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W. G. FEGAN, M.Ch., F.R.C.S.I.

In the minds of many doctors varicose veins and chronic venous insufficiency are the same basic disease, the only difference being the degree of severity. In our opinion, varicose veins do not necessarily lead to chronic venous insufficiency, nor must chronic venous insufficiency be succeeded by varicose veins. Varicose veins and chronic venous insufficiency are fundamentally different and the confusion is caused by their frequent association. It is possible to eradicate all the superficial varices and still not restore the pumping mechanism responsible for the venous clearance of the limb. Conversely, one can restore the mechanism responsible for the venous clearance and rid the limb of ulceration, oedema and bursting pain, but not necessarily completely clear up the varicose veins scattered over the surface of the limb.

The specific characteristic pattern of the pressure measurement tracing which indicates an efficient pumping system shows a big gap between the systolic and diastolic pressure with each step after one begins walking (Pegum and Fegan, 1967).

The hypotensive periods in the main veins are rapidly reflected by the hypotension which develops in the venules necessary for the production of a favourable hydrostatic-osmotic pressure gradient. Venular hypotension is essential to effect fluid clearance. The capacity of the osmotic pressure of the plasma proteins to clear tissue fluid is completely neutralized by high venular pressure. To produce low tension in the venules it is obviously necessary to have a powerful ejection of blood from the large veins between the myofascial compartments of the limb. Valvular damage in the perforating veins permits an abnormal see-saw of blood between the superficial and deep venous systems.

The adverse effects of this reversed see-saw are, first, to rob the ejection phase of its full force and, secondly, to prevent the development of the normal profound hypotension in the large intracompartment veins and, consequently, in the venules. A limb with chronic venous insufficiency will therefore show a gently undulating pressure tracing without the normal jagged peaks and troughs which are necessary both for the ejection of blood from the limb and for the clearance of tissue fluid.

Venous clearance from a limb can also be influenced either by an increase or decrease in the arterial supply or by proximal obstruction to the venous outflow. It is necessary to consider the perfusion arc in toto from the external iliac artery back to the external vein in every position of the limb relative to gravity, horizontal, elevated, dependent and ambulant.

At the start of pregnancy the arterial inflow is increased and pumps which were defective, but nevertheless compensating, may well become clinically inadequate and signs and symptoms of chronic venous insufficiency develop. This is commonly seen in our clinic and occasionally even before the patient has missed a period (Fegan and Henry, 1968).

When dealing with proximal venous obstruction, from whatever cause, it must be understood that clearing proximal obstruction in the presence of a deranged pumping system distal to the obstruction will serve little purpose. If the derangements of the limb pumps can be pin-pointed and corrected, it is very likely that the potential venous by-passes, which can open up quite rapidly (Fegan and Doporto, 1967), will allow adequate venous return, provided that high systolic peaks have been restored by the correction effected in the distal pumps.

The point of valvular damage and incompetence permitting the reversed see-saw flow must be located and obliterated. The good effects of such accurate diagnosis and correction of the points of primary valvular damage are reflected in the improved nutrition of the muscles and skin due to improved tissue fluid clearance, and the disappearance of claudication as well as the improvement in the signs of venous congestion of the skin. We have recorded many patients who presented with generalized tiredness, dyspnoea, cyanosis and arterial inadequacy as well as venous symptoms, who not only showed improved venous clearance in the limb following adequate restoration of the pumping systems, but also a marked improvement in the general symptoms.

Following thrombosis and recanalization of the central collecting veins of the lower limb, the valves are usually damaged. To date there is no satisfactory known method of repairing or replacing these valves. The best we can do at the moment is to locate the sites of retrograde filling into the superficial tissues, to obstruct these sites and, thereby, reduce the reversed pressure see-saw.

If, after this procedure, proximal obstruction still prevents adequate return of blood, then it is reasonable to attack the proximal obstruction. It must, however, be kept in mind that the fundamental lesion of valvular damage in the deep veins has not been overcome and that the relief of proximal obstruction only permits return of blood from the lower limb under the influence of gravity (that is when the patient is lying down with the legs elevated) and contributes nothing to the pumping capacity of the venous muscle pumps in the dynamic state.

In the present treatment of chronic venous insufficiency our primary object should be to locate valvular damage wherever it may be and to restore it as completely as possible because, although a clinical cure can be effected by the obliteration of leaking perforators to the superficial tissues and by the opening of proximal by-passes, the circumstances in the deep vein pumping compartment are still very abnormal. Compensation is stretched to its limits and the likelihood of valves in perforating veins becoming incompetent in the near future is very great.

In our opinion, varicosity per se is due to retrograde turbulent flow in superficial veins in the areas of the leg where the superficial veins are either superficial to Sherman's fascia or where Sherman's fascia has become thinned out. Sherman's fascia is a condensation of superficial fascia between the skin and the deep fascia (Sherman, 1949). For example, varices are more common in the lower half of the thigh where Sherman's fascia is less well defined than in the upper half where Sherman's fascia is well demonstrated. The veins which are deep to this layer can be compressed by it and can therefore be emptied by movement of the leg.

It is known that the conversion of linear flow into turbulent flow greatly alters the forces acting on the walls of the vessel. Turbulence is accepted as the cause of post-stenotic dilation in arteries. It is reasonable that turbulence in a vein should also be accepted as the cause of dilitation.

Palpation of veins in a patient's leg, which has been switched through 180 degrees into the vertical or standing position, will demonstrate an easily palpable thrill. This thrill is confined to the area of varicosity and is not palpable over the non-varicose segments. In our opinion the presence of turbulence alone is the major factor in the development of varicosities.

It should be remembered that signs and symptoms of chronic venous insufficiency due to valvular damage do not become apparent until the limit of the reserve pumping capacity has been transgressed, and that in a small percentage of cases one can have considerable derangement, even past the point of compensation, without the development of marked retrograde flow. Although it is usual for people with chronic venous insufficiency to develop some varicose veins, these few do not.

In the young man with gross superficial veins and no signs of chronic venous insufficiency the turbulence is as spectacular as the veins; and the presence of retrograde turbulent flow down the superficial veins, is accounted for by the ability of the pumps to produce adequate hypotension due to the fact that they have an adequate reserve pumping capacity. It is fundamental to distinguish between downward retrograde turbulent flow in superficial unsupported veins and inefficiency of the multiple pumping units in the leg; their association is not essential and not sequential or independent.

We believe that the common sequence of events in the development of varicose veins is as follows. Initially, the limb sustains a minor injury (the barked shin) and an area of traumatic thrombophlepitis is established opposite an ankle perforator. Following recanalization of this thrombophlebitis the valve in the perforating vein may or may not become incompetent. If it becomes incompetent, an abnormal retrograde see-saw flow is established in the perforating vein. This does not mean that more blood flows up the superficial veins, but that in the segment of vein opposite the leaking perforator immediate and profound venous hypotension can o longer be achieved on walking.

As the leak increases, the abnormal pressure pattern in the superficial compartments spreads to affect the adjacent intra-valvular segments. This spread of abnormal pressure can only be upward in the direction permitted by the valves. The abnormal ascending factor is not increased flow of blood, but spread of abnormal pressure. The essential pressure abnormality that spreads upwards is failure to achieve a rapid profound venous diastole which permits recovery of the tone and nutrition of the vein wall. This is an insidious and often unnoticed process.

At a critical point the valves become secondarily incompetent and at this point retrograde flow across their unequal cusps becomes established. It is this inequality of the valve cusps that gives rise to turbulent retrograde flow and changes the uniform dilatation into saccular aneurysmal dilatation.

This retrograde turbulent flow is the cause of varicose veins. These, however, are relatively unimportant in patients in whom the venous clearance is deranged. It is, however, a different clinical entity form the congested leg of the pregnant woman, which, in our opinion, is due to generalized inhibition of the smooth muscle in the vein walls and valves in the entire limb, permitting a reduction in the efficiency of each individual valve.

This hypothesis is supported by clinical observation and by the spontaneous disappearance in some cases of saphenous varices following treatment of the lower perforators (Quill, 1967).

Varicose veins and chronic venous insufficiency are not the same disease; nor does one necessarily progress to the other. The fundamental disorder in chronic venous insufficiency is derangement of the pumping system in the leg, due to destruction of the valves or perforating veins. Because of this, adequate venous hypotension cannot be achieved. As it is impossible to replace these damaged valves, permanent obliteration of the damaged perforating veins is the best method that is possible to restore the efficiency of the pumps. Varicosity of veins is caused by retrograde turbulent flow in those superficial veins which are unsupported by Sherman's condensation of superficial fascia. These two widely different disturbances are not necessarily sequential, associated or interdependent.

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