ABOUT VEINS

SURGICAL ANATOMY OF VENOUS SYSTEM OF LOWER LEGS:

The venous system comprises of (1) deep veins (2) superficial veins (3) perforators.The deep veins of the lower limbs consist of veins below the knee viz. anterior tibial, posterior tibial and peroneal, soleus and gastrocnemius veins. These join in the upper part of the calf to form the POPTITEAL VEIN. This vein enters the adductor canal to become the SUPERFICIAL FEMORAL vein. The deep femoral vein joins it 5-10 cm below the inguinal ligament to form the common femoral which drains into the external iliac.Characteristics of the deep veins are---

THEY ACCOMPANY THE ARTERIES AND THEIR BRANCHES--- The pulsatile action of the arteries aid in the upward movement of blood in the veins

They HAVE MANY VALVES--- These aid in the upward movement of blood and prevent backflow. The SOLEAL VENOUS PLEXUS LIES WITHIN THE SOLEUS MUSCLE. Therefore the contraction of the muscle

aids in propelling the blood to the heart.

The superficial veins lie in the subcutaneous tissue and comprise of the LONG AND SHORT SAPHENOUS VEINS AND THEIR TRIBUTARIES.

LONG SAPHENOUS VEIN: it begins in the medial marginal vein of the foot . it then ascends in front of the tibial malleolus, runs upwards crossing the medial surface of the tibia to gain the medial border of the tibia. It then ascends upwards behind the medial condyles of the tibia and femur to reach the saphenous opening about 3.5 cm below and lateral to the pubic tubercle. Here it pierces the cribiform fascia and drains into the femoral vein. IT HAS 10-20 VALVES. TRIBUTARIES ARE:

MEDIAL MARGINAL VEIN OF THE SOLE POSTERIOR ARCH VEIN (LEONARDO’S VEIN)—This arch is important because it has 3-4 constant perforating

veins (COCKETT’S PERFORATORS) at the posterior border of the tibia linking it to the posterior tibial vein (deep vein of the leg).

ANTERIOR SUPERFICIAL TIBIAL VEIN – ascends along the shin MEDIAL AND LATERAL ACCESORY SAPHENOUS VEIN--- Runs postermedially and anterolaterally along the thigh. SAPHENOFEMORAL JUNCTION TRIBUTARIES—superficial inferior epigastric, superficial circumflex iliac and

superficial external pudendal. PERFORATOR VEINS --- present above and below the knee and in the mid thigh.

SHORT SAPHENOUS VEIN: It begins in the lateral marginal vein. It ascends behind the lateral malleolus, then along the lateral border of the tendo Achilles and then along the midline of the back of the leg. It perforates the deep fascia and passes between the two heads of gastrocnemius in the lower part of the poptiteal fossa and ends in popliteal vein 3-7.5 cm above the level of knee joint. IT HAS 7-13 VALVES. ITS TRIBUTARIES ARE:

It sends several tributaries upward and medially to join the long saphenous veins.

PERFORATING AND COMMUNICATING VEINS: these veins are a link between the superficial and deep veins. They always pierce the deep fascia. There are valves in these veins that prevent backflow of blood from the deep to the superficial veins. Incompetence of the perforator valves lead to VARICOSE VEINS. When calf muscles contract, high pressure is generated in the deep veins—this forces the blood upwards--- the perforators and the valves inside them help to prevent the blood from reaching the superficial veins during this time. During relaxation of the muscles, blood is aspirated from the superficial to the deep veins. If the valves of perforators become incompetent, these veins become ‘high pressure leaks’ during muscular contraction--- blood backflows into the sup. Veins--- varicosity. In LSV: the perforators are arranged in 3 sets--------

DODD’S PERFORATORS: these occur in relation to the subsartorial canal at the medial aspect of the midthigh. BOYD’S PERFORATORS: these occur in relation to the calf muscles COCKETT’S PERFORATORS: These are present just above the ankle joint at the medial aspect.

In SSV: the perforators are BASSI’S PERFORATORS: these are present 5 cm above the calcaneous and connects the SSV to the

peroneal vein SOLEUS POINT PERFORATOR: connects the soleus vein to the SSV. GASTROCNEMIUS POINT PERFORATOR: CONNECTS THE gastrocnemius vein to the SSV.

VENOUS THROMBOSIS OR THROMBOPHLEBITIS: The presence of thrombus in the superficial or deep vein and the accompanying inflammatory response is termed as VENOUS THROMBOSIS OR THROMBOPHLEBITIS. The factors that predispose to venous thrombosis were given by VIRCHOW ( virchow’s triad)

STASIS: IMMOBILISATION in debilitating illness, orthopedic surgery of hip and knee. VASCULAR DAMAGE: sclerosing agents, IV fluids, ionizing radiation, inflammatory process in the

neighbourhood, injuries eg. tibial fracture, bacterial endotoxin, malignant disease ( carcinoma pancreas, lungs, GIT, stomach, breast.

HYPERCOAGULABILITY: antithrombin III, protein C, protein S deficiency; antiphospholipid syndrome, SLE, DIC, myeloproliferative disorders.

Venous thrombosis also occurs in pregnancy particularly in the THIRD TRIMESTER AND 1ST MONTH OF PEURPERIUM. Also occurs in individuals taking OCP and HRT.

DEEP VEIN THROMBOSIS: The onset of thrombosis is usually SILENT. THE PROCESS OCCURS AT ABOUT THE 7th TO 10th

day AFTER OPERATION, PARTURITION OR ONSET OF INFECTION. 1/3rd to 2/3rd of all patients complain of--- UNILATERAL LEG SWELLING, WARMTH, PAIN AND ERYTHEMA especially over the calf. ANKLE OEDEMA There may be INCREASED TISSUE TURGOR, DISTENTION OF THE SUPERFICIAL VEINS AND THE APPEARANCE OF

PROMINENT VENOUS COLLATERALS. In some patients deoxygenated hemoglobin in the stagnant veins imparts a cyanotic hue--- PHLEGMESIA

CERULEA DOLENS. In markedly oedematous limbs , the interstitial pressure is very high to compress the capillary perfusion

pressure--- PHLEGMESIA ALBA DOLENS. CHEST PAIN OR CARDIAC ARREST: GRAVE SIGN: PULMONARY EMBOLISM. ON EXAMINATION: DIRECT PRESSURE OVER THE CALF OR ALONG THE COURSE OF THE DEEP VEINS--- ELICITS

DIRECT TENDERNESS. A CORD MAY BE PALPABLE.

CONSEQUENCES: PROXIMALLY the thrombus can extend---- may get detached to form emboli--- pulmonary embolism. LOCALLY the thrombus gets organized into fibrous tissue and in this process the valves may get destroyed. DISTALLY the thrombosis and destruction of valves may involve the perforators and superficial veins. This may

lead to OEDEMA, VARICOSITY, VENOUS HYPERTENSION, VENOUS ECZEMA, VENOUS ULCERATION. If pressure increases to such an extent that it exceeds the arterial pressure, blood flow ceases and VENOUS GANGRENE OCCURS.

DIAGNOSIS: BIPEDAL ASCENDING PHLEBOGRAPHY: It is the most accurate method of confirming the diagnosis and

determining the best method of treatment. IT DETECTS FUNCTIONAL VALVES AND THE UPWARD PROGRESSION OF THE CONTRAST. This test is not frequently available.

DUPLEX ULTRASOUND: It is good only for the thrombosis in ABOVE CALF VEINS. The accuracy is not much for detecting thrombi in the calf veins.

RADIOACTIVE FIBRINOGEN TEST WITH I-125: This test is positive during the active formation of thrombus (but not effective after the thrombus is formed).

PLETHYSMOGRAPHY: It is good to detect calf vein thrombosis. It measures the rate at which calf veins empty when pressure in a proximally placed pneumatic cuff is released.

D-DIMER FIBRIN DEGRADATION PRODUCTS: detects the presence of intravascular coagulation.

PREVENTION: 1. ELEVATION OF LEGS UPTO 20 DEGREE.2. ACTIVE EXERCISE OF THE LEG SEVERAL TIMES A DAY.3. GRADUATED COMPRESSION STOCKINGS: VERY EFFECTIVE POSTOPERATIVELY4. INTERMITTENT PNEUMATIC COMPRESSION.5. LOW DOSE UNFRACTIONATED HEPARIN: 5000 UNITS PRIOR TO SURGERY AND THEN 5000 UNITS

EVERY 8-12 HOURS POSTOPERATIVELY.6. DANAPAROID, A LMW heparin: more effective with less incidence of bleeding.7. WARFARIN: in a dose that yields a prothrombin time equivalent to an INR of 2-3 is effective in

preventing DVT.

TREATMENT: 1. PATIENT SHOULD BE IN BED WITH LEG ELEVATED2. UNFRACTIONATED HEPARIN SHOULD BE ADMINISTERED INTRAVENOUSLY AS AN INITIAL BOLUS OF 7500-

10,000 IU, FOLLOWED BY CONTINOUS INFUSION OF 1000-1500 IU/HR. THE RATE OF INFUSION SHOULD BE ADJUSTED TO MAINTAIN A aPTT of twice the control.

3. LMW HEPARIN is a better alternative: ENOXAPARIN: 1 mg/kg SC BID.4. WARFARIN SHOULD BE ADDED ALONGWITH IT SINCE IT TAKES TIME TO ACT AND CAN LATER BE USED AS

MAINTENANCE DRUG. IT SHOULD BE ADJUSTED TO A INR of 2-3. HOW LONG?

3-6 MONTHS---- for patients with ACUTE IDIOPATHIC DEEP VEIN THROMBOSIS LIFE LONG--- FOR THOSE WITH RECURRENT DEEP VEIN THROMBOSIS.

5. If there is small amount of calf vein thrombosis, anticoagulants will suffice but if there is a large amount of loose clot, then it can be potentially embolic---- INSERT UMBRELLA FILTER INTO THE IVC.

6. THROMBOLYTIC THERAPY IS USEFUL IN CASE OF FRESH CLOT (it is unsuccessful if used after 9 days of clot). Drugs are: STREPTOKINASE, UROKINASE, t- PA. An initial dose of 250000-750000 units of streptokinase is given IV over 30 min and continued at the rate of 70000-100000 units per hour.

VARICOSE VEINS:

These are dilated and elongated tortous superficial veins and their tributaries. Causes are: Primary varicose veins: these result from inherited defect in the veins. THEY ARE MORE COMMON IN WOMEN.

These defects are Absence of valves

Weakness of the walls of the blood vessels (more common)--- there is altered amount of collagen and mucopolysaccharide.

Secondary varicose veins result from---- Post- thrombotic damage to the valves of deep veins and perforator veins. Pregnancy--- INCREASED BLOOD VOLUME, PRESSURE OF THE UTERUS, EFFECT OF PROGESTERONE ON

THE SMOOTH MUSCLE OF VENOUS WALL. PELVIC TUMOR compressing the veins RETROPERITONEAL FIBROSIS AV fistula CAVERNOUS HEMANGIOMA.

PREDISPOSING FACTORS: PROLONGED STANDING: effect of gravity, absent calf muscle activity OBESITY: excess of fat provide poor support to the venous wall PREGNANCY: OLD AGE: Collagen degradation--- poor wall support. ATHLETES: Forceful contraction of calf muscle---- generates high pressure that may destroy

the valves and lead to varicose veins. E.g. RICKSHAW PULLERS.COMPLICATIONS OF VARICOSE VEINS:

THROMBOPHLEBITIS HEMORRHAGE PIGMENTATION LIPODERMATOSCLEROSIS STASIS ECZEMA VENOUS ULCER. PULMONARY EMBOLUS.

CLINICAL FEATURES: UNSIGHTLINESS without any symptoms TIRED AND ACHING SENSATION in the affected lower limb particularly in the calf, at the end of the day. NIGHT CRAMPS ESPECIALLY AFTER RETIRING TO BED--- this may be the result of sudden change in the caliber

of the vessels--- this stimulates the muscles through which they pass--- cramps. ANKLE SWELLING TOWARDS EVENING ECZEMA ULCERATION +VE COUGH IMPULSE BRODIE- TRENDELENBURG TEST.

TREATMENT: PERIODIC LEG ELEVATION AVOID PROLONGED STANDING ELASTIC COMPRESSION STOCKING FOR SMALL SYMPTOMATIC VARICOSE VEINS---- SCLEROTHERAPY FOR VERY SYMPTOMATIC CASES, PATIENTS WHO SUFFER FROM RECURRENT SUPERFICIAL VEIN THROMBOSIS

AND/OR DEVELOP SKIN ULCERATION+ ALSO FOR COSMESIS ----- EXTENSIVE LIGATION AND STRIPPING OF THE LSV AND SSV.

CONSEQUENCES OF POST- PHLEBITIC CHRONIC VENOUS INSUFFICIENCY: DAMAGED VALVES OF THE DEEP AND PERFORATOR VEINS LEADS TO STASIS OF BLOOD IN THE SUPERFICIAL VENOUS SYSTEM--- OEDEMA ANF FIBRIN EXUDATION. FIBRIN GETS ORGANIZED IN DUE COURSE TO CAUSE SCLEROSIS. THE LYMPHATICS ARE UNABLE TO DRAIN THE TISSUE FLUID LOAD. ALSO THE SCLEROSIS PROCESS DESTROYS THE LYMPHATIC CHANNELS--- MORE AND MORE TISSUE FLUID ACCUMULATES AND GET ORGANISED--- THICKENED INDURATED MASS INCIRCLING THE LOWER THIRD OF THE LEG--- CHAMPAINGE GLASS APPEARANCE. FURTHERMORE, SMALL AMOUNT OF BLOOD LEAKS OUT THE WEAKENED WALL OF THE VEINS DURING INCREASED VENOUS PRESSURE--- HEMOSIDEROSIS. THIS ELICITS SCRATCHING WHICH MAY LEAD TO ECZEMA FORMATION. ULCERATION OCCURS ON MINOR TRAUMA. UNDER NORMAL CIRCUMSTANCES, THE LYMPHATICS CLEAR THE TOXIC METABOLITES FROM THE INTERSTITIAL SPACE--- SINCE THESE LYMPHATICS ARE DESTROYED IN THIS CASE--- THE TOXIC METABOLITES MAY ACCUMULATE AND CAUSE TISSUE INFLAMMATION--- ECZEMA. THE COMBINATION OF PIGMENTATION, INDURATION AND INFLAMMATION IS CALLED LIPODERMATOSCLEROSIS.

VENOUS ECZEMA:Synonym: Gravitational eczema Stasis eczema Varicose eczema

Definition: Eczema secondary to venous hypertension.

Pathogenesis: Venous hypertension ----- transmitted to the capillary circulation in the skin and SC tissues of the calf ---- this distends the local capillary bed and widens the endothelial pores thus allowing fibrinogen molecules to escape into the interstitial fluid where they form a fibrin sheath around the capillaries. This layer of fibrin forms a precapillary barrier to the diffusion of oxygen and other nutrients that are essential for the normal vitality of the skin. At the same time there is increased sequestration of WBCs in the venules ---- release of proteolytic enzymes and free radicals which produce tissue damage.

C/F: it is an erythematous scaly and often exudative eruption usually seen around the ankle and lower legs. It is often accompanied by other manifestation of venous hypertension ----- varicose veins, oedema, purpura, hemosiderosis,

ulceration or small patches of white atrophic telangiectatic scarring (atrophie blanche). Venous lakes on the dorsum of foot and ankles

There may be subepidermal vascular proliferation producing purple papules around the ankle which may resemble Kaposi sarcoma.

Secondary dissemination may occur It can be complicated by secondary contact dermatitis, infection and rubbing. Allergic contact dermatitis is a common complication probably because of the presence of large numbers of APCs in the

inflamed skin.

D/D : allergic contact dermatitis, infective eczema, discoid eczema, asteatotic eczema, atopic dermatitis, psoriasis, hypertrophic LP, Dermatophyte infection, profuse actinic keratoses.