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Harry Ma MD, PhD Assistant Professor of Surgery University of Oklahoma Tulsa, Oklahoma Department of Surgery.

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Presentation on theme: "Harry Ma MD, PhD Assistant Professor of Surgery University of Oklahoma Tulsa, Oklahoma Department of Surgery."— Presentation transcript:

1 Harry Ma MD, PhD Assistant Professor of Surgery University of Oklahoma Tulsa, Oklahoma Department of Surgery

2 Disclosures None

3 Outline and Objectives Defining chronic venous disease Clinical manifestations Diagnostic evaluation Treatment Non-operative Operative

4 Spectrum of Disease Spider veins (telangiectases) Reticular veins Varicose veins Edema Chronic skin changes Ulcers

5 Impact of CVD Most common form of vascular disorder Chronic Venous Disease: 25 million people in US Health care cost: $1 to 3 Billion dollars annually Indirect cost: ~2 million work days lost annually

6 Definitions Telangiectasias - are a confluence of dilated intradermal venules less than one millimeter in diameter. Reticular veins - are dilated bluish subdermal veins, one to three millimeters in diameter. Usually tortuous. Varicose veins - are subcutaneous dilated veins three millimeters or greater in size. They may involve the saphenous veins, saphenous tributaries, or nonsaphenous superficial leg veins.

7 Definitions of Skin Changes Lipodermatosclerosis: localized chronic inflammation and fibrosis of the skin and subcutaneous tissue Atrophie blanche: localized, often circular whitis and atrophic skin areas surrounded by dilated capillary spots and hyperpigmentation Venous Ulcer: full thickness skin defect

8 CEAP classification Clinical Etiology Anatomy Pathophysiology

9 Clinical Classification C0: no visible or palpable signs of venous disease. C1: telangiectasies 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.

10 Etiologic Classification Ec: congenital (<5%) Ep: primary (65-80%) Es: secondary (postthrombotic 15-28%).

11 Valvular Dysfunction Primary valvular dysfunction: weakness in leaflets or vessel wall Secondary to previous DVT or phlebitis Increases retrograde flow Results in reflux Increased hydrostatic pressure Not just deep or superficial valves but perforators

12 Diagnostic Evaluation Venous Duplex (New Gold Standard) Phlebography or Venography (Old Gold Standard) Air Plethysmography Photophlethysmography Venous pressure (hemodynamic gold standard)

13 Venous Duplex Can rule out thrombosis and obstruction Quantify reflux in veins Visualize anatomy

14 Venous Duplex Vast majority have superficial incompetence only. Sensitivity 95 % for identifying the competence of the saphenofemoral and saphenopopliteal junctions. Less sensitive for identifying incompetent perforators (40 to 60 percent)

15 Risk Factors for varicose veins Morbid obesity Advanced age Sex/Hormonal changes Family history/Genetics History of DVT or phlebitis Occupational risks

16 Clinical Manifestations Veins are prone to thrombophlebitis Common symptoms: Pain Swelling Ulcerations Skin changes Cramping Fatigue

17 Clinical Manifestations Itching Burning Pain after standing Relieved with leg elevation Vague pain Complications: Ulceration Bleeding Skin changes

18 Patient Assessment History History of symptoms and onset History of venous complications Desire for treatment Comorbidities Rule out secondary cause including DVT and HEART Failure Examination Patient in general Pedal pulses Groins Veins Studies Venous Duplex

19 Non-operative management Leg elevation Compression therapy Treatment of ulcer: local wound care NOT DIURETICS

20 Non-operative management LEG ELEVATION – heart level for 30 minutes 3-4 times daily improves micro-circulation reduces edema, and promotes healing of venous ulcers. EXERCISE – daily walking and simple ankle flexion exercises.

21 Compression Therapy Compression bandages Compression Stockings Intermittent Pneumatic Compression Contraindications Active infection Significant arterial occlusive disease ABI < 0.6-0.8

22 Compression Stockings CLASSPRESSURESTRENGTHINDICATIONCEAP OTC< 15mmHGMinimalMinimal symptoms0,1 I15-20mmHgMildMinor varicosities, minor edema1,2,3 II20-30mmHgModerate Moderate varicosities, phlebitis, moderate edema, post-op ablation 3,4 III30-40mmHgFirmSevere varicosities, active or history of ulcers, DVT4,5,6 IV>40mmHgExtra FirmLymphedemaN/A

23 Compression Bandages Elastic In-elastic Types: ACE wrap Easier to use Higher pressures at rest Can cause pressure ulcers Minimal increase in pressure when ambulatory Types: Profore multi-layer wraps High stiffness Exert about 40mmHg Can lose pressure quickly due to limb volume reduction Difficult to apply Better for ambulatory patients

24 Benefits of Compression Increased ulcer healing 30-40mmHg compression resulted in 93% ulcer healing rate by 6 months Prevention of recurrence with compliance: 29% recurrence at 5 years Disadvantages: Compliance

25 Operative Management Ligation and Stripping Ablative therapy Radiofrequency Laser Sclerotherapy

26 Ligation and Stripping Traditional surgical approach Reduced recurrence rates compared to high ligation alone

27 Ablation Laser Use a bare tipped optical fiber which applies laser light energy to the vein. Therapy based on photothermolysis (light induced thermal damage). Laser light heats the target tissue inducing thermal injury Wavelength of light is chosen based on the target structure's chromophore Radiofrequency A high frequency alternating current resulting in energy that heats the adjacent vein walls to the probe which alters the protein structure of the vein effecting its closure

28 Complications of ablation Nerve injury <2% Skin injury <1% Failure of closure <5% Thrombotic complications <1%

29 Which is Better? Equivalent therapy Similar outcomes Success rates >95% for both (N=159) Improvement in QoL surveys and VVQ surveys Cochrane review in 2014 13 randomized trials included 3081 patients total Complication rates equivalent Efficacy: equivalent for laser, RFA, foam sclerotherapy and ligation and stripping

30 Sclerosing Agents Hypertonic Saline Chromated glycerin Nonchromated glycerin Monoethanolamine oleate Sotradecol (STS) Polidocanol Foam

31 Mechanism of action and use Endothelial damage Thrombosis Resultant sclerosis and closure of the vein For telangiectasias Reticular veins Perforator veins More recently incompetent GSV

32 Ultrasound Guided Foam Sclerotherapy First reported in 1995 Mixed with air or CO2 Bubble size of 100 µm or less Ration of sclerosant to air or CO2 is usually 1:4

33 Limitations and complications Large veins Phlebitis 3-8% Embolus (CVA) Visual disturbance DVT Failure or recurrence Anaphylaxis

34 Short term outcomes 1 year follow-up equivalent QoL improvement 72% success rate (vs 89% for EVLA) Two year follow-up in patients with ulcers 85% healing rate

35 Long term outcomes 5-8 year follow-up of 285 patients 89% had improvement in QoL survey and AVSS 15% required repeat treatment

36 References André P, Hartwell D, Hrachovinová I, Saffaripour S, Wagner DD. Pro-coagulant state resulting from high levels of soluble P-selectin in blood. Proc Natl Acad Sci U S A 2000;97:13835-40. PMID: 11095738Beebe-Dimmer JL, Pfeifer JR, Engle JS, Schottenfeld D. The Epidemiology of Chronic Venous Insufficiency and Varicose Veins. Ann Epidemiol 2005;15:175-84. PMID: 15723761 Bradbury A, Evans C, Allan P, Lee A, Ruckley V, Fowkes FG. What are the symptoms of varicose veins? Edinburgh vein study cross sectional population survey. BMJ 1999;318:353-6. PMID: 9933194. Bradbury A, Evans CJ, Allan P, Lee AJ, Ruckley CV, Fowkes FG. The relationship between lower limb symptoms and superficial and deep venous reflux on duplex ultrasonography: The Edinburgh Vein Study. J Vasc Surg 2000;32:921-31. PMID: 11054224 Browse NL. The diagnosis and management of primary lymphedema. J Vasc Surg 1986;3:181-4. PMID: 3510325 Burnand KG, Whimster I, Naidoo A, Browse NL. Pericapillary fibrin in the ulcer-bearing skin of the leg: the cause of lipodermatosclerosis and venous ulceration. BMJ (Clin Res Ed) 1982;16;285:1071-2. PMID: 6812751 Cardinal M, Eisenbud DE, Phillips T, Harding K. Early healing rates and wound area measurements are reliable predictors of later complete wound closure. Wound Repair Regen 2008;16:19-22. PMID: 18211575

37 References 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 population-based study in France. J Vasc Surg 2004;40:650-9. PMID: 15472591 Carpentier PH, Poulain C, Fabry R, Chleir F, Guias B, Bettarel-Binon C; Venous Working Group of the Société Française de Médecine Vasculaire. Ascribing leg symptoms to chronic venous disorders: the construction of a diagnostic score. J Vasc Surg 2007;46:991-6. PMID: 17980285 Christopoulos D, Nicolaides AN, Szendro G. Venous reflux: Quantitation and correlation with the clinical severity of chronic venous disease. Br J Surg 1988;75:352-6. PMID: 3359149 Comerota AJ, The ATTRACT Trial: Rationale for early intervention for iliofemoral DVT. Perspect Vasc Surg Endovas Ther 2009; 21(4): 221-4. Epub 2010 Jan 3. PMID: 20047905 Comerota AJ, Throm RC, Mathias SD, Haughton S, Mewissen M. Catheter-directed thrombolysis for iliofemoral deep venous thrombosis improves health-related quality of life. J Vasc Surg 2000;32:130-7. PMID: 10876214 Cornu-Thenard A, Boivin P, Baud JM, De Vincenzi I, Carpentier PH. Importance of the familial factor in varicose disease. Clinical study of 134 families. J Dermatol Surg Oncol 1994;20:318-26. PMID: 8176043 Corriere MA, Suave KJ, Ayerdi J, Craven BL, Stafford JM, Geary RL, Edwards MS: Vena cava filters and inferior vena cava thrombosis. J Vasc Surg 2007;45:789-94. PMID: 17398389


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