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Jeannouel van Leeuwen , surgeon Chirurgen Maatschap Emma Care Courtesy of Servier 25 january 2012
Incidence
annual incidence of varicose veins is about 2% life-time prevalence of varicose veins approaches 40% Varicosities are more common in women (about 2-3 times as prevalent in women than in men) 10-20% actually are symptomatic enough to complain about their lower leg varicose veins and seek treatment.
Normal Flow Superficial veins drain into the deep veins From the foot up to the heart
Superficial vein disease always starts with abnormal valves and interruption to normal flow called venous reflux
Risk factors
Female, age, ethnicity, occupation, pregnancy, obesity, smoking ASK about history of abdominal complaints/cancer, DVT, previous & other venous complaints
So the examination
Inspection Auscultation Palpation
cough test tap test
Tourniquet Tests
Trendelenberg Tourniquet test Perthes
Doppler
Sapheno-femoral junction Sapheno-popliteal junction
Anatomy
Superficial System arises from foot and ends at Sapheno- femoral junction (spiderhead) Long saphenous vein- medial leg up to SFJ Short saphenous vein- lateral malleolus , up calf to meet popliteal vein behind knee Sapheno- femoral junction- 4 cm lateral and 4cm below the pubic tubercle Communication veins: connecting deep and superficial system through piercing deep fascia, with valves to direct blood from superficial to deep viens. Perforator veins: there are 3 perforators on the medial side and 1 on the lateral side of the leg
2. Thrombophlebitis- superficial red painfull lump 3. Brown pigmentation- haemosiderin deposition 4. Venous Eczema 5. Venous Ulcers- over medial ankle 6. Lipodermatosclerosis-progressive sclerosis
of cutaneous fat- ankle becomes thin and hard- area above becomes oedematous
Atrophy blanche
Inspection
Venous ulcers/eczema
Pitting oedema
Spider veins
Inspection
Lipodermatosclerosis
Literally "scarring of the skin and fat A slow process that occurs over a number of years and has 2 phases:
1.
Acute
Venous pooling chronic venous hypertension RBC forced into surrounding tissue Haemoglobin broken down into brown haemosiderin Chronic haemosiderin formation leads to fibrin deposition Skin becomes thickened and shiny Skin around ankle constricts and the inverted champagne-bottle shape is seen
2.
Chronic
0 - no symptoms; 1 - heavy feet syndrome; 2 - intermittent edema; 3 - persistent edema, hyper- or hypopigmentation, lipodermatosclerosis, eczema; 4 - venous ulcer.
Causes Primary
Theories of Aetiology:
Weak wall theory Congenital valvular incompetence
Aggravating factors:
Female sex High parity Occupation requiring prolonged standing Marked obesity Constricting clothes Estrogen intake Deep venous thrombosis
Secondary Anything that raises intra-abdominal pressure or raises pressure in superficial/deep venous system so:
Pregnancy Abdominal/pelvic mass Ascites obesity constipation thrombosis of leg veins (DVT) AV fistula Vena cava thrombose Large liver cysts
Auscultation
Auscultate over any varicosities for bruits due to A-V malformation
Palpation
Palpate the veins to confirm they are infact veinswill refill if if gently pressed and released Next- find the sapheno-femoral junction (SFJ)
Find Pubic Tubercle just lateral to pubic symphisis 4 cm lateral then 4cm below Palpate for a sapheno varix- localised distension of the long saphenous vein in the groin
Cough Test- Fingers over SFJ, ask patient to cough can you feel a thrill, if yes suggest incompetence Tap Test- tap over the SFJ and feel further down long saphenous vein for any transmitted sounds, if yes suggest incompetence
Trendelenberg/Tourniquet tests
Aim- to localise the valve/s that are incompetent Trendelenberg Lie patient down and raise leg attempting to drain varicosities of blood. Using either a tourniquet or fingers put pressure over SFJ to occlude it Ask patient to stand If varicosities DO NOT refill indicates SFJ incompetence If DO refill the leaky valve is lower down I will now try and locate the incompetent perforator using the tourniquet test
Spider Veins
The proper term is Telangiectasia These are non raised dilated veins located in the Dermis (deep layer of the skin) Single layer endothelium, minimal muscle Can be Red or Blue in color depending on the origin Do not cause major medical complications
Spider Veins
Etiology: Multifactorial
Venous Hypertension associated with varicose veins Congenital: vascular nevi, neonatal hemangiomatosis, others.. Collage Vascular Disease: lupus, Hormonal factors: pregnancy, estrogen therapy, topical steroids
Affects over 1 million people in the US 100,000 are disabled from this More common in elderly population
2. Edema 3. Biological factors Leakage of proteins impedes diffusion O2 Aggregation of white cells
Block capillary flow Release on inflammatory proteins
Management
Conservative/Medical
Graded compression bandaging, Compression hosiery Paste Gauze (Unna) Boots Diuretics? Zinc? Phlebotrophic/Hemorheologi c agents? Aspirin/NSAIDs etc
Surgical
Ankle-to-groin saphenous vein stripping (with stab avulsion) Segmental saphenous vein stripping (with stab avulsion) Saphenous vein ligation: high, low, or both Saphenous vein ligation and sclerotherapy Saphenous vein ligation (with stab avulsion) Stab avulsion of varices without saphenous vein stripping (phlebectomy) Endoluminal occlusion of the saphenous vein by radiofrequency (RF) or laser energy
Surgical treatment
Crossectomy or/and vein stripping till below knee better than compressive therapy alone Other techniques : Endovas.burning or foam injection
Vein Ablation
Laser Ablation (EVLA ) Uses light to heat the vein Radio Frequency (VNUS Procedure) Uses radio frequency to heat the vein
Office based procedure Done under local anesthesia One needle puncture at the level of the
knee Takes about 1 hour Patient resumes normal activity same day
EVLA Results
Sclerotherapy
Cumulate vein with needle Inject Sclerosing Solution
Ethoxysclerol Hyper tonic Saline Foam (Mix STS with air and make bubbles)
Sclerotherapy Use
Neovascularization Perforators Clean up after Phlebectomies Spider veins Reticular veins GSV: can closure the, but has high recurrence rate
Sclerotherapy results
Skin grafting can be put on a non infected granulating skin defect of a venous ulcer
Treatment complications
Major complications following VV surgery are relatively rare Up to 20% morbidity
Infection Hematoma Pain Nerve damage
Saphenous nerve (LSV surgery) Sural, peroneal nerve (SSV surgery)
Oral medication
Effect on edema , hematocrit , augmentation capillary permeability , inflammation , less fibrinolysis , leukocyte function en erythrocytes No evidence for monotherapy only in addition effect on ulcer healing Daflon , Trental , Aspirine
hlebotropic drugs
Daflon Venal Venoruton Doxium
Rheologic hemocorrectors
acetylcalicylic acid, dipiridamol pentoxyphylline low-molecular dextranes