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Prolongation of the INR by argatroban is consider-
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24
ably greater than with lepirudin,
which can complicate
argatroban-warfarin overlap. Argatroban’s greater e ect on
the INR results from its relatively low a nity for thrombin, and thus the need for greater molar concentrations
(approximately twenty-fold) to double the APTT, compared with lepirudin. Plasma concentrations of argatroban
(~1.0 µmol/L) are similar to the theoretical maximum
amount of thrombin generated in the INR reaction.
BIVALIRUDIN
Bivalirudin (Angiomax) is a twenty-amino acid hirulog (analogue of hirudin) that unites a C-terminal seg-
ment of twelve amino acids (dodecapeptide) derived from
hirudin to an active site-binding tetrapeptide sequence
(d-Phe-Pro-Arg-Pro) at its N-terminus, bridged by four gly-
25
cines (2,180 Da).
Indeed, bivalirudin connotes this bivalent
binding to thrombin. Unlike hirudin, however, bivalirudin
interaction with thrombin is transient, as plasma proteases
cleave bivalirudin near its N-terminus. e a nity of bivalirudin for human thrombin (Ki=2nmol/L) is between that
observed for lepirudin and argatroban; accordingly, its ability to prolong the INR is intermediate in comparison with
24
these other two DTIs.
Bivalirudin has undergone o -label
use in HIT, particularly in the setting of o -pump and
25
on-pump (cardiopulmonary bypass) cardiac surgery.
DANAPAROID ORGARAN
Danaparoid (Orgaran) is a “heparinoid” (mixture of anticoagulant glycosaminoglycans) that has both anti-Xa and antithrombin (anti-IIa) activity (anti-Xa/anti-IIa ratio = 22;
6,000 Da [mean]). It is available in Canada and Europe, but
was withdrawn from the United States in 2002. It is e ective for treatment and prevention of thrombosis in HIT, but
its long half-life (25 h), lack of an antidote, and inability to
inhibit clot-bound thrombin make it less than ideal for anticoagulation during vascular surgery.
FONDAPARINUX ARIXTRA
Fondaparinux (Arixtra), a synthetic indirect (AT-dependent)
inhibitor of factor Xa, is modeled a er the AT-binding
pentasaccharide region of heparin (1,727 Da). Despite its
small size (compared with natural heparin), anti-PF4/heparin antibodies are generated as o en during fondaparinux
26
therapy as with LMWH.
However, the antibodies formed
do not cross-react with PF4/fondaparinux, suggesting that
fondaparinux causes HIT even less o en than LMWH,
and probably is e ective for treatment of HIT-associated
17,23
thrombosis
contraindicated
(a situation for which LMWH is considered
8
). Since fondaparinux is FDA-approved
for prevention and treatment of venous thromboembolism
(2.5 mg and 7.5 mg once daily by SC injection, respectively,
for average-sized adults), it is appropriate for many patients
with a previous history of HIT, in which repeat use of heparin usually is avoided. As with danaparoid, the long half-life
of fondaparinux (17 h), the lack of an antidote, and its
inability to inhibit clot-bound thrombin make it less than
ideal for anticoagulation during vascular surgery.
M A N A G E M E N T O F T H E
ISCHEMICLIMB
EVALUATION OF LIMB ISCHEMIA
e clinician must determine whether there is large and
medium-size artery thrombosis that could be amenable to
surgical thromboembolectomy, or whether limb ischemia
re ects microvascular thrombosis, thus indicating a medical rather than surgical emergency (see Figure41.1). O en,
microvascular thrombosis is associated with proximal DVT
in the same limb, but can also be associated with arterial
thrombosis particularly in the setting of overtDIC.
A r t e r i a l romboembolectomy
e vascular surgeon who manages a patient with
limb-threatening ischemia due to artery occlusion in HIT
faces the dilemma of how to anticoagulate such a patient during potentially limb-salvaging thromboembolectomy, as UFH
is at least relatively contraindicated. However, for patients
with acute (or recent) HIT requiring thromboembolectomy,
it is unknown whether nonheparin anticoagulation achieves
better outcomes over intraoperative anticoagulation with hep-
27
Afurther issue is that in the emergency setting of throm-
arin.
boembolectomy for critical limb ischemia, there may not be
su cient time to obtain HIT antibody test results, consult a
hematologist, or even organize alternative anticoagulation.
Section B of Table41.4 lists various nonheparin options
28
for intraoperative anticoagulation.
However, experience
during vascular surgery with any of these approaches is
minimal, and so risk-bene 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 unknown.
Venous Limb Ischemia
Medical Management
Severe venous limb ischemia is a medical emergency,
as e ective anticoagulation may prevent its progression.
Vitamin K (e.g., 10 mg IV over 30–60 min) is recommended
for the patient who has received warfarin, or who has an elevated INR, since vitamin K antagonism or de ciency can
explain venous limb ischemia.
masia cerulea dolens can be prodromal for venous gangrene, and prompt institution of e ective anticoagulation
12–15
e syndrome of phleg-
338 • VENOUS THROMBOEMBOLISM
could avoid critical limb ischemia. 12 Sometimes systemic
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or catheter-direct thrombolysis is given, but a caveat is that
brin(ogen) degradation products produced by thrombolysis will bind and protect thrombin from its physiologic
inhibitors, potentially worsening consumptive coagulopathy. us, in my opinion, at least moderate-dose anticoagulation should be given to a patient who is receiving
thrombolysis (e.g., lepirudin, 0.05–0.10 mg/kg/h or danaparoid 100–200 U/h a er an initial danaparoid 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. ere 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-to-moderate doses) can be appropriate.
R E F E R E N C E S
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 thrombo-
cytopenia , 5e. Boca Raton, FL:CRC Press. 2013:24 –76 .
3. Warkentin TE , Roberts RS , Hirsh J , Kelton JG . An improved de nition of immune heparin-induced thrombocytopenia in postoperative
orthopedic patients , Arch Intern Med . 2003 . 163 : 2518–2524 .
4. Linkins LA , Lee DH . Frequency of heparin-induced thrombocytopenia. In: Warkentin TE , Greinacher A , eds. Heparin-induced thrombo-
cytopenia , 5e. Boca Raton, FL:CRC Press. 2013:110 –150 .
5. Warkentin TE , Kelton JG . A 14-year study of heparin-induced
thrombocytopenia , Am J Med . 1996 . 101 : 502–507 .
6. Lo GK , Juhl D , Warkentin TE , Sigouin CS , Eichler P , Greinacher
A . Evaluation of pretest clinical score (4 T’s) for the diagnosis of
heparin-induced thrombocytopenia in two clinical settings , J romb
Haemost . 2006 . 4 : 759–765 .
7. Warkentin TE , Kelton JG . Temporal aspects of heparin-induced
thrombocytopenia , N Engl J Med . 2001 . 344 : 1286–1292 .
8. Linkins LA , Dans AL , Moores LK , Bona R , Davidson BL , Schulman
S , etal. Treatment and prevention of heparin-induced thrombocytopenia: Antithrombotic erapy and Prevention of rombosis, 9th
ed: American College of Chest Physicians Evidence-Based Clinical
Practice Guidelines , Chest . 2012 . 141 ( Suppl 2 ): e495S–e530S .
9. Warkentin TE , Kelton JG . Delayed-onset heparin-induced thrombocytopenia and thrombosis , Ann Intern Med . 2001 . 135 : 502–506 .
10. Warkentin TE . Management of heparin-induced thrombocytopenia:Acritical comparison of lepirudin and argatroban , romb Res .
2003 . 110 : 73–82 .
11. 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 .
12. Warkentin TE , Elavathil LJ , Hayward CPM , Johnston MA , Russett
J I , K e l t o n J G . e pathogenesis of venous limb gangrene associated
with heparin-induced thrombocytopenia , Ann Intern Med . 1997 .
127 : 804–812 .
13. Smythe MA , Warkentin TE , Stephens JL , Zakalik D , Mattson JC .
Venous limb gangrene during overlapping therapy with warfarin and
a direct thrombin inhibitor for immune heparin-induced thrombocytopenia , Am J Hematol . 2002 . 71 : 50–52 .
14. Warkentin TE . Should vitamin K be administered when HIT is
diagnosed a er administration of coumarin?, J romb Haemost .
2006 . 4 : 894–896 .
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 . Heparin-induced thrombocytopenia. In: Ho man
R , Benz EJ Jr, Silberstein LE , Heslop HE , Weitz JI , Anastasi J , eds.
Hematology:Basic principles and practice, 6e. Philadelphia : Churchill
Livingstone Elsevier . 2013:1913 –1924 .
17. Warkentin TE . Agents for the treatment of heparin-induced thrombocytopenia , Hematol Oncol Clin North Am . 2010 . 24 : 755–775 .
18. Warkentin TE , Greinacher A . Heparin-induced anaphylactic and
anaphylactoid reactions:Two distinct but overlapping syndromes ,
Expert Opin Drug Saf . 2009 . 8 : 129–144 .
19. Greinacher A , Warkentin TE . e direct thrombin inhibitor hirudin , romb Haemost . 2008 . 99 : 819–829 .
20. Warkentin TE , Sheppard JI . Testing for heparin-induced thrombocytopenia antibodies , Transfus Med Rev . 2006 . 20 : 259–272 .
21. Warkentin TE , Sheppard JI , Moore JC , Sigouin CS , Kelton JG .
uantitative interpretation of optical density measurements using
PF4-dependent enzyme-immunoassays , J romb Haemost . 2008 .
6 : 1304–1312 .
22. Warkentin TE , Sheppard JI , Moore JC , Cook RJ , Kelton JG . Studies
of the immune response in heparin-induced thrombocytopenia ,
Blood . 2009 . 113 : 4963–4969 .
23. Warkentin TE , Pai M , Sheppard JI , Schulman S , Spyropoulos AC ,
Eikelboom JW . Fondaparinux treatment of acute heparin-induced
thrombocytopenia con rmed by the serotonin-release assay: A
30-month, 16-patient case series . J romb Haemost . 2011 . 9 :
2389–2396 .
24. Warkentin TE , Greinacher A , Craven S , Dewar L , Sheppard JI ,
Ofosu FA . Di erences in the clinically e ective molar concentrations of four direct thrombin inhibitors explain their variable prothrombin time prolongation , romb Haemost . 2005 . 94 : 958–964 .
25. Warkentin TE , Greinacher A , Koster A . Bivalirudin , romb
Haemost . 2008 . 99 : 830–839 .
26. Warkentin TE , Cook RJ , Marder VJ , etal. Anti-platelet factor 4/
heparin antibodies in orthopedic surgery patients receiving antithrombotic prophylaxis with fondaparinux or enoxaparin , Blood .
2005 . 106 : 3791–3796 .
27. Warkentin TE , Pai M , Cook RJ . Intraoperative anticoagulation and
limb amputations in patients with immune heparin-induced thrombocytopenia who require vascular surgery, J romb Haemost . 2012 .
10 : 148–150 .
28. Warkentin TE . Heparin-induced thrombocytopenia and vascular
surgery , Acta Chir Belgica . 2004 . 104 : 257–265 .
29. Warkentin TE , Greinacher A . Appendix 4:Six treatment principles
of HIT. In: Warkentin TE , Greinacher A , eds.
thrombocytopenia , 5e. Boca Raton, FL : CRC Press . 2013: 625.
Heparin-induced
DIAGNOSIS AND MANAGEMENT OF HIT • 339
42.
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OPERATIVE VENOUS THROMBECTOMY
Anthony J. Comerota and Steven S. Gale
INTRODUCTION
Contemporary venous thrombectomy has the potential of
o ering patients with extensive iliofemoral and/or infrainguinal deep vein thrombosis (DVT) an opportunity for
rapid resolution with signi cant reduction in postthrombotic morbidity. Early experience with venous thrombectomy was enthusiastically received because of reports of
excellent patency without severe postthrombotic sequelae.
1
Mahorner et al.
and Haller and Abrams 2 reported
excellent patency rates in patients operated on 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
3
incompetence.
is damaging report was a 5-year follow-up
of patients originally described by Haller and Abrams. ey
reported that 94% of patients returning for follow-up had
signi cant edema and skin changes, which required elastic stockings and leg elevation. Patients who underwent
follow-up phlebography were found to have incompetent
valves, although this represented only approximately 25%
3
of the patients initially treated. Lansing and Davis
brought
attention to the fact that two of the three postoperative
deaths (in the thirty-four patients initially operated) were
from pulmonary embolism (PE) and that there was a 30%
wound complication rate, an average transfusion requirement of 1,000 ml, and a mean hospital stay of12d.
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, o en with 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 e ort to either identify or
correct underlying venous pathology. Arteriovenous stulae were not constructed, and it is unclear to what degree
patients were anticoagulated either during the procedure or
postoperatively.
e report by Lansing and Davis su ered from a selection
bias, since it is likely that the patients with the most severe
postthrombotic sequelae were returning for follow-up and
therefore were the most heavily represented in their series.
Furthermore, the patients reported represented only 50%
of those initially operated on, with phlebographic examination in far fewer. Another damaging report was that of Karp
4
and Wylie,
who reported uniform rethrombosis following
iliofemoral venous thrombectomy. Although the patients’
clinical symptoms appeared to be improved, the predischarge phlebographic documentation of rethrombosis led
to further disinterest in venous thrombectomy.
Subsequent reports of successful thrombectomy from
5–12
European centers,
with success rates reported as high as
88% without mortality, were for the most part ignored by
surgeons in the United States. Moreover, until 2008, guideline authors overlooked a multicenter randomized trial
evaluating contemporary venous thrombectomy versus stan-
13–15
dard anticoagulation.
Patients underwent systematic
follow-up with routine venous imaging and physiologic measurements. Peer-reviewed reporting occurred at 6months,
14
5years,
and 10years 15 of follow-up. Patients randomized
13
to venous thrombectomy demonstrated improved patency
(P < 0.05), lower venous pressures (P < 0.05), less leg
swelling (P < 0.05), and fewer postthrombotic symptoms
(P < 0.05) compared with anticoagulation.
Fortunately, a number of vascular centers have per-
12,16
sisted in using thrombectomy,
experience and re nement of technique,
and with the ongoing
17
the results have
markedly improved. Most notable among these technical
improvements are the use of a venous thrombectomy catheter (large balloon), uoroscopic-guided thrombectomy
with completion intraoperative phlebography, correction
of an underlying venous stenosis, construction of an arteriovenous stula (AVF), and immediate and prolonged therapeutic anticoagulation, o en catheter-directed.
340
RESULTS OF OPERATIVE
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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
18
mortality was observed. Eklof and Juhan
reported their
large experience in 230 patients undergoing venous thrombectomy for iliofemoral venous thrombosis. ey reported
no fatal PE and only one operative death. It is apparent that
the application of venous thrombectomy now can be based
on its e ectiveness 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 signi cantly reduces
early morbidity in patients with phlegmasia cerulea dolens
and phlegmasia alba dolens. e patients’ pain and edema
quickly subside and the discoloration resolves. e de nition of bene 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 continued.
In our experience, thrombectomy has failed only when our
own treatment guidelines were not observed. Although several patients may not have bene ted, no patient has been
made clinically worse, and we have yet to observe a symptomatic PE following the procedure.
e long-term bene ts of venous thrombectomy relate
to its ability to achieve proximal patency and maintain distal valve competence. Both are in uenced by initial technical success and the avoidance of recurrent thrombosis.
Initial success in achieving patency is, in turn, in uenced
by timely intervention and attention to technical detail.
Pooled data from a number of contemporary reports on
iliofemoral venous thrombectomy (Tables42.1, 42.2) have
indicated that the early and long-term patency for the iliofemoral venous segment is in the 75–80% range compared
with 30% patency in patients treated with anticoagulation
19
alone,
and femoral-popliteal venous valve function is pre-
served in the majority of patients.
TECHNIQUE
e incremental goals that we believe are important for
successful venous thrombectomy are summarized in
Table 42.3. During the past two decades, the technique
of venous thrombectomy has been re 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 modi cations have evolved, however, beginning
with the accurate preoperative de nition of the extent of
thrombus (both proximally and distally) and whether the
thrombus has embolized to the pulmonary vascular bed.
e proximal extent of thrombus can be clearly de ned
by contralateral iliocavagraphy. It is especially important
Table42.1 VENOUS THROMBECTOMY WITH ARTERIOVENOUS
FISTULA:LONGTERM ILIAC VEIN PATENCY
AUTHOR/YEAR
REFERENCE NO.
Plate etal. 1984 (13) 31 6 76
Piquet etal. 1985 (5) 57 39 80
Einarsson etal. 1986 (6) 58 10 61
Vollmar 1986 (7) 93 53 82
Juhan etal. 1999 (8) 150 102 84
Torngren etal. 1988 (9) 54 19 54
Rasmussen etal. 1990 (10) 24 20 88
Eklof etal. 1996 (12) 77 48 75
Neglen etal. 1991 (11) 34 24 88
Meissner etal. 1996 (25) 27 12 89
Pillny etal. 2003 (26) 97 70 90
Hartung etal. 2008 (27) 29 63 86
Holper etal. 2009 (28) 25 68 84
TOTAL 756 55 mo (mean) 80% (mean)
Adapted from Comerota AJ, Gale SS. Surgical venous thrombectomy for iliofemoral deep vein
thrombosis. In:Greenhalgh RM, ed. Towards vascular and endovascular consensus . London:BIBA
Publishing. 2005. Used with permission.
NO. FOLLOWUP MO PATENT ILIAC VEIN %
OPERATIVE VENOUS THROMBECTOMY • 341
Table42.2 VENOUS THROMBECTOMY WITH ARTERIOVENOUS
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FISTULA:LONGTERM VALVE COMPETENCE OF FEMOROPOPLITEAL
VENOUS SEGMENT
AUTHOR/YEAR
REFERENCE NO.
Plate etal. 1984 (13) 31 6 52
Einarsson etal. 1986 (6) 53 10 42
Ganger etal. 1989 (29) 17 91 82
Neglen etal. 1991(11) 37 24 56
Kniemeyer etal. 1993 (30) 37 55 80
Juhan etal. 1999 (8) 150 60 80
Meissner etal. 1996 (25) 27 60 30
TOTAL 352 45 mo (mean) 63% (mean)
From Comerota AJ, Gale SS. Surgical venous thrombectomy for iliofemoral deep vein thrombosis.
In:Greenhalgh RM, ed. Towards vascular and endovascular consensus . London:BIBA Publishing. 2005.
Used with permission.
NO. FOLLOWUP MO FEMORALPOPLITEAL
to determine whether thrombus has extended into the
vena cava. Magnetic resonance venography (MRV) with
gadolinium or spiral computerized tomography (CT) scan
with contrast may obviate the invasive procedure in some
Table42.3 TECHNIQUE OF CONTEMPORARY VENOUS
THROMBECTOMY
1. Identify etiology of extensive venous thromboembolic process
a. Complete thrombophilia evaluation
b. Rapid CT scan of head, chest, abdomen, and pelvis
2 . D e 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 cava lter (if nonocclusive caval clot)
c. Balloon occlusion of vena cava during thrombectomy
d. Positive end-expiratory pressure during thrombectomy
4. Perform a complete thrombectomy
a. Iliofemoral (vena cava) thrombectomy
b. Infrainguinal venous thrombectomy (if required)
5. Ensure unobstructed venous in ow to and out ow from
thrombectomized iliofemoral venous system
a. Infrainguinal venous thrombectomy (if required)
b. Correct iliac vein stenosis (stent)
6. Prevent recurrent thrombosis
a. Arteriovenous stula
b. Continuous therapeutic anticoagulation
c. Catheter-directed postoperative anticoagulation
(ifinfrainguinal venous thrombectomy is required)
d. Extended oral anticoagulation
MRV, magnetic resonance venography; CT, computerized tomography
VALVE CO MP ET ENC E
patients. Our preference is spiral CT scan with contrast of
the head, chest, abdomen, and pelvis. Extending the imaging not only localizes the proximal extent of thrombus, but
also screens for other 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 o en leads to
recurrent venous thrombosis. erefore, it must be identi ed and corrected. Aproperly 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.
e more recent modi cations, which include balloon
catheter thrombectomy of the vena cava during suprarenal
caval balloon occlusion for nonocclusive caval clot, 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. e 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 tests. ese can be reliably performed
in patients who are already being treated with heparin. e
342 • VENOUS THROMBOEMBOLISM
results of the hypercoagulable evaluation are important
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for appropriate recommendations regarding duration of
anticoagulation. Ablood sample is also sent for type and
cross-match.
2. Delineate the full extent of thrombus. It is always
important to know whether clot is involving the vena cava.
A contralateral iliocavagram frequently is performed to
assess the vena cava (Figure 42.1). Additionally, a rapid
spiral CT scan with contrast of the head and chest examines for PE as well as brain and thoracic pathology. e
subsequent abdominal and pelvic CT scans during the
same contrast infusion can identify the proximal extent
of thrombus and any intra-abdominal or pelvic pathology that may be etiologically associated with the DVT
(Figure42.2). 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.
3. erapeutic anticoagulation with unfractionated
heparin (UFH) or low molecular weight heparin (LMWH)
is initiated a er the blood samples are drawn for the thrombophilia evaluation. UFH is used during the procedure and
early postoperative period. Although LMWH is as e ective
as UFH, intravenous UFH o ers better temporal control of
the degree of anticoagulation.
4. Vena caval ltration is not routinely required. An
exception may be those patients with nonocclusive thrombus extending into the vena cava (Figure42.1). e recently
introduced optional (nonpermanent) vena cava 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. e protective vena caval balloon is positioned during preoperative iliocavagraphy from the contralateral femoral vein using uoroscopic guidance. A er
positioning, the balloon remains de ated until the time of
thrombus extraction (Figure42.3).
5. e operating room is prepared for 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 femorisvein
(Figure42.4A).
8. A longitudinal venotomy is made in the common femoral vein at about the level of the saphenofemoral junction.
e precise location of the venotomy depends on the extent
and location of the thrombus. Since the common femoral
vein is dilated, closure of the longitudinal venotomy with
A B
clot
Figure 42.1 Contralateral iliocavagrams showing nonocclusive thrombus in the vena cava illustrate the value of imaging to detect proximal extent of
thrombus.
Used with permission.
From:Comerota AJ, Gale SS. Surgical venous thrombectomy for iliofemoral deep vein thrombosis. In:Greenhalgh R M, ed. Towards vascular and endovascular consensus . London :BIBA Publishing. 2005.
OPERATIVE VENOUS THROMBECTOMY • 343
A B
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Figure 42. 2 Asymptomatic PE (arrow, A) and renal cell carcinoma (arrow, B) identi ed with CT scan of chest as part of the evaluation of patients
with iliofemoralDVT.
Publishing. 2005. Used with permission.
From:Comerota AJ, Gale SS. Surgical venous thrombectomy for iliofemoral deep vein thrombosis. In:Greenhalgh R M, ed. Towards vascular and endovascular consensus . London:BIBA
ne mono lament suture can be achieved without compromising veinlumen.
9. e infrainguinal venous thrombectomy is performed
rst. e leg is elevated and compressed from the toes proximally with a tightly wrapped rubber bandage. e foot is
dorsi exed and the leg squeezed and milked to remove the
clot frombelow.
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 (Figure 42.4B).
A #3 or #4 balloon catheter is passed proximally from
below to exit from the common femoral venotomy
(Figure42.5A). e stem of a plastic IV catheter (12–14
A B
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 syringes attached to the two catheters by a single operating surgeon; this secures the balloons inside the sheath. e
#4 balloon catheter is guided distally through the venous
valves and clotted veins (Figure42.5B) to the level of the
posterior tibial venotomy (Figure42.5C). e infrainguinal
venous thrombectomy is then performed with a #4 or #5
balloon catheter, if necessary (Figure42.5, D and E), repeating catheter passage as required until no further thrombus
is extracted.
11. Following the infrainguinal balloon catheter throm-
bectomy, the infrainguinal venous system is vigorously
C
Figure 42.3 Preoperative iliocavagram shows nonocclusive thrombus extending from the le iliofemoral venous system into the vena cava (A).
Asuprarenal balloon catheter was placed from the contralateral femoral vein and inserted under uoroscopy. e balloon is in 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).
Clot
From Reference 17. Used with permission.
344 • VENOUS THROMBOEMBOLISM
A
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Figure44.4 Exposure of the common femoral, femoral, and profunda femoris veins (A). Exposure of the posterior tibial vein(B). From:Comerota AJ, GaleSS.
Contemporary venous thrombectomy. In:Fischer JE, Bland KI, eds . Mastery of surgery , 5e. Philadelphia, PA:Lippincott Williams & Wilkins. 2006. Used with permission.
B
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 ushing
with a bulb syringe (Figure42.6). A er ushing, a vascular clamp is applied below the femoral venotomy, and the
infrainguinal venous system is then lled with a dilute plasminogen activator solution using approximately 4–6 mg of
rt-PA in 200 cc of saline. e 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,
i f r e q u i r e d .
12. e 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. e proximal thrombectomy is performed under uoroscopy using
a contrast-saline solution to expand the balloon. is is
especially important if a vena cava lter is present, there
is clot in the vena cava, or resistance to catheter passage is
encountered. e anesthesiologist should apply positive
end-expiratory pressure during the iliocaval thrombectomy
to further reduce the risk of PE. If there is clot in the vena
cava, the caval thrombectomy can be performed with a protective balloon catheter in ated above the thrombus and the
thrombectomy performed under uoroscopy (Figure42.3).
13. A er completion of the iliofemoral thrombectomy,
the iliofemoral venous system is examined with intraoperative phlebography/ uoroscopy to ensure unobstructed
venous drainage into and through the vena cava (Figure42.7).
Any underlying iliac vein stenosis is corrected with balloon
angioplasty using a stent if venous recoil occurs. If a stent is
used, a diameter of 12mm or greater is recommended.
14. A er closing the venotomy with ne mono 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 of the super cial
femoral artery (Figure42.8A). e anastomosis should be
limited to 3.5–4.0mm in diameter. Frequently the proximal
saphenous vein requires thrombectomy to restore patency
prior to theAVF.
15. A piece of polytetra uoroethylene (PTFE) or a silastic band is placed around the saphenous AVF and a large
permanent mono lament suture (#0) looped and clipped,
leaving approximately 2 cm in the subcutaneous tissue
(Figure 42.8A). is will guide future dissection in the
event that operative closure of the AVF becomes necessary;
however, most donot.
16. Common femoral vein pressures are measured
before and a er the AVF is opened. Pressures should not
change. If the venous pressure increases when the AVF is
opened, the iliac veins should be reevaluated for residual
stenosis or obstruction, and the proximal lesion corrected.
If the pressure remains elevated, the AVF is constricted to
decrease ow and normalize pressure.
17. If there appears to be notable serous uid in the
wound, a search for transected lymphatics is performed and
they are ligated or coagulated. A#7 Jackson-Pratt drain (or
other similar closed suction drain) is placed in the wound
to evacuate hematoma or serous uid that may accumulate
postoperatively. e drain exits through a separate puncture
OPERATIVE VENOUS THROMBECTOMY • 345
E
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D
A
B
C
Figure 42. 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. Asilastic IV sheath is placed halfway onto the catheter and another #4 balloon catheter
inserted into the other end of the sheath (A). e balloons are in ated to 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). e thrombectomy catheter balloon is gently in ated as the catheter is pulled proximally (D)to exit the femoral venotomy, extracting
thrombus(E).
From Reference 17. Used with permission.
Figure 42. 6 A red rubber catheter (largest diameter possible) is placed into the posterior tibial vein and vigorously injected with a heparin-saline
solution using a bulb syringe to ush residual thrombus. A er ushing, the femoral vein is clamped and the leg veins injected with 150–200 cc of a
dilute UK or rt-PA solution.
From Reference 17. Used with permission.
346 • VENOUS THROMBOEMBOLISM
A
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B
After thrombectomy,
Figure 42. 7 A er thrombectomy, the right common iliac vein shows residual stenosis (A). Following iliac vein venoplasty, the stenosis is corrected,
restoring unobstructed venous drainage into the vena cava(B).
Towards vascular and endovascular consensus . London:BIBA Publishing. 2005. Used with permission.
site adjacent to the incision. e wound is closed with multilayered running absorbable sutures to achieve a hemostatic
and lymphostatic wound closure.
18. e distal posterior tibial vein is ligated. An infusion catheter (typically a pediatric feeding tube) is brought
into the wound via a separate stab incision in the skin and
before balloon dilation
From:Comerota AJ, Gale SS. Surgical venous thrombectomy for iliofemoral deep vein thrombosis. In:Greenhalgh R M, ed.
inserted and xed in the proximal posterior tibial vein
(Figure42.8B). is catheter is used for postoperative heparin anticoagulation and a follow-up (predischarge) phlebogram. is ensures maximal heparin concentration into
the a ected venous segment. A2-0 mono lament suture is
looped around the posterior tibial vein (and catheter) and
After balloon dilation
Figure 42. 8 e venotomy is closed with ne mono lament suture, and a 3.5- to 4.0-mm AVF is constructed sewing the transected end of the saphenous
vein to the side of the super cial femoral artery. Apiece of PTFE (5-mm gra ) or similar wrap is placed around the saphenous AVF, looped with #0
mono lament suture and the ends clipped, leaving approximately 2–2½ cm in the subcutaneous tissue to guide surgical closure of the AVF, should it be
necessary (A). e distal posterior tibial vein is ligated. An infusion catheter (pediatric NG-tube) is brought into the wound through a separate stab wound
in the skin and inserted and xed in the proximal posterior tibial vein. e proximal posterior tibial vein and catheter is looped with #0 mono lament
suture and xed to the skin through a sterile button, which is used to snugly occlude the posterior tibial vein at the time of catheter removal(B).
Reference 17. Used with permission.
B
A
F r o m
OPERATIVE VENOUS THROMBECTOMY • 347
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