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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 specically 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 dier­ence 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 etal. 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 dierence 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 signicantly 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 dierence 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 etal. 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 etal. presented a review article in 2009 and found that duplex ultrasonography exhib­ited a sensitivity of 78%–100% and a specicity 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 conrm diagnosis. Finally, venography remains the gold standard for the diag­nosis of central vein thrombosis.
For patients with pacemaker wires, MRV is oen con­traindicated, and as such, another option for diagnosing thrombosis is transesophageal echocardiogram (TEE). In their 2010 study, Korkeila etal. performed TEE at 6 months
10
25.9 Conclusion 321
https://t.me/med1917
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 signicantly 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 eect, and we may need to consider measuring anti-Xa levels. In addition, novel oral anticoagulants have proved their eectiveness 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 debrillation 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 ecacy of thrombolyt­ics and thrombectomy are not clearly established based on the available data. eir use may be benecial 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 identication of the role of anticoagulation for prophylaxis.33 In the study by D’Ambrosio etal., 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 dierent series of patients, the 1994 study by Monreal etal. 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 etal. demonstrated that polyethylene catheters are more thrombogenic than polyurethane catheters.10 Furthermore, the authors found that rigid catheters may damage venous walls, whereas soer 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 dierence 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 conrmed, 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 proles 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.
 ●
3. Kuter D. Thrombotic complications of central venous catheters in cancer patients. Oncologist 2004;9:207–16.
4. Raad I etal. The relationship between the throm­botic and infectious complications of central venous catheter. JAMA 1994;271(13):1014– 6.
 ●
5. Munoz F etal. 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 etal. 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 etal. 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 etal. Central venous access sites for the pre­vention of venous thrombosis, stenosis and infection. Cochrane Database Syst Rev 2012;(3):CD004084.
10. Murray J, Precious, E., and Alikhan R. Catheter­related thrombosis in cancer patients. Br J Haematol 2013;162:74 8 –57.
11. Baskin J etal. 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 etal. 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 etal. Upper-extremity deep venous thrombosis and pulmonary embolism. Chest 1991;99:280–3.
 ●
19. Monreal M etal. 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 etal. Central vein catheter-related thrombosis in intensive care patients. Chest 1998;114(1):2 07–13 .
21. Horattas M etal. 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 etal. Peripherally inserted central cath­eter usage patterns and associated symptomatic upper extremity venous thrombosis. J Vasc Surg 2012;55(3):761–7.
24. Chopra V etal. 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 etal. The incidence of catheter-asso­ciated venous thrombosis in noncritically ill children. Hosp Pediatr 2015;5:59–66.
27. Williams E etal. Symptomatic deep venous throm­bosis of the arm associated with permanent transve­nous pacing electrodes. Chest 1978;73:613 – 5.
28. van Rooden C etal. Incidence and risk factors of early venous thrombosis associated with perma­nent pacemaker leads. J Cardiovasc Electrophysiol 20 04;15:1258 – 62.
29. Korkeila P etal. Clinical and laboratory risk fac­tors of thrombotic complications after pacemaker implantation: A prospective study. Europace 2010;12:817–24.
30. Kearon C etal. 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 etal. 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 etal. Placement issues for hemodialysis cath­eters with pre-existing central lines and catheters. J Vasc Surg 2010;52(3):805.
35. Boersma R etal. 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 etal. Characterization and probability of upper extremity deep venous thrombosis. Ann Vasc Surg 2004;18(5):552–7.
37. Kleinjan A etal. 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 etal. Characterizing resolution of cath­eter-associated upper extremity deep venous thrombosis. J Vasc Surg 2010;51(1):108 –13.
39. Ascher E etal. 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 etal. 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 filterplacement 328
26.5 Filter characteristics—which one is an idealfilter? 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 signicant thromboemboli without causing complete occlusion of the IVC. e advent of retrievable IVC lters has played a signicant part in broadening the indications for the use of IVC lters to include prophylactic placement. Although this practice remains controversial, appropriately selected patients can benet from IVC lter placement. In this chapter, we discuss the indications, clini­cal use, ecacy, 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 filterplacement 334
26.10 Follow-up of IVC filters 336
26.11 Complications of IVC filters 336
26.12 Comparison of performance between IVCfilters 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 signicant pulmonary hypertension, right heart failure, and associated oxygenation decits, and thus was associated with unacceptably high mortality, rang­ing from 4% in low-risk patients to 39% in patients with sig­nicant cardiac disease.4 Morbidity from the procedure was also substantial and included lower extremity edema, stasis ulceration, and post-thrombotic syndrome. Also of signi­cance, 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 eort to preserve channels for blood ow in the IVC while entrapping signicant 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 ecacy
1
When these
325
326 Indications, techniques, and results of inferior vena cava filters
https://t.me/med1917
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 eectively 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 signicant 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 Greeneld 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 Greeneld 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 signicant 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 identication of the appro­priate site for placement. is naturally led to the develop­ment of lower-prole 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 reected 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 oen associated with the inactivation of the clotting cascade as indicated by an elevated international normalized ratio (INR). Patients with signicantly 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 ecacy 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 suciently 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 inuence 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 conrmed 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 benet 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 benet 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 oers 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
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26.3.3 Prophylactic indications (noVTErequired)
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 benet 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 benet 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 oered no benet for protection from PE.25 e rate of PE aer spinal surgery is reportedly as high as 13%; therefore, this patient popula­tion may benet 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 signi­cantly 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 benet 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 ecacy 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 FILTERPLACEMENT
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-prole delivery devices may be useful in these cases. Careful evaluation of the risks versus benets 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 eects and the durability of the lters. Again, retrievable lters may have a role in these patients depending on the specics 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 eciency (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 Greeneld 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-prole system. In addition to the Greeneld 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 Greeneld lter has a conical conguration 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 signicant 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