMATICSUPERFICIAL VENOUS DILATATIONTelangiectasias (intradermal)Reticular veins (subdermal)
5PROGRESSION OF VEIN DISEASE ASYMPTOMATIC VS SYMPTOMATICVARICOSE VEINS (subcutaneous)
6PROGRESSION OF VEIN DISEASE CHRONIC VENOUS INSUFFICIENCYLeg edema
7PROGRESSION OF VEIN DISEASE CHRONIC VENOUS INSUFFICIENCYSkin changesHyperpigmentation
8PROGRESSION OF VEIN DISEASE CHRONIC VENOUS INSUFFICIENCYSkin changesStasis dermatitis
10PROGRESSION OF VEIN DISEASE CHRONIC VENOUS INSUFFICIENCYLipodermatosclerosisa form of panniculitis just above the ankles. 9.
11PROGRESSION OF VEIN DISEASE CHRONIC VENOUS INSUFFICIENCYVenous stasis ulceration(s)
12EVALUATION CHARACTERISTICS VENOUS ARTERIAL APPEARANCE LOCATION Irregular, dark pigmentation, sometimes fibrotic, granulation, usually shallow.Irregular, smooth edge, minimum to no granulation, usually deep with a punched out appearance.LOCATIONDistal lower leg, medial malleolus.Distal lower leg/feet/toes, lateral malleolus, anterior tibial area.PEDAL PULSESUsually present.May be diminished or absent.PAINMay be present. Usually improves with leg elevation.Usually painful especially with leg elevation.DRAINAGEModerate to large.Minimal to none.TEMPERATUREMay be increased.May be decreased.SKIN CHANGESFlaking, dry, hyperpigmented.Thin, shiny, hairless, yellow nails. 3.
13EVALUATIONCONSIDER A BIOPSY TO EVALUATE FOR POSSIBLE MALIGNANCY VS INFECTIOUS OR INFLAMMATORY PROCESS.DOPPLER ULTRASOUND - VENOUS. CONSIDER ARTERIAL DOPPLER IF THERE IS ANY CONCERN OF SIGNIFICANT ARTERIAL OCCLUSIVE DISEASE.
14EVALUATION VENOUS DOPPLER ULTRASOUND Evaluate for deep and superficial venousthrombosis.Evaluate for incompetent veins withsignificant reflux disease.Evaluate for incompetent perforatingveins and tributaries.
18CLASSIFICATION VEIN DISEASE CEAP – an international consensus conference initiated the Clinical-Etiology-Anatomy-Pathophysiology classification.C 0 – no evidence of venous disease.C 1 – telangiectasias/reticular veins.C 2 – varicose veins.C 3 – edema associated with vein disease.C 4a – pigmentation or eczema.C 4b – lipodermatosclerosis.C 5 – healed venous ulcer.C 6 – active venous ulcer.E c – congenitalE p – primary venous disease.E s – secondary venous disorder.E n – not specified.A s – superficial veins.A d – deep veins.A p – perforating veins.A n – not specified.P r – venous reflux.P o – venous obstruction.P n – not specified. 7.
19MANAGEMENT OF CVILEG ELEVATION – heart level for 30 minutes 3-4 times daily improves micro-circulation reduces edema, and promotes healing of venous ulcers.4.EXERCISE – daily walking and simple ankle flexion exercises.
20MANAGEMENT OF CVI Compression therapy - avoid contraindications such as cellulitisor significant arterial occlusive disease.
21MANAGEMENT OF CVI – COMPRESSION THERAPY Compression bandages – elastic or non-elastic with single or multi-layers.
23MANAGEMENT OF CVI – COMPRESSION STOCKINGS4. CLASSPRESSURELEVEL OF SUPPORTINDICATIONCEAPOTC<15 mmHgMinimalAsymptomatic,comfort only.0, 1I15-20 mmHgMildMinor varicosities, tired aching legs, minor swelling.1, 2, 3II20-30 mmHgModerateModerate to severe varicosities, moderate swelling,phlebitis, following ablation.3, 4III30-40 mmHgFirmSevere varicosities, swelling, management of ulcerations, following DVT, post surgery.4, 5, 6IV>40 mmHgExtra firmLymphedema.NA
24PNEUMATIC COMPRESSION THERAPY MANAGEMENT OF CVIPNEUMATIC COMPRESSION THERAPY
26MANAGEMENT OF CVI - MEDICATIONS Diuretics – one of the most inappropriate treatments.Aspirin – may accelerate the healing of chronic ulcers.Pentoxifylline – more effective for complete or partial ulcer healing then placebo.Stanozolol – an anabolic steroid that stimulates fibrinolysis and improves lipodermatosclerosis and possibly ulcer healing.Escin (horseshoe chestnut) – 50mg twice daily reduces leg volume and edema. It stimulates the release of F series prostaglandins which induce venoconstriction, decreasing the permeability of vessel walls to low molecular proteins, water, and electrolytes.Hydroxyethylrutoside, Sulodexide, Prostacyclin Analogues – not available in the United States. 4.
27MANAGEMENT OF CVI – SKIN CARE Skin cleansing – wash with a mild non-soap cleanser (e.g. Dove, Olay, Caress).Emollients – provides a film of oil to lubricate the skin (e.g. Vaseline, Lubriderm, Aveeno).Barrier preparations – physically block chemical irritants and moisture.(e.g. Zinc oxide, Vaseline).Topical corticosteroids – often used to treat stasis dermatitis. 4.
28MANAGEMENT OF CVI – VENOUS STASIS ULCERS Surgical debridement – used to remove devitalized tissue.Enzymatic agents – used to break down necrotic tissue (e.g. Santyl).Growth factors – synthesized by many cell types such as platelets, neutrophils, and epithelial cells (e.g. Regranex).Bioengineered tissue – used for a variety of non-healing ulcers (e.g. Apligraf, Dermagraft).Skin grafting – an option for non-healing ulcers. 4.
29MANAGEMENT OF CVI – VENOUS STASIS ULCERS Dressings – depend upon the ulcer characteristics, frequency of dressing changes, and cost.-Occlusive dressings may be fully occlusive (impermeable to gases and liquids) or semi-impermeable (impermeable to liquids and partially permeable to gases and water vapor).It stimulates collagen synthesis, angiogenesis, and speeds reepithelialization.-Low adherent gauze dressings – frequent changes but inexpensive.-Hydrogels and alginate dressings are highly absorbent to handle heavily exudative ulcers, while hydrocolloids can help with wound debridement and skin protection.-Silver can be incorporated if the ulcer is infected. 4.
30MANAGEMENT OF CVI – ABLATION THERAPY Indications – patients with persistent signs/symptoms of venous disease after a minimum of 3 months of medical therapy (e.g. compression) and documented reflux (e.g. >0.5 seconds of reflux GSV).Absolute contraindications – acute DVT or phlebitis and pregnancy. 5,6.Radiofrequency versus laser endovenous ablation therapy.
31MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY Radiofrequency devices – generate a high frequency alternating current for which the energy heats the adjacent vein walls to the probe which alters the protein structure of the vein effecting its closure. 5.Superficial veins include – Great Saphenous Vein, Small Saphenous, and incompetent perforator veins.
34MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
35MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
36MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
37MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
38MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
39MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
40MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY
41MANAGEMENT OF CVI – RADIOFREQUENCY ENDOVENOUS ABLATION THERAPY BEFORE AFTER
42MANAGEMENT OF CVI – ENDOVENOUS LASER ABLATION THERAPY Lasers emit a single, coherent wavelength of light. Laser therapy of venous structures is based upon the concept of selective photothermolysis (ie, selective thermal confinement of light induced damage). Vein wall injury is mediated directly by absorption of photon energy by the vein wall and indirectly by thermal convection from steam bubbles, and from heated blood.Superficial veins include – Great Saphenous Vein, Small Saphenous Vein, incompetent perforator veins, telangiectasias and reticular veins. 6.
43MANAGEMENT OF CVI – ENDOVENOUS LASER ABLATION THERAPY
44MANAGEMENT OF CVI – MECHANICAL ABLATION Physical destruction of a vein with its partial or complete removal.- Vein ligation/stripping- Stab phlebectomy- Powered phlebectomy- Open or endoscopic perforator ligation.
47MANAGEMENT OF CVI - SCLEROTHERAPY Chemical irritants injected to close unwanted veins. Preparations include liquid and foam. It is used primarily in the treatment of telangiectasias, reticular veins, and small varicose veins.These substances cause endothelial damage by their actions as either osmotic or detergent agents. Osmotic agents achieve their effect by dehydrating endothelial cells through osmosis. Detergents are surface active agents which damage the endothelium by interfering with cell membrane lipids. 8.
50REFERENCES2012 Vascular Disease Foundation Leesburg Pike, suite 301, Vienna VirginiaAlguire PC, Scovell S. Overview and medical management of lower extremity chronic venous disease UpToDate.Venous stasis and arterial ulcer comparison. February 1,Alguire PC, Mathes BM. Medical management of lower extremity chronic venous disease UpToDate.Scovell S. Radiofrequency ablation for the treatment of lower extremity chronic venous disease UpToDate.Ihnat DM. Endovenous laser ablation for the treatment of lower extremity chronic venous disease UpToDate.Collins KA. Classification of lower extremity chronic venous disorders UpToDate.Greenberg DL, Scovell S. Liquid and foam sclerotherapy techniques for the treatment of lower extremity veins UpToDate.Alguire PC, Mathes BM. Pathophysiology of chronic venous disease UpToDate.