Endoscopic and ultrasonographic observations of damaged venous valves



by F. Calotă, Romania

Firmilian CALOTă, MD, PhD
University of Medicine
and Pharmacy
The 2nd General Surgery
Department, Craiova
Romania

The significant impact of lower limb venous lesions upon a patient’s quality of life explains why knowing about the mechanisms of chronic venous disease is of such value. With the impressive evolution in investigative methods, we now have the opportunity to explore new pathophysiological concepts that have been postulated. The latest imaging investigations—endoscopy and ultrasound—have distinct roles. Endoscopy is currently an invasive procedure used for research purposes, but with great potential for use in minimally invasive endovenous surgery. Information obtained with this investigation method—regarding endovenous morphology, valvular morphology and dynamics, and pathological changes relating to these—is genuinely new and has led to the introduction of new venous concepts, such as valvular segments, commissural slits, commissural reflux channels, etc. Ultrasound examination, a noninvasive method, provides exceptional data about venous anatomy (eg, valve position and dynamics) and transvalvular hemodynamics (reflux and turbulence). Ultrasound procedures can show reflux gates in the deep venous system, venous reflux eccentricity or axiality, and the length and duration of reflux. In addition, the effectiveness of treatments can be determined with this investigative technique. The importance of ultrasound is illustrated by the fact that a phlebological intervention cannot be performed without this examination. Endoscopy and ultrasound for the morphological and dynamic evaluation of the venous system are indisputable means of advancing the development of phlebology and of helping make the most appropriate treatment decisions for patients with venous lesions of the lower limb.

Medicographia. 2016;38:141-147 (see French abstract on page 14

Before addressing the main topic of the paper, it is necessary to clarify some essential notions and concepts for an accurate understanding of vein structure and function under normal and pathological circumstances. Venous circulation is a subsystem of the circulatory system. Its functionality develops in three phases: stability, oscillatory, and chaotic. As paradoxical as it may seem, the chaotic phase contributes to the adjustment of flow rhythms under variable stress conditions. By exploiting chaotic oscillations with a low energy intake, flow rate is brought back to the dynamic stability phase, after passing through the oscillatory phase.

Just as the body, as a dynamic system, extracts negentropy from the surrounding environment in order to amplify its internal structural stability, the venous system in the same way uses deterministic chaos as a reservoir of potentiality. It is important that the ratios of the durations of the above mentioned phases stay in balance; the dynamic stability phase needs to be prevalent, as the oscillation phase is transitional in nature. Changes in the structure of the valvular segment lead to the alteration of venous flow patterns, which amplifies parietal valvular structure changes, both locally and within the whole venous system.

The older the venous disease, the greater the extent of venous remodeling. Multisequential, accurate, and early treatment provides the best results and impedes the progress of chronic venous disease of the lower limb towards later stages associated with disability. The pathogenic cycle starts with local hemodynamic phenomena (stasis and temporary increase in venous pressure at the transversal, pumping reflux gates), progresses with morphological changes of the valvular segments and venous walls, and finishes with longitudinal, gravitational reflux.1 This pathogenic cycle is a strange attractor (chaos theory), and it is proof of dynamic system destabilization of venous flow.

Sequential treatment has the objective of extracting the venous system from the attractor basin in order to stabilize it. Sequential treatment starts with inhibiting endothelial-leukocyte activation (eg, by using Detralex, flavonoids, etc) and reducing venous distention (compression). Next, it progresses through to controlling transversal, pumping reflux (femoral-saphenous and popliteal-saphenous, via the perforating veins) and ends with improving longitudinal, gravitational reflux (via ablations and sclerosis of saphenous trunks using various methods and technologies). The use of any single treatment has proven to be insufficient to interrupt disease progress due to multiple pathogenic mechanisms.1

The valvular segment, a distinct venous structure, is composed of the valvular system (cuspids, anchoring ring) and the valvular sinus, and it represents, in our opinion, the morphofunctional “unit” of the peripheral venous system.2 It is the key element responsible for the performance of antigravitational venous return. Valvular segments are hemodynamic singularities; it is at the valvular segment level that the cyclic chaos-stability balance is determined. The valvular segment is composed of the following morphological components2:

Valvular insertion ring. This is a dense, muscular collagenous structure; at this level, the diameter is smaller than the rest of venous section. It represents the point at which blood enters the valvule. Its position may be studied by ultrasound exam, while endoscopy may visualize the ring as a circular threshold in the venous lumen,3 during the open valvule stage.4
Entrance orifice. The entrance orifice leads into the valvular defile, which is lined by the valve’s inferior contours and commissures.
Valvular defile. The valvular defile is limited by the cusp sides and has the shape of a flat cone, with the base diameter parallel to the skin surface. Its length is determined by the valve size. The open-section area is approximately elliptic in shape, with obvious angulation towards the commissures. This caliber constraint (at least 1/3 of the venous lumen) induces an increase in venous flow speed and a consequent drop in static pressure on the luminal side of the cusps, which is transmitted across the cusps into the sinus.

Valvules may be considered flow accelerators.1,2 The increase in dynamic pressure in the valvular channel encourages the flow of blood from collateral veins and perforating veins (the Venturi effect). Valvules also have the role of flow stabilizers; in the narrow section of the valvule, laminar flow is partially restored.1-3 Downstream valvular flow can be easily highlighted via ultrasound (“flow line clusters”—linear ordering of red blood cells).5 The simultaneous drop in static pressure within the sinus leads to the attraction of blood that exerts force on the cusps1,2,5 and impedes their lining to the venous wall (the intermediary position of cusps during flux as revealed by echo-Doppler examination).5

Valvular sinus formation is obviously determined by hemodynamics, and not gravity. In the superior vena cava, the valvular sinuses are open towards the heart. The jugular sinus is very well represented and easy to picture. In decathletes and marathon runners, the narrow valvular section is longer due to valvular hypertrophy that occurs as a result of adaptation to high dynamic pressure (high shear stress).

The exit orifice of the valvular defile corresponds to a closed curved line tracing the free side of the cusps found in different cross-sectional areas. Upstream valvular flow can be described as a jet produced by constriction down the free side of the cusps. Flow speed is increased by constriction at the valvular gap and also by other mechanisms, eg, vis a tergo (force driving the venous return of peripheral blood) and efficient dynamics of the musculovenous pumps. The increase in flow speed is followed by an additional reduction in the cross-section of flow (via a drop in pressure on the luminal side of the cusps). Soon after exiting the valvular narrowing, the flow lines compress, the respective flow cross-section being minimized (“constriction index” in fluid mechanics). Subsequently, the area of action of the flow widens via aspiration into the surrounding fluid (the efflux phenomenon).

At the frontier of the laminar flux that leaves the valve into the surrounding blood, inertial resistance appears that inverts the marginal flow vectors, resulting in vortices towards the venous wall that lead to the emergence of a “dead water” area. Flow in this area has a circular motion that increases in line with the speed of efflux. Intrasinus rotational flow represents a stabilizing influence for the sinus endothelium of the cusps and, at the same time, a protective, antigravitational hemodynamic phenomenon for the cusp-parietal channel, where the commissural clefts are under low pressure.1,2,4 The long valves and their terminal marginal “icicles” amplify the valvular efflux phenomenon and protect the valvular sinuses. In the closed position with the cusps in contact,4 the gravitational and stress pressure vectors of the valves are redirected towards the sinus wall.

The valvular sinus is the space limited by the parietal sides of the cusp, cusp-parietal angle, and venous wall. It is shaped like a bulb, with the maximal diameter above the cusp’s insertion ring. The valvular sinus is filled with blood, which, contrary to general opinion, does not stagnate, but flows in a circular pattern. This circular flow prevents blood stasis and the concentration of procoagulant factors, possibly to counterbalance the high expression of C-reactive protein and thrombomodulin receptors.6 Moreover, it provides shear stress at a physiological level necessary for the trophicity and stability of sinus endothelial cells and of the glycocalyx film in the sinus. The ultrasound sections in natural contrast highlight turbulence dynamics in the valvular sinus. The presence of blood in the valvular sinuses allows the cusps to maintain an “on hold” position, allowing prompt valve closure at flow reversion.1,2,5

Our endoscopic observations established that there is dynamic pattern of valve opening and closing in normal valves: opening has an eccentric, commissural debut, which continues along the venous axis4; retrograde flow causes closure, which follows the same order as opening, but in reverse.3,5

The open valve, with its diaphragm-like particularity, firstly amplifies movement resistance and secondarily contributes to the increase in inertial resistance of the system. In the closed position, it exerts a clack valve effect on subvalvular flow, with consequences on flow rate.5 At the time of complete closure of the valvule, under the action of hydraulic (hemodynamic) shock, a Windkessel-like phenomenon is produced.

Turbulence resulting from the reversal of flow is produced both on the cardial side of the valve and under the valve, with mainly hemodynamic consequences (stasis and turbulence), but also thermodynamic ones that have not yet been clarified (energy conversion, heat transfer to the venous wall, possibly the inhibition of α2 adrenal receptors).5 Without the existence of ultrasound, all these phenomena would not be known.

The above description is also valid when the valvular system is placed in a horizontal position. In the case of valves in the saphenous and perforator veins, the valves are approximately positioned in the sagittal plane, perpendicular to the axis of flow. In the first case, deterioration of the valvular component leads to longitudinal, gravitational reflux. In the second case, reflux is transverse, generated by the increase in pressure within the “venous room,” which is closed and driven by the abdominal pump. This is an argument for describing the two distinct types of reflux in terms of direction and mechanism: (i) a longitudinal, gravitational reflux; and (ii) a transverse, pumping reflux.1,5 Gravitational reflux takes place preferentially in the superficial venous system (due to particularities of tissue texture and composition) and also in the deep venous system, when valves are insufficient or destroyed. Pumping reflux transfers blood from the deep venous system to the superficial venous system (Figure 1).1,5

Figure 1. Pumping reflux during calf contraction in ostial valve
insufficiency of a Cockett III perforating vein.
Abbreviation: C.F., Calotaă Firmilian [author’s initials]

Acquired venous pathology emergesdue to structural changes in the valvular segment components, followed by the progressive perturbation of venous reversion. The morphological processes are, most frequently, degenerative ones, which explains the high incidence of primary varicosity in adults and the elderly.

Primary inflammatory changes are less common in terms of incidence, but their severity is greater and they have important functional consequences, seriously affecting patients’ lifestyle. Postthrombotic syndrome, which principally affects the deep veins of the lower limbs, progresses in an oscillatory manner, with recurrences and no permanent disappearance of inflammatory phenomena.3,5,6

Venous endoscopy

Venous endoscopy, a recent method of exploring the vascular system, has provided genuinely new information about endovenous morphology, the valvular system, valvular dynamics, and transvalvular blood flow. Even though venous endoscopy does not yet benefit from dedicated equipment, it has real potential for promoting minimally invasive endovenous procedures in deep, extended thromboses in primary valvular insufficiency.5-7 This invasive method, which has only been used in research so far, has introduced new concepts of functional anatomy and pathology, eg, the valvular segment, commissural reflux cleft, commissural reflux channel, endophlebitis, etc.

Following endoscopic observations, we proposed a pathogenic classification of valvular lesions5,6:
Functional valvular lesions (type I)
Functional valvular lesions are dysplastic and determined by progressive prolonged increases of retrograde venous pressure. Obviously, the valvular segment suffers most because of the mechanic effect of blood stasis during prolonged standing. However, the involvement of inherited, hormonal, nutritional, and behavioral (eg, fashion) factors cannot be excluded from the pathogenic picture. There are two distinct types of functional valvular lesion:

Commissural reflux slit (type Ia)
This appears as a small commissural opening of the valve. Upon standing, static and dynamic pressures are directed along the valve slopes toward the cuspid-parietal groove. The venous cross-section geometry changes from an ellipsoid to cylindrical shape. Consequently, circumferential movement of cusp insertion generates a tennis racket–shaped commissural slit with its tail directed toward the venous axis, through which a progressively larger volume of blood drains back transvalvularly. The valvular commissures are the valvular feature most at risk from damage from a progressive and prolonged increase in venous pressure.

Commissural reflux channel (type Ib)
The commissural reflux channel (Figure 2) represents an obvious increase in the reflux cleft. It is delimited by the valve commissure, the sinus wall, the cranial surface of the valvular insertion ring, and axial side of the cusps. Refluent blood is often projected from the threshold ring toward the opposite venous wall, leading to asymmetrical development of venous enlargement under the valve.

The difference between these two subtypes is morphological and clearly correlates with reflux volume.

Traumatic organic valve lesions (type II)
Valvular ruptures
Valvular ruptures may occur with large, sudden stress, which leads to a significant increase in short-term retrograde venous pressure on the cardial side of the valves. The following types can be distinguished:

Commissural ruptures: clefts and tears (type IIa)
These ruptures flutter in the flow of moving liquid. Depending on the severity of the lesion, ultrasound imaging may reveal eccentric transvalvular reflux, which is more clearly identifiable in transverse cross-sections although this can sometimes be identified in longitudinal cross-sections as well.

Cusp insertion lesions: linear perforations close to the cuspparietal insertion (type IIb), without any hemodynamic consequences
Valvular ruptures are not purely traumatic in origin, with leukocyte infiltration on the cusp cranial side8 and stimulation of endothelial cell apoptosis also determining breaches in their structure.5,7 Nevertheless, trauma is the most important factor, which explains why ruptures occur in the valve insertion or nearby, where the strength of the dynamic reflux force is greatest. In these cases, lesion direction is perpendicular to the direction of reflux.

Figure 2. The commissural reflux channel, in which the threshold
of the valvular insertion ring is visible.
Abbreviation: C.F., Calota Firmilian [author’s initials]
Modified from reference 2: Calota F et al. Rom J Morphol Embryol. 2010;51:
157-161. © 2010, Romanian Academy Publishing House.

Valvular ruptures,which aremost frequently located in the commissures or, more rarely, at the insertion base, lead to valvular failure. The presence of ruptures at this level is an indicator of high hemodynamic stress at the cusps. In line with other endoscopicobservations, inflammatory alterations of the valves were not particularly apparent, maybe due to the absence of vascularization at the cusp level (bradytrophic structure).

Inflammatory organic lesions (type III)
The inflammatory structural remodeling of valves has only been observed in the context of a more extended involvement of the venous wall, with changes in caliber, shape, and parietal stiffness. However, there are some who believe that inflammatory valvular damage is of a primitive and solitary type, arguing that there is a highly significant increase in the expression of adherence molecules and subendothelial traces of monocytes on the cardial side of valves.8

Valvular vestiges (type IV)
Here, we have included the valvular debris that appears as a consequence of the dysplastic process and/or iterative traumas caused by the increase in intrathoracic abdominal pressure. They are most often mistaken for endothelial folds and fringes. The sinuses are missing and the venous tracts are almost entirely tubulated.

In postthrombotic syndrome, the valvular segment and extrasegmentary venous wall are polymorphic lesions, in various stages of development. Lesion severity, established en- doscopically, is greater in distal segments, where venous hypertension and stasis are permanent, with consequences in neighboring tissues (extravenous hypertension, intratissue hypertension).9,10 In seriously affected veins, valvular segment vestiges can hardly be recognized.

At the confluence of the important tributaries of large saphenous vein, I have sometimes seen pearl-colored polyps. Their aspect is similar to that of a champagne cork blocking the collateral vein ostium, and they impede the passage of the endoscope.5,6 It is possible that valvular polyps might have developed on an adherent thrombus that has subsequently undergone fibrous remodeling and endothelialization. Their accidental discovery is connected with the introduction of endoscopy.

Ultrasound

Ultrasound is a modern method for noninvasively investigating the venous system. Ultrasonography is capable of highlighting changes in the valvular segment, venous trajectory (sinuosities, elongations), and diameter (venodilation) as well as the hemodynamic consequences—reflux and turbulence— of these changes.11 As mentioned before, the valvular segment represents an essential “piece” of the venous system in order for proper venous function to occur. With natural contrast, in B mode, under physiological conditions, ultrasonography highlights the Windkessel-like phenomenon in the inguinal “venous junction,”10,11 with valvular continence, both in the great saphenous vein junction and in the femoral (superficial) vein, situated immediately under the confluence with the deep femoral vein. When intra-abdominal pressure increases—eg, during the Valsalva maneuver—the retrograde wave determines the rise in pressure in the upstream valvular segment. The special morphology and positioning of the cusps transfer maximum pressure into the valvular sinus. The cusps, found in an intermediary position, are medially pushed; they come into contact on their axial side and close firmly, at the same time as plateau descent. Both the closedvalvule stage and the open-valvule stage are oscillatory, occurring in synchronization with flux-induced oscillations. Sometimes, one can visualize the transvalvular retrograde shock wave transfer through the plateau, as subvalvular turbulence.

Venous diameter measured in the sinus clearly increases, with the venous wall elastically expanding and storing the kinetic energy of the reflux wave blocked by the continent valves. When flow restarts, the potential energy transfers to the flow, which increases in speed, and the diameter goes back to its original size before the Valsalva maneuver.9-11

Ultrasonography can be performed in various ways (B mode, color duplex, power-Doppler, spectral-Doppler) to investigate the following:

Functional hemodynamic events. These events include axial reflux, transvalvular reflux, reflux/flux collision, and reflux turbulence at a transvalvular level. With color duplex ultrasound imaging, in a transverse cross-section, eccentric transvalvular reflux may be easily highlighted.

Figure 3.
Jugular valvular
sinus – an
open valve
(A). Valsalvamaneuver
(B)
showing a
“fractured
wing” floppy
cusp (top)
and a frozen
cusp (bottom).

Structural changes. These changes can include venous diameter, loss of the valvular sinus, and “fractured,” amputated, inverted, “frozen,” or floppy valves (Figure 3). We systematically explored the Cockett perforators and all the insufficient perforators. In the inguinal “venous junction,” we frequently found an interesting hemodynamic phenomenon in patients with old, voluminous varices in the great saphenous vein region: the transfer of blood from the deep femoral vein directly into the saphenous vein junction (Figure 4). The saphenous junctions are highly distensible (Ø >20 mm) and offer favorable conditions for the transfer of venous blood during the Valsalva maneuver directly from the deep femoral vein, situated posteromedially, into the anteromedial saphenous vein junction. The saphenous junction acts as a “reception area” as a result of its remarkable capacity to distend, its compliance to thermic stress being twelve times higher (358%) than that of the common femoral vein (29%).9

Figure 4. Complex longitudinal and transverse reflux in the inguinal
“venous junction” during the Valsalva maneuver. With dynamic imaging,
one observes that deep femoral venous flow runs through
the femoral vein to the saphenous junction, from the beginning to
the end of the Valsalva maneuver.
Abbreviations: DFV, deep femoral vein; FV, femoral vein; GSV, great saphenous vein.

Figure 5. A synthetic patch (indicated by the two arrows) wound
around the femoral vein acts as a “fixed splint” that maintains
valvular continence.
Abbreviations: DFV, deep femoral vein; FV, femoral vein.

Postoperative functional results. Ultrasonographically, the postoperative success of therapeutic procedures—eg, valve continence, “fixed splint” (Figure 5), and relapses—can be checked.

Obtaining ultrasound evidence for both cusps is not always possible under similar resolution conditions due to the variability of their position in distinct planes. Most commonly, with venous section enlargement, “polychromatic” reflux (turbulence) is highly suggestive of valvular failure. Such an image, even in only some sections, is evidence of valve insufficiency.

Conclusion

Venous endoscopy and ultrasound are relatively recent and highly effective procedures for the morphological and dynamic evaluation of the venous system. They undoubtedly represent a means of developing knowledge in the medical specialty of phlebology, with practical importance for accurate diagnosis. Through the information these techniques provide, they help provide important evidence for helping clinicians make the most adequate therapeutic decisions. Venous endoscopy is likely to become a major procedure in minimally invasive endoluminal therapy, with the continuing technological development of endoscopes and adequate instruments. Ultrasound is a complementary procedure and the ideal posttreatment method for evaluating the results of venous interventions.

References

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8. Ono T, Bergan JJ, Schmid-Schönbein GW, Takase S. Monocyte infiltration into venous valves. J Vasc Surg. 1998;27:158-166. 
9. Calota F. Venous hemodynamics. In: Calota F, ed. Phlebopathology [in Romanian]. Bucharest, Romania: Romanian Academy Edition; 2011:97-113. 
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Keywords: venous endoscopy; ultrasound; valvular segment