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10310 Ambulator y Phlebec tomy
Powered Phlebectomy
Powered phlebectomy allows the user to target the
vein using an irrigated illuminator, ablate the target
vein using a powered resector, and visually con fi rm
the vein’s removal. The use of powered phlebec-
tomy has steadily increased since its inception,
with an estimated 11,670 procedures performed in
2006 [ 21 ] . The proprietary name for the powered
phlebectomy device is the TriVex™ System
(Endoscopy Division, Smith & Nephew, Inc,
Mississauga, Ontario, Canada). The development
of this device began in 1966, when Greg Spitz, a
surgeon, took an arthroscopic shaver and applied it
for the removal of varicose veins. Through many
derivations, including transillumination and a deliv-
ery method for tumescent anesthesia, the present
system was complete. The system contains a
modi fi ed arthroscopic shaver and a transillumina-
tor coupled with an irrigator that can also deliver
tumescent anesthesia. The concept was developed
to decrease the time for ambulatory phlebectomy.
Table 10.1 Potential complications arising from ambu-
latory phlebectomy
Anesthetic
complications
Allergic reaction, e.g., to preservative,
lidocaine
Emotionally labile patient
Technique related, e.g., placement of
injection
Skin
complications
Blister
Dimpling
Hypo- or hyperpigmentation (incision)
Induration
Infection
Pigmentation, transitory or permanent
Complications
of compres-
sion bandage
Blisters
Contact dermatitis
Ischemia
Skin necrosis
Swelling
Vascular
complications
Bleeding, seroma
Deep venous thrombosis
Matting
Pulmonary embolism
Super fi cial thrombosis
Telangiectasias
Lymphatic
complications
Lymphocele
Lymphorrhea
Persistent edema
Neurological
complications
Dysesthesia (temporary or permanent)
Nerve damage- saphenous, sural,
peroneal, etc. nerves
Temporary hypoesthesia
Traumatic neuroma
This list is compiled from the experience of several physi-
cians: Jose Olivencia [
27 ] , Robert Muller [ 24 ] , Stefano
Ricci [
33 ] , Michael Ombrellino and Lowell Kabnick [ 13 ]
a
b
c
d
Fig. 10.11 ( a ) Transillumination of varicose veins. ( b )
Tumescence hydrodissects vein for easy removal. ( c ) Skin
over the varicosity is held taut using a sponge. ( d ) Suction/
morcellation of targeted vein
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104
L.S. Kabnick
Although there have been many modi fi cations, the
procedure still remains virtually the same. Varicose
clusters are transilluminated, anesthetized, morcel-
lated, and aspirated (Fig.
10.11a–d ).
Study Results
Studies of the TriVex
™
System describe several
modi fi cations of the procedure to improve patient
outcomes. Investigators have often compared
manual phlebectomy to powered phlebectomy.
Most authors indicate that the number of incisions
are less with TriVex
™
, and operating time is faster.
Ray-Chaudhuri et al. [ 32 ] compared postopera-
tive pain scores, with the results after 14 days
being 2.6 (manual) and 1.9 (TriVex
™
); a differ-
ence that was not statistically signi fi cant. Cosmetic
scores were also equal. In two randomized trials,
Aremu et al. [ 2 ] and Scavée et al. [ 34 ] demon-
strated no difference in patient cosmetic scores or
satisfaction. These conclusions were fi rst recog-
nized by Spitz and coworkers [ 37 ] in their original
reported fi ndings. At 52 weeks, in the TriVex
™
cohort, there was a higher number of recurrences
compared with the ambulatory phlebectomy
cohort of 21.2% and 6.2%, respectively [ 2 ] . In the
initial postoperative period of a 14 patient study
(by the author) comparing consecutive ambula-
tory phlebectomy and TriVex
™
, 100% of the
patients would prefer ambulatory phlebectomy
over TriVex
™
if repeating the procedure in the
future. The reasons listed for the preference for
manual ambulatory phlebectomy were the differ-
ence in early recovery, pain, anesthesia, and
amount of bruising.
In addition, Passman et al. [ 30 ] studied vein
stripping with concomitant ambulatory phlebec-
tomy compared to vein stripping with concomi-
tant powered phlebectomy and found that patients
undergoing powered phlebectomy experienced
more hematomas (5.6% v. 16.3%, respectively).
Although TriVex
™
has proven to be an effective
and fast procedure, the data suggests higher
recurrence and complication rates when com-
pared to ambulatory phlebectomy. Other limiting
factors are that the procedure requires general or
regional anesthesia and is not an of fi ce-based
procedure.
Conclusions
Ambulatory phlebectomy has now been
adopted by physicians as the standard proce-
dure for the removal of varicose veins. This
simple procedure has added a highly accept-
able cosmetic dimension to the medical indi-
cation. Using accepted technique—ambulatory
setting, local anesthesia, 2-mm incisions, hook
technique, and compression—patients will
experience minimal recovery time and few if
any complications (Fig. 10.12a, b ).
Fig. 10.12 Preop vv
https://t.me/med1917
10510 Ambulator y Phlebectomy
Clinical Guidelines
Ambulatory phlebectomy should be staged •
and treated after truncal re fl ux [
12 , 22 ]
Local or tumescent anesthesia should be used •
when performing ambulatory phlebectomy
[ 14 , 15 , 17 ]
Powered phlebectomy (TriVex •
™
) is effective
in treating varicose veins [ 2 , 34 , 37 ]
Phlebectomy is superior to sclerotherapy for •
varicose veins [ 6 ]
Preoperative mapping with transillumination •
in the recumbent position is more accurate
[ 40 ]
References
1. Adams F. The Genuine Works of Hippocrates 1849
Translated from the Greek with a preliminary dis-
course and annotations by Francis Adams. London:
The Sydenham Society; 1849. p. 808–9.
2. Aremu MA, Mahendran B, Butcher W, et al.
Prospective randomized controlled trial: conventional
versus powered phlebectomy. J Vasc Surg. 2004;39:
88–94.
3. Celsus AC. Medicinae Libri Octo, Patavii. Typis
Seminarii Apud Joannem Manfrè. Rome: Liber
Septimus; 1749. p. 473–4.
4. Cohn MS, Seiger E, Goldman S. Ambulatory phle-
bectomy using the tumescent technique for local anes-
thesia. Dermatol Surg. 1995;21:315–8.
5. Constancias-Dortu I. Indications for ambulatory
phlebectomy. Phlebologie. 1987;40:853–8 (In
French).
6. De Roos KP, Nieman FH, Neumann HA. Ambulatory
phlebectomy versus compression sclerotherapy: results
of a randomized controlled trial. Dermatol Surg. 2003;
29:221–6.
7. Dortu J, Raymond-Martimbeau P, editors. Ambulatory
phlebectomy. Houston: PRM Editions; 1993.
8. Gauthier Y, Derrien A, Gauthier O. Ambulatory phle-
bectomy. Ann Dermatol Venereol. 1986;113:601–3
(In French).
9. Gillet F. Die Ambulante Phlebectomie. Schweiz
Rundsch Med (Prax). 1980;69:1398–404.
10. Gordy T, et al. Current procedural terminology 2007.
Chicago: American Medical Association; 2006. 175p.
11. Homans J. The operative treatment of varicose veins
and ulcers, based upon a classi fi cation of these lesions.
Surg Gynecol Obstet. 1916;22:143–58.
12. Kabnick L. Should we consider a paradigm shift for
the treatment of GSV and branch varicosities? In: UIP
world congress phlebology chapter meeting, San
Diego; 2003 (abstract).
13. Kabnick LS, Ombrellino M. Ambulatory phlebec-
tomy. Semin Interv Radiol. 2005;22:218–24.
14. Klein JA. The tumescent technique for liposuction
surgery. Am J Cosmet Surg. 1987;4:263–7.
15. Klein JA. Tumescent technique for regional anes-
thesia permits lidocaine doses of 35 mg/kg for lipo-
suction. J Dermatol Surg Oncol. 1990;16:248–63.
16. Klein JA. Tumescent technique chronicles. Local
anesthesia, liposuction, and beyond. Dermatol Surg.
1995;21:449–57.
17. Klein JA. Tumescent technique for local anesthesia.
Epitomes. Dermatology. 1996;164:51.
18. Mayo CH. Treatment of varicose veins. Surg Gynecol
Obstet. 1906;2:385–8.
19. Mekako A, Hat fi eld J, Bryce M, et al. Combined
endovenous laser therapy and ambulatory phlebec-
tomy: re fi nement of a new technique. Eur J Vasc
Endovasc Surg. 2006;32:725–9.
20. Merriam-Webster’s Online Dictionary 2007.
www.m-
w.com/cgi-bin/dictionary?book=Dictionary&va=tum
escent
. Last accessed 23 Jan 2007.
21. Millennium Research Group. US markets for varicose
vein devices 2006. Toronto: Millennium Research
Group, Inc.; 2006.
22. Monahan DL. Can phlebectomy be deferred in the
treatment of varicose veins? J Vasc Surg. 2005;42:
1145–9.
23. Muller R. Treatment of varicose veins by ambulatory
phlebectomy. Phlebologie. 1966;19:277–9 (In
French).
24. Muller R. Ambulatory phlebectomy. Phlebologie.
1978;31:273–8 (In French).
25. Muller R. Clari fi cation on ambulatory phlebectomy
according to Muller. (A.P.M.). Phlebologie.
1996;49:335–44. In French.
26. Muller R. History of ambulatory phlebectomy. In:
Ricci S, Georgiev M, Goldman MP, editors.
Ambulatory phlebectomy. 2nd ed. Boca Raton: Taylor
Francis Group; 2005, xxxiii–xl.
27. Olivencia JA. Ambulatory phlebectomy of the foot.
Review of 75 patients. Dermatol Surg. 1997;23:279–80.
28. Olivencia JA. Complications of ambulatory phlebec-
tomy. Review of 1000 consecutive cases. Dermatol
Surg. 1997;23:51–4.
29. Olivencia JA. Ambulatory phlebectomy turned
2400 years old. Dermatol Surg. 2004;30:704–8.
30. Passman M, Dattilo J, Guzman R, et al. Combined
endovenous ablation and transilluminated power phle-
bectomy: is less invasive better? Vasc Endovascular
Surg. 2007;41:41–7.
31. Ramelet AA. Complications of ambulatory phlebec-
tomy. Dermatol Surg. 1997;23:947–54.
32. Ray-Chaudhuri SB, Huq Z, Souter RG, McWhinnie
D. A randomized controlled trial comparing transil-
luminated powered phlebectomy with hook avulsions:
an adjunct to day surgery? J One Day Surg. 2003;
13:24–7.
33. Ricci S. Ambulatory phlebectomy. Principles and
evolution of the method. Dermatol Surg.
1998;24:459–64.
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106
L.S. Kabnick
34. Scavée V, Lesceu O, Theys S, et al. Hook phlebec-
tomy versus transilluminated powered phlebectomy
for varicose vein surgery: early results. Eur J Vasc
Endovasc Surg. 2003;25:473–5.
35. Schmidt RM, Rosenkranz HS. Antimicrobial activity
of local anesthetics: lidocaine and procaine. J Infect
Dis. 1970;121:597–607.
36. Smith SR, Goldman MP. Tumescent anesthesia in
ambulatory phlebectomy. Dermatol Surg.
1998;24:453–6.
37. Spitz GA, Braxton JM, Bergan JJ. Outpatient varicose
vein surgery with transilluminated powered phlebec-
tomy. Vasc Surg. 2000;34:547–55.
38. Trauchessec J-M, Vergereau R. Outcomes after ambu-
latory phlebectomy. J Med Esthetics Chir Dermatol.
1987;14:337–43 (In French).
39. Weiss R, Feied C, Weiss M. Vein diagnosis and treat-
ment. New York: McGraw-Hill; 2001. 198p.
40. Weiss RA, Goldman MP. Transillumination mapping
prior to ambulatory phlebectomy. Dermatol Surg.
1998;24:447–50.
41. Weiss RA, Ramelet AA. Removal of blue periocular
lower eyelid veins by ambulatory phlebectomy.
Dermatol Surg. 2002;28:43–5.
42. Welch H. Endovenous ablation of the great saphenous
vein may avert phlebectomy for branch varicose veins.
J Vasc Surg. 2006;44:601–5.
https://t.me/med1917
107
N.S. Sadick et al. (eds.), Practical Approach to the Management and Treatment of Venous Disorders,
DOI 10.1007/978-1-4471-2891-5_11, © Springer-Verlag London 2013
1 1
Introduction
Perforating veins are valved venous conduits that,
with rare exception, direct blood to travel from
the super fi cial to the deep venous system. There
are 100–150 perforating veins in the lower
extremities. Direct perforators connect to the
deep axial veins and are more predictable in their
locations. Indirect perforating veins that connect
with intramuscular veins are more variable in
location.
Perforating veins that are associated with
pathology have been labeled with name tradition-
ally related to physicians involved in determining
their signi fi cance. However, as discussed in Chap. 2 ,
using the new nomenclature perforators are now
described by their location [ 1 ] . Re fl ux in several
of these perforating vein groups has been associ-
ated with the development of varicose veins with
other groups classically described as part of the
pathophysiology of medial calf and ankle skin
injury. Perforator re fl ux is thought to be particu-
larly important since these conduits conduct very
high intramuscular pressures directly to the
super fi cial veins. The intramuscular pressures are
substantially higher than the hydrostatic pressure
caused by a re fl uxing saphenous vein.
Re fl ux in perforating veins may be caused by
a primary defect in the perforating vein valves or
may be secondarily caused by (1) increased pres-
sure in the contiguous deep vein overwhelming
the ability of the valve to control fl ow (either
from severe deep vein re fl ux or upstream deep
vein obstruction) or (2) as a result of volume
overload leading to perforating vein dilation and
secondary incompetence by being a major re-
entry point of large volume super fi cial venous
re fl ux back to the deep system. This later, so
called overload induced re fl ux in re-entry perfo-
rating veins can then allow the higher deep vein
pressure to be propagated locally to the super fi cial
veins just like the other mechanisms of re fl ux.
Perforating Veins in Disease
Perforating Veins Causing Varicose
Veins
Incompetent perforating veins (IPV) causing var-
icose veins are easy to identify with DUS.
Although the criteria for signi fi cant re fl ux has
been determined to be outward fl ow lasting
between 0.3 and 0.5 s after compression of a
lower venous segment, generally the re fl ux asso-
ciated with IPV leading to varicose veins have
substantial duration. The re fl ux usually occurs
during calf muscle diastole (relaxation) but in
more severe cases may also occur during systole
Treatment of Incompetent
Perforating Veins
Steve Elias
S. Elias , M.D.
Dept of Surgery, Division of Vascular Surgery,
Columbia University ,
New York , NY , USA
NY Presbyterian – Columbia University Medical Center ,
New York , NY , USA
e-mail: veininnovations@aol.com
https://t.me/med1917
108
S. Elias
(contraction). With DUS tracing the re fl uxing
fl ow to the perforator is suf fi cient to make the
diagnosis. Usually the IPV will have an enlarged
diameter but with small varicosities the perfora-
tor may be quite small. Occasionally the IPV will
cause a trucnal vein to re fl ux below the point
where the perforator joins the truncal vein. This
is most commonly seen with the femoral canal
medial thigh perforating vein previous known as
a Hunterian IPV. Usually this IPV will cause
GSV re fl ux below the IPV for a variable length of
involvement.
Treatment of these IPV and related varicose
veins is governed by the vein size, location and to
what it is connected to as well as to the experi-
ence of the operator. Treatment of mid thigh IPV
and GSV re fl ux with associated varicose veins
often employs EVTA to ablate the GSV begin-
ning somewhat above its in fl ow into the GSV and
ablating the entire incompetent venous segment.
The varicose veins can then be treated with either
AP or liquid sclerotherapy.
Treatment of the relatively common lateral
thigh IPV and its associated varicose veins is
accomplished successfully and durably with AP.
Liquid sclerotherapy has been used but may be
anecdotally associated with a higher recurrence
rate. The use of US guided foam sclerotherapy
may improve the outcome over liquid sclerother-
apy but this is again anecdotal.
Posterior popliteal IPV are usually located in
the lateral popliteal fossa and are usually derived
directly from the popliteal vein although occa-
sionally they appear more like an incompetent
proximal branch off an incompetent SPJ. By
DUS these can be distinguished from incompe-
tent branches off sciatic nerve related varicies.
The popliteal fossa varicose veins can be effec-
tively treated with AP as long as care is taken to
avoid the common peroneal nerve which is
located more super fi cially along the lateral
popliteal fossa and then again super fi cial just
below the fi bular head. If the IPV can be avulsed
to the popliteal vein or close to it the incidence of
recurrence is low. Some operators will combine
AP with an injection of a small amount of foamed
sclerosant into the proximal end of the vein after
it is divided directing the injection toward the
source. Liquid sclerotherapy may be effective
with small IPV. However as the vein diameter
gets larger its success is less effective. Foam scle-
rotherapy may again be an alternative but its risk
and success rate are not quanti fi ed.
Perforating Veins Associated with
Ulceration
Propagation of high muscular compartment pres-
sures to the veins in the area of the medial calf
and ankle through local IPV is felt to have a large
role in initiating the pathophysiology ultimately
leading to venous ulceration. However, not all
incompetent perforating veins are pathologic [ 2 ] .
Not all incompetent perforator veins need
treatment.
Most incompetent pathologic perforator veins
need treatment. Some questions which will be
discussed in this section are:
1. What are the criteria for an incompetent perfo-
rating vein?
2. What are the criteria for a pathologic perforat-
ing vein?
3. When should a pathologic perforator vein be
treated (indications)?
4. What techniques are available for treating
pathologic perforating veins?
5. What are the results of current treatments?
6. Where in the algorithm of treatment for
advanced venous disease (C4–C5) does perfo-
rator treatment fall?
Incompetent Perforating Veins
(IPV) versus Pathologic Perforating
Veins (PPV)
Until recently the idea of a true distinction
between an incompetent, abnormally functioning
perforator vein and an incompetent, pathologic
perforator vein was not considered by many prac-
titioners. The accepted criteria for incompetence
have been elucidated by many [
3, 4 ] . In general,
a perforator vein with reversal of fl ow greater
than 0.5 s has been considered incompetent. At
times a size at the fascial level of 3.5 mm or
greater with reversal of fl ow has been an added
criteria [ 3 ] .
https://t.me/med1917
10911 Treatment of Incompetent Perforating Veins
Just because a perforator vein is incompetent,
it does not automatically qualify as a pathologic
perforator vein. This distinction is quite impor-
tant. One does not need to always treat an incom-
petent perforator but one should almost always
treat a pathologic perforator. By de fi nition a
pathologic perforator is adding to the patient’s
venous disease. As O’Donnell has stated, “An
enlarged IPV diameter at the fascial level greater
than 3.5 mm. as well as duplex evidence of high
volume and prolonged outward fl ow may indi-
cate an IPV with signi fi cant pathophysiology”
[
5 ] . The need to better de fi ne pathology has lead
to the American Venous Forum/Society for
Vascular Surgery consensus statement that the
de fi nition of a pathologic perforator is: (SE [ 34 ] )
1. A perforator equal to or greater than 3.5 mm.
at the fascial level
2. Re fl ux greater than 0.5 s
3. CEAP 5 or 6 patients
4. IPV under or in proximity to an ulcer or healed
ulcer
5. All four of the above criteria need to be pres-
ent to be a PPV
Whether this de fi nition is accepted by all prac-
titioners remains to be seen. For this section we
will accept this de fi nition. This author (SE) feels
that the great majority of pathologic perforators
warrant treatment as they are present in advanced
disease venous patients. At times, some incom-
petent perforators may also need treatment such
as those that are the source of painful
varicosities.
Indications for Treatment
As described above most pathologic perforator
veins are considered for treatment. These PPV’s
are present in the C5 and C6 patients. When con-
sidering treatment of PPV’s in C5 and C6 patients,
it is assumed that all other super fi cial axial re fl ux
has been treated and the possibility of proximal
deep venous obstruction has been evaluated [ 6 ]
and treated when appropriate [ 7 ] . The timing of
treatment (i.e. concomitant or staged) of PPV’s
will be discussed in the algorithm section.
There are certain clinical scenarios when IPVs
should be treated. Remember, an IPV in disease
states less than C5 should not be termed “patho-
logic” but merely “incompetent”. In this authors
practice large (>4.0 mm) IPVs that are the source
of symptomatic varicose veins or the source of
pain are treated as discussed above. Many times
large IPVs of the thigh are underlying cause of
recurrent varicose veins.
Treatment Choices
(i) The fi rst treatments for IPV in patients with
C5 and C6 CVD involved their open liga-
tion using a medial calf incision through
areas that often had signi fi cant lipoderma-
tosclerosis. This procedure known as the
Linton procedure and its modi fi cations of
open perforator ligation have a relatively
high incidence of wound complication
ranging from 20% to 40% and was associ-
ated with a high ulcer recurrence rate [ 8, 9 ] .
These procedures, which are no longer per-
formed, required general or regional anes-
thesia and involve an in-hospital stay of
3–5 days. Postoperative pain was signi fi cant
and required narcotics.
(ii) With the development of endoscopic tools,
the ligation of perforators with incisions in
healthy skin away from the lipodermato-
sclerosis encouraged a resurgence of inter-
est in IPV ligation to manage venous
ulceration. Subfascial endoscopic ligation
of perforating veins (SEPS) overcomes
some of the limitations of the Linton proce-
dure but has some of its own. Wound infec-
tion rates are dramatically lower; ranging
from 3% to 5% [ 10 ] . This is due to inci-
sions made remote from the affected skin at
the perimalleolar area [ 11 ] . The ability to
access and ligate perforators located close
to the malleolus can be limited by the angu-
lation of the working instruments involving
“sword fi ghting” in the subfascial space, a
large edematous extremity, and the inability
of the operator to open and explore the deep
posterior compartment. Attempts to impact
these shortcomings have been addressed in
the past, but some have not been commer-
cially available or adopted on a widespread
basis [ 12, 13 ] . Although SEPS is usually
performed on an outpatient basis, it still
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110
S. Elias
requires regional or general anesthesia and
can be associated with moderate pain and
nerve injury [ 14 ] . SEPS certainly is an
advance in perforator treatment compared
with open perforator ligation techniques
[
15, 16 ] . Yet despite the adoption and use of
SEPS since the mid-1990s, challenges have
been encountered. The learning curve of
SEPS may have hindered a more global
adaptation.
(iii) As mentioned, several minimally invasive
approached to management of IPVs have
been developed and have been described as
a group using the recently coined term per-
cutaneous ablation of perforators or PAPS
[ 17, 18 ] . All methods of PAPs have certain
commonalities: (1) ultrasound-guided per-
cutaneous intraluminal access; (2) applica-
tion of a drug or some energy source within
the lumen leading to vein wall contraction
and/or occlusion; (3) local anesthesia with
possibly some form of sedation (oral or
intravenous); (4) an outpatient of fi ce loca-
tion and no incisions; and (5) simple retreat-
ment, if needed.
Although the term PAPs may be relatively
new, the concept is not. As early as 1974, liquid
sclerosant has been used it close IPV with fairly
good clinical results [ 19– 21 ] . The indications for
PAPS are the same as other methods used to treat
pathologic perforators. However, three assump-
tions are made: (1) pathologic perforator incom-
petence is a signi fi cant source of venous
hypertension, (2) it is important to treat PPVs,
and (3) other methods of perforator treatment
have some limitations regarding technique.
Assumptions 1 and 2, although arguable, have
been supported by others [
22– 24 ] . Assumption 3,
the limitations of other techniques, is overcome
by the concept of PAPS. Of course, PAPS has its
own inherent issues and limitations, which are
discussed later.
PAPs is performed in an of fi ce or ambulatory
center setting with local and/or oral intravenous
sedation. Most PAPs procedures are done with
local anesthesia alone. This overcomes the neces-
sity for general or regional anesthesia.
Theoretically, a percutaneous approach should
decrease wound or infection complications to
near zero. Dissection of tissue is nonexistent,
thus not separating and stretching tissue (SEPS)
or cutting and undermining tissue (open ligation).
Postoperative pain is minimal and generally can
be managed with nonsteroidal anti-in fl ammatory
drugs or no pain medication whatsoever. If, in the
course of lifelong follow-up, patients develop
new or recurrent perforators, PAPs is easily
repeatable, with minimal morbidity. New or
recurrent perforator disease is a well-described
entity, and these patients may require multiple
interventions lifelong [
25, 26 ] . One of the main
technical issues of SEPS is access to distal (close
to malleolus) perforators. The location of perfo-
rators does not matter with PAPS; as long as a
perforator is visualized, it can be accessed and
ablated. Even inframalleolar perforators can be
treated. A fi nal theoretical advantage is better
physician and patient acceptance of this mini-
mally invasive procedure. However, no procedure
is without real or theoretical disadvantages.
Other theoretical disadvantages of PAPS
include skin injury, nerve injury, and deep vessel
injury, as well as recanalization and recurrence of
IPVs. This author’s experience and others have
shown that using current technology and current
technique, skin, nerve, and deep vessel injury
does not occur [ 27 ] . Yet this still remains a mini-
mal but real theoretical disadvantage until long-
term data become available. Of course, both open
ligation and SEPS procedures also have deep
vessel and nerve risk.
Lastly, PAPS may share a theoretical disadvan-
tage with SEPS—the learning curve. To access
the relatively small PPVs (4–6 mm on average),
one needs to be quite facile with ultrasound-
guided percutaneous access. PPVs, although two
to three times larger than competent perforating
veins, are still relatively small [ 3 ] . In summary,
we feel that most of the theoretical disadvan-
tages of PAPS can be overcome with experience:
nerve injury, deep vessel injury, skin injury, and
access failure.
The basic method, no matter what energy source
is used, involves (1) ultrasound-guided intralumi-
nal access; (2) instillation of some ablative source
(chemical or thermal); (3) con fi rmation of initial
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11111 Treatment of Incompetent Perforating Veins
treatment success; and (4) follow-up of treatment
success. Thus far, the energy used has been either
chemical; sodium tetradecyl sulfate [STS], aethox-
ysclerol, or sodium morrhuate [
21, 27 ] or thermal
(radiofrequency [RF] or laser) [ 28, 29 ] .
With sclerotherapy access can be made into the
varicose tributaries or directly into the IPV. Access
into the tributaries is usually easier and safer mini-
mizing inadvertent arterial infusion, either accom-
plished visually or with US guidance. Since the
devices are non- fl exible, the access for thermal
abaltion needs to be directly into the IPV. Ultrasound-
guided access can be made by needle, angiocath, or
specialized probe. The issue of con fi rmation of
access in the lumen of the IPV or thermal abaltion
can be addressed in various ways. Of course, ultra-
sound intraluminal visualization and aspiration of
blood are the sine qua non of access. The radiofre-
quency; stylet (RFS) catheter (VNUS Medical) also
has the ability to measure impedance in ohms. This
allows con fi rmation of the visual, intraluminal
placement. As of this writing, using laser or sclero-
sant only, visual and blood aspiration is the method
used to document intraluminal placement. This
author performs PAPS with RF, laser, or chemical
energy with equal access success.
When access with the thermal device is
attained, the tip of the device should be at or just
below the fascia to minimize deep vessel and
nerve injury (Fig.
11.1 ). This is analogous to
SEPS when clips are placed just below the fascia
level to minimize nerve and deep vessel injury
(Fig.
11.2 ). The patient is placed in a reverse
Trendelenberg position to fully dilate the vein for
access. For access, the RF catheter, a 16-gauge
angiocath (for a 600- m m laser fi ber), or a 21-gauge
micropuncture needle (for a 400- m m laser fi ber)
can be used. For chemical ablation, a 25- or
27-gauge needle is used.
After access is attained the energy or drug is
delivered (RF, Laser, or Chemical) to ablate the
PPV. The particulars of technique for each modal-
ity have been elucidated elsewhere and interested
readers are encouraged to review this paper [ 30 ] .
The full discussions of speci fi c techniques are
beyond the scope of this chapter [ 31 ] . Post PAPS
signi fi cant changes are seen by ultrasound
con fi rming successful PPV occlusion (Figs. 11.3 ,
11.4 , and 11.5 ) .
Results
Evaluating the clinical bene fi t of the different IPV
ablative techniques has been dif fi cult. For SEPS
the combined effects of truncal vein ablation
along with SEPS confound the outcomes data for
SEPS [ 32 , 34 ]. For the newer PAPS procedures
most of the data involves short-term follow-up of
Fig. 11.1 PAPS access at
fascial level
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112
S. Elias
patients evaluated primarily with surrogate end-
points such as occlusion rates of the IPV.
SEPS has proven to be a safe procedure
with a low wound complication and DVT
rate. Unfortunately despite evaluation in ran-
domized trials the bene fi ts of SEPS in accel-
erating ulcer healing and minimizing their
recurrences when compared to graduated
compression stockings (GCS) have not been
proven. As mentioned, treatment of GSV
re fl ux in these trials was performed in about
half of the patients and confounded interpre-
tation. This is important to consider as other
randomized data comparing GSV treatment
with follow-up GCS to GCS alone suggest
that GSV treatment led to a lowered ulcer
recurrence rate.
Sclerotherapy with liquid and foam have con-
sistently been shown to close IPVs in over 90%
of cases although their recanalization occurs in
up to one-third. The published and presented
data of thermal PAPS [
17 ] shows an 80–90%
average ef fi cacy rate at the 6 month to 1 year
level of follow up. Some centers have followed
patients longer with equal long term success
[ 31 ] . However many of the patients treated in
these studies had less signi fi cant disease (C2–C4)
Fig. 11.3 Post PAPS
changes at arrow (gray scale)
Fig. 11.2 Perforator clipped at fascial level post SEPS
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