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Venous Insufficiency: Nuts and Bolts Venous Insufficiency: Nuts and Bolts

Venous Insufficiency: Nuts and Bolts - PowerPoint Presentation

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Venous Insufficiency: Nuts and Bolts - PPT Presentation

Harry Ma MD PhD Assistant Professor of Surgery University of Oklahoma Tulsa Oklahoma Department of Surgery Disclosures None Outline and Objectives Defining chronic venous disease Clinical manifestations ID: 699393

pmid venous surg veins venous pmid veins surg skin vasc ulcer clinical symptoms compression chronic varicose leg disease vein

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Slide1

Venous Insufficiency: Nuts and Bolts

Harry Ma MD, PhDAssistant Professor of SurgeryUniversity of OklahomaTulsa, Oklahoma

Department of SurgerySlide2

Disclosures

NoneSlide3

Outline and Objectives

Defining chronic venous diseaseClinical manifestationsDiagnostic evaluationTreatmentNon-operativeOperativeSlide4

Spectrum of Disease

Spider veins (telangiectases)Reticular veinsVaricose veinsEdemaChronic skin changesUlcersSlide5

Impact of CVD

Most common form of vascular disorderChronic Venous Disease: 25 million people in USHealth care cost: $1 to 3 Billion dollars annuallyIndirect cost: ~2 million work days lost annuallySlide6

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.Slide7

Definitions of Skin Changes

Lipodermatosclerosis: localized chronic inflammation and fibrosis of the skin and subcutaneous tissueAtrophie blanche: localized, often circular whitis and atrophic skin areas surrounded by dilated capillary spots and hyperpigmentationVenous Ulcer: full thickness skin defectSlide8

CEAP classification

ClinicalEtiologyAnatomyPathophysiologySlide9

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.Slide10

Etiologic Classification

Ec: congenital (<5%) Ep: primary (65-80%)Es: secondary (postthrombotic 15-28%).Slide11

Valvular Dysfunction

Primary valvular dysfunction: weakness in leaflets or vessel wallSecondary to previous DVT or phlebitisIncreases retrograde flowResults in refluxIncreased hydrostatic pressureNot just deep or superficial valves but perforatorsSlide12

Diagnostic Evaluation

Venous Duplex (New Gold Standard)Phlebography or Venography (Old Gold Standard)Air PlethysmographyPhotophlethysmographyVenous pressure (hemodynamic gold standard)Slide13

Venous Duplex

Can rule out thrombosis and obstructionQuantify reflux in veinsVisualize anatomySlide14

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) Slide15

Risk Factors for varicose veins

Morbid obesityAdvanced ageSex/Hormonal changesFamily history/GeneticsHistory of DVT or phlebitisOccupational risksSlide16

Clinical Manifestations

Veins are prone to thrombophlebitisCommon symptoms:PainSwellingUlcerationsSkin changesCrampingFatigueSlide17

Clinical Manifestations

ItchingBurningPain after standingRelieved with leg elevationVague painComplications:UlcerationBleedingSkin changesSlide18

Patient Assessment

HistoryHistory of symptoms and onsetHistory of venous complicationsDesire for treatmentComorbiditiesRule out secondary cause including DVT and HEART FailureExaminationPatient in generalPedal pulsesGroinsVeins

StudiesVenous DuplexSlide19

Non-operative management

Leg elevationCompression therapyTreatment of ulcer: local wound careNOT DIURETICSSlide20

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.Slide21

Compression Therapy

Compression bandagesCompression StockingsIntermittent Pneumatic CompressionContraindicationsActive infectionSignificant arterial occlusive diseaseABI < 0.6-0.8Slide22

Compression Stockings

CLASSPRESSURESTRENGTH

INDICATIONCEAPOTC

< 15mmHG

Minimal

Minimal symptoms

0,1

I

15-20mmHg

Mild

Minor varicosities, minor edema

1,2,3

II

20-30mmHg

Moderate

Moderate varicosities, phlebitis, moderate edema, post-op ablation

3,4

III30-40mmHgFirmSevere varicosities, active or history of ulcers, DVT4,5,6IV>40mmHg

Extra Firm

Lymphedema

N/ASlide23

Compression Bandages

ElasticIn-elasticTypes: ACE wrapEasier to useHigher pressures at restCan cause pressure ulcersMinimal increase in pressure when ambulatoryTypes: Profore multi-layer wrapsHigh stiffnessExert about 40mmHgCan lose pressure quickly due to limb volume reduction

Difficult to applyBetter for ambulatory patientsSlide24

Benefits of Compression

Increased ulcer healing30-40mmHg compression resulted in 93% ulcer healing rate by 6 monthsPrevention of recurrence with compliance: 29% recurrence at 5 yearsDisadvantages: ComplianceSlide25

Operative Management

Ligation and StrippingAblative therapyRadiofrequencyLaserSclerotherapySlide26

Ligation and Stripping

Traditional surgical approachReduced recurrence rates compared to high ligation aloneSlide27

Ablation

LaserUse 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 injuryWavelength of light is chosen based on the target structure's chromophoreRadiofrequencyA 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 closureSlide28

Complications of ablation

Nerve injury <2%Skin injury <1%Failure of closure <5%Thrombotic complications <1%Slide29

Which is Better?

Equivalent therapySimilar outcomesSuccess rates >95% for both (N=159)Improvement in QoL surveys and VVQ surveysCochrane review in 201413 randomized trials included3081 patients totalComplication rates equivalentEfficacy: equivalent for laser, RFA, foam sclerotherapy and ligation and strippingSlide30

Sclerosing Agents

Hypertonic SalineChromated glycerinNonchromated glycerinMonoethanolamine oleateSotradecol (STS)PolidocanolFoamSlide31

Mechanism of action and use

Endothelial damageThrombosisResultant sclerosis and closure of the veinFor telangiectasiasReticular veinsPerforator veinsMore recently incompetent GSVSlide32

Ultrasound Guided Foam Sclerotherapy

First reported in 1995Mixed with air or CO2Bubble size of 100 µm or lessRation of sclerosant to air or CO2 is usually 1:4Slide33

Limitations and complications

Large veinsPhlebitis 3-8%Embolus (CVA)Visual disturbanceDVTFailure or recurrenceAnaphylaxisSlide34

Short term outcomes

1 year follow-up equivalent QoL improvement72% success rate (vs 89% for EVLA)Two year follow-up in patients with ulcers85% healing rateSlide35

Long term outcomes

5-8 year follow-up of 285 patients89% had improvement in QoL survey and AVSS15% required repeat treatmentSlide36

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: 15723761Bradbury 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: 11054224Browse NL. The diagnosis and management of primary lymphedema. J

Vasc Surg 1986;3:181-4. PMID: 3510325Burnand 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

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18211575Slide37

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: 15472591Carpentier 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: 17980285Christopoulos 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: 3359149Comerota 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: 10876214Cornu-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: 8176043Corriere 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