State University of Medicine and Pharmacy Nicolae Testemitanu [301636]

State University of Medicine and Pharmacy “Nicolae Testemitanu”

from Republic of Moldova

FACULTY OF MEDICINE N.2

DIPLOMA THESIS

RUPTURED VARICOSE VEINS OF THE LOWER LIMBS

Student: [anonimizat]: M1043

Scientific advisor: Dr. Vasile Culiuc

Chișinău 2016

[anonimizat]. They are very common and do not cause medical problems in most people. [anonimizat]. [anonimizat], [anonimizat]. All these veins contain valves which should only allow the blood to flow upwards. If the veins become widened and varicose these valves no longer work properly. Blood can then flow backwards down the veins and produce a [anonimizat], or sitting. Lying down or "putting your feet up" relieves this head of pressure and usually makes the legs feel better. [anonimizat].

In a [anonimizat], sometimes with scarred white areas. Eczema can also develop. [anonimizat], an ulcer may result

Other problems which varicose veins can occasionally produce are phlebitis and bleeding. Phlebitis (sometimes called thrombophlebitis) [anonimizat] (clotting of blood) [anonimizat]. [anonimizat] a [anonimizat] “oozing” from site of injury. [anonimizat] a fall, hit or scratch .

Varicose vein:-

General data

The tow main superficial veins of the lower extremity are the great saphenous vein (GSV) and the small saphenous vein (SSV), and they are located in the subcutaneous tissue layer under the skin and above the deep fascia layer that covers the muscles of the legs. The deep venous system (DVS) of the lower limbs is located beneath the fascia layer and in the muscle compartments and runs along the same track as the main arteries in the legs. [anonimizat].

[anonimizat], the pressure in the DVS increases and helps pump the blood towards the heart. [anonimizat] a [anonimizat]. [anonimizat]. As blood flows through the venous systems of the legs back to the heart, 1-way bicuspid valves that are located in the deep veins, the perforating veins, and the superficial veins promote the unidirectional flow of blood and prevent backflow [1].

Epidemiology:-

Approximately 23% of adults in the United States have varicose veins. This figure rises to 80% for men and 85% for women if reticular veins and spider telangiectasias are included.

Worldwide:-

The frequency of venous disease is higher in Western society and industrial countries, most likely due to alterations in activity and lifestyle .

Sex:-

Due to hormonal factors, varicosities and telangiectasia are more frequent in women rather than in men.

Age related :

Majority of the varicose veins in adults have their genesis in childhood. Serial of examinations for children from 10-12 years and another in 4 and 8 years later shows that symptoms are experienced (and venous test results are abnormal) before any abnormal veins are visible at the surface of the skin.

When abnormality in veins becoming visible, reticular veins becomimg first to appear and are followed after a number of years by incompetent perforators. Smaller telangiectatic and big varicose veins usually become visible only in adulthood, many years after the true onset of disease.

Although varicosities progress to worsen over the time and to appear a new areas of involvement through during life, a small number of cases appear after the pregnancy years [2].

S, Schmid-Shonbein GW, Bergan JJ. Leukocyte activation in patients with venous insufficiency. J Vasc Surg 1999;30:148– 56

Causes :-

Majority of the varicose disease is a result to increasing superficial venous pressure, but some people have a weakness of vein walls(hereditary) and leading to develop varicosities even if threr is no elevated venous pressures. Some patients with varicose veins of the lower extremity also have abnormally” weak-wall” veins in the forearm and hand veins [3].

B-  inheritance characteristic is important in the determination susceptibility to primary valvular failure, but the exact genetic factors that responsible for varicosities not yet been illustrated .the reflux at the sapheno-femoral junction (where the superficial greater saphienous vein join the deep common femoral vein) is twice as likely when a parent had a similar condition. Monozygotic twins are concurrent with regard to varicose veins in 75% of cases. The propagation of varicose veins is 43% for female relatives of patients with varicose veins but is 19% in male relatives [3].

C- standing for long time can leads to elevation hydrostatic pressures that can cause chronic venous enlargement and secondary valvular incompetence anywhere within the superficial venous system. If proximal junctional valves become impaired, high pressure passes from the deep veins into the superficial veins and this event rapidly progresses to become irreversible. Women are especially susceptible to this type of varicose problem because vein walls and valves periodically become more distensible because of the influence of cyclic increases in progesterone [4].

D- Pregnancy is one of the common cause of varicosities. During pregnancy period, the circulating hormonal factors lead to increase the dispensability of vein walls and leading the valve leaflets to soften. in the same time, the veins must accommodate a greatly expanded circulating blood volume. Later in pregnancy, the enlarged uterus compresses the inferior vena cava, causing further venous hypertension and secondary distension of leg veins. Depending on the relative contributions of these mechanisms, varicose veins of pregnancy may or may not spontaneously regress after delivery. Treatment of existing varicose veins prior to pregnancy has been shown to prevent the progression of disease and reduce the recruitment of other veins during pregnancy [5].

Pathophysiology :-

In healthy veins, one-way valves direct the flow of venous blood upward and inward. Blood is collected in superficial venous capillaries, flows into larger superficial veins, and eventually passes through valves into the deep veins and then centrally to the heart and lungs. Superficial veins are suprafascial, while deep veins are within the muscle fascia. Perforating veins allow blood to pass from the superficial veins into the deep system.

Elevated venous pressure most often is the result of venous insufficiency due to valve incompetence in the deep or superficial veins. Chronically increased venous pressure can also be caused by outflow obstruction, either from intravascular thrombosis or from extrinsic compression [6].

Most commonly, superficial venous valve failure results from excessive dilatation of a vein from high pressure of reverse flow within the superficial venous system. Valve failure can also result from direct trauma or from thrombotic valve injury. When exposed to high pressure for a long enough period, superficial veins dilate so much that their delicate valve leaflets no longer meet [7].

Varicose veins of pregnancy most often are caused by hormonal changes that render the vein wall and the valves themselves more pliable. The sudden appearance of new dilated varicosities during pregnancy still warrants a full evaluation because of the possibility that these may be new bypass pathways related to acute deep vein thrombosis [7].

Varicose veins usually result from venous hypertension owing to incompetence of the major communications between the superficial and deep veins of the lower extremity. In a significant number of patients, there is no demonstrable truncal saphenous reflux and varicosities are the result of isolated perforating and nonsaphenous vein incompetence. The clinical and histological features of VVs are the result of disruption of the normal architectural structure of the venous wall as a consequence of remodeling of the extracellular matrix (ECM) in response to increased venous distention and altered hemodynamic shear stress. Although a number of genes, growth factors, proteases, and their inhibitors known to modulate the ECM have been implicated in the pathogenesis of VVs, their etiology remains unknown. The complex variations in venous anatomy in patients with VVs require detailed vein mapping to determine the source and drainage locations of reflux if the rates of residual and recurrent varicosities are to be reduced [8] .

Labropoulos N, Leon L, Kwon S, et al. Study of venous reflux progression. J Vasc Surg 2005;41:291– 5

Bergan JJ, Schmid-Schonbein GW, Coleridge-Smith PD, Nicolaides AN, Boisseau MR, Eklof B. Chronic venous disease.

Classification :-

In order to standardize the reporting and treatment of the diverse manifestations of chronic venous disorders, a comprehensive classification system (CEAP) has been developed to allow uniform diagnosis.

[9]. – frank, HS berganjji et, al, the fundamental of phlebolgy ,venous disease for clinicians .

Physical examination :-

The physical examination of the venous system is replete with difficulty. In most regions of the body, the deep venous system cannot be perform inspection, palpation, auscultation, or percussion. Examination of the superficial venous system should be serve as an indirect guide to the deep system.

The venous system (lower extremity) and its connections becoming gradually more better defined through inspection, percussion ,palpation, and hand-held Doppler examination to form a venous map that later guides treatment. The courses of all the dilated veins that are identified may be marked along the leg with a pen and later transcribed into the medical record as a map of all known areas of superficial reflux.

Inspection

the Inspection is usually performed in an organized manner, usually from distal to proximal and from front to back. The perianal region, pubic region, and abdominal wall must also be inspected.

Inspection may reveal such findings as telangiectasias, ulceration, atrophy blanche, interdigital mycosis, acrocyanosis, eczematous lesion, micro ulcers, stasis dermatitis, flat angiomata, prominent varicose veins, scars from a prior surgical operation, or evidence of previous sclerosant injections. Measuring and photographing lesions(before and after) is recommended, because patients undergoing treatment for varicose and spider veins often forget the original appearance of their legs and feet and may report that preexisting lesions were caused by treatment.

Normally, veins typically are visible as distended at the foot and ankle and occasionally in the poplieteal fossa. In other regions of the leg(e.g. thigh), visible distension of superficial veins usually implies disease. Translucent skin may allow normal veins to be visible as bluish sub-dermal reticular pattern, but dilated veins above the ankle usually are evidence of venous pathology.

Discolored skin(dark red, purpule) often is a sign of chronic venous stasis, particularly if it is localized along the medial ankle and the medial aspect of the lower leg. Non-healing ulcers in this area are most likely due to theunderlying venous stasis. Skin changes or ulcerations that are localized only to the lateral aspect of the ankle are more likely to be related to prior trauma or to arterial insufficiency than to pure venous insufficiency.

Palpation

The entire surface of the skin is gently palpated with the fingertips because dilated veins may be palpable even where they are not readily observed. Palpation helps to indicate both normal and abnormal veins. After gentile palpation to identify superficial vascular anomalies, more deep palpation is helpful to elucidate the causes and sources of the superficial problems.

Palpation begins with the antero-medial surface of the lower limb (the territory of the long saphenous vein), proceeds to the lateral surface (collateral varicose veins of large trunks and non-saphenous varicose veins), and finally focuses on the posterior surface (territory of the short saphenous vein) of both lower limbs. The location, size, shape, and course of all varicosities are establish, and the diameter of the largest vessel is measured as accurately as possible [10].

Both distal and proximal arterial pulses should be also palpated. An ankle-brachial index is vereyuseful if any suspicion that arterial insufficiency exists.

The arch of the long saphenous vein may be palpable in some patients who do not have varicose veins, but it is particularly well appreciated in patients with truncal reflux at the sapheno-femoral junction. It is best palpated tow finger breadths down to the inguinal ligament and just medially to the femoral artery. If a reflux is exist, a forced coughing maneuver may produce a palpable vibration or sudden expansion at this level.

The short saphenous vein may be palpable in the popliteal-fossa in some of slender patients. Other normal superficial veins above the foot usually are not palpable even after prolonged standing.

Palpation over an area of tenderness or an area of leg pain may reveal a firm , thrombosed ,thickened vein. These palpable abnormally thrombosed vessels are superficial, but may associated with deep vein thrombosis which exist in 40% of patients with superficial phlebitis. When the veins completely thrombosed, the popliteal vein (is a continuation of the femoral vein which is passes behind the knee and into the calf) may sometime be palpated in the popliteal fossa, and the same is true of the common femoral vein at the thigh. Palpation for deep thrombosis is not reliable because the majority of cases do not produce any palpable abnormality [11].

Varicose veins of recent onset are easily distinguished from chronic varicose by palpation. Newly dilated vessels appear on the surface of the muscle or bone, chronic varicose erode into underlying muscle or bone, creating deep boggy or spongy pockets in the calf muscle and deep palpable bony notches, especially over the anterior tibia.

Palpation often reveals fascial defects in the calf along the course of an abnormal vein at sites where superficial tributaries emerge through openings in the superficial fascia. Incompetent perforating veins may connect the superficial and deep venous systems though these fascial defects, but the finding is neither sensitive nor specific for perforator incompetence.

Percussion

Venous percussion is useful to determine whether different venous segments are directly interconnected. Percussion can be used to trace the course of veins already detected on palpation, to discover varicose veins that could not be palpated, and to assess the relationships between the various varicose vein networks.

With the patient in a standing position, a vein segment is percussed at one position while an examining hand feels for a pulse wave at another position. The propagation of a palpable pulse wave demonstrates a patent superficial venous segment with open or incompetent valves connecting the 2 positions. The examination findings can be misleading because prolonged standing causes even a normal vein to become distended. If valves have floated open, a pulse wave may be propagated even in a normal vein. The technique is most valuable when a bulging venous cluster in the lower leg has no obvious connection with veins in the upper thigh, yet a palpable pulse wave demonstrates the existence of an unseen connection.

Percussion can be used to elucidate the course of any significant superficial vein. With the patient standing, the lowest portion of the vein is percussed while the opposite hand searches above for a percussion wave. The procedure is repeated along the entire course of the vein and then along every identifiable superficial vein until a clear anatomic picture has been elucidated [12] .

Perthes maneuver

The Perthes maneuver is a traditional technique intended to distinguish antegrade flow from retrograde flow in superficial varices. Antegrade flow in a variceal system indicates that the system is a bypass pathway around deep venous obstruction. This is critically important because, if deep veins are not patent, superficial varices are an important pathway for venous return and must not be sclerosed or surgically removed.

To perform the Perthes maneuver, a Penrose tourniquet is placed over the proximal part of the varicose leg in such a way as to compress superficial varicose veins but not the deep veins. The patient walks or performs toe-stands to activate the calf muscle pump. The calf muscle pump normally causes varicose veins to be emptied, but if deep system obstruction exists, then the varicose veins paradoxically become more congested.

If the result of the Perthes maneuver is positive (ie, distal varices have become engorged), then the patient is placed supine with the tourniquet in place and the leg elevated (Linton test). If varices distal to the tourniquet do not drain after a few seconds, deep venous obstruction must be suspected. These maneuvers are not consistently reliable and are of primarily historical interest [13].

Trendelenburg test

The Trendelenburg test can often be used to distinguish patients with superficial venous reflux from those with incompetent deep venous valves.

The leg is elevated until the congested superficial veins have all collapsed. An examining hand is used to occlude a varicose vein just below the saphenofemoral junction or at another point of suspected reflux from the deep system into the superficial varicosity. The patient stands with the occlusion still in place.

If the distal varicosity remains empty or fills very slowly, the principal entry point of high pressure into the superficial system has been identified. Rapid filling despite manual occlusion of the suspected high point of reflux means that some other reflux pathway is involved [14].

Doppler auscultation

The physical examination as described thus far cannot differentiate dilated veins of normal function from true varicosities that carry venous blood in a retrograde direction. Doppler examination is an adjunct to the physical examination that can directly show whether flow in a suspect vein is antegrade, retrograde, or to-and-from.When used as part of the physical examination, a Doppler transducer is positioned along the axis of a vein with the probe at an angle of 45° to the skin. Gentle tapping on the underlying vessel produces a strong Doppler signal and confirms the correct positioning of the transducer.An augmentation maneuver is performed by compressing and then releasing the underlying veins and muscles below the level of the probe. Compression causes forward flow in the direction of the valves. Release of compression causes backward flow through incompetent valves, but no Doppler signal is noted if the valves are competent and the blood cannot flow backwards [15]. These compression-decompression maneuvers are repeated while gradually ascending the limb to a level where the reflux can no longer be appreciated.

Each superficially visible or palpable is investigated in this way. If no visible or palpable dilated varices exist, the presence or absence of retrograde flow is documented at the top, middle, and bottom of long and short saphenous veins on each leg.

Doppler flow assessment adds a great deal of information to the physical examination findings, but patients with significant varicosities should also be evaluated by duplex ultrasonography, which combines Doppler flow detection with 2-dimensional ultrasound imaging.

RAPTURED VARICOSE VEINS

Varicose veins are a common entity presenting a worldwide distribution. Although they are usually benign, sometimes are proved to be a threatening condition. Massive hemorrhage is an unusual complication of this common venous pathology that demands immediate medical intervention [16].

When varicose veins near the skin’s surface become weakened, the pressure caused by pooling blood can cause the vein to rupture. These ruptures can occur suddenly, causing blood to seep into surrounding tissue beneath the skin. If the skin over your varicose vein has thinned, which is common, you may bleed through your skin (Think of what happens when a fluid-filled blister breaks open.). Sometimes there’s just a small amount of blood; other times the bleeding can be significant, even life-threatening [17]. It occurs in most of the cases in superficial vein or intradermal varicose veins or in venous ulcers [18].

Most patients describe that it occurs during or after a warm shower (warm water causes veins to relax and dilate, allowing more blood to pool within the veins) or during sleep. It is painless and patients report that they notice it because they feel something wet in bed.  Patients who are on blood thinners can lose large amounts of blood, especially if it occurs while they are sleeping. Some people have required blood transfusions. The small blue spider veins around the ankle are equally at risk of rupture as are the larger bulging veins [19].

Risk factors :-

1. chronic heart disease – which lead to increases the pressure on the veins ,it also make the bleeds more difficult to stop.

2. Liver dysfunction (cirrhosis)- This has two negative consequences. It increases the pressure in the leg veins as well as potentially effecting the livers ability to produce blood clotting factors [20].

3. coagulopathy – Some problems are genetic or acquired while others are the result of medications. The genetic and acquired conditions include  Von Willebrands Disease and hemophilia. Medically induced situations that ‘thin the blood’ include the taking of aspirin, NSAIDS, coumadin and Eliquis.  Some of these actually do ‘thin the blood’ but more likely they make clotting and clot formation times longer.  If they are being used it’s assumed that they are medically necessary for other diseases [20].

4. Social isolation and dementia- Unfortunately in some cases nobody is around to help someone who is bleeding.

5. decreasing mobility- As the legs merely ‘hang,’ the blood pools more due to gravity and there is increased pressure on the veins. Any activity where there is compression of the legs muscles, walking or running for example, helps return blood towards the heart and lessens the venous pressure [22].

Pattern and nature of bleeding

The rupture of the varicose veine is consider acute and small if it is less than 5 mm [23].

Bleeding from venous blood system and its bloodstain pattern is distinguished from arterial bleeding with arterial gushing and splashing [23].

In case of high intravascular venous pressures (e. g. right heart failure),also

venous pulsatile bleeding can occur, which can simulate an arterial blood pattern [24].

In many cases reported , in fatal varicose hemorrhage the doctors or the police who arrive to scene the mistaken with a homicide due the large quantity of blood , and the pattern of “splashing “ , because normally the low blood pressure in the superficial vein cannot make such a miss ,but they presuming that the cause of death was arterial bleeding .

In this image show hemorrhage from ruptured varicose vein :

[25]. -G. Weyrich, Statistische Untersuchungen u¨ ber den plo¨ tzlichen Tod aus natu¨ rlicher Ursache beim Erwachsenen, Beitr. Gerichtl. Med. 12 (1932) 146–237.

[26]. – N Morrow PL, Hardin NJ, Karn CM, Beloin R, McDowell RW. Fatal hemorrhage caused by varicose veins. Am J Forensic Med Pathol 1994;15:100–4.

Classically, arterial bleeding is associated with a projected bloodstain pattern with significant volume and spines (the pointed edges that radiate out from the center of stains due to the volume and force of the haemorrhage). Clusters of large elliptical stains and drip patterns occur with significant lacerations or incisions of large arteries causing an arterial spurt or gush that differs from impact spatters or low-velocity, free-falling droplets of blood. Lesser injuries to smaller arteries may produce a much finer pattern from smaller droplets. As blood that escapes from veins is under much lower pressure it tends to pool until gravitational forces acting on it exceed the surface tension of the blood. This results in the formation of spherical droplets in freefall that produce approximately circular stains upon impact with a horizontal surface such as a floor. These stains are characterized by their large size (13–21.5 mm) and their lack of directional indicators[27].

Causes of varicose vein bleeding .

Vein rupture can occur spontaneously or can be caused by a minor trauma. Predisposing factor is the localization of the varicose veins (lower leg and malleolus region) above a protuberance. Especially in case of altered skin by chronic venous stasis, the skin is vulnerable and may very easily be injured by trivial minor trauma. A risk factor is sclerotic alterations of the vessel wall that may lead to higher vulnerability [28].

Evans et al. classified venous ulcerations in two types: acute perforating ulcers smaller than 5 mm in diameter with only slight alterations in skin and chronic ulcers with diameters of 1–10 cm with significantly altered skin. Acute perforating ulcers occur in the early stages of chronic venous insufficiency and therefore they are accompanied by only minor alterations in the skin and subcutaneous fibrosis. Acute perforating ulcerations are healing well. In contrast, chronic ulcerative types are associated with distinctive subcutaneous fibrosis. These ulcers heal poorly. Browse and Burnard suggest an elevation of the intravascular venous pressure followed by conditional porous endothelium with subsequent accumulation of fibrin in the subcutaneous tissue. It is supposed that fibrin acts as an oxygen diffusion barrier which leads to necrosis and ulcerations in the tissue [29].

In chronic venous insufficiency, superficial veins respond to increased pressure by dilating. In muscle contraction, high compartmental pressures that normally occur within the calf muscle pump is transmitted directly to the superficial veins and subcutaneous tissues drained by communicating veins[30].

When this occurs, venous pressure in the coetaneous venules may reach 100 mmHg in the erect position. Bleeding under such high pressure may be so intense that it can easily be mistaken for arterial hemorrhage; consequently, if the ligature is applied inappropriately, the venous bleeding is exacerbated rather than halted.Such an incorrect application of the ligature can be just as harmful as a general lack of knowledge concerning what to do in such situations [31].

Massive varicose vein bleeding could be due to congenital peripheral soft tissue vascular malformation (an arteriovenous communication) [32].

The ruptured varicose is not fatal considering the amount and the quantity of the loosing blood , for instance in patient that can handle their task without need for help , meaning people less than 75 -80 years old , if they had an episode of bleeding they can compress the site of injury while they calling for help , or they can “notice” the hemorrhage [34].

but in the other hand , in very old people this situation is difficult for them , so they facing a prolonged bleeding from the vein till death , that’s why the majority of registered death cases is belong to elderly and properly live alone . (34)

so the best way for avoiding this complication is by diagnose the condition and take percussion measures [35].

This a picture from “YouTube” of a patient filming bleeding varicose vein after a minor trauma.

Diagnosis

Color duplex ultrasound

Duplex ultrasound is widely used to investigate chronic venous disease of the lower limbs. In recent years, there has been a much better understanding of the ultrasound images of superficial veins and how these relate to venous disease [36].

Orthograde flow (blue)

Return with valve aperture insufficiency during Valsalva press test (red).

Evaluation of venous pump function

Using plethysmography , recording changes in volum and pressure in affected extremity, with the help of infrared light assessing the capillary filling dyring exercise , increasing capillary filling inactivate venous reflux , meaning incompetent veins [37].

Probe application in light reflection

rheography.

No disruption to the venous pump. Venous (pump) insufficiency

Continouse wave Doppler

In which the transducer emits and receives the ultrasound wave contiusly , allowing mwsurment of high velocity of blood flow , and estimate valvue function. Like recording in aortic stenosis [38].

Normal electrical current, Pathological current, Breathing-dependent.

Not breathing-dependent

Managements :-

What to tell patient calling with varicose veins hemorrhage?

• Press the bleeding point with a finger.

• Don’t stay sitting or standing. Lie down on your back, elevate the leg.

• Apply a paraffin dressing, cover with a thick stack of gauze or folded tissues.

• Roll a bandage over the gauze pad in order to apply a pressure equivalent to the previous finger pressure, no more. Do not apply a tourniquet (must apply at hospital). If you have no bandage, use elastic suspenders or any garment of elasticated material.

• If you are breathless or dizzy: call emergency.

• If you are not, ask someone to drive you to the hospital .

There are a variety of treatments available for varicose veins including compression stockings, injection sclerotherapy (injection of an irritant substance), as well as surgical methods of treatment. Many surgical treatments are practiced. These may involve ligation (tying) of the affected vein (long or short saphenous veins), stripping of the affected trunk veins and avulsions (removal) of the varicosities (dilated segments) [39].

The most common surgical operation is ligation of the saphenofemoral vein, stripping of the long saphenous vein (LSV) and avulsions.

The operation can be associated with significant blood loss, especially if it is a bilateral procedure [40].

A-Tourniquets .

There is a potential for large blood loss during surgery, especially if both legs are operated on at the same time. Tourniquets on the upper leg during surgery may be useful to minimize blood loss.

Tourniquet have been used as a means to exsanguinate (remove all blood from) limbs where there can be a risk of significant blood loss such as in orthopaedic surgery, and arterial bypass surgery.

But the usage of tourniquets has some complication , such as thrombosis and nerve damage [41].

– Corbett R, Jayakumar KN. Clean up varicose vein surgery– use a tourniquet. Annals of the Royal College of Surgeons of England 1989;71(1):57–8. [MEDLINE: 627]

In this picture , we can see how the tourniquet stop the blood flow , this exactly what happen during surgical repair of varicose vein .

B-Subfascial ligation

is a procedure that involves cutting through the skin and deep fascia , and tying off the incompetent perforating veins that link the veins in the skin to the deep veins in the muscle [42].

ligation of saphenofemoral vein :-

The most common surgical operation in which stripping of the long saphenous vein (LSV) andavulsions. The operation can be associated with significant bloodloss, especially if it is a bilateral procedure [43]

Sclerotherapy

clerotherapy is the targeted elimination of varicose veins by injection of a sclerosing substance into the vein lumen. Sclerosing agents cause a chemical irritation of the venous intima that produces an inflammation of the endothelial lining of the vessel.1 Subsequently, a secondary, wall-attached local thrombus is generated and, in the long term, the veins will be transformed into a fibrous cord, ie, sclerosis. According to their potency, sclerosing agents can be classified as major (alcohol, iodine, sodium tetradecyl sulfate), intermediate (sodium salicylate, polidocanol), or minor (chromate glycerin). Polidocanol, sodium teradecyl sulfate, sodium morrhuate, and ethanolamine oleate are detergent agents. They contain a hydrophilic and a hydrophobic pole and act by altering the surface tension around endothelial cells. The hydrophobic pole binds to the cell surface, whereas the hydrophilic portion attracts water into the cell, resulting in a rapid and intense cell hydration [44].

Sclerofoam is obtained by mixing a liquid with a gas. For sclerotherapy, detergent sclerosing agents such as Polidocanol (POL) and Sodium Tetradecyl Sulfate (STD or STS) are the most logical ingredients. The usual gas is air, although many others have been tried or are being used. Foam is obtained after repeated alternate passages from one syringe to another through a connector that may have a reduced diameter to decrease the size of each foam bubble [45].

[46].

( External appearance of polidocanol microfoam; its interna cohesion gives it manageability)

The foam is its ultrasound echogenicity. Liquid/air interfaces act like refl ectors and foam appears as an excellent contrast medium, even when only a few bubbles are present , This characteristic is helpful in following foam when injected from a remote injection point [47].

The most common method of making foam uses two 5 ml Luer-lock siliconized syringes. One syringe contains 1 ml of sclerosing agent at the desired concentration, the other 4 ml of (sterile, filtered) room air [48].

Sclerofoam is mostly used for large veins, thus it is usually injected with duplex guidance and duplex control of efficacy [49].

The main advantage of Sclerofoam is that it fills up the varicose vein without being diluted with blood. It is important to adjust the injected volume to the length and diameter of the vein. This can be estimated by a simple calculation using the formula of the cylinder: V · (D/2)2 · L

(V  volume, D diameter, L Length) [50].

Two groups of different methods are used to inject sclerofoam :-

Open-vein access allows injection of any volume and repeat injections with additional syringes if necessary. It is important to emphasize the fact that open-vein access allows preparation of the foam at the last minute, and rapid injection of fresh foam. Short catheters and butterfl y needles have almost the same utility [51].

Long catheters are still uncommon but will open a new perspective. The tip can be placed at any level, for example the (SFJ) junction. After positioning, the leg can be elevated and an Esmarch bandage applied. This empties the vein and then the foam is injected while pulling back the catheter. This technique, in principle, is comparable to endovenous ablation, but is much cheaper. Preliminary results are encouraging but the technique is more complicated than open-vein access. Its advantages remain to be demonstrated [52].

[53].

– Naylor CD. Systolic propulsion of the eyeballs in tricuspid regurgitation. Lancet 1995; 346: 1706.

[54]

– Sepulveda G, Lukas DS. The diagnosis of tricuspid incompetence: clinical features in 60 cases with associated mitral valve disease. Circulation 1955; 11: 552–63.

Its simplicity, reproducibility, low cost, safety, make sclerotherapy the treatment of choice for the anatomic and functional elimination of a pathologic venous area [55].

It has shown better outcomes than surgery (both conventional surgery and new less aggressive techniques), and it does not have the limitations or the morbidity of other endovascular procedures that are theoretically less invasive, such as endovenous lase [56].

Sclerotherapy is an effective treatment method with a low incidence of complications, eg, allergic reaction, skin necrosis, excessive sclerosing reaction (thrombophlebitis), pigmentation, matting, nerve damage, scintillating scotomas , etc [57].

Compression therapy:-

Compression therapy, despite significant improvements in dressing materials and other methods, remains the cornerstone of conservative treatment. This is because of its ease of use, non-invasive nature [58].

The most common forms of therapeutic leg compression are elastic stockings, including tights, non-elastic and elastic bandages (short and long stretch), and intermittent pneumatic compression. The mechanisms of action include compression of superficial and deep veins and improvement of the muscle pump function, both leading to reduction of ambulatory venous pressure and reduction of oedema [59].

[59]. Cabrera J, Redondo P, Becerra A, et al: Ultrasound-guided injection of polidocanol microfoam in the management of venous leg ulcers. Arch Dermatol 140:667-673, 2004

Elastic stockings and bandage in the form of graduated compression have been the cornerstone of conservative management of chronic venous disease C0-C4 for decades. They compress varicose veins, reduce venous reflux, and improve calf muscle pump function. More recently it has been shown that progressive graduated compressive stockings (higher pressure at the calf compared with the ankle) are more effective than the usual degressive graduated compressive stockings (higher pressure at the ankle) in improving pain and lower leg symptoms. Furthermore, they were easier to apply.elastic stockings require proper fitting and, to remain effective, should be replaced at intervals of 3-4

months, according to the manufacturers’ instructions [60].

[60].

Guex J-J. Foam sclerotherapy: An overview of use for primary venous insuffi ciency, Semin Vasc Surg. 2005. 18: 25–29.

Graduated compression stockings have been designed to deliver a gradient of external pressure, which is highest in the ankle region and lowest in the upper thigh region, applying a pressure which gradually decreases up the leg. These pressures are defined as 18 mmHg at the ankle, 14 mmHg at the mid-calf and 8-10 mmHg at the thigh. These pressures may vary slightly depending on the manufacturer of the hosiery and the circumference of the patient’s limb. The pressures are therefore approximate and are reported by the manufacturers as a range [61].

Compression Stockings Classifications:

light compression—16 to 20 mm Hg

class I stockings—20 to 30 mm Hg

class II stockings—30 to 40 mm Hg

class III stockings—40 to 50 mm Hg [62].

Breu FX, Guggenbichler S. European consensus meeting on foam sclerotherapy, Dermatol Surg. 2004. 30: 709–717. [63].

Compression stockings are contraindicated in patients with several peripheral arterial occlusive disease, massive leg oedema or pulmonary oedema due to heart failure and extreme leg deformity [64].

Compression hosiery or stockings are often the first line of treatment for varicose veins in people without either healed or active venous ulceration. Evidence is required to determine whether the use of compression stockings can effectively manage and treat varicose veins in the early stages [65].

TIRS technique:-

When the pressure gets too high in the venous system, chronic venous insufficiency occurs. The increased pressure can occur in the superficial system, deep system or both. With long standing high venous pressure, ulceration and other undesirable complication can occur.

This technique mainly aimed towered healing the ulcer .

Ronald G. Bush, MD FACS, Midwest Vein & Laser Center, Dayton, Ohio, has developed a technique called ‘Terminal Interruption of Reflux Source’ (TIRS).

With the using of ultra sound , vessels that are causing the high pressure, and it’s corrected for treatment and to prevent recurrence .

ultrasound guidance, 1% Sotradecol foam is injected into a venous branch or branches in close proximity to the ulcer bed. The branch may course under the ulcer or lead directly to it. Although more than one outflow source may be localized, all targeted veins must have documentation of reflux and have continuity with the primary source [66]

CONCLUSION

Rupture varicose vein is a serious complication because it can bleed after a minor trauma such as cat scratch. If not treat the predisposing factor and the risk factor the incidence of rupture will increase and in some cases could be fetal especially in elderly because they cannot control the bleeding.

It’s important to do a conservative treatment such as sclerotherapy and compression therapy to control the varicose vein and to prevent further bleeding by minor trauma.

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