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320 Acute central venous thrombosis in the setting of central lines, pacemaker wires, and dialysis catheters
https://t.me/med1917
that thrombosis formation with pacemaker leads was likely
to involve the three components of Virchow’s triad: stasis,
hypercoagulability, and endothelial damage.
29,30
e same
nding has been echoed by other studies.
25.4.5 Site selection
ere have been a number of studies that have addressed
site selection for CVC-related complications and specically
thrombosis. In one of these studies, the internal jugular
vein route had a decreased incidence of malposition as compared to the subclavian vein route: 5.3% versus 9.3% (RR:
0.66; 95% CI: 0.44–0.99).31 e study also found no dierence in thrombotic events. In another study, Martin et al.
addressed the risk of UEDVT in a prospective controlled
trial with axillary vein cannulation and found the incidence
of CVT to be 11%.
25.4.5.1 LATERALITY
Debourdeau et al. presented a review article and found
three studies that included CVCs and thrombosis in cancer patients.33 One study was a prospective controlled trial
in solid cancers among patients with tunneled catheters. It
evaluated 5447 patients and found le-sided subclavian and
jugular vein versus right subclavian vein access routes carry
an increased RR of 2.6 (P < 0.001). Another study examined
122 patients with solid tumors or hematological malignancies and found that the risks of thrombosis in le-sided versus right-sided access equaled 19% versus 5%, respectively
(RR: 4.4; P = 0.04). Finally, the third study sampled 334
patients with solid tumors or hematological malignancies
and also found le-sided versus right-sided CVC thrombosis, which resulted in rates of UEDVT of 25.6% versus 6.8%,
respectively (P < 0.001). us, le-sided access may carry a
higher risk of catheter-associated UEDVT in cancer patients.
25.4.5.2 JUGULAR OR SUBCLAVIAN
A Cochrane review completed in 2012 by Ge etal. attempted
to ascertain which vascular access site was associated with
thrombosis.9 ey found three randomized controlled trials
relevant to this topic. In comparing the internal jugular vein
route versus the subclavian route for long-term access in
cancer patients, the authors found no dierence in thrombotic complications (n = 240; RR: 1.97; 95% CI: 0.87–4.48).
Comparing femoral versus subclavian routes for shortterm CVCs, the results showed that femoral access (21.55%,
25/116 patients) had signicantly increased thrombotic
complications compared to subclavian access (1.87%, 2/107)
(n = 223; RR: 11.53; 95% CI: 2.80–47.52). Finally, by comparing the femoral site to the internal jugular vein in hemodialysis patients for short-term needs, the analysis found
that there was no dierence in thrombotic events between
these groups. is analysis demonstrated that subclavian
and internal jugular vein routes have similar long-term
catheter-related thrombotic complications. e subclavian
route was preferred to the femoral route for short-term
CVC access. ere were no randomized controlled trials
32
addressing CVT and catheter site location for either pacemaker or long-term hemodialysis catheter needs.
25.4.5.3 PRE-EXISTING CENTRAL LINES
AND CATHETERS
ere has been a traditional fear of inserting a hemodialysis
catheter on the ipsilateral side as a pacemaker or other CVC
due to the risk of venous thrombosis or wire dislodgement.
However, Jung etal. presented interesting ndings during
their retrospective review of 600 dialysis catheters over 10
years.34 ey found that in all 39 patients with preexisting CVCs (n = 19) or pacemaker wires (n = 20), the inser-
tion of a tunneled dialysis catheter ipsilateral to the side of
other CVC or pacemaker wires failed to reveal malfunction,
infection, or dislodgement of the lines or wires. us, the
authors recommended that in patients with anticipation of
a need for arteriovenous stula placement on one side, it is
safe to place a hemodialysis catheter on the side ipsilateral
to the cardiac pacing wire or CVC.
34
25.5 DIAGNOSIS
Determination of thrombosis using duplex ultrasonography
can demonstrate an acute UEDVT by the absence of augmentation of ow with respiration and other augmentation
maneuvers, inability to compress the vein whenever applicable, and hypoechoic signals.6 Baskin etal. presented a review
article in 2009 and found that duplex ultrasonography exhibited a sensitivity of 78%–100% and a specicity of 86%–100%
for the diagnosis of symptomatic UEDVT in an adult population.11 In another study, a prospective analysis was performed
in 66 children with acute lymphoblastic leukemia.11 e study
compared bilateral venography and duplex ultrasonography
in the diagnosis of asymptomatic UEDVT. e authors demonstrated that UEDVT occurred in 29% of patients and the
sensitivities of duplex ultrasonography and venography were
37% and 79%, respectively. ey postulated that the lower
duplex ultrasonography sensitivity was due to its inability to
detect subclavian thrombosis, while venography may miss
internal jugular thrombosis. e authors suggested using
a combination of methods if suspicion remained elevated.
In addition, a 2013 review article by Murray et al. of cancer
patients with thrombosis demonstrated that the sensitivity of
duplex ultrasonography may drop to 56% if proximal subclavian or brachiocephalic veins need to be assessed.
Nevertheless, due to its noninvasive nature and cost
advantage, duplex ultrasonography is initially recommended. If the duplex examination fails to reveal any
thrombosis and clinical suspicion remains high, either
computed tomography venography or magnetic resonance
venography (MRV) may be needed to conrm diagnosis.
Finally, venography remains the gold standard for the diagnosis of central vein thrombosis.
For patients with pacemaker wires, MRV is oen contraindicated, and as such, another option for diagnosing
thrombosis is transesophageal echocardiogram (TEE). In
their 2010 study, Korkeila etal. performed TEE at 6 months
10

25.9 Conclusion 321
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post-implantation of pacemakers and found approximately
9% of patients to have either thrombus in the right atrium or
the central veins.29 However, routine evaluation by TEE is of
limited value due to its invasive nature and cost. erefore,
duplex ultrasonography is suggested as the rst-line tool for
the investigation.
25.6 PREDICTING PROBABILITY
While there is no clear way of knowing if a patient wi ll develop
catheter-related thrombosis, there have been attempts to use
biomarkers, hematological tests, and clinical examination to
identify patients who may be at higher risk of thrombosis.
In a prospective study enrolling 212 patients with hematological malignancy undergoing intensive chemotherapy,
Boersma et al. found that the incidence of symptomatic
CVC thrombosis is approximately 9%. High factor VIII levels (P = 0.023), leukocytosis (P = 0.042), and plasminogen
activator inhibitor-1 levels above the 75th percentile of the
population (P = 0.008) were all signicantly related to symp-
tomatic thrombosis. e authors suggested the use of further
thromboprophylactic measures in this subset of patients.
35
In another study, the authors conducted a retrospective
review of all patients over a 5-year period who underwent
duplex ultrasonography of the upper extremity to evaluate
for thrombosis. Forty of 177 (23%) upper extremities that
underwent scanning were found to have UEDVT. History of
prior central venous catheterization predicted UEDVT with
an OR of 7.0 (P = 0.0 01).
36
In a separate study, Constans’ Clinical Decision Score for
predicting UEDVT assessed the risk as 12%, 20%, and 70%
based on 1 point being assigned for each of the following
three risk factors: presence of a CVC or pacemaker wire in
the venous system; localized pain; and unilateral edema. A
reduction of 1 point is assigned if some other diagnosis is at
least as likely to be present as thrombosis.
37
25.7 TREATMENT OF CVT
Most of the data for UEDVT treatment has been extrapolated
using what we know from lower extremity DVT. As such,
anticoagulation has historically been the treatment of choice.
e standard for anticoagulation is heparin as a bridge
to vitamin K antagonists. In pediatrics, low-molecularweight heparin may be unpredictable in its eect, and we
may need to consider measuring anti-Xa levels. In addition,
novel oral anticoagulants have proved their eectiveness in
lower extremity DVT and should be strongly considered as
enhanced alternatives.
UEDVT associated with catheters or wires should be
treated with 3–6 months of anticoagulation. If the patient
does not need a central line, including a PICC, the recommendation is to remove it.
ing and debrillation need not be removed. Finally, in those
patients who are unable to complete anticoagulation, one
may consider placement of a superior vena cava (SVC) lter
to prevent PE.
12,33,39
30,33,38
Furthermore, wires for pac-
e American College of Chest Physicians guidelines
recommend against the use of compression in symptomatic
patients. Furthermore, the safety and ecacy of thrombolytics and thrombectomy are not clearly established based on the
available data. eir use may be benecial for phlegmasia.
40
25.8 PREVENTION OF CATHETER-
RELATED CVT
e French National Federation of Cancer Centers workgroup on Standards, Options, and Recommendations
reviewed 36 publications (studies between 1990 and 2007)
in order to establish their guidelines on the prevention of
CVC-related thrombosis. eir analysis found that catheter
position is the most important factor, and recommended
that the distal tip of all CVCs should be at the junction of
the right atrium and SVC.
17
While some studies have advocated the routine use of anticoagulation for the prevention of thrombosis,
12,19
most recent
data fail to replicate the data that were published in the original trial, and routine anticoagulation for prophylaxis is not
recommended.33 Similarly, there is also no role for anticoagulation in the pacemaker population. Although studies have
showed that anticoagulation prophylaxis trended towards
less thrombosis in a small series, there has not been clear
identication of the role of anticoagulation for prophylaxis.33
In the study by D’Ambrosio etal., the authors performed a
meta-analysis and found that anticoagulation use in cancer
patients with CVCs had a lower risk of symptomatic CVCrelated venous thrombosis than the control group (RR: 0.61;
95% CI: 0.42–0.88).13 In a dierent series of patients, the
1994 study by Monreal etal. showed that prophylaxis with
dalteparin starting 2 hours before CVC insertion in cancer
patients reduced the risk for UEDVT.19 Catheter thrombogenecity has also been discussed. Murray etal. demonstrated
that polyethylene catheters are more thrombogenic than
polyurethane catheters.10 Furthermore, the authors found
that rigid catheters may damage venous walls, whereas soer
ones may be more compliant and remain in the optimal location, leading to improved thrombotic outcomes.
Data on heparin-bonded catheters are scarce and largely
inconclusive regarding thrombus prophylaxis.
41
Indeed, heparin-bonded catheters have not been demonstrated to be prophylactic against UEDVT in adult patients.42 In the pediatric
population, a Cochrane review examined two studies: one
with 97 patients and the other with 209 patients. Both studies randomized participants to heparin-bonded catheters and
non-heparin-bonded catheters. e review found no dierence
in catheter-related thrombosis (RR: 0.34; 95% CI: 0.01–7.68).
43
25.9 CONCLUSION
Virchow’s triad is of importance in the development of
CVT. Indwelling catheters inherently contribute to each of
the components of the triad. ey are foreign objects to the
venous system and may contribute to its local hypercoagulability. Furthermore, catheter or pacemaker wire presence

322 Acute central venous thrombosis in the setting of central lines, pacemaker wires, and dialysis catheters
placement.
https://t.me/med1917
Guidelines 3.9.0 of the American Venous Forum for the management of acute central venous thrombosis in the setting of
central lines, pacemaker wires, and dialysis catheters
No. Guideline
3.9.1 To decrease the risk of central venous thrombosis, we recommend
placement of the tip of the central venous catheter at the
junction of the right atrium and superior vena cava.
3.9.2 We recommend 3–6 months of anticoagulation for the
treatment of symptomatic acute central venous thrombosis in
the setting of central lines, pacemaker wires, or dialysis
catheters. Removal of the central line or catheter is
recommended only if they are no longer needed.
in the lumen may cause stasis due to low ow in the vessel
lumen. In addition, their initial insertion and presence carries the potential to cause endothelial damage.
Acute CVT is usually asymptomatic. Diagnosis starts with
a clinical examination, followed by duplex ultrasonography.
Once the diagnosis of UEDVT is conrmed, the mainstay
of treatment is anticoagulation. ere are limited roles for
Central venous
thrombosis diagnosed
Phlegmasia of
upper extremity
thrombectomy or thrombolysis. Furthermore, prevention of
thrombosis is best achieved by placing the CVC tip at the
junction of the right atrium and SVC. Finally, improving
catheter and wire proles to be less thrombogenic may have
a role in decreasing the prevalence of CVT. Treatment algorithm for CVT associated with pacemaker wires, CVCs or
dialysis catheters are presented in Figure 25.1.
REFERENCES
●
= Key primary paper
★
= Major review article
◆
= Guideline
Grade of
recommendation
(1: strong; 2:
weak)
1 B
1 B
Grade of evidence
(A:high quality;
B:moderate quality;
C:low or very low quality)
Yes
Consider
thrombolysis/
thrombectomy
Do not remove
*If patient unable to undergo anticoagulation, consider SVC filter
Central venous
catheter/
dialysis catheter
Is catheter
needed?
Yes
catheter
Recommend
anticoagulation
for 3–6 months
No
Pacemaker
wires
Do not remove
wires
No
Remove
catheter
Figure 25.1 Treatment algorithm for CVT associated with
pacemaker wires, CVCs or dialysis catheters.
1. McGee D and Gould M. Preventing complications
of central venous catheterization. N Engl J Med
20 03;348(12):1123 – 33.
★
2. Korkeila P et al. Venous obstruction after pacemaker implantation. Pacing Clin Electrophysiol
2007;30(2):199–206.
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3. Kuter D. Thrombotic complications of central
venous catheters in cancer patients. Oncologist
2004;9:207–16.
4. Raad I etal. The relationship between the thrombotic and infectious complications of central venous
catheter. JAMA 1994;271(13):1014– 6.
●
5. Munoz F etal. Clinical outcome of patients with
upper-extremity deep vein thrombosis: Results from
the RIETE registry. Chest 2008;13 3(1):143– 8.
6. Hingorani A etal. Upper extremity deep venous
thrombosis and its impact on morbidity and mortality rates in a hospital-based population. J Vasc Surg
1997;26(5):853–60.
7. Hingorani A et al. Risk factors for mortality in patients
with upper extremity and internal jugular deep
venous thrombosis. J Vasc Surg 2005;41(3):476–8.
8. Hingorani A etal. Upper extremity deep venous
thrombosis: An underrecognized manifestation of a hypercoagulable state. Ann Vasc Surg
2000;14(5):421–6.

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9. Ge X etal. Central venous access sites for the prevention of venous thrombosis, stenosis and infection.
Cochrane Database Syst Rev 2012;(3):CD004084.
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10. Murray J, Precious, E., and Alikhan R. Catheterrelated thrombosis in cancer patients. Br J Haematol
2013;162:74 8 –57.
11. Baskin J etal. Management of occlusion and
thrombosis associated with long-term indwelling
central venous catheters. Lancet 2009;374(9684):
159 – 69.
12. Joffe H and Goldhaber S. Upper-extremity deep
vein thrombosis. Circulation 2002;106:1874 – 8 0.
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13. D’Ambrosio, L, Aglietta M, and Grignani G.
Anticoagulation for central venous catheters in patients with cancer. N Engl J Med
2014;371(14):1362–63.
14. Prescott S and Tikoff G. Deep venous thrombosis
of the upper extremity: A reappraisal. Circulation
1979;59(2):350–5.
15. Tilney N and Griffiths H. Natural history of major
venous thrombosis of the upper extremity. Arch Surg
1970;101:79 2–6.
16. Gloviczki P, Kazmier F, and Hollier L. Axillarysubclavian venous occlusion: The morbidity of a
nonlethal disease. J Vasc Surg 1986;4:333–7.
17. Patel N etal. Multimodal endovascular–open surgical
approach to phlegmasia cerulea dolens of the upper
extremity: A case report. Presented at: 20th Annual
Meeting of the American Venous Forum. Charleston,
SC, 2008.
18. Monreal M etal. Upper-extremity deep venous
thrombosis and pulmonary embolism. Chest
1991;99:280–3.
●
19. Monreal M etal. Pulmonary embolism in patients
with upper extremity DVT associated to venous
central lines—A prospective study. Thromb Haemost
1994;72(4):548–50.
20. Timsit J-F etal. Central vein catheter-related
thrombosis in intensive care patients. Chest
1998;114(1):2 07–13 .
21. Horattas M etal. Changing concepts of deep
venous thrombosis of the upper extremity—Report
of a series and review of the literature. Surgery
1988;104(3):561–7.
22. van Rooden CJ et al. Infectious complications of
central venous catheters increase the risk of catheter-related thrombosis in hematology patients:
A prospective study. Journal of Clinical Oncology
2005;23(12):2655–60.
23. Liem T etal. Peripherally inserted central catheter usage patterns and associated symptomatic
upper extremity venous thrombosis. J Vasc Surg
2012;55(3):761–7.
24. Chopra V etal. Risk of venous thromboembolism
associated with peripherally inserted central catheters: A systematic review and meta-analysis. Lancet
2013;382(9889):311–25.
25. Nifong TP and McDevitt TJ. The effect of catheter to
vein ratio on blood flow rates in a simuated model of
peripherally inserted central venous catheters. Chest
2011;140(1):48–53.
★
26. Smitherman A etal. The incidence of catheter-associated venous thrombosis in noncritically ill children.
Hosp Pediatr 2015;5:59–66.
27. Williams E etal. Symptomatic deep venous thrombosis of the arm associated with permanent transvenous pacing electrodes. Chest 1978;73:613 – 5.
28. van Rooden C etal. Incidence and risk factors of
early venous thrombosis associated with permanent pacemaker leads. J Cardiovasc Electrophysiol
20 04;15:1258 – 62.
★
29. Korkeila P etal. Clinical and laboratory risk factors of thrombotic complications after pacemaker
implantation: A prospective study. Europace
2010;12:817–24.
◆
30. Kearon C etal. Antithrombotic therapy for VTE
disease: American College of Chest Physicians
evidence-based clinical practice guidelines. Chest
2012;141(2):e419S–e494S.
★
31. Ruesch S, Walder B, and Tramer, M. Complications
of central venous catheters: Internal jugular versus
subclavian access—A systematic review. Crit Care
Med 2002;30(2):454–60.
32. Martin C, Viviand X, Saux P, and Gouin F. Upper
extremity deep vein thrombosis after central venous
catheterization via the axillary vein. Crit Care Med
1999;27(12):2626–9.
◆
33. Debourdeau P etal. 2008 SOR guidelines for the
prevention and treatment of thrombosis associated with central venous catheters in patients with
cancer: Report from the working group. Ann Oncol
2009;20(9):1459–71.
34. Jung D etal. Placement issues for hemodialysis catheters with pre-existing central lines and catheters.
J Vasc Surg 2010;52(3):805.
35. Boersma R etal. Biomarkers for prediction of central
venous catheter related-thrombosis in patients
with hematological malignancies. Clin Appl Thromb
Hemost 2015; doi: 10.1177/1076029615579098 [Epub
ahead of print].
36. Schmittling Z etal. Characterization and probability
of upper extremity deep venous thrombosis. Ann
Vasc Surg 2004;18(5):552–7.
37. Kleinjan A etal. Safety and feasibility of a diagnostic
algorithm combining clinical probability, D-dimer
testing, and ultrasonography for suspected upper
extremity deep venous thrombosis: A prospective
management study. Ann Intern Med 2014 ;16 0 : 4 51–7.
38. Jones M etal. Characterizing resolution of catheter-associated upper extremity deep venous
thrombosis. J Vasc Surg 2010;51(1):108 –13.
39. Ascher E etal. Lessons learned from a 6-year clinical
experience with superior vena cava Greenfield filters.
J Vasc Surg 2000;32(5):881–7.

324 Acute central venous thrombosis in the setting of central lines, pacemaker wires, and dialysis catheters
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40. Usoh F etal. Long-term follow-up for superior vena cava filter placement. Ann Vasc Surg
2009;23(3):350–4.
41. Long D and Coulthard M. Effect of heparin-bonded
central venous catheters on the incidence of catheter-related thrombosis and infection in children and
adults. Anaesth Intensive Care 2006;34(4):481–4.
42. Lee A and Kamphuisen P. Epidemiology and prevention of catheter-related thrombosis in patients with
cancer. J Thromb Haemost 2012;10:1491– 9.
★
43. Shah P and Shah N. Heparin-bonded catheters for
prolonging the patency of central venous catheters in children. Cochrane Database Syst Rev
2014;(2):CD005983.

26
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Indications, techniques, and results of inferior
vena cava filters
SCOTT T. ROBINSON, VENKATARAMU N. KRISHNAMURTHY, AND JOHN E. RECTENWALD
26.1 Introduction 325
26.2 Background 325
26.3 Indications for IVC filter placement 326
26.4 Contraindications to IVC filterplacement 328
26.5 Filter characteristics—which one is an
idealfilter? 328
26.6 Types of IVC filters 328
26.7 Temporary filters 333
26.1 INTRODUCTION
e majority of pulmonary emboli (PE) arise from thrombosis in the deep veins of the legs and pelvis. e rst-line therapy for venous thromboembolism (VTE) is pharmacologic
anticoagulation, but in instances where anticoagulation is
contraindicated or therapeutic anticoagulation cannot be
achieved, an alternative treatment strategy is required. is
subset of patients requires placement of venous lter devices
that provide partial interruption of the inferior vena cava
(IVC) to prevent PE. e goal of IVC lter placement is to
trap clinically signicant thromboemboli without causing
complete occlusion of the IVC. e advent of retrievable
IVC lters has played a signicant part in broadening the
indications for the use of IVC lters to include prophylactic
placement. Although this practice remains controversial,
appropriately selected patients can benet from IVC lter
placement. In this chapter, we discuss the indications, clinical use, ecacy, insertion techniques, and complications of
IVC lters.
26.2 BACKGROUND
John Hunter introduced one of the earliest techniques for
the management of lower extremity thrombophlebitis in
the 1700s with ligation of the femoral veins to prevent clot
propagation. However, it was not until 1846, with Rudolph
Virchow’s suggestion that thrombus in the pulmonary
venous system was of embolic origin, that venous occlusion
26.8 Permanent or optionally retrievable? 333
26.9 Techniques of IVC filterplacement 334
26.10 Follow-up of IVC filters 336
26.11 Complications of IVC filters 336
26.12 Comparison of performance between IVCfilters 337
26.13 Suprarenal IVC and superior vena cava filters 338
26.14 Conclusion 338
References 339
was approached as a strategy for PE prevention. Bottini is
credited with the rst successful caval ligation in a setting of
trauma, but Homan was the rst to hypothesize that embolization of lower extremity thrombus could be prevented
through bilateral ligation of the femoral veins.
techniques failed to prevent recurrent PE, Collins and
Nelson,2 and subsequently Homan,3 proposed infrarenal
ligation of the IVC as a strategy for PE prevention. Early
IVC ligation involved a laparotomy under general anesthesia in patients with signicant pulmonary hypertension,
right heart failure, and associated oxygenation decits, and
thus was associated with unacceptably high mortality, ranging from 4% in low-risk patients to 39% in patients with signicant cardiac disease.4 Morbidity from the procedure was
also substantial and included lower extremity edema, stasis
ulceration, and post-thrombotic syndrome. Also of signicance, ligation of the IVC was associated with an incidence
of recurrent PE of up to 15% through the development of
collateral vessels around the ligated segment. Surgical vena
caval interruption techniques involving suture or staple
grids, and external caval clips were also later developed
in an eort to preserve channels for blood ow in the IVC
while entrapping signicant thrombus within caval segments. ese techniques, although improvements from IVC
ligation, were also fraught with complications, yet remained
standards of therapy until less morbid treatments became
available.
In the late 1960s, the Mobin–Uddin umbrella was intro-
duced and became widely utilized because of its ecacy
1
When these
325

326 Indications, techniques, and results of inferior vena cava filters
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and ease of placement compared to the contemporary
surgical treatment options. e Mobin–Uddin umbrella
consisted of a silicone disc with multiple holes and six
stainless steel struts to maintain the appropriate geometry when deployed. Although it eectively prevented PE,
it did so at the expense of caval patency and was associated with an IVC occlusion rate as high as 65%.5 ere
were also signicant problems with caval xation that
resulted in migration of the device into the right heart
or pulmonary artery. As a result, it was later withdrawn
from the market.
e Greeneld lter was rst used in 1972 to provide
protection against PE and is the benchmark to which all
other lters are currently compared. e long-term patency
rate of the Greeneld lter is as high as 95%,6 which is likely
due to the conical design that enables a high thrombus volume to area reduction ratio. is design allows up to 70%
of the cone volume to be occupied with thrombus before a
50% obstruction in IVC cross-sectional area and signicant
reduction in blood ow occurs. e original 24-French (Fr)
stainless steel lter was developed for operative insertion
via a femoral or internal jugular venotomy under local anesthesia. e operative procedure required general anesthesia
with a pre-operative venacavogram performed to assess for
caval anomalies and to allow identication of the appropriate site for placement. is naturally led to the development of lower-prole systems that allowed for rapid and
safe percutaneous delivery and deployment of the lter. e
increasing convenience and reduced procedural cost of IVC
lter placement has led to a surge in use of these devices,
with an increase of 111% over the 10-year period prior to
7
2008.
26.3 INDICATIONS FOR IVC FILTER
PLACEMENT
It is well established that the rst-line therapy for the
treatment of VTE is anticoagulation.
most widely accepted indications for IVC lter placement
require the presence of a VTE and contraindication to
systemic anticoagulation. Indications for IVC lter placement are traditionally divided into absolute indications,
relative indications, and prophylactic indications. Absolute
indications for IVC lter placement are well established
and follow common sense. ese indications include the
presence of VTE and one of the following: a baseline contraindication to anticoagulation, a complication from anticoagulation, or a recurrent deep venous thrombosis (DVT)
or PE despite adequate (therapeutic) anticoagulation.
ere is considerable controversy surrounding numerous
relative and prophylactic indications for IVC lter placement, which is reected by variation in guidelines from
the American College of Chest Physicians (ACCP), the
American Heart Association (AHA), and the Society of
Interventional Radiology (SIR). e indications for IVC lter placement are summarized in Table 26.1, and discussed
in detail below.
8,9
Consequently, the
Table 26.1 Indications for inferior vena cava filter
placement
• Common indications:
• Contraindication to anticoagulation in patients
with pulmonary embolism (PE)/deep venous
• Complications of anticoagulation
• Failure of anticoagulation due to progression of
DVT, recurrent PE, or noncompliance
• Massive, life-threatening PE with residual DVT
despite anticoagulation
• Free-floating thrombus in inferior vena cava (IVC)
iliac, or pelvic veins
• Chronic, recurrent PE with pulmonary hypertension
and cor pulmonale
• Indications specifically for prophylactic IVC filter:
• Patients with prior PE with significantly increased
risk for second PE or those with poor
cardiopulmonary reserve
• Patients with a significant burden of proximal DVT
or free-floating thrombus
• Patients at high risk for complications of
thromboembolism like malignancies and major/
multiple trauma
• Patients who cannot receive anticoagulants, such
as those with internal organ injury or active internal
bleeding
• Multiple risk factors for DVT in a pre-operative
patient
26.3.1 Absolute indications (requires
presence of VTE)
Contraindication to anticoagulation is the most frequently
cited reason for selecting IVC lter placement over standard
anticoagulation therapy. Major contraindications to anticoagulation are serious active bleeding, recent spinal cord or
brain injury, recent stroke, surgery, or trauma. Advanced
age and pregnancy are also considered as relative contraindications to anticoagulation, but remain controversial.
Many contraindications to anticoagulation therapy are
self-limited or are reversed over time, allowing a course of
anticoagulation to be completed at a later time. e latter
advocates the increased use of retrievable IVC lters.
Complications secondary to anticoagulation include
bleeding or, in rare cases, an adverse reaction to the anticoagulant used. Up to 5%–10% of patients treated with
intravenous heparin will develop a bleeding complication over the duration of therapy. e severity of bleeding is variable, but appears to be dose dependent and
varies with the patient’s inherent risk (i.e., prior surgery
or trauma, predisposing clinical factors, or underlying
hemostatic conditions).
cations, heparin-induced thrombocytopenia develops in
1.1%–2.9% of patients receiving unfractionated heparin.12
10,11
In addition to bleeding compli-

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Should this occur, all heparin must be discontinued, even
that which is used for ushing lines and catheters, as the
condition responds to cessation of therapy. Rarely, patients
may develop sensitivity to heparin with the development
of a cutaneous rash or anaphylaxis. e incidence of these
complications is much lower with the use of low-molecularweight heparins, but they do occur. Alternatives to heparin
should be considered.
Bleeding may also occur in up to 10% of patients treated
with warfarin (Coumadin). e degree of bleeding is most
oen associated with the inactivation of the clotting cascade
as indicated by an elevated international normalized ratio
(INR). Patients with signicantly elevated INRs are more
likely to develop major hemorrhagic complications than
those with mildly elevated levels.13 Routine monitoring and
dietary counseling will help to prevent such complications.
Monitoring should also be undertaken when there has
been a change in concomitant medications. Several drugs
have either a synergistic or antagonistic interaction with
warfarin, resulting in decreased ecacy or increased risk
of adverse events. In addition to bleeding complications, a
small number of patients develop warfarin-associated skin
necrosis, which usually is seen early and in the absence of
adequate concurrent heparin treatment. is is most likely
to occur in areas of increased subcutaneous fat and may
also be associated with the “blue toe” syndrome. Should this
develop, the drug must be promptly discontinued.
14
Recurrent VTE while on therapeutic anticoagulation
is considered a failure of anticoagulation, and is another
common indication for lter placement. Prior to determining that anticoagulation has failed, it should be established
that the patient was adequately anticoagulated to begin
with. Many times, failures of anticoagulation are failures
to reach therapeutic drug levels. e patient who develops
recurrence or extension of thromboembolism while anticoagulated may, in fact, not be adequately anticoagulated or
simply non-compliant. In order to reduce this risk, patients
should be monitored closely during the initiation of therapy
with heparin to ensure that they are therapeutic within the
rst 24 hours. For low-molecular-weight heparin, patients
become therapeutic with an appropriate weight-based dose.
Nomograms have been developed to ensure that this takes
15,16
place.
For patients on warfarin, the INR must be closely
monitored to ensure that patients remain suciently anticoagulated for the duration of their treatment course. A
subset of patients with warfarin resistance who demonstrate
an inability to achieve a therapeutic INR should also be considered for IVC lter placement.
Recently, several new oral anticoagulants (NOACs) have
been developed for treatment of VTE. ese NOACs include
the direct thrombin inhibitor dabigatran and the direct
anti-Xa inhibitors rivaroxaban, apixaban, and edoxaban.
All of these drugs are currently approved for both stroke
prevention in atrial brillation and the treatment of VTE.
e increasing use of NOACs for the treatment of VTE is
relevant to this chapter for several reasons. Like heparinderived products and warfarin, the primary complication
of NOAC therapy is bleeding; thus, IVC lters may be indicated in patients taking NOACs. Additionally, there is no
standard method of monitoring patient response to NOAC
therapy. One of the purported advantages of this new class
of drugs is that, unlike warfarin, regular monitoring of
these drugs is not required. However, the inability to assess
for therapeutic drug levels makes it extraordinarily challenging to establish whether a patient with a recurrent VTE
on NOAC therapy was adequately anticoagulated at the
time of the VTE event. Lastly, the growing use of NOACs
for VTE treatment may inuence future guidelines regarding the management of VTE. At present, failure of a single agent has been considered an indication for IVC lter
placement. However, as more oral therapies emerge for the
treatment of VTE, future guidelines may require failure of
multiple pharmacologic modalities prior to use of an IVC
lter.
26.3.2 Relative indications (VTE required)
e relative indications for IVC lter placement also
require the conrmed presence of VTE, in addition to risk
factors for future PE or cardiopulmonary compromise.
Such indications include individuals with a DVT and poor
cardiopulmonary reserve such as pulmonary hypertension
or cor pulmonale, who are unlikely to tolerate the hemodynamic and respiratory stress of a PE. Similarly, patients
with residual DVT who have experienced a massive PE
may not tolerate additional pulmonary insult, and therefore may benet from IVC lter placement. Patients with
a large, free-oating iliocaval thrombus (typically greater
than 6 cm) may also be considered for lter placement, as a
large thrombus with high embolic risk could lead to a massive PE. Other relative indications for IVC lter placement
include patients with a VTE and relative contraindications
to anticoagulation, as is demonstrated by poor adherence
to medications or by those with ataxia or a high fall risk.
Additionally, patients with a high peri-procedural risk of
PE, including those undergoing pulmonary thromboembolectomy, and patients with DVT and a large clot burden
undergoing thrombolysis, could benet from IVC lter
placement.
ere is ongoing debate with regard to the relative
indications for IVC lter placement. Current AHA guidelines identify just one relative indication for IVC lter
use: an acute PE in a setting of poor pulmonary reserve.
Additionally, the AHA guidelines state that IVC lters
should not routinely be used as an adjunct to anticoagulation or in a setting of brinolysis. e ACCP has slightly
more liberalized guidelines, with relative indications for
IVC lter use including unstable patients with acute PE,
massive PE treated with thrombolysis/thrombectomy, or
chronic PE treated with thromboendarterectomy.8 e SIR
oers the most inclusive set of recommendations for IVC
lter use, with the multidisciplinary consensus conference
guidelines from 2007 and quality improvement guidelines
from 2011 identifying all of the above indications.
9

328 Indications, techniques, and results of inferior vena cava filters
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26.3.3 Prophylactic indications
(noVTErequired)
Indications for prophylactic IVC lter placement remain
highly controversial. Only the SIR guidelines recommend
the use of IVC lters in a prophylactic setting, and the
ACCP guidelines explicitly recommend against the use of
prophylactic IVC lters. Nevertheless, there are certain
populations that may benet from the placement of an IVC
lter, even in the absence of DVT. ese indications are discussed below.
Certain trauma patients may be at excessively high risk of
DVT, and thus are possible candidates for prophylactic IVC
lters.17 e constellation of traumatic injuries that constitutes high risk includes brain injury, spinal cord injury, and
pelvic and lower extremity long bone fractures. ese injuries carry a 50-fold increase in thromboembolic complications compared to other trauma patients.
lters in these patients has been criticized. By itself, the lter
protects against PE, but does nothing to prevent additional
episodes of thrombosis or to treat existing DVT. ere are
also concerns about increased health care costs and procedural morbidity/mortality.
18,20–2 4
Certain surgical patients that may benet from prophylactic IVC lter placement include patients undergoing
bariatric surgery or spinal surgery. e incidence of PE in
bariatric surgery patients is reported to be 1%–4%, but may
be even higher in super-obese patients. is has remained
unchanged despite the near-universal institution of pharmacomechanical prophylaxis measures. Several small
retrospective studies have suggested IVC lter placement
reduces the incidence of PE in bariatric surgery patients, but
the practice remains controversial, and a recent systematic
review concluded IVC lter placement oered no benet for
protection from PE.25 e rate of PE aer spinal surgery is
reportedly as high as 13%; therefore, this patient population may benet from pre-operative prophylactic IVC lter
placement. Several small retrospective studies support this
contention
26,27
; however, the quality of evidence at this time
is low.
Malignancy has long been known to carry a signicantly increased risk of VTE. e reported incidence of
PE in the literature is somewhere between 7% and 50% in
patients with malignancy.28 Two studies have estimated the
risks of PE in cancer patients to be approximately 3.6-fold
higher than in patients without malignancy.
patients that are at increased risk of VTE also appear to be
at increased risk of bleeding while receiving anticoagulation
therapy.
29,31,32
Debate regarding the use of IVC lters in the
setting of malignancy has persisted since the 1990s. Despite
frequent use for this indication and continued attempts to
clarify their role, the proper use of IVC lters in the setting
of malignancy remains a point of contention.
Immobility is an established risk factor for VTE, with
prolonged immobility leading to a 4.9-fold increased risk
33
of PE.
While pharmacoprophylaxis and sequential com-
pression devices may reduce the incidence of PE, certain
18,19
e use of IVC
29,30
ese same
individuals that have a contraindication to anticoagulation may benet from IVC lter placement. For example,
patients with severe stroke can have prolonged immobility
and, due to risk of intracerebral hemorrhage, cannot receive
anticoagulation. ere are limited data demonstrating the
ecacy of IVC lters in preventing PE in patients with
restricted mobility. However, given the low risk of complications associated with IVC lters, these devices should
be considered in immobilized patients who cannot receive
anticoagulation.
34
26.4 CONTRAINDICATIONS TO IVC
FILTERPLACEMENT
e only absolute contraindications to IVC lter insertion
are complete thrombosis of the IVC and inability to gain
access to the IVC due to severe venous obstruction. A relative contraindication is uncorrectable, severe coagulopathy
or thrombocytopenia, in which case surgical venotomy and
surgical placement may be safer, although IVC lters with
low-prole delivery devices may be useful in these cases.
Careful evaluation of the risks versus benets of lter placement should be done in such patients. Special situations
requiring caution prior to lter placement include: patients
with untreated or uncontrolled bacteremia, who should be
treated with immediate and appropriate antibiotic treatment, and lter placement in pediatric patients and pregnant women, due to uncertain long-term eects and the
durability of the lters. Again, retrievable lters may have
a role in these patients depending on the specics of these
cases. If an IVC lter must be placed in a pregnant woman
or woman of child-bearing age, placement of the lter in
the suprarenal position should be considered to avoid the
potential complication of compression of the lter by the
enlarging uterus.
26.5 FILTER CHARACTERISTICS—WHICH
ONE IS AN IDEAL FILTER?
Several designs of lters in various size and shapes are available for clinical use. e availability of such a wide range of
lters suggests that not one type is by itself ideal. e characteristics of an ideal lter are described in Table 26.2. e
most important desirable factors are high ltering eciency
(large and small emboli) without impedance of blood ow,
stability of positioning and structure, and a low rate of associated morbidity.
26.6 TYPES OF IVC FILTERS
26.6.1 Permanent filters
Permanent lters are placed with the intention of providing life-long protection from PE, and are thus designed with
caval xation in mind. e rst widely used IVC lter was
the Greeneld lter, which was originally introduced in
1972 as a permanent lter (Figure 26.1). It is constructed of

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Table 26.2 Characteristics of an ideal filter
1. High filtering efficiency for both large and small
emboli without impedance of blood flow
2. Stability of position/fixation and structural integrity
3. Low procedural morbidity, no mortality, and low cost
4. Ideal biomechanical property: biocompatible,
non-thrombogenic, and magnetic resonance imaging
compatible
5. Ideal delivery system: small caliber and easy
deployment with ability to reposition
6. Safe retrievability when no longer needed
Figure 26.1 The original stainless steel Greenfield filter
first used in 1972. (Used with permission from Rutherford
RB, Ed., Vascular Surgery (4th Ed), W.B. Saunders
Company, Philadelphia, 1995.)
stainless steel and was originally intended for open surgical placement via a 28-Fr sheath. It has been discontinued
from clinical use and replaced with a lower-prole system.
In addition to the Greeneld lter, several other permanent
IVC lters are available for clinical use (Table 26.3). Brief
descriptions of available permanent IVC lters are included
below and in Figure 26.2.
26.6.2 Titanium Greenfield filter
e titanium version of the Greeneld lter has a conical
conguration consisting of six struts that is compressed
into a 12-Fr carrier (14.3-Fr outer diameter) sheath. e
sheath is inserted with a guidewire, but actual lter deployment occurs without the use of a guidewire, unlike the
original and stainless steel over-the-wire design. e lter is
designed for IVC diameters smaller than 28 mm. e lter
comes in femoral and jugular versions.
26.6.3 Stainless steel over-the-wire
Greenfield filter
e lter has six stainless steel struts that are press-tted
into a cylindrical cap with a hole that the guidewire can
pass through. is lter is placed over a centering guidewire to address frequently encountered instances of lter
tilting and asymmetry with the titanium version. e hooks
of four of the legs point superiorly, and two opposite hooks
point inferiorly to prevent migration. e hooks are also
“recurved,” forming a complete circle before protruding to
decrease the degree of hook penetration. ere are separate
femoral and jugular versions of this lter. e lter is safe
for magnetic resonance imaging, but causes a signicant
amount of artifact.
Table 26.3 Permanent inferior vena cava filters
Name Manufacturer Year introduced FDA approval
Titanium Greenfield Boston Scientific/Medi-tech, Natick, MA 1988 1989
Over-the-wire stainless
steel Greenfield
VenaTech/LGM B. Braun Medical, Evanston, IL 1986 1989
Low-profile VenaTech B. Braun, Boulogne, France 2000 2001
Simon Nitinol Bard, Covington, GA 1988 1990
TrapEase Cordis, Miami, FL 1998 2000
Bird’s nest Cook, Bloomington, IN 1982 1989
Name
Titanium Greenfield 14.3 Fr 38 mm 47 mm Titanium Compatible
Over-the-Wire stainless
steel Greenfield
VenaTech/LGM 14.6 Fr 30 mm 38 mm Phynox Compatible
Low-profile VenaTech 9 Fr 40 mm 43 mm Phynox Compatible
Simon Nitinol 9 Fr 28 mm 45 mm Nitinol Compatible
TrapEase 8 Fr 35 mm 50–65 mm Nitinol Compatible
Bird’s nest 14 Fr 40 mm 70–110 mm Stainless Not compatible; creates
Boston Scientific/Medi-tech, Natick, MA 1994 1995
Delivery
system size
15 Fr 32 mm 49 mm Stainless steel Not compatible
Maximum
diameter Length Material MRI compatibility
large artifacts
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