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
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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
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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
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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
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