Chronic Venous Insufficiency

Chronic Venous InsufficiencyPrepared by Gihan Hany NakhlehMed III-Balamand UniversitySGHUMCOutlineDefinitionPrevalenceAnatomy ReviewPathophysiologyRisk FactorsClinical FeaturesDiagnosisTreatmentDefinitionA condition that affects the venous system of the lower extremities with venous hypertension causing various pathologies including pain, swelling, edema, skin changes, and ulcerations.

Occurs when valves become dysfunctional and impairs venous blood return.Affects up to 20% of adultsBy age 50 approximately 40% of women and 20% of men have significant vein problems3PrevalenceFemale : male 3:1

Affects up to 5-30% of adults

By age 50, 40% of women and 20% of men have significant vein problemsVenous anatomySuperficialGreat SaphenousSmall SaphenousDeepAnterior & Posterior TibialPeronealPoplitealFemoralPerforating

Venous anatomy

Muscle pumps

Venous pathophysiology and dysfunctionValvular incompetence reflux

Venous obstruction

Exacerbated by muscle pump dysfunction

Proper outflow of venous blood from the lower extremities depends on three factors: vein patency, competence of valves and proper calf function. All disturbances in these 3 components result in venous hypertension and chronic venous insufficiency. Failure of the muscle pump seems to be the most under-estimated pathophysiological factor bcz doppler sonography and phlebography cannot assess its function. Check for insufficiency standing and supine.Calf muscles and the muscles in the feet need to contract with each step to squeeze the veins and push the blood upward. Muscle atrophies with ageabnormal squeezing of the vein insufficiency.To keep blood flowing up, and not back down veins have one way valves. When valves become damaged blood leaks backward. Valve damage can be due to aging, extended sitting or standing or a combination of aging and reduced mobility. When veins and valves are weakened to the point where it is difficult for blood to flow up to the heart BP in veins rises for a long time leading to CVI.CVI most commonly occurs due to a blood clot in the deep veins of the legs DVT. 30% of ppl with DVT will develop this problem within 10 years after diagnosis.Venous obstruction: pelvic tumors 8Valvular incompetenceCongenital: Klippel Trenaunay and Parkes Weber syndromesPrimary: preexisting weakness in vessel wall or valve leaflet (uncertain cause)Secondary: Direct injuryPhlebitisExcessive venous distention due to hormonal effects Post-thrombotic syndromeValvular incompetence

Venous obstructionIntrinsicPrevious DVT with inadequate recanalizationVenous stenosisExtrinsicMay-Thurner syndrome (compression of left common iliac vein as it traverses between the right common iliac artery and lumbosacral region)Pelvic tumorsIliac compression syndrome

Muscle pump dysfunctionAge

Neuromuscular conditions or muscle wasting syndromes

ImmobilityRisk factorsAdvancing ageFamily history of venous diseaseLigamentous laxity (eg, hernia, flat feet)Prolonged standing or sittingIncreased BMISmoking

Sedentary lifestyleLower extremity traumaPrior venous thrombosis (superficial or deep)High estrogen statesPregnancy

Clinical featuresPain most commonlyAnkle and calf edema (relieved by foot elevation)Pruritus and brownish pigmentation (due to hemosiderin deposits)Stasis dermatitisLipodermatosclerosisUlceration: above the medial malleolus, wet, painlessInsufficient venous return results in increased pressure in the capillaries with the result that both fluid and cells may "leak" out of the capillaries. This results in red cells breaking down, with iron containing hemosiderin possibly contributing to the pathology of this entity.Mech: hypoxia, fibrin deposits, and MMPs.

Lipodermatosclerosis: inflammation of subcutaneous fat.15CEAPC- Clinical7 categories +/- symptomsE- EtiologyCongenital, primary, or secondaryA- AnatomySuperficial, deep, or perforatingP- PathophysiologyReflux, venous obstruction, calf muscle dysfunctionC- Clinical classification

DiagnosisHistory Physical ExamNoninvasive testingDuplex, APG, PPGInvasive testingPhlebography, AVPPhysical exam findings

TelangiectasiaPhysical exam

Varicose veinsPhysical exam

HyperpigmentationPhysical exam

Stasis dermatitisPhysical exam

Lipodermatosclerosis and atrophie blanchePhysical exam

Physical exam

Venous duplex imaging - reflux

Reflux in the saphenofemoral junction. The common femoral vein and greater saphenous vein (GSV) tributaries in the groin were normal. (B) The GSV at the knee is mildly dilated. The mild dilatation in the center of the image and the reflux pattern (blue color in each valve cusp) during the release of the compression indicate the presence of a valve. (C) The GSV in the lower calf has a small diameter, but a high velocity, very prolonged retrograde flow. (D) Varicose tributaries of the GSV from the lower thigh to the calf. This particular segment is actually one vein, although there appears to be many due to the tortuosity of the tributary. The patient underwent endovenous thermal ablation of the GSV from the upper calf to a point 2 cm from the saphenofemoral junction and phlebectomies of the tributaries. The remaining GSV was treated with foam sclerotherapy.Abbreviation: GSV, great saphenous vein.Secondary venous disease is less common than primary CVD and is caused by either a thrombotic event or arteriovenous fistula (AVF). Trauma has been mentioned as a cause of secondary CVD, but this occurs through deep venous thrombosis (DVT) of an AVF that can occur after trauma. Increasing venous pressure secondary to AVF formation creates local venous hypertension causing endothelium damage, vein wall weakening, and dilation faster but similar to that observed in primary CVD26Venous duplex imaging - dvt

Chronic obstruction with partial recanalization and reflux in a 58-year-old female patient with previous caval, iliofemoral, and popliteal vein thrombosis.She had significant thigh and calf swelling bilaterally. (A) Chronic thrombosis of the common femoral vein. Echogenic material is seen in the lumen and there is a lack of compressibility.(B) Irregular flow channels are seen in the lumen. Flow is detected in collateral veins on either side of the thrombosed segment. (C) The femoral vein is partially recanalized and has reflux. Chronic thrombus is seen mostly towards the far wall. (D)Reflux in a perforator vein in the lower calf. The vein is dilated with a diameter of 5 mm. Reflux was found in the posterior tibial vein, and the calf posterior accessory tributary. The great saphenous vein was normal at this level, but chronically thrombosed at the saphenofemoral junction. The patient was treated conservatively with compression.27Air plethysmography

phlebography

TreatmentConservative

Elastic compression stockings, ambulation, periodic rest elevation, avoid prolonged standing

Ulcers: multilayer compression bandage, antibiotics PRN, hydrocolloids, aggressive wound care.

Stasis dermatitis: topical steroids, moisturize

Exercise: improve calf muscle functionconservative

Ulcer managementPharmacological treatmentFlavonoids e.g. Daflon Venoactive drug Decreases chronic vein inflammation, promotes ulcer healing, effective in elastic compression

Coumarin Competitive inhibitor of vit K Anticoagulant

Interventional treatmentSclerotherapy

Endovascular therapy (stenting)

Ablative therapy with endovenous radiofrequency and laser

Foam sclerotherapy

Surgical treatmentLigation and stripping and venous phlebectomy

Subfacial endoscopic perforator surgery

Valve reconstructionSurgical treatment

The end