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of varicose veins:from historical background to today’s evi-
https://t.me/med1917
dence, Acta Chir Belg . 2004. 104 :283–289, with permis- sion from  e Royal Belgian Society of Surgeons.
Section III is reprinted in part from Fischer R, Chandler JG, De Maeseneer MG, etal.  e unresolved problem of recurrent saphenofemoral re ux, J Am Coll Surg . 2002. 195 :80–94, with permission from  e American College of Surgeons.
R E F E R E N C E S
1. Fischer R , Chandler JG , De Maeseneer MG , etal.  e unresolved
problem of recurrent saphenofemoral re ux , J Am Coll Surg. 2002 .
195 : 80–94 .
2. De Maeseneer MGR .  e role of postoperative neovascularisa-
tion in recurrence of varicose veins:From historical background to
today’s evidence , Acta Chir Bel. 2004 . 104 : 283–289 .
3. von Langenbeck B . Beitrage zur chirurgischen Pathologie der Venen ,
Arch Klin Chir. 1861 . 1 : 47 . 4 . H o m a n s J .  e operative treatment of varicose veins and ulcers,
based upon a classi cation of these lesions , Surg Gynecol Obstet.
1916 . 22 : 143–158 .
5. Sheppard M . A procedure for the prevention of recurrent sapheno-
femoral incompetence, ANZ J Surg. 1978 . 48 : 322–326 .
6. Glass GM . Neovascularization in recurrence of the varicose
great saphenous vein following transection , Phlebology. 1987 .
2 : 81–91 .
7. Glass GM . Neovascularization in recurrence of varices of the great
saphenous vein in the groin:Surgical anatomy and morphology , Vasc
Surg. 1989 . 23 : 435–442 .
8. Jones L , Braithwaite BD , Selwyn D , Cooke S , Earnshaw JJ .
Neovascularisation is the principal cause of varicose vein recur-
rence:Results of a randomised trial of stripping the long saphenous
vein , Eur J Vasc Endovasc Surg. 1996 . 12 : 442–445.
9. De Maeseneer MG , Ongena KP , Van den Brande F , Van Schil PE ,
De Hert SG , Eyskens EJ . Duplex ultrasound assessment of neovas-
cularization a er sapheno-femoral or sapheno-popliteal junction
ligation , Phlebology. 1997 . 12 : 64–68 .
10. De Maeseneer MG , Tielliu IF , Van Schil PE , De Hert SG , Eyskens
EJ . Clinical relevance of neovascularisation on duplex ultrasound
in the long term follow up a er varicose vein operation , Phlebology.
1999 . 14 : 118–122 .
11. Nyamekye I , Shephard NA , Davies B , Heather BP , Earnshaw
JJ . Clinicopathological evidence that neovascularisation is a
cause of recurrent varicose veins , Eur J Vasc Endovasc Surg. 1998 .
15 : 412–415 .
12. van Rij AM , Jones GT , Hill GB , Jiang P . Neovascularization and
recurrent varicose veins:More histologic and ultrasound evidence ,
J Vasc Surg. 2004 . 40 : 296–302 .
13. Stücker M , Netz K , Breuckmann F , Altmeyer P , Mumme A . Histomorphologic classi cation of recurrent saphenofemoral re ux , J Vasc Surg. 2004 . 39 : 816–821 .
14. Hollingsworth SJ , Powell GL , Barker SGE , Cooper DG . Primary varicose veins: Altered transcription of VGFE and its receptors (KDR,  t-1, soluble  t-1) with sapheno-femoral junction incompe­tence ,
15. Lemasle P , Lefebvre-Vilardebo M , Uhl JF , Vin F , Baud J .
Eur J Vasc Endovasc Surg.
Postoperative recurrence of varices:What if inguinal neovascularisa­tion was nothing more than the development of a pre-existing net­work?, Phlebologie. 2009 . 62 : 42–48 .
16. Chandler JG , Pichot O , Sessa C , Schuller-Petrovic S , Osse FJ , B er g a n J J . D e ning the role of extended saphenofemoral junc­tion ligation: A prospective comparative study , J Vasc Surg. 2000 . 32 : 941–953 .
17. Pichot O , Kabnick LS , Creton D , Merchant RF , Schuller-Petrovic S , Chandler JG . Duplex ultrasound  ndings two years a er great saphenous vein radiofrequency endovenous obliteration , J Vasc Surg. 2004 . 39 : 189–195 .
18. Pittaluga P , Chastanet S , Guex JJ . Great saphenous vein stripping with preservation of sapheno-femoral con uence: Hemodynamic and clinical results , J Vasc Surg. 2008 . 47 : 1300–1305 .
19. De Maeseneer MG , Philipsen TE , Vandenbroeck CP , etal. Closure of the cribriform fascia:An e cient anatomical barrier against post­operative neovascularisation at the saphenofemoral junction? Apro­spective study , Eur J Vasc Endovasc Surg. 2007 . 34 : 361–366 .
20. De Maeseneer MG , Vandenbroeck CP , Van Schil PE . Silicone patch saphenoplasty to prevent repeat recurrence a er surgery to treat saphenofemoral incompetence:Long-term follow-up study , J Vasc Surg. 2004 . 40 : 98–105 .
21. van Rij AM , Jones GT , Hill BG , et al. Mechanical inhibition of angiogenesis at the saphenofemoral junction in the surgical treat­ment of varicose veins , Circulation. 2008 . 118 : 66–74 .
22. Heim D , Negri M , Schlegel U , De Maeseneer M . Resecting the great saphenous stump with endothelial inversion decreases neither neo­vascularisation nor thigh varicosity recurrence , J Vasc Surg. 2008 . 47 : 1028–1032 .
23. Merchant RF , Pichot O , Closure Study Group. Long-term outcomes of endovenous radiofrequency obliteration of saphenous re ux as a treatment for super cial venous insu ciency, J Vasc Surg. 2005 . 42 : 502–509 .
24. Ravi R , Traylor EA , Diethrich EB . Endovenous thermal ablation of super cial venous insu ciency of the lower extremity:Single center experience with 3000 limbs treated in a 7-year period , J Endovasc  er. 2009 . 16 : 500–505 .
25. De Maeseneer M , Pichot O , Cavezzi A , et al. Duplex ultrasound investigation of the veins of the lower limbs a er treatment for varicose veins:UIP consensus document , Eur J Vasc Endovasc Surg. 2011 . 42 : 89–102.
26. De Maeseneer MG , Vandenbroeck CP , Hendriks JM , Lauwers PR , Van Schil PE . Accuracy of duplex evaluation one year a er varicose vein surgery to predict recurrence at the sapheno-femoral junction a er  ve years , Eur J Vasc Endovasc Surg. 2005 . 29 : 308–312 .
2004 . 27 : 259–268 .
198 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
25.
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THE CHANGING IMPORTANCE OF THE
SAPHENOUSVEIN
TREATING VERSUS NONTREATMENT
Paul Pittaluga , S. Chastanet , and T.  Locret
INTRODUCTION
 e saphenous vein (SV) has been the main target for the treatment of varices for decades. Indeed, the traditional physiopathological concept of varicose disease relies on the descending theory of evolution of the super cial venous insu ciency (SVI) that describes a development starting from junctions between the deep venous system and saphe­nous axes, with the re ux spreading progressively along the SV to reach the collateral veins on which the varices develop.  us, for numerous decades, the so-called radical therapeutic principle of varicose disease has the goal of elim­inating saphenous axis re ux with surgical treatment com­bining crossectomy with stripping (CS).  e new thermal or chemical endovenous treatment techniques are based on the same physiopathological principle and have the same goal of eliminating SV re ux.
However, the analysis of the long-term results of tradi­tional surgery, the absence of crossectomy when carrying out endovenous treatments, the recent etiopathogenic stud­ies of SVI, and the clinical studies on the extension of the super cial venous re ux led to new physiopathological con­cepts of SVI that question traditional therapeutic designs focused on the treatment of the SV and the relevance of the treatment of the SV itself.
CRITICAL ANALYSIS
TRADITIONAL CONCEPT OF SVI
AND THERAPEUTIC DESIGNS
Described for the  rst time in 1890, the concept of SVI is based on the existence of points of re ux from the deep venous network toward the super cial venous network, the principal vector of this re ux being the SV starting from the
saphenofemoral junction (SFJ) according to the retrograde extension theory of the re ux.
 e saphenous re ux would progress by retrograde val­vular decompensation from the ostial valve (OV) to the malleolar region, furthered by orthostatism.  is venous hyperpressure progressing from the deep venous system toward the super cial system causes a dilation of the collat­erals of the re uxing SV, and in some cases the appearance of skin damages of chronic venous disease.
 is concept justi es the traditional surgical treatment by CS described at the start of the twentieth century. goal of the surgical treatment is rigorous elimination of all the re ux points, from the SFJ and all its a erents to the re uxing perforating veins (PV), by going through the resec­tion of the SV, of course.  is surgical treatment remained the gold standard for the choice of “radical” therapy of the SVI up to ourtime.
L O N G  T E R M R E S U L T S
OF THE TRADITIONAL
TREATMENTBYCS
As one of the main goals of the treatment of the SVI is to remove the varices, the presence of varices is an objective component for evaluation of the e cacy of this treatment. According to the authors, studies of results of more than 5years report an extremely variable level of clinical varicose recurrence (6 to 93%), and of the time, the technique of the procedure, the length of follow-up, and the method of con­trol (Table25.1).
Analysis of the literature regarding the principal factors for recurrence shows an evolution:the oldest studies men­tion surgical defects, anatomical error, and tactical error, while gradually junctional neovascularization appears as a new nosologic entity
9–12
1,2
3,4
 e
5–8
to become the most frequent factor
199
Table25.1 FREQUENCY OF RECURRENCE AFTER TRADITIONAL CROSSECTOMY AND STRIPPING
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OF THE SAPHENOUSVEIN
AUTHOR REFERENCE
NUMBER
Fischer R [9] 2001 125 34 y 48%
Van Rij AM [10] 2003 137 5 y 47.1%
Kostas T [11] 2004 113 5 y 25% Clinical
Winterborn RJ [12] 2004 133 11 y 62% Clinical
for recurrence in publications in the early 2000s.
YEAR OF PUBLICATION
N FOLLOWUP FREQUENCY OF
13–15
 is evolution could be attributed to the specialization in surgi­cal training, with the enlarged practice of crossectomy, per­fectly codi ed for vascular surgeons.  us, the number of residual junctions has decreased, being accompanied by an increase in the frequency of inguinal neovascularization as the principal source of postsurgical recurrence.
However, in spite of a standardization of the surgi­cal procedure, the frequency of postsurgical recurrences has not decreased, only its assumed origin has changed. Moreover, the proportion of surgical procedures carried out on recurring varices still represents approximately 20% of the volume of venous surgery in the literature with the pass
16–19
of time,
even in the early 2000s, with the initial strip-
ping including an enlarged crossectomy.
CONSERVATION OF THE
SFJ AFTER ENDOVENOUS
TREATMENT OR MINIMALLY
INVASIVE SURGERY
RECURRENCE
60%
93% 66%
MEAN OF ASSESSMENT
Clinical Ultrasound Duplex-scan
Clinical Ultrasound Duplex-scan Air plethysmograph
that it was acceptable to preserve a stump of approximately
22–24
2cm upstream of the OV.
 e study of the evolution of the untreated SFJ shows that it is the site of an anterograde  ux from the collaterals toward the deep vein in 88 to 95.7% with a follow-up vary-
25–30
ing from 1 to 5years.
 us, an e ective occlusion of the SV endovenously leads to the disappearance of the junction re ux in the great majority of cases (Table25.2).
 e results obtained a er RF or endovenous laser (EVL) treatment have led some authors to propose a mini-invasive surgical approach on the same principle, stripping without crossectomy (SWC), which associates the achievement of surgical stripping by invagination under tumescent local anesthesia, associated with the conservation of the SFJ by ligature of the great saphenous vein (GSV) at 2cm from its ostium. At minimum, the results of the SWC con rm those of the RF or the EVL with abolition of the re ux of the SFJ in more than 98% of the cases a er stripping of the GSV at
31
2years
and even at 5years. 32
 e physical principle of the endovenous techniques is the delivery of endovenous thermal energy, the purpose of which is to occlude the SV, ideally leading to the elimina­tion of the treated venous axis by resorption, thus realizing a real “ablation.”
20–21
So, in principle, the procedure is similar to that of sur­gical ablation by stripping, with the common purpose of eliminating the re uxing saphenous axis, based on the same 100-year-old descending theory of evolution of the SVI. Moreover, the  rst protocols of endovenous treatments o en combined crossectomy to treat the source of the re ux.
However, the search for less invasiveness, which was the main motivation of the endovenous principle, led to avoid­ing the inguinal incision in order to attempt an “endovenous crossectomy,” in particular with radiofrequency (RF) treat-
21
 e existence of a thromboembolic complication
ment. related to the risk of heating the femoral vein has encour­aged the practitioners of endovenous techniques not to treat the subostial portion of the SFJ. Most authors agreed
VARICOSE RECURRENCE AFTER
THERMAL ENDOVENOUS
TREATMENT
 e series a er endovenous treatment unreliably report the frequency of clinical varicose recurrence, in particular a er EVL treatment where this data is o en not mentioned, the principal result criterion being the closure of theSV.
On the other hand, the frequency of recurrences accord­ing to the PREVAIT de nition (presence of clinical varices on a lower limb [LL] that has already been treated, whatever
33
the mean of treatment)
is reported in the series with treat­ment by RF, with  gures that vary between 22 and 30% at 3 and 5years, while the persistence of saphenous re ux var-
27,28,30
ies between 12 and 15% for these same series,
meaning that the majority of clinical recurrences appear while the GSV is occluded and while it no longer presents re ux.
We had reported the same observation in a surgical
series in which out of 203 LL operated on for poststripping
200 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
Table25.2 ABSENCE OF REFLUX OF THE SFJ AFTER SAPHENOUS ABLATION BY RF
https://t.me/med1917
OR EVL TREATMENT ORBYSWC
AUTHOR REFERENCE
NUMBER
Pichot [26] 2004 104 2 y RF 95.2 %
Merchant [27] 2005 406 5 y RF 83.8 %
Nicolini [28] 2005 68 3 y RF 88 %
Min RJ [25] 2003 121 2 y EVL 93.4 %
Proebstle T [29] 2006 188 1 y EVL 95.7%
Casoni [32] 2008 62 5 y SWC 98.4%
Pittaluga [31] 2008 195 2 y SWC 98.2%
(From Reference32)
YEAR OF
PUBLICATION
recurrence, the source of re ux was a neojunction in less than 40% of the cases, while the great majority of clinical recurrences were independent of the saphenous axis that
34
had been stripped.
REVERSIBILITY OF THE
REFLUX OF THE GSV AFTER
PHLEBECTOMIES
N FOLLOWUP TECHNIQUE ABSENCE
•
Morphological studies:decrease in the elastin/collagen
50,51
ratio
•
Biochemical studies:decrease in proteolytic activity,
parietal hypoxia
or increase in the connective tissue in the media 52
53,54
REFLUX JSF
 us, Labropopulos et al. con rm that “the parietal
venous modi cations may appear in any venous segment,
55
whatever its localization and quality of its valves.”
Some authors have reported that simple phlebectomies could modify the hemodynamics and the diameter of the
35–41
saphenous vein.
We reported our experiment with this approach through the ASVAL method (ambulatory selective varices ablation under local anesthesia) with short-term abolition of the saphenous re ux in 70% of
42
the cases,
a result that remains stable with a frequency of
freedom from varicose recurrence of 91.5% and 88.5% at
43,44
3 and 4years respectively, frequency of freedom for recurrence a er surgical
equivalent to or less than the
45,46
or
endovenous ablation treatment of the GSV with the same
27,28,30
follow-up.
ETIOLOGY AND PATHOGENY OF
ESSENTIAL VARICES
 e descending theory relies on an insu ciency of the ter­minal valves of the SV or valves of femoral perforating veins as the origin of the insu ciency of the SV upstream of its
2,47
secondary dilation.
 is theory has been predominant for a long time, but it is currently questioned by partisans of the “parietal hypoth­esis” with well-supported arguments. Indeed, numerous publications bring to fore the importance of parietal modi­ cations in the etiology of the varices:
•
Functional studies:presence of venous dilations under
continent valves
48,49
TYPOLOGY AND EXTENSION
OF THE SUPERFICIAL
VENOUSREFLUX
Faced with re ux of the SV, it has been established that the ostial valve was o en continent.  e frequency of an iso­lated subostial or truncular re ux is estimated to be around
56,57
50% in the literature.
 e incontinence of the ostial valve is thus not necessary for the development of distal SVI. Moreover, it is thought that the SVI is associated with
57,58
a deep venous re ux in only 2 to 10% of cases.
More and more publications mention a progres-
sion of the super cial venous re ux from the suprafascial
55,56,58,59
veins.
Some authors also con rm that these observa-
tions contradict the assumption that the re ux is developed
60–62
from the saphenous junction retrogradely.
In a retrospective study based on 2,275 echo-Doppler mappings, we had noted that there was a positive correla­tion between the patient’s age, the clinical stage of the SVI, and the extent of the super cial venous re ux, and these observations speak in favor of an anterograde or multifocal development of the super cial venous insu ciency, prob-
63
ably from the suprafascial venous network
(Figure25.1).
In 2010, Labropoulos et al. provided additional evi­dence that the frequency of varicosities is lower in the saphenous trunk than in the tributaries or accessory veins.  ey also established a correlation between the CEAP clas­si cation and the extent of the re ux and the saphenous
64
trunk diameter.
THE CHANGING IMPORTANCE OF THE SAPHENOUS VEIN • 201
A
https://t.me/med1917
Age
63 yrs
55 yrs
50 yrs
43 yrs
Isolated VV Saph. reux +
junct. compet.
Saph. reux +
junct. incomp.
Whole saph.
reux
All dierences are signicant (p<0.05)
B
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
Figure25.1 Correlation of the venous re ux progression with age (A)and signs and symptoms (B)according to a retrospective study on 2,275 echo-Doppler mappings (From Reference63).
Isolated VV Saph. reux +
QUESTIONS ABOUT THE IMPORTANCE OFTHESV
Freq. of symptoms Freq. of C4–C6
61.1%
3.1%
junct. compet.
66.5%
7.6%
9.8%
Saph. reux +
junct. incomp.
•
How does one interpret the clinical observations that
87.3%
73.2%
16.6%
Whole saph.
reux
All dierences are signicant (p<0.05)
report the frequent existence of a suprafascial SVI in the absence of re ux of theGSV?
 e analysis of the above studies raises several questions:
•
Why does the frequency of varicose recurrences remain
as high in spite of carrying out a “radical” treatment with CS of the GSV that has been perfectly codi ed for several decades?
•
How does one explain the abolition of the re ux of the
SFJ in spite of the absence of crossectomy a er removal of the GSV by RF or EVL treatment or bySWC?
•
How can truncular re ux of the GSV be abolished a er
DESCENDING THEORY AND THE
It is not possible to answer these questions without ques­tioning in depth the principle of the descending theory starting from junctions and saphenous axes. Indeed, the tra­ditional descending theory does not enable any of the previ­ous questions to be answered.
QUESTIONING THE
TREATMENT OFTHESV
simple phlebectomies?
•
Why did more than half of the clinical recurrences
observed in the medium term a er treatment with RF appear while the GSV was occluded and no longer presented re ux?
•
What is the physiopathological incidence in studies
on the etiopathogeny of the essential varices that favor a parietal, not valvular, hypothesis of the origin of the disease?
 e initial notion of a surgical defect (absence of resection of the SFJ) as the predominant explanation for the recur­rence of the retrograde pathway occurring a er CS, has regressed because of the extensive practice of crossectomy.  e concept of inguinal neovascularization has become the predominant explanation of recurrence a er CS.  is
ON THE FREQUENCY OF
RECURRENCES AFTERCS
202 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
neovascularization may be considered as a healing of the
https://t.me/med1917
crossectomy zone, and some authors question its role as a
65
recurrence factor,
particularly as Perrin etal. 66 report that there is only a single “source” of re ux during a poststrip­ping recurrence in less than 10% of cases.  e ablation of the saphenous axis to treat the origin of the SVI, in keeping with the descending theory, thus has very serious limits.
hypothesis seriously contradicts the descending theory based on the successive rupture of the junctional or saphenous valves leading to “the  ooding” of suprafascial collaterals.
ON THE EXISTENCE OF PRIMITIVE
VARICES IN THE ABSENCE OF REFLUX
OF THE SFJ, EVEN OF THEGSV
ON THE REVERSIBILITY OF
AREFLUX OF THE SFJ AFTER RF OR
EVL TREATMENTORSWC
 e absence of treatment of an SFJ that presents an ostial re ux should logically lead to the persistence of the junction re ux or at the very least to its reappearance in the medium or long term in the logic of the descending theory. However, the studies of the results of RF treatment at 5years show that the absence of re ux at the level of the untreated SFJ is main-
27,30
tained when the GSV is occluded.
 e results reported
a er SWC are similar, with an absence of re ux at the level
31,32
of the SFJ in 98.2% at 2 years
and 98.4% at 5 years.  us, the treatment of ostial re ux, a key component of the descending theory for which the irreducible corollary is the enlarged crossectomy, is solidly brought back into question.
ON THE ABOLITION OF AREFLUX
OF THE GSV AFTER PHLEBECTOMIES
And yet, the descending theory of evolution following successive valvular lesions cannot explain this observed phenomenon, because a single functional valvular incom-
39–44
petence can explain a reversibility of the re ux.
ON THE PROBLEM OF CLINICAL
VARICOSE RECURRENCES AFTER
ENDOVENOUS TREATMENT
If the endovenous techniques have shown their e ectiveness for obliteration of the GSV and the elimination of the re ux of the SFJ, that has not resolved the frequency of clinical varicose recurrences that remain at about 30% at 5years,
45,46
close to the  gures obtained a er CS.
 erefore, the
27,30
elimination of the saphenous re ux endovenously or by stripping, even if it is a complete success, does not enable varicose recurrence to be avoided.
A certain number of clinical studies show that in the presence of varices not only is the SFJ competent in more than 50%
56,57
of cases or totally competent SV.
but what is more, there is frequently a partially
58,59,63
Moreover, the studies that are involved with progression of re ux certainly recognize the involvement of the SV in the development of the SVI but without assigning any responsibility to the SV forit.
58–64
NEW HEMODYNAMIC CONCEPT
CALLING INTO QUESTION THE
IMPORTANCE OFTHESV
 is in-depth questioning of the descending theory leads to a very di erent hypothesis:that of ascending theory of evolution of the SVI from the suprafascial venous network, ascendingly or multifocally toward the SV.  e extension of the SVI on the super cial venous network is done centrip­etally:the evolution begins on the suprafascial tributaries at the bottom, where the hydrostatic pressure is higher, caus­ing the dilatation of the vein wall.  is evolution initially remains within the suprafascial plane, creating a dilated and re uxing venous network and progressing following the decreasing hydrostatic pressure gradient. In addition, this re uxing network, when becomes su ciently important, creates a “varicose reservoir” (VR) with a  lling e ect in the intrafascial saphenous axis, causing functional incom­petence of the saphenous valves, then a dilatation of the SV, evolving anterogradely up to the SFJ also following the
61,62
decreasing hydrostatic pressure gradient.
 e concept of the ascending theory makes it possible
to outline answers to the questions mentioned previously:
ON THE FREQUENCY OF
RECURRENCES AFTERCS
O N T H E P R O G R E S S I V E
ABANDONMENT OF THE VALVULAR
HYPOTHESIS TO THE BENEFIT OF
THE PARIETAL HYPOTHESIS
 e descending theory is based on an insu ciency of the terminal valves of the SV or valves of the femoral perforat­ing veins as being at the origin of the insu ciency of the SV by retrograde pathway.  is theory is currently ques­tioned by numerous studies parietal modi cations prior to valvular lesions.  e parietal
Treatment as speci c as CS cannot eradicate varicose recur­rence, which would be more or less irreducible because of the natural evolution of the disease starting from the col­lateral veins themselves.
ON THE REVERSIBILITY OF
AREFLUX OF THE SFJ AFTER RF OR
EVL TREATMENT ORBYSWC
48–54
that show the existence of
Since re ux of the SFJ is a consequence of the re ux upstream, it can be understood that abolition of the re ux of the GSV
THE CHANGING IMPORTANCE OF THE SAPHENOUS VEIN • 203
by RF or EVL treatment or by SWC could restore an antero-
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grade  ow with it by virtue of the anastomosis of the collat­erals of the SFJ that have an anterograde  ow.  e enlarged crossectomy, removing an important physiological drainage pathway of the inguinal region could even be deleterious, as the very low rate of neovascularization appears to demon-
26–28, 31
strate a er preservation of the SFJ (0 to 1.7%) trast to the surgical series with crossectomy (20 to 52%).
ON THE ABOLITION OF A
REFLUX OF THE GSV AFTER
PHLEBECTOMIES
in con-
46,65
According to the ascending theory, the ablation of the VR may lead to abolition of the saphenous re ux with the elimination of the  lling e ect and the disappearance of the functional incompetence of the saphenous valves.
39–44
Furthermore, Lurie suggested the possibility of functional insu ciency of the saphenous valves in the absence of any anatomical lesions.  e closing of the valves would be caused by the existing pressure in the valvular sinus, which pressure would increase in direct proportion to the velocity of the anterograde  ow. If this velocity fails to reach a criti­cal value that allows pressure to reach a level su cient to
67
close the valve, the valve will not close.
 is is why a re ux may be present that passes through healthy valves when a patient is in the decubitus position, because the velocity of the anterograde  ow is slight. Because ablation of the VR makes it possible to improve the saphenous hemodynamics, it may also make it possible to eliminate a functional valvu­lar insu ciency by increasing the anterograde velocity.
according to a personal evolution factor.  us, the endove­nous treatments or the mini-invasive surgery can decrease the aggressiveness of the initial treatment compared with the CS, but its prognosis would not be changed in the medium or long term, with an irreducible rate of clinical recurrences (Table25.3).
O N T H E P R O G R E S S I V E
ABANDONMENT OF THE VALVULAR
HYPOTHESIS TO THE BENEFIT OF
THE PARIETAL HYPOTHESIS
 e parietal etiopathogenic hypothesis of the origin of the SVI gets its clinical illustration with the development of the disease starting from suprafascial veins, the wall of which is most fragile, causing an initial extension within this supra­fascial network.
ON THE EXISTENCE OF PRIMITIVE
VARICES IN THE ABSENCE OF
REFLUX OF THE SFJ, EVEN THEGSV
 e GSV is the super cial vein, the wall of which is thickest and most muscular, protected moreover by the doubling of
63,64
the subcutaneous fascia in which it  ows.
 us, it could logically be the last to be decompensated, which makes it possible to explain the presence of a suprafascial SVI with an absent or partial re ux in theGSV.
PERSPECTIVES
ON THE PROBLEM OF CLINICAL
VARICOSE RECURRENCES AFTER
ENDOVENOUS TREATMENT
In spite of the abolition of the re ux of the GSV, the natural evolution of the SVI is not a ected in the medium or long term, and the varices appear again more or less obviously
Table25.3 FREQUENCY OF VARICES RECURRENCES PREVAIT REFERENCE34 AFTER CS, ENDOVENOUS ABLATION BY RF, SWC, ANDASVAL
AUTHOR
REFERENCE
NUMBER
Van Rij AM [10] 2003 5 y CS 47.1 %
Kostas T [11] 2004 5 y CS 25 %
Merchant [27] 2005 5 y RF 27.4 %
Nicolini [28] 2005 3 y RF 22.8 %
Pittaluga [31] 2003 2 y SWC 6.7 %
Casoni [32] 2008 5 y SWC 11.1 %
Pittaluga [43] 2006 4 y ASVAL 11.5 %
(From Reference 32)
YEAR OF PUBLICATION
FOLLOWUP TECHNIQUE REVAS
N E W T H E R A P I E S
 e ascending theory validates the new therapeutic approaches:
•
 e RF or EVL treatment with conservation of the SFJ,
which is no longer considered to be the origin of the
204 • PRIMARY SUPERFICIAL VENOUS INSUFFICIENCY
SVI, and which even becomes a useful functional entity
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for venous drainage of the inguinal region.
•
Foam echosclerotherapy, which makes it possible to have
great  exibility in treatment adaptation according to the evolutive stage of the patient since it will be capable of treating the GSV but also theVR.
•
Mini-invasive surgery, whether it is ablative (SWC)
for the same reasons as RF or EVL treatment, or conservative (ASVAL) since it limits the treatment to the VR, starting point of the SVI according to the ascending theory.
NEW STRATEGIES FOR TREATMENT
However, apart from the ASVAL, all the new SVI treat­ments up to now, whether they are surgical, thermal, or chemical, have the goal of obliterating the re uxing SV, which is the principal, and sometimes only, criterion for evaluation of the result of these techniques in the literature.
 e traditional descending theory bases its entire thera­peutic position on the presence of a saphenous re ux with its elimination as a goal, without real analysis of the subtle­ties of this re ux (re ux of the junction, extent of the re ux, hemodynamic pro le) or analysis of the relationship of this re ux to the patient’s complaint.  us, the result is assessed on the quality of the elimination of the saphenous re ux. It is paradoxical to observe that one could consider that treatment by stripping, RF, or EVL is a success because the saphenous re ux no longer exists, while varices or symp­toms are present.
If we accept the ascending theory as an explanation of the SVI in the majority of cases, the treatment of the SV can no longer be considered to be the goal with priority or even the only goal of the therapy. It is the treatment of the VR
43,68
that becomes the treatment goal with priority.
In addition, the ascending theory leads to the ques­tion of treatment of varices preserving the SV in earlier stages, especially for young patients, which might avoid or slow down the progression to the higher stages of disease,
64
toward skin damage.
Obviously the answer to this ques-
tion requires longitudinal cohort studies.
Much work remains to be done, because if the VR is an essential component for the treatment and prognosis of the SVI, it is indispensible to integrate it as an assessment crite­rion in all studies of treatment of the SVI. However, there are no reliable means currently for assessing theVR.
C O N C L U S I O N
 e traditional descending physiopathological description can no longer be considered to be the only explanation of the SVI. More and more it appears that the evolution of the SVI develops from the distal network ascendingly or
multifocally toward the saphenous axes.  us, the system­atic treatments of ablation of the saphenous vein or crossec­tomy are widely questioned. Treatment should be focused on the VR and personalized according to the hemodynamic and clinical checkup, but also according to the wish of the patient.  e scienti c studies necessary to validate the dif­ferent therapeutic choices are indispensible with a long-term follow-up.
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