VARICOSE VEINS

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<h1>VARICOSE VEINS</h1><strong> Author: <a href='http://www.articleseen.com/profile_pinku.aspx'>pinku</a></strong><br /><p>Anatomy Veins bring blood back to the heart against gravity (when erect), a distance of 3-4 ft. The main system carrying 95% of the venous return is the deep system situated near the bones. The superficial system is present below the skin and dilates (varicose veins). There are also interconnecting veins between these two systems, called perforators. The deep system comprises: • Soleal sinusoids • Tibial veins • Popliteal vein • Femoral vein The superficial system comprises: • Dorsal venous arch • Long saphenous vein • Short saphenous vein • Posterior arch vein • Perforator veins • Giaccomini vein • Other tributaries. • Veins of the legs have one way valves. How veins work Blood moves in the arteries by the pumping action of the heart. When lying, gravity is eliminated and blood is pushed back by the pressure of the arterial blood. When walking it has to move against gravity. The calf muscles (external heart) compress the venous sinusoids and force blood back in the deep veins. During relaxation of the muscles the blood would fall to the feet but this is prevented by the presence of one way valves in the veins. Abnormal valves Venous insufficiency can occur due to problems in the veins themselves or weakness of the pumping mechanism of the calf. The two can cause leaky valves. Turbulent flow may cause weakness of the vein at various points causing them to varicose. The main causes are: • Congenital abnormalities of veins • DVT damaging valves of deep system • Superficial vein incompetence. DVT causes inflammation of the vein, damaging the valves. So when clot dissolves it leaves a damaged leaky valve. Now the muscles of the calf have to do more work to pump the blood back. Ultimately they weaken and lead to pooling of the blood - swelling, varicose veins, dermatitis and ulcers. DVT is more common in: • Major illness or surgery • Cancer • Pregnancy • Major accidents • Prolonged immobility • Any cause leading to prolonged major vein compression • Blood abnormalities • Metabolic causes – dehydration, high lipids & cholesterol, CHF) • Drugs – pill • SMOKING Classification of VVs It depends on the therapeutic approach to primary VVs 1. Spider angiomata – cluster of small subcuticular veins which may be associated with a superficial feeder vein. 2. Varicose Veins a) Segmental VVs – not associated with saphenous or perforator valvular incompetence b) Varicose veins associated with perforator incompetence but not SF incompetence c) Incompetent Saphenous system varicosities j) LSV  Competent SF jn valve but incompetent LSV valves BK  Incompetent SF jn valve – 66% ii) SSV  Competent SP valve but incompetent SSV valves below the mid calf.  Incompetent SP valve There may be a combination of the above conditions. If the saphenous system is not involved then there is the possibility of local valve incompetence or weakness of the vein wall. This can be differentiated by color Doppler study by an experienced operator. Very often the LSV below the knee is incompetent. Here the SF valve and the SP valve are competent but Giocomini’s vein (connecting LSV to SSV) .This is seen in 1.4% patients. Due to the spoilage of the valves, veins dilate and reflux → leading to tortuosity and large sacs form in the veins → turbulent flow is seen → thrombosis may occur (superficial phlebitis). Diagnosis & Evaluation The diagnosis is fairly obvious but may be missed in morbid obese. The diagnostic challenge therefore does not lie in identification but to identify the site of valvular incompetence and extent of segmental involvement. Clinical evaluation One has to separate patients who come for cosmetic reasons from those needing treatment for pain at the fag end of the day relieved by elevation. Thus the common symptoms & signs are:  Leg ache relieved by elevation  Tender varicosities  Ankle swelling  The complications of long standing VVs are:  Bleeding  Statis dermatitis  Ulcers  Phlebitis CVI or very long standing VVs may give rise to the following sequence of events: Brawny oedema → stasis dermatitis → subcutaneous fibrosis → cutaneous atrophy → pigmentation → ulceration Non-invasive testing Bed-side Doppler – is fairly accurate in picking up SF or SP incompetence or perforator incompetence. However it needs a skilled operator. Color Doppler study – the results and findings are the same as the above study except it is more accurate in identifying deep and superficial valvular incompetence, especially if present together. Summary Evaluation of VVs is anatomic and physiological. DVT must be excluded to be sure that the veins are not secondary VVs. Indications for therapy  Pain  Aching  Phlebitis  Swelling  Progressive VVs Surgery is more successful for incompetent veins and sclerotherapy for smaller varices and spider angiomata. Treatment Multiple ligation & local excision The site of the venous reflux is identified with a doppler and marked pre-op. Vertical incision is made over the site and veins extracted by blunt dissection followed by avulsion without ligation. Should bleeding persist, it means the incompetent perforator has not been identified. Finger tip compression over the site of depression stops the bleeding. Another incision over the site is made and the vein ligated. Wound is closed by sub-cuticular absorbable sutures and leg wrapped with elastic crape bandage. Saphenous ligation + stripping Since the entire LSV is pathological the vein has to be removed after high ligation. It is exposed at the groin by an incision parallel to the groin and just below it. The LSV is exposed just anterior to the medial malleolus at the ankle. The distal end of the LSV is ligated with non-absorbable and divided. The stripper is inserted at the ankle. If the stripper is arrested along the length then another incision is made at the site to help it progress. All branches of LSV in groin are identified by blunt dissection and ligated. The LSV is never ligated at the SFJ till the stripper is felt in the LSV and you are very sure that femoral vein is not being ligated. A clamp is placed on the saphenous vein so as not to compromise the FV in the ligature. The vein is transfixed. Compression over the stripped LSV is applied for 5 mins. After this the clotted blood is milked at either end and sub-cuticular sutures are applied to the incisions. Now compression bandage is applied to the thigh and the leg. Legs are elevated for 12 hours after surgery and total bed-rest is ordered. Then patient is encouraged to walk but sitting is discouraged and he must wear compression stockings till reviewed in two weeks time. Any bruising seen will normally settle in 6/52. Normal bathing is allowed during recovery. Segmental or distal saphenous varicosities Here sclerotherapy may be beneficial but long term results are awaited. The LSV above the knee may be normal but BK may be incompetent. If the segment is long it may be stripped but if not multiple ligations and avulsions may be done. Short saphenous varicosities Here the SSV is ligated behind the knee. It is divided, stripped and multiple avulsions of the branches are done. VNUS CLOSURE – This is a new technique where the main vein is heated to 85 C via a thin catheter introduced into the LSV just above the knee. This denatures the proteins in the wall of the vein and leading to their fusion and the vein can never open again. Long term results are awaited. Post-op complications  DVT  Saphenous nerve damage  Infection  Bleeding  Ecchymosis. Varicose Ulcers 90% of all ulcers are venous. 1% of the entire population suffers from these ulcers some time along their lives. Many of these ulcer patients have varicose veins associated. Do all patients with VVs develop ulcers? NO! Far fewer patients and it is related to the muscle pump failure and the valve destruction. This leads to ‘water logging’ within the calf muscles and their poor efficiency. Normally pressure decreases in the veins while we walk but here a chronic damage to the veins leads to increase pressure in the capillaries causing leakage of plasma and blood into the tissues. Blood contains enzymes and chemicals causing inflammation and the skin and underlying fat becoming itchy, sore and swollen. Blood leaking into tissues also contains fibrinogen which converts into insoluble fibrin which is laid down in large amounts and gets converted to scar tissue which contracts choking underlying tissue of its blood supply. The skin now becomes frail and breaks down into ulcers at the least trauma. This ulcer will never heal unless the chain of events leading up to its formation is reversed. The skin around the ulcer becomes patchy brown due to the breakdown of insoluble products of RBC (hemosiderin). 10% of the other leg ulcers are due to: • Arterial disease • AV fistulae • Diabetes • Neuropathic ulcers • Malignancy Treatment of Deep veins DVT is normally controlled by anticoagulants though they normally do not dissolve the clot but prevent the propagating thrombus which can become dangerous as it is friable and can easily dislodge into the lungs giving rise to the fatal PE. </p><strong>About the Author:</strong><br />I am Rajnish Kumar, in this time I am working a job on SEO. Now I am Permotting an http://vascularclinic.in/ site that is related from health and as far as I know about this site this is one of the best sites in health category. So please visit this site and gain a lot of knowledge about vascular. I am doing job in Aninfosolutions LTD.<p> Article Source: <a href='http://www.articleseen.com/Article_VARICOSE-VEINS_140737.aspx'> http://www.articleseen.com/Article_VARICOSE VEINS_140737.aspx</a></p>

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