Dr \u00a0Meera Narendran BHMS,MD(Hom)
\nThe lower limbs has superficial and deep veins; the superficial veins are in subcutaneous tissue, and the deep veins are in to the deep fasica and accompany all major arteries. The veins of lowerlimb act as a complex pumping meachanism capable of returning venous blood to the heart against the force of gravity in the upright position.<\/p>\n
Superficial veins of the lower limb The great saphenous <\/strong>veins is formed by the union of the dorsal vein of the great toe and the dorsal venus arch of the foot. The great saphenous vein.<\/p>\n The small Saphenous vein. Although many tributaries are received by the saphenous veins, their diameter remains remarkably uniform as they descend the limb. This is possible because the blood they received is continuously shunted from these superficial veins in the subcutaneous tissue to the deep veins by means of the many perforating veins. Deep veins of the lower limb Creation of flow within veins Disorderd venous function Signs of venous abnormality in the lower limb with patient standing 2. Saccules on the veins 3. Inky-blue-black veins 4. Distended Subdermal and intradermal venules 5. Cough impulse 6. Increased warmth in veins Varicose veins, arise in 3 circumstances of unnatural flow. 1. Simple (or primary) varicose veins Signs of venous hypertension Venotensive change Symptoms of venous disorder 1. Pruritus – May be the early change Diagnosis Special investigations Management Homoeopathic Medicines
\n<\/strong>The two major superficial veins in the lower limb are the great and small saphenous veins.<\/p>\n\n
\n<\/strong><\/p>\n\n
\nThe perforating veins, penetrate the deep fasia close to their origin from the superficial veins and contains valves that when functioning normally, only allow blood to flow from the superficial veins to the deep veins. The perforating veins pass through the deep fascia at an oblique angle so that when muscle the deep fascia, the perforating veins are compressed. This also prevents blood from flowing from the deep to the superficial veins.<\/p>\n
\n<\/strong>Deep veins contained within the vascular sheath with the artery, whose pulsations also help to compress and move blood in the veins.
\nThe dorsal digital veins of the foot receive tributaries from the plantar venous arch and join to form common dorsal digital veins that terminate in the dorsal venous arch.
\nMedial and lateral plantar veins pass close to the arteries and after communicating with the great and small suphenous veins, form the posterior fibial veins posterior to the medical malleolus. The deep veins communicate with the superficial veins through perforating veins. Because of the effect of gravity, bloodflow is markedly reduced when a person stands quietly. During exercise blood received is propelled by muscular contraction to the femoral and then the internal iliac veins, flow in the reverse direction away from the heart or from the deep to the superficial veins is prevented if venous valves are competent.<\/p>\n
\n<\/strong>Only three forces create movement of venous blood in the limbs.
\n1. Aretrial pressure across the capillary beds
\n2. Musculovenous pumps.
\n3. Gravity :- If the limb is elevated above the horizontal flow towards the heart occurs by simple gravitational downflow.<\/p>\n
\n<\/strong>Venous insufficiency, a state of inadequate venous return in the upright position and accompanied by venous hypertension, may occur in the following circumstances.
\n1. Deficient or defective valves in superficial veins, causing massive downflow:- See in simple varices veins.
\n2. Active venous thrombosis (acute deep vein thrombosis) with imapairment of musculovenous pumping mechanism.
\n3. Post-thrombotic Syndrome
\nVenous thrombosis causing obstruction or deformity in the venous circuits.
\n4. Loss of deep vein valve competence or replacement of the deep veins by enlarged, valves, collateral veins as occurs in post thrombotic states.
\n5. Valveless and abak vein Syndrome.
\nIn born deficiency of deep vein valves or inherent weakness in the vein wall with valve failure.
\n6. Prolonged in activity of the muscles with the limbs in a dependent position, as in paralysis or disease states innibiting use of muscles.
\nArteriovenous fistula by direct arterial in flow to the venous side can cause venous hypertension and the characteristic venotensive changes resulting from it.<\/p>\n
\n<\/strong>1. Tortuosity
\nThis is the most significiant visible sign of abnormality. This is mostly seen in superficial valve incompetence, where strong gravitational downflow occurs. High flow in a normal direction at increased pressure, intermiftently or continuously, will cause enlargement but seldom accompanied by tortousity.<\/p>\n
\nSince saphenous vein is too robust, seldom become tortous, instead one or more saccules may be seen or palpated along its length. Usually a saccule is immediately below valve cusps and which are leaking heavily and the gross turbulence this causes on coughing give rise to a characteristic, palpable thrill, readily confirmed by Doppler flowmetry and functional phelebography. The presence of a saccules is a clear indication of a incompetent valve.<\/p>\n
\nVaricose commonly become adherent to overlying skin and may so stretch it that the dark blue venous blood shows through very clearly. This fragile covering will be vulnerable to minor trauma which may cause heavy haemarrhage.<\/p>\n
\nExtensive patterns of radiating venules are commonly seen around the ankle and on the foot (corona phlebectatica). These flares of veins indicate venous congestion with increased venous pressure. They occur more readily in the weakened tissues of the elderly and are not necessarly the precursons of ulceration. (These veins must be distingushed from small elustens of intradermal venules (thread or spider veins). Seen on the thigh or upper leg increasingly as middle age approaches these may signify underlying venous disorder.<\/p>\n
\nVaricose veins give a palpable impulse when the patient coughs, because of the absence of functioning valve between the abdomen and the vein, and it confirms incompetence in the valves of deep and superficial veins leading to this point.<\/p>\n
\nVeins carrying a strong reversed flow of blood that has just emerged from a deep vein at true body temparature, as in simple varicose veins. This is valuable confirmation of the vein\u2019s abnormal state. This sign is also seen in Arteriovenous fistula.
\nWith the patient lying
\nHollows and grooves in the elevated limb.
\nWhen the limb is elevated the veins wil empty and space occupied by large varicose veins becomes a hollow or a groove readly palpable or even visible.
\nThe nature of varicose veins<\/p>\n
\n<\/strong>I. Simple (or primary)
\nII. Secondary
\nIII. Arteriovenous fistula<\/p>\n
\nThese occur only in the superficial veins of the lower limbs and are by far the most common variety of varicose veins. Such veins have no competent valves and are subject to substantial upright and moving. Due to inadequate valves.
\n2. Secondary varicose veins
\nTortuisty is often seen in superficial veins carrying reversed flow as a part of collateral mechanism compensating for obstruction in a neighbouring deep vein. Tortousity is seen in normal veins.
\nEg:- Suprapubic veins acting as collaterials to iliac vein oesophageal varices in portal hyperation.
\n3. Arteriovenous fistula
\nTortuosity is often present in lesser veins inthe vicinity of an A.V. fistula but major veins leading from it enlarge without totuosity.<\/p>\n
\n<\/strong>Venous hypertension is a common consequence of venous disorder. Raised venous pressure cause an increase in capillary pressure & will cause characteristic changes in skin and subcuteneous tissues. These are mainly the result of excess capillary transudation carrying with it protein molecules and leading to deposition of fibrin which forms a barrier to nutritional exchange between capillaries and the surrounding tissues. Other substances are also extravasated including haemosiderin which eventually gives the characteristic brown skin pigmenation of venous hypertension.<\/p>\n
\n<\/strong>1. Swelling
\nMainly due to oedema
\n2. Induration
\nA characteristic diffuse fibrosis in the subcutaneous tissues. These changes may be accentuated by fat necrosis and chronic inflammatory changes. The term \u201clipodermatosclerosis or liposclerosis are often used to describe induration due to venous disorder.
\n3. Pigmentation
\nMost characterstic change, due to accumulation of haemosiderin in the skin.
\n4. Ulceration
\nIf the condition remain untreated, prograssive deterioration in skin nutrition leads to small areas of tissue death, to form an ulcer.
\nAn venous ulcer will be surrounded by pigmented skin and atleast induration. In long standing ulcers the neibouring skin may also show a characteristic white scarring known as \u201catrophie blache\u201d.
\n5. Eczema and dermatitis.
\nSkin is prone to eczema especially the pigmented area. Pruritus will be prominent.<\/p>\n
\n<\/strong>(When venotensive changes are not present)
\n1. Distress and aching after prolonged standing. In women discomfort is most marked over a few days before menstruration.
\n2. Nocturnal cramps
\nAdditional Symptoms when venotensive changes are present include<\/p>\n
\n2. Increased discomfort
\n3. Venous claudication<\/p>\n
\n<\/strong>By clinical history and clinical examination
\nClinical Tests
\n<\/strong>1. Brodie – Trendelenburg test
\n2. Tourniquet test
\n3. Perthe\u2019s test
\n4. Modified Perths test
\n5. Scwartz test
\n6. Pralt\u2019s test
\n7. Morrisey\u2019s Cough impulse test
\n8. Fegan\u2019s method
\n(to indicate the sites of perforators)<\/p>\n
\n<\/strong>1. Phlebography
\n2. Ascending fuctional cinephiebography
\n3. Doppler ultrasonogram
\n4. Duplex imaging
\n5. Ultrasound and CT scan<\/p>\n
\n<\/strong>1. Reassurance
\n2. Use of elastic compression stockings (creep bandage)
\n3. Injection Sclerotherapy
\n4. Surgical treatment<\/p>\n
\n<\/strong>Sulphur, Pulsatilla, Graphitis, Fluric acid, Millifolium, Hammamelis, Cale flur, Ambragrisea Vipera, Lycopodium, Bothrops, Lachesis, Carbo veg, Arnica.<\/p>\n","protected":false},"excerpt":{"rendered":"