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With growing popularity of sclerotherapy di erent tech-
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9
niques have been developed.
Results, however, were o en
unsatisfactory. In 1981 Cockett summarized main causes of
failure in perforator injection as (1) inability to accurately
locate the perforator, (2)potential damage by extravascular
injection of sclerosant, (3)potential damage to posterior tibial
artery, and (4)potential damage to deep veins causingDVT.
10
Advances in ultrasound imaging in the 1980s and 1990s
provided the technical basis for ultrasound-guided procedures. At the same time, reliable identi cation of perforating
veins not only became possible but also was integrated into
11
standard diagnostic protocols.
Together with new sclerosing agents, which can be e ectively used in signi cantly lower
concentrations with less damage to extravascular tissues,
these advances helped to overcome the de ciencies of conventional sclerotherapy of perforating veins. By the late 1990s
ultrasound-guided sclerotherapy (USGS) became popular in
European countries and made its way to the United States.
12–15
Figure54.1 Perforating vessels. e perforating artery (Perf A) is located
next to the perforating vein (Perf V) at the fascial opening.
BASIC CONSIDERATIONS
To perform echosclerotherapy of lower extremity perforating veins, a thorough knowledge of their anatomy and
physiopathology is necessary. Perforator veins connect the
super cial to the deep venous system and to the venous
sinuses within the leg muscles. ese veins usually contain a
series of bicuspid valves, located in their subfascial segment,
which prevent transmission of high pressure from the deep
venous system into the super cial veins. e distribution of
medial perforating veins connecting the super cial and deep
systems in the calf and thigh is relatively constant. However,
the number and anatomy of the numerous perforators to
the muscular venous sinuses is unpredictable. Perforating
veins are accompanied by perforating arteries supplying
the skin and, sometimes, by cutaneous nerve branches and
lymphatic vessels. Perforating arteries are usually smaller in
diameter and located superior to the accompanied vein.
16
e presence of these arteries can o en be con rmed by
17
duplex scan
(see Figure54.1).
e coexistence of perforating veins and arteries in the
lower extremities was described rst by Robert Linton, who
established that “communicating” pedicles have venous
and arterial components. He also described how these vessels run along the intermuscular fascial planes and noted
that “the arteries are so small that it is not necessary to
preserve them.” Identi cation of the perforating arteries, although not always possible, becomes desirable when
ultrasound-guided sclerotherapy of perforating veins is performed. Accidental injection of sclerosing agent into the
arterial bed may possibly cause complications such as skin
necrosis, and can be prevented by visual control, or by performing injections at a distance from the fascial opening
where the perforating artery and vein are not in such close
proximity to each other. e role of perforator arteries in
pathogenesis of venous ulcers and sanogenesis a er treatment is yet to be studied. As they provide blood supply to
skin areas a ected by venous disease, preservation of these
vascular structures during treatment may be desirable. Our
observations indicate that blood ow in perforating arteries
17
increases a er USGS.
If this hyperemia can be shown to be
bene cial in ulcer healing, selective oblation of perforator
veins by USGS could be more desirable than surgical interruption when both veins and arteries are interrupted. e
same logic may be applied to perforating cutaneous nerves.
Perforator vein incompetence usually is associated with
deep and/or super cial venous incompetence, but, if le
untreated, can persist a er successful treatment of saphenous
re ux. Strong association of perforator incompetence with
skin changes and ulceration has been well established, however,
incompetent perforators are o en present in less advanced
stages of the disease, when their role in disease progression
and/or recurrence of varicose veins is less obvious. Following
the cases of persistent perforator veins a er correction of
other sources of re ux at Straub Clinic revealed association
of patients’ symptoms with isolated incompetent perforators,
and relief of these symptoms a er successful USGS. ese
ndings and variations in anatomy support identi cation of
not only perforator veins in areas of skin changes but also all
those potentially clinically important as a treatment target.
Incompetent perforating veins 4 to 7mm in diameter
can be treated with this technique. Smaller veins seldom are
incompetent, and larger veins require larger volumes of sclerosant, which potentially increases the risk of complications.
CLINICAL CONSIDERATIONS
Indications for USGS are not di erent from indications to
surgical interruption of perforating veins. Cases of symptomatic chronic venous disease from C2 to C6 clinical class
458 • CHRONIC VENOUS INSUFFICIENCY
(CEAP) that have demonstrable incompetent perforating
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veins at duplex ultrasound constitute the majority of indications. In primary disease, USGS can be performed at the
time of initial treatment of saphenous re ux, or as a separate stage. In secondary (postthrombotic) disease, careful
consideration should be given to the pathophysiologic role
of incompetent perforators in each individual extremity.
Incompetent perforators can constitute a major out ow
track around an obstructed segment in some cases and be a
contributor to skin ulceration in others.
USGS does not require anesthesia and can be performed
in the o ce as well as in the operatingroom.
Patients with known allergic reactions to sclerotherapy
agents, or who are pregnant or lactating should be excluded.
e presence of severe arterial occlusive disease or active
vasculitis is also a contraindication as inadvertent intraarterial injection potentially can result in limbloss.
SCLEROSINGAGENTS
Sodium tetradecyl sulfate (Sotradecol) and sodium morrhuate are the agents frequently used for therapy of incompetent perforating veins. Polidocanol (Aethoxysklerol)
is another valid drug for this purpose still awaiting FDA
approval in the United States.
e mechanism of action of all these drugs is based on
their detergent properties. Immediately a er injection the
endothelial cells in contact with the drug undergo swelling
and disruption. is irreversible trauma causes localized
thrombosis, vasospasm, and then vein brosis and reabsorption. Larger veins should be treated with increased concentrations rather than larger volumes, since the latter may
cause escape of the drug into the deep veins and potentially
into the systemic venous circulation.
Recent development of foam sclerotherapy opens new
opportunities for treatment of perforating veins. In addition to di erent sclerosing agents and their concentrations, the use of foam introduces variability in type of gas,
gas-to-liquid ratio, time between processing and use, size
of the bubbles, and methods of preparation. is variability complicates analysis of results and development of
guidelines. Until the standardization of sclerosing foams is
developed, foam sclerotherapy continues to be based on the
experience and preferences of a treating physician.
PREOPERATIVEDUPLEX
Duplex ultrasound scan plays the most important role in
evaluation of the patient before USGS. Complete examination of deep and super cial venous systems including
testing for obstruction and valvular incompetence is necessary in every case. Perforating veins should be identi ed by
scanning all aspects of the calf and by following the course
of the great saphenous vein (GSV), the vein of Giacomini,
or any incompetent nonsaphenous vein of the thigh. It is
preferable to examine patients in a standing position, as
the increased hydrostatic pressure makes perforating veins
easier to visualize and evaluate. Incompetence of a perforating vein can be determined by registering of reversed ow
(directed to the super cial veins) longer than 0.4 seconds,
or by the size of the vein at the fascial opening exceeding
11,18
3.5mm, or by the presence of both criteria.
In addition to identi cation of incompetent perfora-
tor veins, ultrasound provides information on which veins
are connected by these perforators, and thus allocates each
perforator to a de ned place in the hemodynamic map of
the venous system of the a ected extremity. At the time
of duplex scan, incompetent perforating veins located in
the areas of skin changes and ulcers, those connected with
corona phlebectatica, or clusters of varicose veins, and those
associated with symptoms should be separated from perforators found in asymptomatic limbs, and from those with a
questionable hemodynamic role in the disease process. is
information is crucial for development of a surgical plan
and for a decision on how to treat each of the incompetent
perforators.
TECHNIQUE
e procedure can be performed under general or local
anesthesia during saphenous and varicose vein ablation, or
as an isolated procedure in the outpatient clinic setting.
When performed as a stand- alone procedure, no sedation
or local anesthesia is required.
e procedure room is warmed to a comfortable tem-
perature in order to avoid venous constriction, and the
patient is positioned in the supine or prone position,
depending on the location of veins to be treated. e skin
is prepped with iodine solution, and a sterile latex cover is
applied to the ultrasound probe. is must be oriented longitudinally, and a er the target vein is identi ed, a 25-gauge
needle connected to a 3-cc syringe is inserted into the skin
close to the ultrasound transducer. e needle tip has to
be oriented toward the perforating vein, along the sagittal
plane of the probe. e target for the injection is the segment of perforating vein above the fascia (see Figure54.2A).
Asmall amount of venous blood is withdrawn in the syringe
to con rm the correct position of the needle, and 1 to 2 cc
of 1% sodium tetradecyl sulfate, or 5% sodium morrhuate
is injected under duplex vision. e sclerosing agent can be
easily seen by B-mode ultrasound imaging, thus monitoring
each injection with ultrasound provides vital information
regarding the precision of injection and volume of sclerosant needed to be injected to close the perforator, but not
to cause damage of deep veins. Pain during injection, among
other causes, can indicate that a perforating artery has been
punctured, and therefore injection should be stopped to
avoid serious complications.
USGS OF PERFORATING VEINS IN CHRONIC INSUFFICIENCY • 459
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Figure54.2 Ultrasound-guided sclerotherapy of the perforating vein. (A) e needle is placed in a vein above the fascia (F). (B)A er an injection the
perforating vein (PV) is lled with an echogenic material and has no ow.
e needle is withdrawn and compression applied for
a few minutes. e vein is reimaged, and sclerotherapy is
considered successful if no residual ow is observed in the
treated perforator (see Figure54.2A).
Larger veins can be treated by foam sclerotherapy. With
this technique conventional sclerosing agent and air are
mixed in order to form ne bubbles. e principle behind
this method is that by displacing blood from the treated
vein and increasing the contact time between the sclerosant
and the vein more e ective treatment can be achieved.
P O S T O P E R A T I V E C A R E
External compression is important for e ective sclerotherapy. Even a er a successful injection, inadequate compression of the treated area may allow blood ow through
a damaged, thrombogenic endothelium, and so thrombophlebitis may develop at that site. Furthermore, adequate
compression may improve the calf muscle pump, thus
preventing propagation of thrombus into the deep veins.
Recurrences may be due to inadequate initial or subsequent
continuous compression until a brous occlusion occurs.
Elastic bandages are applied to the extremity and maintained for 1 to 2 weeks and replaced by classII-III knee-high
compression stockings therea er. Patients with heavy elastic
bandages should be warned to remove them should pain
occur, before ischemia has caused any damage. Patients are
encouraged to ambulate in order to prevent venous stasis
that may lead to deep venous thrombosis.
R E S U L T S
Although available reports on results of USGS consistently
demonstrate bene ts of this treatment modality, their conclusions should be taken with caution.
12–13,15,19–22
Important di erences between USGS and surgical interruption of perforating veins should be considered when
clinical results of perforating vein treatment are analyzed.
e true minimally invasive nature of USGS translates
into minimal impact on patients’ immediate posttreatment
activity and quality of life. Early unrestricted ambulation
can be a contributing factor for the treatment outcome.
Any surgical procedure, including SEPS, results in
in ammation followed by scar formation in the area of
the treated perforator. e impact of these processes on
an extremity with CVI has not been de ned, but presents
theoretical possibilities either for prevention of development
or recurrent perforators. On the one hand, postoperative
scars may act as a mechanical barrier against reconnection
of the deep and super cial systems, but on the other hand,
postoperative in ammation might promote neovascularization, thus recurrence of perforators. In the case of USGS, the
vein remains in place, therefore its recanalization is possible.
Availability of information on objective documentation of
immediate treatment success, and di erentiation between
reopening of treated perforator and development of new vessels can signi cantly impact interpretation of publisheddata.
Utilization of di erent sclerosing agents in a variety of
concentrations with di erences in e ects on the vein and
surrounding tissue contributes to the complexity of interpretation of reported results.
Waiting for a higher level of evidence on USGS success,
and for more precise de nitions of outcome measures, one
can rely only on clinical experience of groups and individuals
performing a high volume of these procedures. e Straub
clinic group performed over 3,000 injections of incom-
15,19–21
petent perforators in the early 2000s.
Immediate
successful obliteration of the treated veins at the time of
injection was obtained in 98% of cases. Skin complications with super cial skin necrosis occurred in six patients.
Recurrence, de ned as the presence of ow in a previously
sclerosed perforating vein at duplex follow-up, was present
in 23% of cases with a mean follow-up of 17months. Venous
clinical severity scores decreased on average from 11.95 pretreatment to 6.5 posttreatment (p < 0.05). Likewise, venous
disability scores dropped from 1.86 pretreatment to 0.81
posttreatment (p < 0.05). Perforator recurrence was more
common in limbs with ulcerations. Except for the rare
460 • CHRONIC VENOUS INSUFFICIENCY
occurrence of skin necrosis, cosmetic results were excellent,
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o en with partial reversal of preexisting skin changes, and
relief of symptoms.
C O M P L I C A T I O N S
Sclerotherapy of perforating veins is associated with minimal
discomfort and pain and thus does not require local or general anesthesia. Occurrence of immediate or delayed pain at
the site of injection or in a larger calf region should alert the
operator against extravascular injection in the so tissue or
in a nearby artery. Intraarterial injection is extremely painful,
whereas extravasation in the subcutaneous tissue may remain
asymptomatic, unless the sclerosant solution had been mixed
with normal saline, or a high concentration of sclerosant
had been used. As a result of extravasation, super cial skin
necrosis may occur. In our experience super cial skin necrosis occurred in less than 2% of patients, and usually resolved
with minimal sequelae in a matter of weeks. Amore serious
complication is intraarterial injection, as this produces a diffuse endotheliitis blocking the arterioles, which may lead
to tissue ischemia and gangrene. Should this complication
occur, injection of procaine around the injected artery, local
cooling, systemic heparinization, and infusion with low
molecular weight dextran are recommended.
As discussed previously, a potential complication of inadequate compression is thrombophlebitis, because residual
ow within a damaged vein predisposes to thrombosis of the
vein and eventual recanalization. DVT, also rare, is probably
due to injection of large volumes of sclerosant. Again, if sclerosing agents are injected in small amounts, only the intima,
not the blood, should be a ected. ese agents are inactivated rapidly by the blood and are, paradoxically, hemolytic
and not thrombotic. Another important point to stress is
that patients must be encouraged to walk immediately a er
treatment and must continue this every day to prevent stagnant blood from collecting in the damagedveins.
It would be prudent to avoid injecting limbs of patients
with known congenital or acquired prothrombotic state
(bedridden, neoplastic, early postthrombosis).
Another possible, although rare, serious complication is
anaphylactic shock. While performing injection sclerotherapy, all the necessary equipment to handle this situation must
be readily available (oxygen, epinephrine, and steroids) as
this could be a life-threatening event. We have not observed
this complication during perforating vein sclerotherapy.
C O N C L U S I O N
Ultrasound-guided sclerotherapy is a minimally invasive,
alternative technique for the treatment of incompetent
calf perforating veins. If a rigorous technique and careful
precautions are undertaken, minimal complication rates
and satisfactory clinical results can be achieved. A er
sclerotherapy, patients can resume their routine activities
and return to work, and this is without doubt one of the
most appealing aspects of this method. We believe that the
adoption of this technique in experienced hands potentially could represent the standard method of treating
incompetent perforators, as it is associated with minimal
discomfort for the patient, acceptable recurrence rates,
and is easily repeatable. ese results are encouraging, but
future research should de ne precise indications, optimal
techniques, and measures for clinical and hemodynamic
success for this procedure.
R E F E R E N C E S
1. Caggiati E , Mendoza M . e discovery of perforating veins , Ann
Vasc Surg . 2004 . 18 ( 4 ): 502–503 .
2 . H om 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 .
3. Hauer G , Barkun J , Wisser I , Deiler S . Endoscopic subfascial discission of perforating veins , Surg Endosc . 1988 . 2 ( 1 ): 5–12 .
4. Gloviczki P , Cambria RA , Rhee RY , Canton LG , McKusick MA .
Surgical technique and preliminary results of endoscopic subfascial
division of perforating veins, J Vasc Surg . 1996 . 23 ( 3 ): 517–523 .
5. Rhodes JM , Gloviczki P , Canton LG , Rooke T , Lewis BD , Lindsey
JR . Factors a ecting clinical outcome following endoscopic perforator vein ablation, Am J Surg . 1998 . 176 ( 2 ): 162–167 .
6. Gloviczki P , Bergan JJ , Rhodes JM , Canton LG , Harmsen S , Ilstrup
DM . Midterm results of endoscopic perforator vein interruption
for chronic venous Insu ciency:Lessons learned from the North
American subfascial endoscopic perforator surgery registry: e
North American Study Group , J Vasc Surg . 1999 . 29 ( 3 ): 489–502 .
7. Fegan WG . Continuous compression technique for injecting veins ,
Lancet . 1963 . 2 : 109–112 .
8 . F eg a n WG . e treatment of varicose veins by injection sclerother-
apy , Edizioni Minerva Medica . 1979 .
9. Goor W . Sclerotherapy of incompetent perforating veins. In: May
R , Partsch H , Staubesand J , eds. Perforating veins . Munich,
Germany:Urban & Schwarzenberg.1981 .
10. Cockett F . Techniques of operations on perforating veins. In: May
R , Partsch H , Staubesand J , eds. Perforating veins . Munich,
Germany:Urban & Schwarzenberg.1981.
11. Labropoulos N , Tiongson J , Pryor L , et al. De nition of venous
re ux in lower extremity veins , J Vasc Surg . 2003 . 38 ( 4 ): 793–798 .
12. Guex JJ . Ultrasound guided sclerotherapy (USGS) for perforating
veins (PV), Hawaii Med J . 2000 . 59 : 261–262 .
13. ibault PK , Lewis WA . Recurrent varicose veins:Part2:Injection
of incompetent perforating veins using ultrasound guidance , J Derm
Surg Onc. 1992 . 18 : 895–900 .
14. Schadeck M . Sclerotherapie des perforantes jambieres , Phlebologie .
1997 . 50 ( 4 ): 683–688 .
15. Puggioni A , Lurie F , Masuda E , Eklof B , Kistner R . Ultrasound-guided
sclerotherapy of incompetent perforators: Technique and duplex
follow-up. Paci c Vascular Symposium on Venous Disease, Kona,
Hawaii, November, 2002 .
16. Ghali S , Bowman N , Khan U . e distal medial perforators of
the lower leg and their accompanying veins , Br J Plast Surg . 2005 .
58 (8):1086–1089.
17. Lurie F , Kessler D , Puggioni A , Masuda E . Blood ow in perforating arteries can change a er oblation of incompetent perforating
veins:Preliminary ultrasound observations:6th European American
Congress on Venous Diseases , Prague, Czech Republic , May 2005,
Praktika ebologie . 2005 . 14 ( 2 ): 55–56 .
USGS OF PERFORATING VEINS IN CHRONIC INSUFFICIENCY • 461
18. Sandri JL , Barros FS , Pontes S , Jacques C , Salles- Cunha SX .
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Diameter-re ux relationship in perforating veins of patients with
varicose veins , J Vasc Surg. 1999 . 30 ( 5 ): 867–875 .
19. Masuda EM , Kessler DM , Puggioni A , Lurie F , Kistner RL , Eklof B .
e e ect of ultrasound-guided sclerotherapy of incompetent perforator veins on venous clinical severity and disability scores , J Vasc
Surg. 2006 . 43 ( 3 ): 551–556 .
20. Puggioni A , Lurie F , Masuda E , Kistner R , Eklof B . Ambulatory treat-
ment of chronic venous disease with ultrasound guided sclerotherapy
of perforating veins . Society for Clinical Vascular Surgery, 31st
Symposium , Miami, Florida, March, 2003 .
21. Eklof B , Kessler D , Kistner R , etal. Can duplex-guided sclerotherapy
replace SEPS in the treatment of incompetent perforating veins? Veith
Symposium , NewYork, NewYork , November 20–23 , 2003 .
22. de Waard MM , der Kinderen DJ . Duplex ultrasonography-guided
foam sclerotherapy of incompetent perforator veins in a patient
with bilateral venous leg ulcers , Dermatol Surg . 2005 . 31 ( 5 ):
580–583 .
462 • CHRONIC VENOUS INSUFFICIENCY
55.
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PERFORATINGVEINS
John J. Bergan , Luigi Pascarella and Nisha Bunke-Paquette
INTRODUCTION
e development of ankle hyperpigmentation, edema,
atrophie blanche, and incipient ulceration, the cutaneous
trophic changes of chronic venous insu ciency (CVI), is
1
linked to a complex microangiopathy.
is, on a macrovascular level is linked to ambulatory venous hypertension,
which is enhanced by super cial and deep re ux. Also, it
is linked to a lesser extent to venous obstruction. us it
appears that venous hypertension is the fundamental patho-
2
genic factor that leads toCVI.
VALVE REMODELING PRODUCES
DISTAL VENOUS HYPERTENSION
Our observations on ultrasound-proven, re uxing saphenous veins have shown that the endothelium of their venous
valves and vein walls contain an in ltration of monocytes
and an associated increased expression of intercellular adhesion molecules (ICAM-1). ere is a statistically signi cant
spatial correlation between CD68-positive monocytes and
ICAM-1 in the various tissue areas of the valves and the
3
vein walls.
e leukocytes and the expression of adhesion
molecules are concentrated more on the proximal venous
wall and valve cusp than on the distal wall and lea et.
is suggests a cause and e ect relationship with venous
hypertension.
e altered hemodynamics that accompany the venous
hypertension change the plasma sheer stress, which, in turn,
stimulates leukocyte pseudopod projection and adhesion of
the leukocytes to the endothelium. It is a reduction, not an
increase, in shear stress that leads to adhesion of the white
4
cells on the endothelium.
Adhesion of the cells is followed
by migration through the endothelium and interstitial macrophage in ltration.
e microscopic alterations, linked to venous hypertension described earlier are accompanied by gross tissue
changes, which result in valve incompetency. Observations
of these changes in primary venous insu ciency reveal
dilation of the valvular annulus, atrophy of the cusp, and
brotic remodeling of the valve and its annulus. Some have
proposed that hemodynamic mechanical injury increases
5
tissue damage to the annulus and cusps.
Others suggest that
activated leukocytes release transforming growth factor-β
(TGF-β
tein production.
) gene expression, which alters environmental pro-
1
6
is might explain the gross observations
seen in a ected valves.
V E N O U S S T A S I S : A N
INAPPROPRIAT ETERM
Although the term “chronic venous insu ciency” (CVI)
is in common usage and is becoming increasingly visible,
the older term, “venous stasis” remains dominant. is is a
tribute to John Homans of Harvard, who introduced the
concept that venous stasis was the ultimate cause of venous
ulceration.
Homans believed that there was a causal relation
between venous ulcerations of the legs and blood stasis in
7
patients with severe chronic venous insu ciency.
Blood
stasis, as proposed by Homans, was determined by a shortage of oxygen content in the skin, and it was this that led
to a condition of tissue hypoxia, necrosis, and ulceration.
Many observations in the last quarter century have demonstrated that shortage of oxygen is not the main cause of
venous ulcers.
It has been hypothesized that presence of cutaneous
arteriovenous stulas might cause a deprivation of oxygen by shunting oxygenated blood away from skin already
hypoxic from stasis. Such arteriovenous connections are eas-
8
ily demonstrated
by arteriography and microdissection in
limbs with severe CVI but are not thought to contribute to
9
the skin changes.
Coleridge Smith and others have shown
that the content of oxygen in the skin and in varicose veins
10
of limbs with venous ulcers is not decreased.
gen content in varicose veins is increased.
In fact, oxy-
11
In addition, the
oxygen di usion defects suspected by histological ndings
of pericapillary brin cu s have been refuted. Studies such
1
7
463
as clearance of Xenon133 through liposclerotic skin have
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12
shown no signi cant oxygen barrier.
PREULCERATIVE CUTANEOUS
CHANGES
In ammation dominates the early skin changes that precede venous ulceration. Increased leukocyte activation and
an increased expression of soluble adhesion molecules have
been demonstrated. ere is a perivascular in ltration of the
papillary plexus capillaries. Granulation tissue composed of
lymphocytes, plasma cells, macrophages, histiocytes, and
broblasts invades the subepithelial layer. is granulation
tissue is responsible for the deposition of collagen bers.
13
Collagen bers appear to have completely lost their normal
orientation in the cutaneous tissue. ese lesions account
for the in ammatory and postin ammatory process of tissue brosclerosis:lipodermatosclerosis.
When skin at the border of CVI is compared to normal skin in the same individual, the strong expression of
ICAM-1 is seen in addition to a dense in ltration by T lymphocytes and macrophages. In some instances, the tissue also
14
is in ltrated by an increased number of mast cells.
is is
the typical picture of a chronic in ammatory reaction with
an upregulation of endothelial adhesion molecules and dermal in ltration by T lymphocytes and macrophages in the
skin of patients withCVI.
THE PERFORATINGVEINS
Incompetent perforating veins are strongly associated with
super cial venous re ux, and it is still controversial whether
incompetent perforating veins are the primary cause of
skin changes of chronic venous insu ciency or whether
the incompetent perforating veins and skin changes are the
result of super cial re ux. e cause of valvular dysfunction in perforating veins is not yet fully understood (see
Figure55.1).
15
Despite the classic studies of Linton
and Cockett, 16 it
is still not known what the exact role of incompetent perforating veins is in the development of venous ulceration. Our
observations suggest that venous hypertension is closely
associated with valve damage and remodeling, which pro-
17
duces subsequent valve incompetence.
erefore, it is use-
ful to relate these ndings to the valves in perforatingveins.
It is well known that muscle contraction produces
muscular compartment pressures in the range of 100mm
18
mercury and higher.
could initiate the cascade of molecular events, which even-
Such pressures exerted over time
tuate in valvular incompetence. is valve incompetence
would then produce the cutaneous “blow out” described
as “spherical dilatations on veins under the skin” by Dodd
19
and Cockett.
Failure of perforating vein valves due to their
remodeling caused by repetitive compartment pressure elevation induced by normal exercise would lead to the skin
changes described earlier.
A NEW HYPOTHESIS
A useful hypothesis is that venous hypertension, caused by
super cial re ux and calf compartment pressure, is transmitted to unsupported venules of the skin. It is this sum of
gravitational and hemodynamic pressure that stimulates the
skin changes of chronic venous insu ciency. If this is true,
a large component of ankle venous hypertension emanates
from normal calf exercise with calf compartment pressures
transmitted directly through the incompetent perforating
vein valves to the skin (see Figure55.2).
AB
Figure55.1 ( A) is ultrasound scan image shows an incompetent perforating vein penetrating the deep fascia and re uxing into the GSV. It is calf
muscle contraction that provides the pressure that is transmitted through a failed valve and elongates and dilates the super cial vein. (B) e IPV in
this image is dilated and measures 7.8mm in diameter.
464 • CHRONIC VENOUS INSUFFICIENCY
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Figure55.2 is perforating vein is shown penetrating the deep fascia. Its
outward ow is demonstrated best by compression of distal so tissues.
Indirect evidence of the importance of perforator veins
in venous ulceration comes from surgical experience in
20
dividing perforating veins in treatment of CVI.
Ashorter
ulcer healing time and improved hemodynamics have been
21
found in limbs subjected to perforating vein surgery.
De Palma showed in a crossover study that failure of
conservative care, mainly consisting of compression, could
be reversed by intervention with division of perforating
22
is report, much like others, 23 is confused by the
veins.
fact that 70% of the limbs had simultaneous stripping of
the long saphenous vein at the time of perforator vein interruption. In fact, the sum of these two maneuvers did reduce
venous hypertensive microangiopathy.
As ancient theories of causation of CVI gradually have
been disproven as indicated earlier, it is no longer thought
that venous blood stasis or ischemia due to arteriovenous
stulas, brin cu development, or leukocyte trappings
are important. Instead, a more logical explanation of the
skin changes of chronic venous insu ciency is credible
(see Table55.1).
In development of the severe changes of CVI, rst,
venous hypertension and super cial venous valve failure
21
are linked.
Sequential venous valve failure may be centrifugal or centripital. is allows venous hypertension
to be transmitted to the ankle by super cial re ux. Next,
perforating vein valves fail through the same mechanisms
of venous hypertension-induced valve remodeling. Or, perforating veins acting as part of the private re ux recirculation can enlarge to the point of valvular incompetence
22
(see Figure55.3).
Subsequent to perforating vein valve failure, subcutane-
ous changes of in ammation are produced by the in amma-
14
tory process,
and these lead to the clinical manifestations
of chronic venous insu ciency.
As suggested previously, therapy of CVI supports
this hypothesis. Compression treatment reduces ambulatory venous pressure and is e ective in healing venous leg
Table55.1 HYPOTHESES EXPLAINING GENESIS OF
ADVANCED CHRONIC VENOUS INSUFFICIENCY
1 . S up e r cial vein valve incompetence* raises distal venous pressure.
2. Perforating vein valve incompetence** raises distal venous
pressure.
3 . A d d it i v e e ects of super cial and perforator incompetence
produce profound distal venous hypertension.
4. Venous hypertension produces venulectasia, edema, leukocyteendothelial interaction, and the in ammatory response.
5 . I n ammation produces hyperpigmentation, brosis, and
ulceration.
*Due to gravitational re ux induced valve remodeling.
**Due to muscle compartment pressure induced valve remodeling.
ulcers. 24 Super cial vein surgery reduces ambulatory venous
pressure, allows healing of venous leg ulcer, and reduces the
25
e ects of CVI.
Perforator vein interruption by the Linton
or endoscopic techniques reduces ambulatory venous pres-
26,27
sure and ameliorates the chronic changes of CVI.
EXIT AND REENTRY
PERFORATINGVEINS
ere are two fundamental facts that confuse understanding of perforating veins. e rst relates to ow direction.
Some perforating veins produce abnormal out ow from
deep circulation to super cial circulation. is is demonstrated in Figure55.1. is can be termed “perforating
vein re ux.” Other perforating veins demonstrate normal
ow from the super cial system to the deep system. is is
shown in the diagram of Figure55.3 and the duplex scan
shown in Figure55.4. In situations of super cial venous
incompetence and re ux, these can be called reentry perforating veins. It was Hach who understood this best, as he
described the private circulation of re ux in super cial veins
reentering to the deep system and the deep system in turn
24
re uxing into the super cial veins.
It is most likely that it is
the reentry perforating veins that disappear a er adequately
performed super cial venous stripping.
Another confusing factor in relating perforating veins
to venous ulceration is the fact that venous ulceration is
not directly related to severity of hemodynamic changes.
e lower limbs in a patient with bilaterally severe varicose
veins might appear to be identical and might have identical
hemodynamic measurements, but one limb might have all
the stigmata of CVI and the other might have none. is
caused by the venous hypertension or other hemodynamic
changes but instead are dependent on leukocyte activation
and the subsequent molecular changes that follow. In the
absence of leukocyte activation, skin changes do notoccur.
However, it may very well be that perforating vein out ow or re ux as detected by color ow Doppler duplex on
25
PERFORATINGVEINS • 465
https://t.me/med1917
Figure55.3 Normal perforating vein blood ow is from the super cial to
the deep venous system. When saphenous vein re ux and varicose veins
are present, the direction of ow is normal, but the perforating veins
that allow reentry of re ux ow may enlarge and become incompetent
as shown in this diagram.
(From Reference 27, with permission.)
release of distal compression creates the hypertension in the
subcutaneous venular network that elongates and dilates
the capillaries, enlarges the intercellular junctions, produces
edema, and triggers the in ammatory reaction that causes
the skin changes.
If this is proven to be true, observations on the e cacy of measures to reduce cutaneous hypertension such
as e ective compression, super cial venous re ux ablation
26
by foam sclerotherapy,
and perforator vein interruption
will rest on a rm foundation. Even e ective pharmacological intervention to moderate leukocyte activation is
foreseeable.
C O N C L U S I O N S
Perforating veins and severe CVI are linked, and descriptions of molecular events associated with venous hypertension explain the relationship. ese validate current medical
and surgical therapy and point the way toward more e ective and less cumbersome treatments in the future.
Figure55.4 is reentry perforating vein has become tortuous because
of increased ow. Distal compression causes its inward directed ow to
stop. is resumes a er distal compression release.
R E F E R E N C E S
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