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Figure56.20 CT image of a crushed right iliac stent. In this case, the
kissing Nitinol stents should have been extended higher into the cava
to prevent this asymmetry. Furthermore, upon rethrombosis, the stent
system should have been revised immediately.
F. DISTAL THROMBUS: e presence of acute and
chronic tibiopopliteal thrombus can threaten the long-term
patency of proximal reconstructions. We rmly believe that
treatment of the entire limb is key to technical and clinical success. Complete understanding of the calf veins and
popliteal in ow is important. Duplex and pedal phlebography are used to provide this information. In the event
of thrombotic obstruction, ow-directed delivery of a
thrombolytic agent can reduce calf and popliteal thrombus (Figures56.21, 56.22). e saphenous vein is intermittently compressed against the malleolus and/or condyle,
to redirect venous ow into the deep veins. e dedicated
tourniquets, designed for this purpose, e ectively promote
thrombolysis of thrombus in the calf and popliteal segments
(Tiger Surgical, Inc., Portland,OR).
G. IVC FILTERS: It is not generally thought to
be necessary to place a caval lter while performing
catheter-directed thrombolysis. e incidence of PE has
been remarkably low, as the thrombus does not fragment
without undue manipulation. However, mechanical thrombectomy for removal of acute thrombus poses the risk of
embolism. In this case, temporary lters have been placed
and subsequently removed. Occluded IVC lters can
be safely and e ectively bypassed. We have passed single
and kissing Wallstents through and alongside all types of
occluded lters without complication (Figures56.6, 56.13,
56.23). Once the exchange guide wire has traversed this
area of occlusion, serial balloon dilation will expand the
tissue and allow stent deployment. Mechanical thrombectomy and thrombolysis can be e ectively and safely used
to restore ow in acutely thrombosed IVC bearing lters.
35
In our iliocaval series, successful recanalization of chronically occluded lters has also been performed with remark-
8
able long-term patency.
Raju and Neglen encountered
twenty- ve patients with occluded IVC lters. eir results
Figure56.21 Contrast venogram shows acute tibial thrombus prior to ow-directed thrombolysis. e diagram shows placement of the DVT
tourniquet, which was speci cally designed for lytic infusions. Compression of the saphenous vein against the malleolus promotes ow into the
deep venous system. In this manner, e ective delivery of the thrombolytic drug can dissolve acute thrombus.
478 • CHRONIC VENOUS INSUFFICIENCY
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Figure56.22 Photograph of a patient with both ankle and knee
tourniquets in place for ow-directed lysis. Adisc is positioned
uoroscopically to strategically compress the super cial vein against
thebone.
also demonstrate the feasibility and low morbidity of stent-
37
ing through a thrombosed lter.
Stent complications are
quite rare, but they can happen.
H. ILIAC STENTS AND PREGNANCY: Young
women undergoing stent procedures during child-bearing
age were understandably concerned about whether or not
an iliac stent would be an issue with pregnancy. On the contrary, treating a DVT or preventing thrombosis by stenting
a May- urner compression mitigates against thrombosis
during pregnancy and a er delivery. Anticoagulation is
managed by a hematologist or high-risk pregnancy specialist. In our experience, four women have delivered seven
healthy children without complication. Hartung reported
that eight pregnancies occurred in six patients in whom a
self-expanding stent had been previously placed for iliac
compression. e recommendation to sleep on the right
side and continue lovenox throughout the conception
40
period and pregnancy parallel our experience.
CLINICAL EXPERIENCE
In 2006, Raju reported a series of 120/4,217 (2.8%)
patients with obstructive lesions of the IVC identi ed
among patients with chronic venous insu ciency examined
1
between 1997 and 2005.
e majority of the lesions were
infrarenal (82%), 14% (14/97) were suprarenal but below
the diaphragm, and four cases extended into the superior
aspect of the intrahepatic IVC. In 93% of cases, lesion
involved the common iliac segment, but in 7%, the lesion
was limited to the IVC. Most of the IVC lesions 85/99
(86%) were stenotic (>60%) and not occlusive. ere were
fourteen occlusions in which seven of the attempted recanalizations were not successful. e CEAP clinical classi cation for the stented limbs included C3 (37%), C4 (26%),
C5 (7%), and C6 (19%). e seven limbs with unhealed
ulcers were found to have residual untreated re ux, which
was predominantly in axial veins. ere were nineteen limbs
with active ulcers that underwent stenting. In twelve limbs
(63%) the ulcers healed and remained healed at 24months.
Re ux was present in seventeen, involving both deep and
super cial systems. Only two of these limbs underwent
concurrent endovascular treatment of saphenous re ux.
Although the other limbs had identi ed re ux, correction of
the obstruction, alone, allowed healing of the ulcer. Stented
patients experienced signi cant clinical improvement. A er
Figure56.23 ree-image sequence showing baseline cavagram and subsequent reconstruction in a patient with IVC occlusion. Note the double
barrel stents are extended parallel to the occluded lter.
ENDOVASCULAR MANAGEMENT OF ILIOCAVAL THROMBOSIS • 479
3.5years, the reduction in pain and swelling was 74% and
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51%, respectively. At 24months, cumulative primary and
primary assisted patency were 58% and 82%, respectively.
is is a valuable series, and the authors are to be commended
for extensive experience and thoughtful review. Ninety percent of patients had symptomatic CVI, while 10% were
essentially asymptomatic, including the four patients who
had no idea there was a venous lesion prior to presenting
with acute thrombosis distal to the IVC. Basically, the utilization of a complete venous investigation, including pelvic
duplex, pressure testing, and transfemoral venography with
IVUS uncovers a lot more venous pathology than anyone
ever estimated. Whereas this degree of diagnostic investigation is not available in many institutions, the authors leave
little doubt that venous obstruction is more prevalent than
previously thought.
rombolytic therapy was not used except in treating
acute DVT. Whereas we use catheter-directed thrombolysis to open and so en chronic thrombotic occlusions, the
Raju and Neglen perform their procedures without thrombolysis. For the most part, thrombolysis was not required
to pass a wire. However, lytic therapy may have facilitated
di cult (unsuccessful) recanalization and diminished the
incidence of residual stenoses that compressed stents and
resulted in reintervention. Most of the lesions in this series
were stenotic and, therefore, did require the opening of a
primary channel. e authors make several technical points
that Ihave similarly emphasized. First, complete stenting
of diseased segments promotes reestablished continuity
of deep venous ow, which is imperative to stent patency.
Understenting should be discouraged in view of the observation that tributary ow passes through Wallstent interstices and traversing the inguinal ligament with overlapping,
self-expanding metallic stents is well tolerated. Moreover,
neither the initial venographic appearance, the extent of
the lesion, nor the duration of the symptoms is a predictor
of success or failure of guide-wire passage through a venous
obstruction. Some chronic lesions are almost impossible
and some are very easy. ere must be genetic issues we do
not yet recognize.
S U M M A R Y
Endovenous therapy represents a signi cant component
in the treatment of chronic venous insu ciency due to
thrombosis. e clinical options for treatment of residual obstruction, following DVT, now favor reconstruction of the native axial veins with self-expanding metallic
stents. e evolution of the tools and techniques is ongoing, as the majority of the procedures have been adapted
from arterial interventions. Because the venous system
is characterized by lower pressure and lower ow state,
compared with the arterial system, manipulations within
veins are thrombogenic, and good technique is essential.
Appreciating that stents represent a form of bypass and,
therefore, require good in ow as well as out ow to remain
patent is fundamental. O en, this is not obvious to the
inexperienced physician, who underestimates the role of
residual thrombus in distal veins or the importance of a
stent extending into the IVC by one centimeter. Chronic
venous insu ciency is that “something old” that seems to
be a renaissance topic in the midst of new pharmaceutical discoveries and the emerging eld of endovenous surgery. Hopefully, continued innovation, multidisciplinary
e orts, and clinical evidence will all support our e orts to
better prevent DVT, to treat acute DVT in a timely manner, and, overall, reduce the incidence of postthrombotic
venous insu ciency.
R E F E R E N C E S
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Duncan JR . Gadolinium, carbon dioxide, and iodinated contrast
material for planning inferior vena cava lter placement:Aprospective trial . J Vasc Interv Radiol. 2003 . 14 ( 8 ): 1017–1022 .
4. David A , Peterson BA , Ella A , etal. Computed tomographic venography is speci c but not sensitive for diagnosis of acute lower extremity deep venous thrombosis in patients with suspected pulmonary
embolus, J Vasc Surg. 2001 . 34 : 798–804 .
5. Jost CJ , Gloviczki P , Cherry KJ Jr, etal. Surgical reconstruction of
iliofemoral veins and the inferior vena cava for nonmalignant occlusive disease , J Vasc Surg. 2001 . 2 : 320–328 .
6. Zollikofer CL , Antonucci F , Stuckmann G , Mattias P , Salomonowitz
EK . Historical overview on the development and characteristics
of stents and future outlooks , Cardiovasc Intervent Radiol. 1992 .
5 : 272–278 .
7. Irving JD , Dondelinger RF , Reidy JF , etal. Gianturco self-expanding
stents:Clinical experience in the vena cava and large veins, Cardiovasc
Intervent Radiol. 1992 . 5 : 328–333 .
8 . orpe P , Osse F , Dang H . Endovascular reconstruction for chronic
iliac vein and inferior vena cava obstruction. In: Gloviczki P , Yao
J , eds. Handbook of venous disorders , 2e. London : Arnold . 2001 .
347–361 .
9. O’Sullivan GJ , Semba CP , Bittner CA , et al. Endovascular management of iliac vein compression (May- urner) syndrome , J Vasc
Interv Radiol. 2000 . 11 : 823–836 .
10. Razavi MK , Hansch EC , Kee ST , Sze DY , Semba CP , Dake MD .
Chronically occluded inferior venae cavae:Endovascular treatment ,
Radiology. 2000 . 1 : 133–138 .
11. Neglén P , Raju S . Intravascular ultrasound scan evaluation of the
obstructed vein, J Vasc Surg. 2002 . 35 : 694–700 .
12. Raju S , Owen SJ , Neglen P . e clinical impact of iliac venous stents
in the management of chronic venous insu ciency , J Vasc Surg.
2002 . 35 : 8–15 .
13. Vedantham S , Vesely TM , Sicard GA, etal. Pharmacomechanical
thrombolysis and early stent placement for iliofemoral deep vein
thrombosis , J Vasc Interv Radiol. 2004 . 15 : 565–574.
14. Allie DE , Hebert CJ , Lirtzman MD , etal. Novel simultaneous combination chemical thrombolysis/rheolytic thrombectomy therapy
for acute critical limb ischemia: e power-pulse spray technique,
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16. te Riele WW , Overtoom TT , Van Den Berg JC , van de Pavoordt ED ,
de Vries JP . Endovascular recanalization of chronic long-segment
occlusions of the inferior vena cava: Midterm results , J Endovasc
er . 2006 . 13 ( 2 ): 249–253 .
17. Raju S , Neglen P . High prevalence of nonthrombotic iliac vein
lesions in chronic venous disease:Apermissive role in pathogenicity ,
J Vasc Surg. 2006 . 44 : 136–144 .
18. Neglén P , Hollis KC , Olivier J , Raju S . Stenting of the venous outflow in chronic venous disease:Long-term stent-related outcome,
clinical, and hemodynamic result , J Vasc Surg. 2007 . 46 : 979–990 .
19. Hilleman DE , Razavi MK . Clinical and economic evaluation of the
trellis-8 infusion catheter for deep vein thrombosis, J Vasc Interv
Radiol. 2008 . 19 : 377–383.
20. Neglén P , Tackett TP Jr, Raju S . Venous stenting across the inguinal
ligament , J Vasc Surg. 2008 . 48 : 1255–1261 .
21. Trabal J , Comerota A , LaPorte F , Kazanjian S , Di Salle R , Sepanski ,
D . e quantitative bene t of isolated, segmental, pharmacomechanical thrombolysis (ISPMT) for iliofemoral venous thrombosis,
J Vasc Surg. 2008 . 48 : 1532–1537 .
22. Raju S , Neglén P . Percutaneous recanalization of total occlusions of
the iliac vein, J Vasc Surg. 2009 . 50 : 360–368 .
23. Hartung O , Loundou AD , Barthelemy P , Arnoux D , Bou M ,
Alimi YS . Endovascular management of chronic disabling ilio-caval
obstructive lesions: Long-term results , Eur J Vasc Endovasc Surg.
2009 . 38 ( 1 ): 118–124 .
24. Cockett FB , o m a s M L . e iliac compression syndrome , Br J
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25. Cockett FB , omas ML , Negus D . Iliac vein compression:Its relation to iliofemoral thrombosis and the post-thrombotic syndrome ,
Br Med J. 1967 . 2 : 14–19 .
26. Labropoulos N , Borge M , Pierce K , Pappas PJ . Criteria for de ning
signi cant central vein stenosis with duplex ultrasound , J Vasc Surg.
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27. Comerota AJ . e ATTRACT trial:Rationale for early intervention
for iliofemoral DVT , Perspt Vasc Surg Endovasc er. 2009 . 4 : 221–224 .
28. Killewich LA , Bedford GR , Beach KW , Strandness DE Jr.
Spontaneous lysis of deep venous thrombi:Rate and outcome , J Vasc
Surg. 1989 .
29. Johnson BF , Manzo RA , Bergelin RO , Strandness DE Jr. Relationship
between changes in the deep venous system and the development of
the postthrombotic syndrome a er an acute episode of lower limb
deep vein thrombosis:Aone- to six-year follow-up , J Vasc Surg. 1995 .
21 : 307–312 .
30. Prandoni P . Risk factors of recurrent venous thromboemboli: e
role of residual vein thrombosis, Pathophysiol Haemost romb.
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31. Markel A , Manzo RA , Bergelin RO , Strandness DE Jr. Valvular
re ux a er deep vein thrombosis:Incidence and time of occurrence ,
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32. Mewissen MW , Seabrook GR , Meissner MH , Cynamon J ,
Labropoulos N , Haughton SH . Catheter-directed thrombolysis for
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Radiology. 1999 . 211 ( 1 ): 39–49 .
33. Nazarian GK , Austin WR , Wegryn SA, etal. Venous recanalization by
metallic stents a er failure of balloon angioplasty or surger y:Four-year
experience, Cardiovasc Intervent Radiol. 1996 . 19 ( 4 ): 227–233 .
34. Neglen P , Raju S . In-stent recurrent stenosis in stents placed in the lower
extremity venous out ow tract , J Vasc Surg. 2004 . 39 ( 1 ): 181–187 .
35. Peter Neglén , MD, PhD, Rikki Darcey , BS, Jake Olivier , PhD,
Seshadri Raju , MD. Bilateral stenting at the iliocaval con uence J
Vasc Surg 2010 ; 51 : 1457–1466 .
36. Neglén P , Oglesbee MD, Raju S . Stenting of chronically obstructed
inferior vena cava lters, J Vasc Surg. 2010 . 51 ( 3 ): 794.
37. Bjarnason H , Kruse JR , Asinger DA, et al. Iliofemoral deep
venous thrombosis:Safety and e cacy outcome during 5 years of
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38. Comerota AJ , Gravett MH . Iliofemoral venous thrombosis:Areview , J Vasc Surg. 2007 . 46 : 1065–1076 .
39. Hartung O , Barthelemy P , Arnoux D , Bou M , Alimi Y S .
Management of pregnancy in women with previous le ilio-caval
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9
: 89–97 .
ENDOVASCULAR MANAGEMENT OF ILIOCAVAL THROMBOSIS • 481
57.
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POPLITEAL VEIN ENTRAPMENT
Seshadri Raju
opliteal vein entrapment is a rare clinical entity.
Anatomic popliteal vein compression, however, can be
P
demonstrated by imaging techniques in 27 to 42% of
asymptomatic individuals with a 34% incidence of bilateral-
1,2
In the frequency of the anatomic lesion and the rarity
ity.
of the clinical expression, the entity perhaps resembles thoracic outlet syndrome. Compression of the popliteal vein
is infrequently (±10%) associated with companion arterial
compression, even though the very rst case reported by
Rich and Hughes in 1967 was.
indistinguishable from other forms of chronic venous disease
(CVD) and easily applicable diagnostic testing is lacking.
Diagnosis currently depends on awareness of the entity and
elimination of other causes of chronic venous insu ciency.
Invasive monitoring of dynamic popliteal venous pressure
with ankle maneuvers in suspected cases may be speci c.
INCIDENCE
e estimated incidence is less than 4% of all cases of CVD,
probably much less. Sporadic case reports
2,16
series
Contrary to expectations, the disease is not con ned to
the young; there appears to be no age or sex predilection.
Like other forms of CVD, common symptoms and signs are
swelling, pain, and stasis skin changes including ulceration.
Limb swelling extending above the knee joint probably
rules out the condition as the primary pathology. Venous
claudication may be present in some but not all. Cutaneous
hyperpigmentation may extend more proximally beyond
the gaiter area in some patients. Isolated popliteal valve
re ux when symptomatic should arouse clinical suspicion
of entrapment, as the former by itself is seldom symptomatic. Entrapment may result in popliteal vein thrombosis.
can be found in the literature.
CLINICAL FEATURES
3
Clinical features are o en
2
4–15
and two
2
17
I N V E S T I G A T I O N S
Popliteal vein compression on ascending venography is sensitive, but not speci c. Popliteal vein compression should
be demonstrated on active plantar exion; passive dorsi exion may also reproduce the lesion in some (see Figure57.1).
e site of compression is variable (high popliteal 11%, mid
popliteal 39%, low popliteal 18%, and di use 32%), thus
suggesting varied compressive mechanisms.
Like venography, duplex with ankle maneuvers can also
demonstrate popliteal vein compression without any inference to causality of symptoms.
compression with ankle maneuvers is present in about half
of the limbs without clinical features of arterial insu ciency. Demonstration of arterial compression does not signify functionally signi cant associated venous compression.
Magnetic resonance imaging
features of the gastrocnemius muscle, which is frequently a
part of the compressive mechanism, and it can help rule out
other causes of compression such as the Baker’s cyst.
Abnormalities on ambulatory venous pressure measurement (pedal vein) and out ow fraction by occlusive plethysmography may be suggestive, but these tests are neither
sensitive nor speci c.
tion fraction and residual volume measurements with air
plethysmography(APG).
Dynamic popliteal vein pressure measurements (see
Figure57.2) with ankle maneuvers appear to be diagnostic
and useful in assessing outcome a er entrapment release.
e most frequent compressive mechanism is the gastrocnemius muscle due to abnormalities in the origin of the
medial head (see Table 57.1). Postnatal extension of the
medial head of the gastrocnemius muscle from the medial
femoral condyle to involve portions of the adjacent femoral
sha is a normal event; excessive migration appears to result
2
Similar comments apply to ejec-
P A T H O L O G Y
1
Associated popliteal artery
18,19
may display abnormal
9,14
2
482
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Figure57.1 Popliteal vein compression with ankle maneuvers:mid
popliteal (le ). Discrete lesions at high and low popliteal locations as
well as di use lesions (not shown) alsooccur.
Table57.1 PATHOLOGICAL FEATURES IN THIRTY
CASES OF ENTRAPMENT UNDERGOING RELEASE
COMPRESSIVE ENTRAPMENT MECHANISM NUMBER
Gastrocnemius medial head anomalous origin
Additional third head of gastrocnemius
Gastrocnemius lateral head origin from medial
Condyle
Soleus sling
ick perivenous fascia
Abnormal course of vascular bundle lateral to the
Lateral head
Unknown
PATHOLOGICAL CHANGES IN
THE POPLITEAL VEIN
Sclerosis
Prestenotic Dilatation
Poststenotic Dilatation
Postthrombotic Changes
*One case associated with atrophic lateralhead.
**Two saccular aneurysms.
†Associated with other entrapment mechanisms.
(From Reference 2, with permission)
18*
1
5
3
13†
2
l
NUMBER
13
1
4**
2
in compression of the vein. Compression by other muscles
such as the lateral head of the gastrocnemius or the soleal
sling are relatively rare. Compression of the vein by the tibial nerve may occur rarely.
e compressed vein segment o en becomes sclerosed
and stenotic. Both prestenotic and poststenotic dilatations occur, occasionally large enough to be classi ed as
aneurysms. Athick perivenous fascia attached to the gastrocnemius muscle is an integral part of the compressive
mechanism, which may explain the varied location of vein
compression noted on venography. e entrapment mechanism likely involves prolonged spasm of the vein initiated
by external compression by adjacent muscle. Elevation of
the popliteal vein pressure persists long a er cessation of
active muscle contraction (see Figure 57.3). Entrapment
2
may eventually lead to popliteal valve re ux
20
tor incompetence.
Unlike in popliteal artery entrapment,
A B
and perfora-
anatomic course variations of the popliteal vein are
relativelyrare.
S U R G I C A L T R E A T M E N T
e posterior approach 20 or the medial approach 2 to the
popliteal fossa may be used. e posterior approach is preferable if anatomic course variations of the popliteal vasculature are suspected.
The medial head of the gastrocnemius is taken down
from the bone with particular attention to the muscle
extension beyond the condyle. This extension may be large
11
enough to be described as a third head.
As recurrences
with reattachment of the muscle can occur, resection of
the medial head may be preferable to simple detachment
of the muscle from its origin. Other compressive elements
Figure57.2 Calf exercise with percutaneously inserted Millar Probes. (A) e 2-Fr catheters have tip-mounted pressure transducers. (B) e catheter
tip is positioned in the popliteal vein under uoroscopy.
POPLITEAL VEIN ENTRAPMENT • 483
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Figure57.3 Simultaneous pressure tracings in the dorsal foot vein and popliteal vein with calf exercise. Note elevation in popliteal pressure and
decrease in foot venous pressure a er exercise. Popliteal pressure elevation persists for 100 seconds a er cessation of exercise before slowly declining
to baseline.
(From Reference 2, with permission).
when present should be lysed as well. The vein should be
cleared of its perivenous sheath and tributaries over a generous 10-cm length centered on the compressive point.
Aneurysmal and stenotic segments should be resected
and the vein repaired without any hint of tension, using
a saphenous graft if necessary. The popliteal valve should
be repaired if refluxive, particularly when skin changes
are present. Axillary vein transfer may be required if pri-
2
mary valve reconstruction is not possible.
Perioperative
antithrombotic prophylaxis including use of low molecular weight heparin, meticulous hemostasis, and closed
drainage are necessary to achieve clean primary healing without local complications that may predispose to
recurrenc e .
CLINICAL RESULTS
Excellent clinical results with relief of pain, swelling,
and stasis skin changes have been reported particularly
Popliteal Vein
Dorsal Vein
% Increase
Unchanged
% Decrease
Figure57.4 Elevated popliteal vein pressure a er exercise decreases
a er entrapment lysis. Dorsal vein pressure (post exercise) shows little
change.
(From Reference 2, with permission).
Pre-Op Post-Op
80
60
40
20
0
–20
–40
–60
–80
–100
when the diagnosis is firmly established on the basis
of dynamic popliteal vein pressure measurements (see
2
Figure57.4).
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cyst, desmoid tumor and fabella syndrome ], J Mal Vasc . 1990 .
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484 • CHRONIC VENOUS INSUFFICIENCY
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chronic venous insu ciency , J Vasc Surg . 1993 . 18 ( 5 ): 760–766 .
18. Fermand M , Houlle D , Cormier JM , Vitoux JF , Lignieres G .
Popliteal vein entrapment shown by MR imaging , AJR Am J
Roentgenol . 1990 . 155 ( 2 ): 424–425 .
19. Di Cesare E , Marsili L , Marino G, etal. Stress MR imaging for evaluation of popliteal artery entrapment , J Magn Reson Imaging . 1994 .
4 ( 4 ): 617–622 .
20. Di Marzo L , Cisternino S , Sapienza P, etal. [ Entrapment syndrome
of the popliteal vein:results of the surgical treatment ], Ann Ital Chir .
1996 . 67 ( 4 ): 515–519 ; discussion 519–520.
POPLITEAL VEIN ENTRAPMENT • 485
58.
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VALVULOPLASTY IN PRIMARY VENOUS
INSUFFICIENCY
DEVELOPMENT, PERFORMANCE,
AND LONGTERM RESULTS
Robert L. Kistner , Elna Masuda , and Fedor Lurie
idespread interest in the occurrence of deep
vein re ux, its clinical e ects, the technique of
W
valve repair followed the demonstration in 1968 that direct
surgical repair of the femoral venous valve was feasible. is
chapter will review the background on which the rst repair
was based and highlights that have evolved in this eld since
the rst repair was reported in1968.
e rst valve repair 1 was the result of curiosity in a clinical
case of swelling, pain, and work disability in a patient who
su ered le leg deep venous thrombosis (DVT) following a
high voltage electricalburn.
Two years following the injury this patient was unable
to return to work due to swelling and pain in the extremity.
An ascending venogram revealed the unexpected nding
of patency of the entire deep venous system with traces of
postthrombotic scarring in the popliteal vein and the lower
thigh portion of the femoral vein. Since this nding did not
o er an adequate explanation of the patient’s symptoms
(swelling above the knee), it was reasoned that the problem
was due mainly to re ux rather than obstruction, and this
led to the concept of descending venography to determine
the valvular status in this extremity. e descending venogram showed full axial re ux of contrast from the common
femoral vein (CFV) down through the popliteal vein and
into the calf. It also showed a well-formed but incompetent
valve at the upper end of the femoral vein (formerly termed
the super cial femoral vein). Other valves were identi ed in
the distal femoral vein. Evidence of postthrombotic scarring
in the popliteal and super cial femoral veins wasnoted.
direct valve repair, and the long-term results of
THE FIRST VALVEREPAIR
With the diagnosis of axial re ux as the cause of the
patient’s symptoms, it was elected to treat the patient a er
the teachings of Robert Linton
saphenous and perforator re ux, followed by control of the
deep vein re ux by interrupting the upper end of the femoral vein just distal to the origin of the deep femoral vein in
the groin. e patient previously had the saphenous vein
stripped. e perforators of the calf were interrupted 3 d
prior to exploration of the femoral vein, and the femoral
vein was approached as a separate procedure.
Prior to surgery on the femoral vein, the nding of a
normal-appearing valve in the upper femoral vein on the
venogram resulted in the decision to explore the valve to see
if it might be repairable prior to ligation of the femoral vein.
When this exploration at surgery revealed a morphologically normal vein and valve structure with the single nding of elongation of the valve cusp, it was elected to attempt
repair of this defect by shortening the leading edge of the
two cusps. When this was done the valve appeared normal
and it resulted in a totally competent valve upon closure of
the vein. It was decided to accept this newly competent femoral valve as replacement for the originally intended ligation
of the femoral vein. e patient was managed with full heparinization for the rst postoperative week, then switched
to Coumadin.
e clinical result was dramatic relief of his symptoms
from the rst postoperative day when he spontaneously
remarked that his leg felt relieved of its congestion. He
remained free of unilateral symptoms in this extremity for
the remaining 13years of hislife.
is successful surgical repair of an incompetent femo-
ral vein valve in 1968 led to a series of seventeen repairs that
were the substance of the rst national report of the procedure in 1975.
3
is series consisted of advanced venous
2
by controlling greater
486
insu ciency cases evaluated with ascending and descend-
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ing venography to identify instances where severe clinical
venous insu ciency was associated with axial deep vein
re ux rather than deep obstruction.
BACKGROUND KNOWLEDGE
OF NONTHROMBOTIC REFLUX
DEEP VEIN DISEASE
Except for the publications of Gunnar Bauer in the 1940s, 4
clinically important deep vein re ux disease had been attributed to postthrombotic disease. Bauer was a brilliant investigator surgeon who worked in a small hospital in Mariestad,
Sweden, in the mid-1900s. He experimented with venography in patients suspected of having venous disease and
devised a method of performing descending venography,
described in 1948. ese venograms were performed with
a needle in the CFV and with the patient in the 45-degree
erect position. Static lms were obtained to document ndings. Bauer was the rst to report nonthrombotic cases with
high-grade axial re ux in the deep veins, and to associate
these cases with advanced stages of clinical venous insu ciency. He treated these cases with popliteal vein ligation
and reported early clinical success, but later follow-up of
some of these cases by his peers in Sweden discredited the
long-term value of popliteal vein ligation.
Bauer’s descending venography resulted in activity in
other sites around the world, as re ected by reports that
5,6
appeared in the early 1950s.
Confusion arose from these
reports when it was found that deep re ux was associated
with symptoms in some cases, whereas other cases were
asymptomatic. As a result of this confusion with descending
venography and the report that popliteal vein ligation was
a questionable procedure, this entity, which Bauer called
“idiopathic nonthrombotic re ux,” apparently lost credibility as an important cause of venous insu ciency in the
1950s and lay dormant until venous valve repair surfaced
in1975.
e description of the re ux entity that Bauer termed
4
“idiopathic nonthrombotic venous insu ciency”
is identical to the present-day primary venous insu ciency. is
entity is fundamentally di erent from postthrombotic disease since there is no element of gross in ammation or scarring of the vein or valve, or intraluminal obstruction with
wall thickening as found in the postthromboticcases.
TREATMENT OF DEEP VEIN
REFLUX PRIOR TO1968
ere was great interest in the aggressive management
of the chronic venous disease (CVD) leg prior to 1960,
which is well summarized in the papers of Robert Linton
2,7
of Boston from 1938 to 1953.
Linton refers to the epic
work of Homans,
8
who drew attention to the importance
of the perforator veins and concentrated on the excision of
the diseased skin and scar tissue in the lower leg. Homans’s
understanding of the pathophysiology of CVD is amazing
in view of the fact that he had no imaging studies to visualize the leg veins and depended entirely on clinical acumen to divine the relationship between the skin changes
of CVD and the venous system. He came to understand
that these changes were related to deep vein disease, which
was attributed to postthrombotic changes in the veins
through clinical examination alone. Linton embraced and
ampli ed this thinking and devised a multipronged surgical e ort to control venous hypertension by removing the
saphenous vein, radically eliminating perforator veins in
the calf, ligating the super cial femoral vein, and removing
a large segment of deep fascia in the posterior calf to facilitate lymph drainage of the extremity. During the 1950s he
was an intense advocate of aggressive surgical treatment for
advanced venous insu ciency, essentially all of which he
attributed to postthrombotic venous disease. His papers
emphasize the importance of re ux in the genesis of postthrombotic sequelae as he describes the progression of the
originally obstructive thrombosis to a re uxive postthrombotic state a er recanalization of the thrombosed channels has occurred. Although his papers cite the work of
Gunnar Bauer, there is little or no mention of ascending or
descending venography or of nonthrombotic venous re ux
disease in Linton’s diagnostic workup of the postphlebitic
patients.
EARLY INFLUENCE OF
VALVULOPLASTY ON THE
STUDY OF VENOUS DISEASE
e realization that there is an entity of primary re ux disease as a cause of axial re ux separate from postthrombotic
re ux stimulated investigation into the frequency of the
two conditions, their diagnostic criteria, and the implications their identi cation would have on management.
Among the questions that stimulated the interest of
investigators were the need to know the frequency with
which axial primary deep vein re ux occurred, the amount
of damage it could contribute to the extremity, and the
near- and long-term results of its repair. With the ability to
repair re ux in the super cial, perforator, and deep veins,
the concept of total repair of re ux was possible, and the
question of which conditions would warrant this more
aggressive treatment required investigation. For the rst
time, thorough knowledge of the pathophysiology in each
segment of the venous tree had become of practical import
because each could be repaired. is ultimately became
a strong stimulus to revise the diagnosis of venous insuf ciency into an objective image-driven study of the entire
deep venoustree.
VALVULOPLASTY IN PRIMARY VENOUS INSUFFICIENCY • 487
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