Varicose Veins Causes and Treatment

Get Rid Varicose Veins Naturally

Here are some sneak previews on what you'll find in this report: Unlike popular belief, common dieting found in other diet books just don't work. You only need this special diet to help improve and lessen the veins discomfort. Forget about paying for expensive gyms for working out your fitness to prevent the horrible looking veins from coming back. Here are 7 simple exercises you can do instantly without costing you a dime. How to use special aromatherapy technique to literally help the blood leave the legs and return to the heart. This will reduce swelling while shrinking the blood vessels near the skin's surface. 3 top herbal therapies to relieve my pain from my veins. How to use 4 types of common homeopathic remedies to ease the pain and soreness that are worse from touch. Secret tips on using specific herbs which are used during naturopathic treatment. One of my favourite remedies to help me relieve aches and pain from varicose veins. This works effectively on spider veins as well. How to mix special juices to help strengthen the walls of the veins, which also help prevent blood clots, one of the serious complications of varicose veins. 5 massage secrets which you can do it yourself to alleviate discomfort associated with varicose veins. I'll even show you how to prepare massage oil treatment effectively. 1 common massage Mistake that could rupture your veins without you knowing. It simply worth knowing how to handle your massaging correctly. Not all yoga exercises can help you. Here are the top yoga exercises which can Worsen your varicose veins without you knowing. Some simple folk natural remedies you can easily prepare for yourself at home. Some of these remedies will either help shrink your varicosities and nourish the veins leaving your legs super smooth Read more here...

Get Rid Varicose Veins Naturally Overview

Rating:

4.7 stars out of 13 votes

Contents: EBook
Author: Diane Thompson
Official Website: www.varicoseveincures.com
Price: $27.00

Access Now

My Get Rid Varicose Veins Naturally Review

Highly Recommended

The author has done a thorough research even about the obscure and minor details related to the subject area. And also facts weren’t just dumped, but presented in an interesting manner.

This ebook does what it says, and you can read all the claims at his official website. I highly recommend getting this book.

Venous Valve Incompetence Causes Varicose Veins

Valves of the venous system frequently become incompetent or sometimes even are destroyed. This is especially true when the veins have been overstretched by excess venous pressure lasting weeks or months, as occurs in pregnancy or when one stands most of the time. Stretching the veins increases their cross-sectional areas, but the leaflets of the valves do not increase in size. Therefore, the leaflets of the valves no longer close completely. When this develops, the pressure in the veins of the legs increases greatly because of failure of the venous pump this further increases the sizes of the veins and finally destroys the function of the valves entirely. Thus, the person develops varicose veins, which are characterized by large, bulbous protrusions of the veins beneath the skin of the entire leg, particularly the lower leg. Whenever people with varicose veins stand for more than a few minutes, the venous and capillary pressures become very high, and leakage of fluid from the...

Varicose Veins

Retrospective examination of this illustration and the accompanying text makes it clear that the occluding thrombus had formed in the ostial valve of a tributary vein and had subsequently protruded into the femoral vein lumen. Because ostial valves are unicuspid, a thrombus that forms in such a valve would be expected to occlude the tributary completely, so the tributary and its sub-tributaries will become distended. Thus, we can predict that ostial valve thrombi will usually, or perhaps always, result in varicose veins. More speculatively, we may propose the converse that all or most cases of varicose veins are attributable to (probably silent) ostial thrombi. This speculation is consistent with recent accounts of chronic venous disease (Bergan et al. 2006).

An Alternative Viewpoint

This hypothesis, which has been experimentally corroborated (e.g. Hamer et al. 1984), explains the frequency of pulmonary embolism and chronic venous disease. Two of its important premises are (1) that venous thrombi can (and usually do) form in blood that is normally coagulable, both systemically and locally (2) that the blood must be flowing, not static, for thrombi to form (Malone and Agutter 2006). In the years following its publication and experimental corroboration, interest in the phenomenon of ischaemia-reperfusion injury (IRI) flourished, not least because IRI is of great significance in transplant surgery. The underlying mechanism of IRI as it is understood today somewhat resembles that described by our alternative model, though the former relates primarily to the heart and arteries, the latter exclusively to the veins.

The Vascular Hypothesisexotic But Persisting

This, of course, is reminiscent of the clonidine treatment that has been found to be effective in two double-blind studies in idiopathic (52) and uremic RLS (53). The response rates in 70 (52) to 80 (53) of the patients even correspond roughly to the rate of improvement (80 ) reported by Ekbom (51). Surprisingly, there is one large open-label study (54) that reported that 98 (111 113) of patients searching treatment for varicose veins and suffering from concomitant RLS reported a complete or near complete relief of RLS symptoms after a few sessions with sclerotherapy, and in approximately 70 of patients this relief lasted for 2 years. Even more recently, a 35-day treatment with enhanced counterpulsation (55) and the wearing of a low-pressure device on the legs (56) ameliorated RLS in individual patients. The actual pressure sensation, however, could account for this independent of any vascular effect. Circumstantial evidence could also be evoked by the link between smoking and RLS in...

Endothelial Hypoxia and the Congregation of Leukocytes

8 Outside the VVP, neutrophils release proteinases and ROS that alter the ECM of the vein wall. Concomitantly, the endothelium releases mitogens that induce the subendothelial smooth muscle cell to dedifferentiate and proliferate (Michiels et al. 1994). Chronic repetition of these processes can eventually lead to alterations in the venous wall such as the ones observed in varicose veins.

Sevitt on the Aetiology of DVT

That venous stasis, another member of Virchow's Triad, also plays a part in the pathogene-sis of thrombosis in the lower limbs and pelvis rests on strong, if circumstantial, evidence. Firstly, the blood may take minutes to pass along the thigh and leg veins when the limbs are supine, horizontal, and immobilised especially in elderly patients secondly, venous thrombosis is particularly common in middle aged and elderly patients confined to bed after operation or injury, or for medical reasons - and, generally speaking, the longer the bed rest, the greater the frequency and extent of thrombosis thirdly, at necropsy, the location of primary thrombi in valve pockets and at vein junctions is consistent with particularly stagnant pools in relatively stagnant channels. Does stasis act mainly through local silting of platelets, leukocytes, and some red cells onto the endothelium or is the endothelium also abnormal Histological examination of recent thrombi indicates that they are laid down on...

Wound Bed Preparation

As advanced ordnance created higher-energy war wounds, as the private sector acquired high-energy weapons, and as vehicles became faster and more pervasive, surgeons have had ample opportunity to apply the lessons of war to the civilian sector. In terms of chronic wounds, people have been living longer and suffering from some of the latter stages of chronic disease. Diabetic foot ulcers were rare prior to the advent of insulin. Paraplegic patients rarely lived for long periods with pressure ulcers, and end-stage venous disease is similarly a latter-day occurrence.

Hypoxic Injury to the VVP Cusp Endothelium Is Potentially Thrombogenic a Proposal

Endothelial Response Venous Injury

Indeed, no one now doubts that thrombosis follows gross injury to the venous intima a subendothelium that has been injured along with its covering endothelium invites platelet activity, which initiates the coagulation cascade at that injury site. Wharton Jones (1851) described the phenomenon clearly and it became clinically useful. The modern surgical procedure of injecting sclerosant (endothelium-killing) agents into segments of dilated varicose veins irritates and kills the intima, thus inducing controlled occlusive thrombosis followed by auto-stenosis and cure of the varicose appearance. 'Injecting varicose veins', in effect, adapts the experimental work of two centuries to the cosmetic treatment of varicose disfigurement.11

Thrombi Originate in the Venous Valve Pockets

Encompassing a wide range of ages and causes of death, he found thrombi in most of the larger leg veins the soleal vein scored particularly highly (see also Sevitt 1973 Sevitt and Gallagher 1961). Thrombi were initiated as microscopic nidi in regions adjacent to the valve cusps, where their main constituents were leukocytes, platelets and fibrin (i.e. they began as 'white thrombi'). The overall composition of a mature thrombus, notably its erythrocyte content, may therefore depend on its age and on the mean local blood velocity during its formation and development but thrombus formation depends on blood movement within and near the VVP, and is initially associated with the local congregation of leukocytes.

Polarographic Demonstration of VVP Hypoxaemia during Non Pulsatile Flow

In anaesthetised human subjects (in preparation for surgical treatment of their varicose veins), streamline flow in the leg veins was presumed when valve cusps were not seen to 'flap' normally when pulsatile flow was temporarily suspended. VVP hypoxaemia was demonstrated directly (Fig. 11.3) and was readily related to the perturbation of normal flow patterns within the pocket (Fig. 11.4). Intravenous (intra-pocket) polarography confirmed that the PO2 fell immediately, invariably and quite precipitously in VVP blood during such periods of streamline flow. It returned instantly to 'normal' each time a single pocket-emptying venous pulse occurred, or massaging external pressure was applied, thus proving that the PO2 within VVP depends on, and reacts to, sequential filling and emptying. After 2 h of sustained non-pulsatile flow in the leg veins of anaesthetised dogs, blood cells had congregated in the VVP and on the parietalis, as predicted by the VCHH, shown in Fig. 11.1(a) and...

Increased Blood Volume Caused by Increased Capacity of Circulation

Volume increases sufficiently to fill the extra capacity. For example, in pregnancy the increased vascular capacity of the uterus, placenta, and other enlarged organs of the woman's body regularly increases the blood volume 15 to 25 per cent. Similarly, in patients who have large varicose veins of the legs, which in rare instances may hold up to an extra liter of blood, the blood volume simply increases to fill the extra vascular capacity. In these cases, salt and water are retained by the kidneys until the total vascular bed is filled enough to raise blood pressure to the level required to balance renal output of fluid with daily intake of fluid.

Femoral Venous Thrombosis and Massive Pulmonary Embolism

Because clotting almost always occurs when blood flow is blocked for many hours in any vessel of the body, the immobility of patients confined to bed plus the practice of propping the knees with pillows often causes intravascular clotting because of blood stasis in one or more of the leg veins for hours at a time. Then the clot grows, mainly in the direction of the slowly moving venous blood, sometimes growing the entire length of the leg veins and occasionally even up into the common iliac vein and inferior vena cava. Then, about 1 time out of every 10, a large part of the clot disengages from its attachments to the vessel wall and flows freely with the venous blood through the right side of the heart and into the pulmonary arteries to cause massive blockage of the pulmonary arteries, called massive pulmonary embolism. If the clot is large enough to occlude both of the pulmonary arteries at the same time, immediate death ensues. If only one pulmonary artery is blocked, death may not...

Types of cardiovascular disease

Types Cardiovascular Diseases

Blood clots in the leg veins, which can dislodge and move to the heart and lungs. Riskfactors Surgery, obesity, cancer, previous episode of DVT, recent childbirth, use of oral contraceptive and hormone replacement therapy, long periods of immobility, for example while travelling, high homocysteine levels in the blood.

Blood Cell Congregation and Blood Coagulation

Site of valve cusp injury just as they do in the circulation (notwithstanding their apparently lower concentrations in the leg veins Woldhuis et al. 1992). When platelets congregate on the dead parietalis, the coagulation process leading to fibrinogenesis may be initiated (Chapter 2). The resulting fibrin web may then begin to entrap red cells. From this, we may imagine that every 'coagulum' embodies a white red alternation of layers (each only a few microns thick) so that every thrombus is composed of multiple, sequential, strata of white cells with thin backings of red cells a venous thrombus is built up like a coal seam rather than as a 'single clot in a basin'. Herein lies the answer to Aschoff's conundrum and his illustration of thrombus histology venous thrombi have layered, 'coralline', structures because of the way they are formed.

Intermittent Positive Pressure Compression IPPC of Feet or Legs

The same considerations relate to the prophylactic use of IPPC. The principle is once again to empty 'stale', deoxygenated blood from VVP, mainly in the leg veins.12 So what might be the ideal frequencies, intervals and pressures at which the IPPC apparatus should be operated Patients wearing such devices complain of the disturbing effect of compression. For some people, tight and aggressive13 squeezing

The Unification of Approaches

Fig. 12.5 The aetiology of DVT - summary of the VCHH. The flow diagram outlines a plausible aetiological scheme. When the parietalis endothelium of a valve cusp becomes hypoxic under conditions of sustained non-pulsatile flow, the elk-1 egr-1 pathway is initiated and the EC pheno-type is changed. As a result, vasodilators are produced, perhaps increasing blood flow through the vasa venarum and helping to sustain the oxygenation of the mural endothelium. Thrombin is activated, enhancing the egr-1 pathway via PAR-1, and anti-coagulation factors such as thrombo-modulin are inhibited. Also, cytokines are secreted that recruit leukocytes and platelets to the injured site when the hypoxaemic VVP is replenished with fresh blood by a brief episode of normal pulsatile flow. Continuation of the streamline flow leads to death necrosis of the affected parietalis, and a (brief) restoration of pulsatility leads to the phagocytic removal of the dead cells. Signals such as VEGF (not shown in the...

Interrupted Flow and Underperfusion of VVP

McLachlin et al. (1960) provided experimental evidence that 'stagnant blood' (they used the term 'stasis') co-exists alongside moving blood in these particular circumstances. An injected radiographic dye was visualised in what the authors presumed to be VVP of leg veins whenever the 'peripheral venous heart' pulsed less frequently and or less forcefully than normal, i.e. when the 'diastole' of the calf-muscle pump was indefinitely prolonged by postponement of the next muscular 'systole'. This resulted in the sequestering of the tracer in VVP as shown by x-ray photographs, implying underperfusion or non-perfusion of the valve cusps, which fluttered half-open and half-closed (Chapter 9).

The Significance of Ostial Valves

Virchow's engraving (Fig. 10.1) suggests that different investigative procedures could reveal different proportions of parietal to ostial valve thrombi, and this might explain the extraordinary difference of opinion between Sevitt and Paterson. Moreover, as the engraving illustrated, the propensity of thrombi to dehisce and or fracture to release emboli, and the tiny residual lesion barely visible in the tributary mouths, show that a search for the primary site of a fatal embolus could be vain, since it is marked only by the trivial little thrombus in, or poking out of, a femoral vein tributary. Such veins would have to be harvested and dissected very much more thoroughly, perhaps after isolation and glutaraldehyde fixation, if accurate knowledge of the true extent of thrombosis in leg veins and their valve-guarded tributaries were to be sought. Several other points arise from Fig. 10.1.

Carbon Monoxide Poisoning and Anaemia

Originating in varicose veins of the legs. Wiskowski (1921) saw extensive thrombosis in the lower right leg of an 11 year old girl . Brack (1928) reported 22 cases of illuminating gas poisoning in which extensive capillary thromboses were scattered throughout the whole heart Our emphasis

Pathology

Embolism in the United States (around 0.1 of all patient mortalities). Emboli are observed in over 10 of unselected autopsies, and recurrent venous thrombotic and thromboembolic episodes are quite common (Freedman 1998). Mortality from untreated pulmonary embolism has been estimated at 30 (Carson et al. 1992). It is worth recalling that Virchow's pioneering scientific study of DVT related entirely to the concept and category of 'embolia' and the novel related phenomenon of metastatic pulmonary embolisation. We shall discuss his work in Chapter 6. (b) Local DVT-associated morbidity is much less discussed than embolism but it may impair a patient's quality of life by causing permanent disability. Morbid sequelae, collectively labelled 'post-thrombotic syndrome', usually begin with limb oedema caused or aggravated by raised venous pressure distal to a thrombus, which increases the rate of capillary filtration. Although this oedema may subside within a few months in about half of all...

Wound Assessment

Before dealing with wound management, we must always consider the underlying cause of the ulcer and ensure an adequate blood supply (or the correction of an impaired blood supply) to the leg and ulcer area. The great majority of ulcers are because of venous disease, arterial disease, or both (16).

The Ancient World

Studies of arteries and veins in Alexandria during the later centuries BC, notably by two pioneers of vascular surgery, Herophilos and Erasistratos, culminated in the work of Galen during the 2nd century AD. Galen used venesection to treat ulcers and varicose veins. His mainly accurate anatomy, and his mainly fanciful physiology, remained virtually unquestioned until the 16th century we shall say more about this in Chapter 8. In 1452, Leonardo da Vinci produced superb anatomical drawings that included illustrations of superficial limb veins. These were important precedents for the revolution in anatomy that was to take place a century later in the school of Vesalius and his successors in Padua.

Get Rid Varicose Veins Naturally Official Download Page

The best part is you do not have to wait for Get Rid Varicose Veins Naturally to come in the mail, or drive to a store to get it. You can download it to your computer right now for only $19.00.

Download Now