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402 Chapter 44/The Diagnosis and Management of Heparin-Induced Thrombocytopenia
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after thromboembolectomy if heparin is used, though this
does not occur in all instances.
Section B of Table 44.4 lists various nonheparin options
for intraoperative anticoagulation.25 However, experience
during vascular surgery with these approaches is minimal,
and so risk-benefi t considerations of any operative intervention must be judged individually. Whether monitoring is best
performed using APTT, activated clotting time (ACT), or
ecarin clotting time (ECT) is unresolved. Physicians should
avoid “incidental” perioperative heparin exposure, for
example, during preoperative angiography or intraoperative
fl ushing of catheters.
Venous Limb Ischemia
Medical Management
Severe venous limb ischemia is a medical emergency, as
effective anticoagulation may prevent its progression.
Vitamin K (e.g., 10 mg i.v. over 30–60 min) is recommended
for the patient who has received warfarin, or who has an
elevated INR, since vitamin K antagonism or defi ciency can
explain venous limb ischemia.
10,14,15
The syndrome of phleg-
masia cerulea dolens can be prodromal for venous gangrene, and prompt institution of effective anticoagulation
can avoid critical limb ischemia.14 Sometimes systemic or
catheter-direct thrombolysis is given, but a caveat is that
fi brin(ogen) degradation products produced by thrombolysis
will bind and protect thrombin from its physiologic inhibitors, potentially worsening consumptive coagulopathy.
Thus, in my opinion, at least moderate-dose anticoagulation
should be given to a patient who is receiving thrombolysis
(e.g., lepirudin, 0.10 mg/kg/h or danaparoid 100–200 U/h
after an initial bolus).
Surgical Management
A surgical role for severe venous limb ischemia is less
certain. Fasciotomy is sometimes performed in patients with
suspected compartment syndrome, but this may delay or
interrupt much-needed aggressive anticoagulation. Further,
it is uncertain to what extent compartment syndromes contribute to limb ischemia in patients with HIT-associated
DVT and associated microvascular thrombosis.
Preoperative and Postoperative Anticoagulation
A patient with HIT-associated thrombosis who requires
intraoperative anticoagulation with a nonheparin anticoagulant may already be receiving this agent during the immediate preoperative period, thus obviating the need for a full
intraoperative dose. There is also the dilemma of whether to
continue the anticoagulant immediately postoperatively, or
whether to suspend infusion until postoperative hemostasis
appears secure. However, the prothrombotic nature of acute
HIT suggests that continuing anticoagulation even during
the immediate postoperative period (at least in low doses)
can be appropriate.
References
1. Warkentin TE. Heparin-induced thrombocytopenia: Pathogenesis and
management, Br. J. Haematol. 2003. 121: 535–555.
2. Warkentin TE. Clinical picture of heparin-induced thrombocytopenia.
In: Warkentin TE, Greinacher A, eds. Heparin-induced thrombocytopenia, 3e. 2004. 53–106. New York: Marcel Dekker, Inc.
3. Warkentin TE, Roberts RS, Hirsh J, Kelton JG. An improved defi nition
of immune heparin-induced thrombocytopenia in postoperative orthopedic patients, Arch. Intern. Med. 2003. 163: 2518–2524.
4. Warkentin TE. An overview of the heparin-induced thrombocytopenia
syndrome, Semin. Thromb. Hemost. 2004. 30: 273–283.
5. Lee DH, Warkentin TE. Frequency of heparin-induced thrombocytopenia. In: Warkentin TE, Greinacher A, eds. Heparin-induced thrombocytopenia, 3e. 2004. 107–148. New York: Marcel Dekker, Inc.
6. Warkentin TE, Kelton JG. A 14-year study of heparin-induced thrombocytopenia, Am. J. Med. 1996. 101: 502–507.
7. Warkentin TE. Heparin-induced thrombocytopenia: Diagnosis and
management, Circulation. 2004. 110: e454–e458.
8. Lo GK, Juhl D, Warkentin TE, Sigouin CS, Eichler P, Greinacher A.
Evaluation of pretest clinical score (4 T’s) for the diagnosis of heparininduced thrombocytopenia in two clinical settings, J Thromb Haemost.
2006. 4: 759–765.
9. Warkentin TE, Kelton JG. Temporal aspects of heparin-induced thrombocytopenia, N. Engl. J. Med. 2001. 344: 1286–1292.
10. Warkentin TE, Greinacher A. Heparin-induced thrombocytopenia:
Recognition, treatment, and prevention. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy, Chest. 2004.
126(Suppl.): 311S–337S.
11. Warkentin TE, Kelton JG. Delayed-onset heparin-induced thrombocytopenia and thrombosis, Ann. Intern. Med. 2001. 135: 502–506.
12. Warkentin TE. Management of heparin-induced thrombocytopenia: A
critical comparison of lepirudin and argatroban, Thromb. Res. 2003.
110: 73–82.
13. Hong AP, Cook DJ, Sigouin CS, Warkentin TE. Central venous catheters and upper-extremity deep-vein thrombosis complicating immune
heparin-induced thrombocytopenia, Blood. 2003. 101: 3049–3051.
14. Warkentin TE, Elavathil LJ, Hayward CPM, Johnston MA, Russett JI,
Kelton JG. The pathogenesis of venous limb gangrene associated with
heparin-induced thrombocytopenia, Ann. Intern. Med. 1997. 127:
804–812.
15. Warkentin TE. Heparin-induced thrombocytopenia: IgG-mediated
platelet activation, platelet microparticle generation, and altered procoagulant/anticoagulant balance in the pathogenesis of thrombosis and
venous limb gangrene complicating heparin-induced thrombocytopenia, Transfus. Med. Rev. 1996. 10: 249–258.
16. Warkentin TE, Kelton JG. Thrombocytopenia due to platelet destruction and hypersplenism. In: Hoffman R, Benz EJ Jr, Shattil SJ, Furie
B, Cohen HJ, Silberstein LE, McGlave P, eds. Hematology. Basic
Principles and Practice, 4e. 2005. 2305–2325. New York: Elsevier;
Churchill Livingstone.
17. Greinacher A, Eichler P, Lubenow N, Kwasny H, Luz M. Heparininduced thrombocytopenia with thromboembolic complications: Metaanalysis of 2 prospective trials to assess the value of parenteral
treatment with lepirudin and its therapeutic aPTT range, Blood. 2000.
96: 846–851.
18. Lewis BE, Wallis DE, Leya F, Hursting MJ, Kelton JG. Argatroban
anticoagulation in patients with heparin-induced thrombocytopenia,
Arch. Intern. Med. 2003. 163: 1849–1856.
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19. Warkentin TE, Sheppard JI, Moore JC, Moore KM, Sigouin CS, Kelton
JG. Laboratory testing for the antibodies that cause heparin-induced
thrombocytopenia. How much class do we need? J. Lab. Clin. Med.
2005. 146: 341–346.
20. Warkentin TE, Cook DJ. Heparin, low molecular weight heparin, and
heparin-induced thrombocytopenia in the ICU, Crit. Care Clin. 2005.
21: 513–529.
21. Greinacher A. Lepirudin: a bivalent direct thrombin inhibitor for anticoagulation therapy, Exp. Rev. Cardiovasc. Ther. 2004. 2: 339–357.
22. Warkentin TE, Greinacher A, Craven S, Dewar L, Sheppard JI, Ofosu
FA. Differences in the clinically effective molar concentrations of four
direct thrombin inhibitors explain their variable prothrombin time prolongation. Thromb. Haemost. 2005. 94: 958–964.
23. Warkentin TE, Koster A. Bivalirudin: A review, Expert Opin. Pharmacother. 2005. 6: 1349–1371.
24. Warkentin TE, Cook RJ, Marder VJ, Sheppard JI, Moore JC, Eriksson
BI. et al. Anti-platelet factor 4/heparin antibodies in orthopedic surgery
patients receiving antithrombotic prophylaxis with fondaparinux or
enoxaparin, Blood. 2005. 106: 3791–3796.
25. Warkentin TE. Heparin-induced thrombocytopenia and vascular
surgery, Acta Chir. Belgica. 2004. 104: 257–265.
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CHAPTER
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45
Operative Venous Thrombectomy
ANTHONY J. COMEROTA and STEVEN S. GALE
INTRODUCTION
Contemporary venous thrombectomy has the potential of
offering patients with extensive iliofemoral and/or infrainguinal deep vein thrombosis (DVT) an opportunity for rapid
resolution with signifi cant reduction in postthrombotic morbidity. It is both surprising and disappointing that vascular
surgeons in the United States have not moved beyond the
criticisms of the venous thrombectomy procedure performed
over 40 years ago. In the most recent ACCP consensus
conference section addressing the management of patients
with venous thromboembolic disease, it is stated that “in
patients with DVT, we recommend against the use of venous
thrombectomy (Grade 1C).”1 They go on to say that “surgical thrombectomy is commonly complicated by a recurrence
of thrombus formation.” Unfortunately, the authors reference an anecdotal experience in patients treated over
40 years ago.2 The follow-up on these patients was
incomplete and biased. Only 50% of the patients
originally treated underwent follow-up and only 25% had
follow-up phlebography.
The early experience with venous thrombectomy was
enthusiastically received because of reports of excellent
patency without severe postthrombotic sequelae. Mahorner
3
and Haller and Abrams4 reported excellent patency
et al.
rates in patients operated upon early for iliofemoral venous
thrombosis. Haller and Abrams reported an 85% patency
rate with 81% of survivors having normal legs without
postthrombotic swelling. However, a subsequent follow-up
report indicated higher rates of rethrombosis with failure to
prevent postthrombotic sequelae, despite a patent deep
venous system, presumably due to valvular incompetence.
This most damaging report was a fi ve-year follow-up of
patients originally described by Haller and Abrams. They
2
reported that 94% of patients returning for follow-up had
signifi cant edema and skin changes, which required elastic
stockings and leg elevation. Patients who underwent followup phlebography were found to have incompetent valves,
although this represented only approximately 25% of the
patients initially treated. Lansing and Davis
tion to the fact that two of the three postoperative deaths
(in the 34 patients initially operated) were from pulmonary
embolism (PE) and that there was a 30% wound complication rate, an average transfusion requirement of 1000 ml, and
a mean hospital stay of 12 days. Critics of operative venous
thrombectomy frequently fail to mention that the early technique was unlike modern thrombectomy procedures, with
patients undergoing cut-downs on their iliac veins, femoral
veins, and vena cava, often with fl ush and irrigation procedures performed to clear the venous system of thrombus,
whereas venous thrombectomy today is performed with
balloon catheters, and autotransfusion devices are available
to minimize the need for blood transfusion. Completion
phlebograms were essentially nonexistent with no effort to
either identify or correct underlying venous pathology. Arteriovenous fi stulae were not constructed and it is unclear to
what degree patients were anticoagulated either during the
procedure or postoperatively.
The report by Lansing and Davis suffered from a selection bias, since it is likely that the patients with the most
severe postthrombotic sequelae were returning for follow-up
and therefore the most heavily represented in their series.
Furthermore, the patients reported represented only 50% of
those initially operated upon, with phlebographic examination in far fewer. Another damaging report was that of Karp
and Wylie,
iliofemoral venous thrombectomy. Although the patients’
clinical symptoms appeared to be improved, the
5
who reported uniform rethrombosis following
2
brought atten-
The Vein Book
405
All rights of reproduction in any form reserved.
Copyright © 2006, Elsevier Inc.
406 Chapter 45/Operative Venous Thrombectomy
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predischarge phlebographic documentation of rethrombosis
led to further disinterest in venous thrombectomy.
Subsequent reports of successful thrombectomy from
European centers,
6–13
with success rates reported as high as
88% without mortality, were for the most part ignored by
surgeons in the United States. However, a number of vascular centers have persisted in using thrombectomy,
13,14
and
with the ongoing experience and refi nement of technique,15
the results have markedly improved.
Most notable among these technical improvements are
the use of a venous thrombectomy catheter (large balloon),
fl uoroscopic-guided thrombectomy with completion intraoperative phlebography, correction of an underlying venous
stenosis, construction of an AVF, and immediate and prolonged therapeutic anticoagulation, often catheter-directed.
The ACCP consensus guideline authors failed to reference a contemporary randomized trial of venous thrombectomy and AVF versus anticoagulation alone in patients with
iliofemoral venous thrombosis.
16–18
These patients underwent systematic follow-up with routine venous imaging
and physiologic measurements. Peer-reviewed reporting
occurred at six months,16 fi ve years,17 and 10 years18 of
follow-up. Patients randomized to venous thrombectomy
demonstrated improved patency (P < 0.05), lower venous
pressures (P < 0.05), less leg swelling (P < 0.05), and
fewer postthrom botic symptoms (P < 0.05) compared to
anticoagulation.
RESULTS OF OPERATIVE
VENOUS THROMBECTOMY
Although the early mortality rate in Haller and Abrams
series was 9%, with two of the three fatalities attributed to
PE, by the mid-1980s a progressive reduction in operative
mortality was observed. Eklof and Juhan19 reported their
large experience in 230 patients undergoing venous thrombectomy for iliofemoral venous thrombosis. They reported
no fatal PE and only one operative death. It is apparent that
the application of venous thrombectomy now can be based
on its effectiveness relative to competitive forms of therapy
in reducing early morbidity and the late sequelae of iliofemoral venous thrombosis, rather than on the concern that
the procedure will fail or be accompanied by complications.
Successful venous thrombectomy signifi cantly reduces
early morbidity in patients with phlegmasia cerulea dolens
and phlegmasia alba dolens. The patients’ pain and edema
quickly subside and the discoloration resolves. The defi nition of benefi t, however, may be masked by the additional
cost of the operation, the need for blood transfusion, incisional discomfort, and wound complications. Interestingly,
even if thrombectomy is not complete or is followed by
some degree of rethrombosis, the limb rarely returns to its
former morbid state if elevation and anticoagulation are
TABLE 45.1 Venous Thrombectomy with Arteriovenous
Fistula: Long-Term Iliac Vein Patency
Follow-up Patent iliac vein
Author/Year No. (mos) (%)
Plate et al. 1984
Piquet et al. 19856 57 39 80
Einarsson et al. 1986
Vollmar 1986
Juhan et al. 19999 150 102 84
Torngren et al. 198810 54 19 54
Rasmussen et al. 199011 24 20 88
Eklof et al. 199613 77 48 75
Neglen et al. 199112 34 24 88
Meissner et al. 199625 27 12 89
Pillny et al. 200326 97 70 90
TOTAL 702 41 mos (mean) 78% (mean)
Adapted from Reference 29. Used with permission.
16
31 6 76
7
58 10 61
8
93 53 82
continued. In our experience, thrombectomy has failed
only when our own treatment guidelines were not observed.
Although several patients may not have benefi ted, no patient
has been made clinically worse, and we have yet to observe
a symptomatic PE following the procedure.
The long-term benefi ts of venous thrombectomy relate to
its ability to achieve proximal patency and maintain distal
valve competence. Both are infl uenced by initial technical
success and the avoidance of recurrent thrombosis. Initial
success in achieving patency is, in turn, infl uenced by timely
intervention and attention to technical detail. Pooled
data from a number of contemporary reports on iliofemoral
venous thrombectomy (see Tables 45.1 and 45.2) have indicated that the early and long-term patency for the iliofemoral venous segment is in the 75 to 80% range compared with
30% patency in patients treated with anticoagulation alone,20
and femoral-popliteal venous valve function is preserved in
the majority of patients.
TECHNIQUE
The incremental goals that we believe are important for
successful venous thrombectomy are summarized in Table
45.3. During the past two decades, the technique of venous
thrombectomy has been refi ned and improved. Most of the
principles of a successful procedure follow those established
for patients undergoing arterial reconstruction for acute arterial occlusion. A number of important technical modifi cations have evolved, however, beginning with the accurate
preoperative defi nition of the extent of thrombus (both
proximally and distally) and whether the thrombus has
em bolized to the pulmonary vascular bed. The proximal
extent of thrombus can be clearly defi ned by contralateral
iliocavagraphy. It is especially important to determine
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TABLE 45.2 Venous Thrombectomy with Arteriovenous
Fistula: Long-Term Valve Competence of Femoropopliteal
Venous Segment
Follow-up Femoral-popliteal
Author/Year No. (mos) valve competence
Plate et al. 1984
Einarsson et al. 1986
Ganger et al. 198927 17 91 82
Neglen et al. 199112 37 24 56
Kniemeyer et al. 199328 37 55 80
Juhan et al. 19999 150 60 80
Meissner et al. 199625 27 60 30
TOTAL 352 45 mos 63% (mean)
(mean)
From Reference 29. Used with permission.
TABLE 45.3 Technique of Contemporary
Venous Thrombectomy
1. Identify etiology of extensive venous thromboembolic process
a. Complete thrombophilia evaluation
b. Rapid CT scan of chest, abdomen, and pelvis
2. Defi ne full extent of thrombus
a. Venous duplex examination
b. Contralateral iliocavagram, MRV, or spiral CT
3. Prevent pulmonary embolism (numerous techniques)
a. Anticoagulation
b. Vena caval fi lter (if nonocclusive caval clot)
c. Balloon occlusion of vena cava during thrombectomy
d. Positive end-expiratory pressure during thrombectomy
4. Perform complete thrombectomy
a. Iliofemoral (vena cava) thrombectomy
b. Infrainguinal venous thrombectomy (if required)
5. Ensure unobstructed venous infl ow to and outfl ow from
thrombectomized iliofemoral venous system
a. Infrainguinal venous thrombectomy (if required)
b. Correct iliac vein stenosis (if present)
6. Prevent recurrent thrombosis
a. Arteriovenous fi stula
b. Continuous therapeutic anticoagulation
c. Catheter-directed postoperative anticoagulation (if infrainguinal
venous thrombectomy is required)
d. Extended oral anticoagulation
MRV, magnetic resonance venography; CT, computerized tomo-
graphy.
16
31 6 52
7
53 10 42
whether thrombus has extended into the vena cava.
Magnetic resonance venography with gadolinium or spiral
computerized tomography (CT) scan with contrast may
obviate the invasive procedure in some patients. Our preference is spiral CT scan with contrast, since a rapid CT scan
of the chest can be performed simultaneously to evaluate for
PE and other pathology, followed by a CT scan of the
abdomen and pelvis, which not only localizes the proximal
extent of thrombus, but also examines for intraabdominal
and pelvic pathology.
During the operation, complete thrombus removal is
ensured by completion phlebography. Correction of an
underlying venous stenosis with balloon angioplasty and
stenting (if needed) is critical to obtain unobstructed venous
drainage into the vena cava. Residual iliac vein obstruction
produces venous hypertension at best and often leads to
recurrent venous thrombosis. Therefore, it must be identifi ed
and corrected. A properly constructed AVF increases venous
velocity through the previously thrombosed iliofemoral
venous system without increasing venous pressure, thereby
decreasing the risk of rethrombosis. Prolonged therapeutic
anticoagulation is important to prevent recurrence.
The more recent modifi cations, which include balloon
catheter thrombectomy of the vena cava during suprarenal
caval balloon occlusion for nonocclusive caval clot and
infrainguinal venous thrombectomy followed by early and
continued postoperative anticoagulation through a catheter
remaining in the posterior tibial vein and construction of an
AVF, are likely to further improve outcome. The sequential
details of the contemporary venous thrombectomy are
described in the following sections.
Preoperative Procedures
1. Evaluate the patient for an underlying thrombophilia.
Since the majority of patients with DVT do not
develop this degree of extensive thrombosis, the
likelihood of identifying an underlying thrombophilia
is high. If the patient is already anticoagulated, blood
is sent for antiphospholipid antibody, factor V Leiden,
prothrombin gene mutation, and homocysteine. These
can be reliably performed in patients who are already
being treated with heparin. A blood sample also is
sent for type and cross-match.
2. Delineate the full extent of thrombus. It is always
important to know whether the clot is involving the
vena cava. A contralateral iliocavagram frequently is
performed to assess the vena cava (see Figure 45.1).
Additionally, a rapid spiral CT scan with contrast of
the chest examines for PE as well as thoracic
pathology. The subsequent abdominal and pelvic
CT scans during the same contrast infusion can
identify the proximal extent of thrombus and any
intraabdominal or pelvic pathology that may be
etiologically associated with the DVT (see Figure
45.2). We have found PE in approximately 50% of
our patients. We have also found renal cell carcinoma
with tumor thrombus extending into the vena cava,
adrenal tumors, retroperitoneal lymphoma, hepatic
metastases from unknown primaries, and iliac vein
aneurysms. Each of these is critically important for
proper patient management and would have been
overlooked had the CT scan not been performed.
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FIGURE 45.1 Contralateral iliocavagrams showing nonocclusive thrombus in the vena cava illustrate the value of
imaging to detect proximal extent of thrombus.29 Used with permission.
FIGURE 45.2 Asymptomatic PE (arrow, A) and renal cell carcinoma (arrow, B) identifi ed with CT scan of chest as
part of the evaluation of patients with iliofemoral DVT.
3. Therapeutic anticoagulation with unfractionated
heparin (UFH) is initiated after the blood samples
are drawn for the thrombophilia evaluation.
Unfractionated heparin is continued throughout the
procedure and postoperatively.
4. Vena caval fi ltration is not routinely required. An
exception may be those patients with nonocclusive
29
Used with permission.
thrombus extending into the vena cava (see
Figure 45.1). The recently introduced optional
(nonpermanent) vena caval fi lters have been used with
plans for early retrieval. Patients with caval thrombus
also have been managed with balloon occlusion of the
proximal vena cava at the time of balloon catheter
thrombectomy. The protective vena caval balloon is
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FIGURE 45.3 Preoperative iliocavagram shows nonocclusive thrombus extending from the left iliofemoral venous
system into the vena cava (A). A suprarenal balloon catheter was placed from the contralateral femoral vein and inserted
under fl uoroscopy. The balloon is infl ated at the time of thrombectomy (B). Schematic of iliocaval thrombectomy
performed with the double balloon catheter technique, protecting the patient from pulmonary embolism (C).
15
positioned during preoperative iliocavagraphy from
the contralateral femoral vein using fl uoroscopic
guidance. After positioning, the balloon remains
defl ated until the time of thrombus extraction (see
Figure 45.3).
5. The operating room is prepared for fl uoroscopy. An
autotransfusion device is made available during the
procedure.
Operative Details
6. General anesthesia is recommended for the majority
of patients.
7. A longitudinal inguinal incision is made with
exposure and control of the common femoral vein,
femoral vein, saphenofemoral junction, and profunda
femoris vein (see Figure 45.4A).
8. A longitudinal venotomy is made in the common
femoral vein at about the level of the saphenofemoral
junction. The precise location of the venotomy
depends upon the extent and location of the thrombus.
Since the common femoral vein is dilated, closure of
the longitudinal venotomy with fi ne monofi lament
suture can be achieved without compromising vein
lumen.
9. The infrainguinal venous thrombectomy is performed
fi rst. The leg is elevated and compressed from the toes
proximally with a tightly wrapped rubber bandage.
The foot is dorsifl exed and the leg squeezed and
milked to remove the clot from below.
10. If infrainguinal clot persists, a cut-down on the medial
portion of the lower leg is performed to expose the
posterior tibial vein in order to accomplish a balloon
catheter infrainguinal venous thrombectomy (see
Figure 45.4B). A #3 or #4 balloon catheter is passed
proximally from below to exit from the common
femoral venotomy (see Figure 45.5A). The stem of a
plastic IV catheter (12–14 gauge) is slid halfway onto
the balloon catheter coming up from below and
another (#4) balloon catheter is placed into the
opposite end of the plastic sheath. Pressure is applied
to the two balloons to secure the catheters inside the
sheath by a single operating surgeon. The #4 balloon
catheter is guided distally through the venous valves
and clotted veins (see Figure 45.5B) to the level of the
posterior tibial venotomy (see Figure 45.5C). The
infrainguinal venous thrombectomy is then performed
with a #4 or #5 balloon catheter, if necessary (see
Figure 45.5D,E), repeating catheter passage as
required until no further thrombus is extracted.
410 Chapter 45/Operative Venous Thrombectomy
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FIGURE 45.4 Exposure of the common femoral, femoral, and profunda femoris veins (A). Exposure of the posterior
tibial vein (B).
30
11. Following the infrainguinal balloon catheter
thrombectomy, the infrainguinal venous system is
vigorously fl ushed with a heparin-saline solution to
hydraulically force residual thrombus (which can be
considerable) from the deep venous system by placing
a #14–#16 red rubber catheter into the proximal
posterior tibial vein and fl ushing with a bulb syringe
(see Figure 45.6). After applying a vascular clamp
below the femoral venotomy, the infrainguinal venous
system is then fi lled with a dilute plasminogen
activator solution using approximately 4 to 6 mg of rtPA in 200 cc of saline. The plasminogen activator
solution remains in the infrainguinal veins for the
remainder of the procedure. If the infrainguinal
venous thrombectomy is not successful due to chronic
thrombus in the femoral vein, the femoral vein is
ligated and divided below the profunda. Patency of
the profunda is ensured by direct thrombectomy, if
required.
12. The proximal thrombectomy is performed by passing
a #8 or #10 venous thrombectomy catheter partway
into the iliac vein for several passes to remove
thrombus before advancing the catheter into the vena
cava. The proximal thrombectomy is performed under
fl uoroscopy with contrast in the balloon, especially if
a vena caval fi lter is present, there is clot in the vena
cava, or resistance to catheter passage is encountered.
The anesthesiologist should apply positive endexpiratory pressure during the iliocaval thrombectomy.
If there is clot in the vena cava, the caval thrombectomy can be performed with a protective balloon
catheter infl ated above the thrombus and the
thrombectomy performed under fl uoroscopy (see
Figure 45.3).
13. After completion of the iliofemoral thrombectomy,
the iliofemoral venous system is examined with
intraoperative phlebography/fl uoroscopy to ensure
unobstructed venous drainage into the vena cava (see
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Figure 45.7). Any underlying iliac vein stenosis is
corrected with balloon angioplasty using a stent if
venous recoil occurs. If a stent is used, a 12 mm
diameter or greater is recommended.
14. After closing the venotomy with fi ne monofi lament
suture, an end-side AVF is constructed using the end
of the proximal saphenous vein or a large proximal
branch of the saphenous vein anastomosed to the side
FIGURE 45.5 Technique of infrainguinal balloon catheter venous thrombectomy begins with passage of a #3 or #4
balloon catheter from the posterior tibial vein proximally, exiting the femoral venotomy. A silastic IV sheath is placed
halfway onto the catheter and another #4 balloon catheter inserted into the other end of the sheath (A). The balloons
are infl ated to fi x the catheter tips inside of the sheath with pressure applied by a single individual guiding them distally
through the clotted veins and venous valves (B). Catheters and sheath exit the posterior tibial venotomy (C). The
thrombectomy catheter balloon is infl ated gently as the catheter is pulled proximally (D) to exit the femoral venotomy,
extracting thrombus (E).
15
of the superfi cial femoral artery (see Figure 45.8A).
The anastomosis should be limited to 3.5 to 4.0 mm
in diameter. Frequently the proximal saphenous vein
requires thrombectomy to restore patency prior to the
AVF.
15. A piece of PTFE or silastic is placed around the
saphenous AVF and a large permanent monofi lament
suture (#0) looped and clipped, leaving approximately
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