Chronic venous disorders

 

Chronic venous insufficiency is severe manifestation of venous disorders that is skin pigmentation and worse. Varicose veins, deep venous reflux come under chronic venous disease.

 

Varicose veins affects about 32% of the population.  Venous ulceration may be seen in 1% of the adult population and thus 1-2% of the health budget is spent on treating advanced venous disease.

 

Pathogenesis:

Venous valvular incompetence, perforator valve incompetence and venous obstruction and muscle pump dysfunction underpin venous insufficiency.

 

In the normal state, venous pressure in the foot drops with calf pumping, slowly returning to steady state. With venous valve incompetence, resting pressures are elevated and the drop with exercise is less pronounced. With venous obstruction, again resting pressures are elevated and there is no drop with exercise.

 

Deep venous valve dysfunction is most often due to DVT.

 

Deep venous obstruction may lead to abnormally elevated venous pressures with exercise and thus secondary calf pump dysfunction.

 

Superficial valve dysfunction may be primary or due to injury, phlebitis, excessive venous distension. Junctional vein valves can become incompetent and allow transmission of high pressures into the lower valves. Perforator incompetence can lead to calf pump energy being fed into the superficial system resulting in localized superficial reflux.

 

These macrocirc changes leads to microcirculatory dysfunction in which there is elongation and dilatation of the capillary beds with thickening of the basement membranes, endothelial damage leading to a leaky endothelium thus there is leakage of fluid molecules, RBCs into the interstitial space. This can lead to secondary damage to the lymphatic network, further embarising drainage mechanisms from the limb. 

 

3 theories f venous microangiopathy:

1)   Fibrin cuff theory: leakage leads to fibrin deposition around capillary hence imparing diffusion of oxegyn into tssue

2)   White blood cell trapping theory: WBC trapped in capillaries leading to activation of leukocytes and inflammation

3)   Growth factor trapping theory: growth factors trapped in capillary and thus unavailable to heal tissues.

 

Genetic disorders with varicose veins:

1)   Lymphoedema-distchiasis syndrome: varicose veins at early age FOXC2

2)   CADASIL: varicose veins at early age

3)   Ehler Danlos Type 4: varicose veins

4)   Haemochromatosis: genetic mutation associated with venous ulceration

5)   Klippel Trenaunay: varicose veins, limb hypertrophy and port wine stains: there may be congenital venous atresia/agenesis valve insuff, venous aneurysms, lymphatic anomlaies

6)   Parke Weber: Lymphatic malformations, capillary malformation, AVF: assoc with muscle pump dysfunction

Clinical:

            History iofedema, ulceration, DVT, phlebitis, previous venous surgery suggest venous aetiology to problems.  Family history of venous ulceration and varicose veins, thrombotic disorders.

            Examination:

1)   Inspect for varocise veins, colour change

2)   limb girth

3)   palpate for vein tenderness

4)   oedema is initially pitting, then becoming a brawny oedma: uncompressible

5)   corona phlebectatica: inframalleolar flair

 

The Trendelenburg Test or Brodie-Trendelenburg test (not to be confused with Trendelenburg's sign) determines the competency of the valves in the superficial and deep veins of the leg. With the patient in the supine position the leg is flexed at the hip and raised above heart level until the veins become empty. A tourniquet is then applied around the upper thigh to compress the superficial veins but not too tight as to occlude the deeper veins. The leg is then lowered by asking the patient to stand. Normally the superficial saphenous vein will fill from below within 35 seconds as blood from the capillary beds reaches the veins; if the superficial veins fill more rapidly with the tourniquet in place there is valvular incompetence below the level of the tourniquet in the "deep" or "communicating" veins. After 20 seconds, if there has been no rapid filling, the tourniquet is released. If there is sudden filling at this point it indicates that the communicating veins are competent but the superficial veins are incompetent.[1] The test is reported in two parts, the initial standing up of the patient (positive or negative based on rapid filling) and the second phase once the tourniquet is removed (positive or negative based upon rapid filling). For example, a possible outcome of the test would be negative-positive meaning that the initial phase of the test was negative indicating competence in the communicating veins and the second phase of the test was positive meaning that there is superficial vein incompetence.

The test can be repeated with the tourniquet at different levels to further pinpoint the level of valvular incompetence:

    above the knee - to assess the mid-thigh perforators

    below the knee - to assess incompetence between the short saphenous vein and the popliteal vein.[2]

    Can add perthes test, where the patient walks on standing up. Incompetent perforators leads to enlargement of varicosities below the tourniquet

Doppler test for reflux: Flow towards the feet lasting more than .5s is indicative of venous reflux.

 


 

Classification systemts:

The CEAP classification :

 

C: clinical classification C3 oedema, C4a pigmentation, C4b: LDP or atrophie blanche, C5 healed ulcer, C6 active ulcer

E: Etilogy: Congenitial (Klippel TReaunay), Primary, secondary

A: Anatomic: Superficial Deep Perforator

P: Pathophysioligic: reflux, obstruction, both

 

The Venous severity score

VSS: venous severity score, made up of, venous clinical severity score, venous segmental disease score, venous disabilty score,

 

Outcome of treatment measures:

            Many different types, VEINEs, SF-36

 

The differential diagnosis for leg swelling is:

1)   Chronic venous insuf

2)   DVT

3)   Systemic causes of leg swelling:

a.     CHF

b.     Nephrotic syndrome

c.      Endocrine diseases

d.     Side effects of medications eg Ca channel blockers. NSAIDs, hypoglycaemic agents

4)   Regional disorders:

a.     Ruptured popliteal cyst,

b.     Haemotoma, muscle tumour

c.      Chronic extertional compartment syndrome

d.     Gastroc tear

e.     Lymphoedema

The differential diagnosis for pigmentation of the lower limb is:

1)   CVI

2)   LDS

3)   Dermatitis

4)   Myxedema

5)   Necrobiosis diabeticorum

6)   Ascities

7)   Morbid obesity

 

The differential of chronic ulceration:

1)   arterial insuf

2)   AVF

3)   Peripheral neuropathy

4)   Vasculitis

5)   Rheumatoid arthritis

6)   Blood dyscrasia eg sickle cell

7)   Infection

8)   Pyoderma gangrenosum,

9)   malignancy

10)          trauma

11)         drug side effects

 

Diagnostic evaluation:

            Duplex gives anatomic information. Air plethysmography and foot pressures give an estimate of disease severity.

 

Duplex: reflux longer than 1 s is considered diagnostic in the deep system and .5s in the superficial system

 

Photoplethysmography:

A light is placed on the foot and light sensor. The more blood in the skin, the weaker then signal picked up by the sensor. Thus Tests:

1)   The calf is pumped to empty the limb The time taken for the foot to refill to 90% of its original signal is calculated. If very quick refill ie less than 20s, indicates venous reflux. If venous refill time is >20s, indicates normal venous function.

2)   A tourniquet is applied to occlude the superficial veins only. The test is repeated and if time is normal, indicates superficial reflux only. Quick time indicates deep reflux.

3)   Calf pump function can be assessed by comparing readings with emptying the leg with gravity times against calf pump times to empty leg,

 

Air plethysmography:

            An empty cuff is placed around calf which measures the volume of the calf.  Tests:

1)   Venous outflow: leg elevated and proximal tuoriquet appied: tourniquet let down and outflow fraction at 1 second calculated: anything under 3*% is diagnostic if impaired outflow

2)   Venous reflux: limb placed in dependant position: venous filling index calculated: measuring the total venous volume and then time taken to fill 90% of the venous volume in upright position. Values above 4ml/s indicate venous reflux

3)   Calf pump function: total calf volume measured and then reduction after toe raising measured. Ejection fraction is the amount ejected divided by total volume

Phlebograhy:

            Can be ascending and descending phlegram

 

Ambulatory venous pressure: gold standard for CVI: art line needle into pedal vein. Pressure measured at rest, after exercise and after placement of an ankle cuff to distinguish deep from superficial disease.

 


 

Management:

Conservative management:

Behaviour Measures:

            Leg elevation

            Foot of bed elevation

            Weight loss

 

Compression therapy: graded external compression reduces residual volume fraction (thus improved calf pump function) and decreases reflux in vein segments

 

Wound and skin care

 

Medications:

            4 classes:

1)   coumarins

2)   flavonoids: benzopyrones: decrease leukocyte action and decrease endothelial permeability

3)   saponosides: Horse chestnut seed extract

4)   other plant extracts

 

Exercise: Graded calf pump exercise: does not decrease reflux but can improve calf pump function as an adjunct

 

Interventional management:

            Sclerotherapy:

                        Sodium tetradecyl sulfate: anionic detergent that damages intima thus leading to sclerosis of vein

                        Aethoxyscerol: Polidocanol

            Can be used to treat telangiectasia, subcut varicose veins, transfascial perf veins and venous malformation. Can be used as a 1:5 foam. Main problem is hyperpigmentation around the sclerosed vessel from haemosiderin in the vein blood clot

 

            RF and Laser: potential complications parasthesia, STP, DVT and PE, bruising, skin burns and infection. .1% lidocaine tumescent analgesia. AS effective as surgery without the pain and swelling

 

            Endovascular: stenting of the illiacs improves outflow. Need close follow up to ensure no instent stenosis.

 

            Surgical Management:

                        Ligation and stripping: reduces recurrence of ulceration in RCT even if they have deep reflux. ESCHAR study: surgery does not heal ulcers quicker but leads to less recurrence and improved ulcer free time.

                        Perforator ligation: endoscopic vs open

                        Valve reconstruction: Primary valve incompetence: valvuloplasty, external stent                                                      

Secondary valve incompetence: neovalve

Varicose Veins

 

Open Surgery

Aetiology: still unclear however the constant associations are previous DVT and genetics. DVT leads to venous hypertension which thus causes diltation of the superficial veins and hence valve incompetence thence varicosities.

 

Telangiectasia: less than 1mm, Reticular veins 1-3mm, Varicose veins >3mm.

Auscultate for an AVF.

 

Natural History: once present, the veins never regress. Complications of varicose veins include STP, acute bleeding, eczema, ulceration.

 

Perforators can be direct or indirect. Indirect join the superficial veins to the deep via a muscular vein. Direct perforators are fairly constant in location.

 

The incision for high ligation is 1cm above and parallel to the groin crease beginning at the femoral pulse and going medial. The junction should be dissected out and 2cm above and below to ensure no other junctions.

 

Treatment of GSV reflux leads to decreased recurrence rates of ulcers and improve quality of life compared to conservative mx alone.

 

In the surgery vs endovenous debate, there is an obvious advantage to EVA in the immediate post procedure window. There does not appear to be any difference in long term results between the two.

 

REcurence after SSV surgery is high about 50%. The U/S is thus critical to locating the junction and  any important local venous branches.

 

Who to still do Surgery on as opposed to EVLT or RF:

            A: GSV or GSV branch that is less than 1cm deep to the skin ie a subcutaneous saphenous tributary

            B: GSV aneurysm or dilatation: usually a proximal segment 2.5-3cm in diameter will not spasm effectively with EV techniques and may even form thrombus that may embolise etc.

            C: chronic thrombophlebitis: where a thickwalled vein or webbing through vein prevent advancement of RF catheter through vein. The vein may not spasm down effectively with EV. These need high ligation and sequatial avulsions.

            D: Excessive tortuosity preventing EV catheter advancement

            E: Acute superficial thrombosis: if the thrombus has extended to the junction they need anticoagulation +/- junction ligation. EV is contraindicated when fresh thrombus is present

            F: Economic

            G: Surgeon choice

 


 

Endovenous surgery:

 

Duplication of the GSV occurs in 25% of calves and 8% of thighs.  True duplications where both veins are in the saphenous compartment is rare. There is about 6 valves in the thigh GSV.

 

The saphenous eye refers to the superior saphenous fascia, vein and muscular fascia beneath.

 

Veins at the junction include SEPV, Superficial epigastric and superficial circumflex illac, anterior and posterior thigh circumflex veins.

 

The SSV lies within its own compartment, starts posterior to the lateral malleolus and the junction is often with 5cm of the pop skin crease. There may be no junction and several deep conenctions up the thigh or a giacomini to connect to the GSV.

 

Perforator Anatomy:

            There are 6 divides to perforator location: foot, ankle, leg, knee, thigh, gluteal region. The medial perforators in the calf are the posterior tibial perforators, lower, middle and upper: connects the posterior arch vein to the posterior tibial vein. Paratibial perforator (anteromedial postio of calf). Inferior femoral canal perforators connect GSV to the pop vein. Superior femoral canal perforators connect GSV to the femoral vein mid thigh. Perforators can be taken out with subfascial endoscopic perforator surgery but in the era of sclera, it seems crap.

           

Reticular veins lie in the superficial compartment and for a lateral subdermic venous system that largely exists in the lateral leg.

 

The RF catheter should be positioned 2cm distal to junction. This proximal bit may require two 20s treatments. Post op patients should be given a grade III above knee stocking and repeat ultrasound in 72 hours.

 

Absolute contraindications to sclerotherapy are a known allergy to the sclerosant, acute cellulitis, acute respiratory or skin disease, severe systemic disease, phlebitis migrans, acute superficial thrombophlebitis, pregnancy, hyperthyroidism, and bedridden status. Foam is best for reticular veins and larger varicose veins where as liquid is better for small reticular veins and telangiectasia. Long term foam results are not as good and EV. Pain during sclerotherapy injection may be due to intra-arterial puncture, and thus the injection has to be stopped immediately. Should such pain occur, injection of procaine around the injected artery, local cooling, systemic heparinization, and infusion with low-molecular-weight dextran are recommended.

 

Cutaneous lasers allow targeting of smaller reticular and telangiectasia.

 

Deep venous surgery: The peroneal and tibial veins have anout 12 valves. The popliteal has 3 valves, most distal. The SFV has 5 valves, the most constant one is 1-2 cms distal to the CFV.