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STATE-OF-THE-ART REVIEW Inferior Vena Cava Thrombosis Mohamad Alkhouli, MD, a Mohammad Morad, MD, b Craig R. Narins, MD, a,c Farhan Raza, MD, d Riyaz Bashir, MBBS d JACC: CARDIOVASCULAR INTERVENTIONS CME This article has been selected as this issues CME activity, available online at http://www.acc.org/jacc-journals-cme by selecting the CME tab on the top navigation bar. Accreditation and Designation Statement The American College of Cardiology Foundation (ACCF) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The ACCF designates this Journal-based CME activity for a maximum of 1 AMA PRA Category 1 Credit(s)Ô. Physicians should only claim credit commensurate with the extent of their participation in the activity. Method of Participation and Receipt of CME Certicate To obtain credit for this CME activity, you must: 1. Be an ACC member or JACC: Cardiovascular Interventions subscriber. 2. Carefully read the CME-designated article available online and in this issue of the journal. 3. Answer the post-test questions. At least 2 out of the 3 questions provided must be answered correctly to obtain CME credit. 4. Complete a brief evaluation. 5. Claim your CME credit and receive your certicate electronically by following the instructions given at the conclusion of the activity. CME Objective for This Article: 1) Identify the clinical context in which inferior vena cava thrombosis should be suspected. 2) Describe the diagnostic tests for inferior vena cava thrombosis. 3) Differentiate the various treatment modalities of inferior vena cava thrombosis with respect to the indications, risks versus benets, technical aspects and patient selection. CME Editor Disclosure: JACC: Cardiovascular Interventions CME Editor Bill Gogas, MD, PhD, has received research grant support from NIH T32, Gilead Sciences, and Medtronic Inc. Author Disclosures: The authors have reported that they have no re- lationships relevant to the contents of this paper to disclose. Medium of Participation: Print (article only); online (article and quiz). CME Term of Approval Issue Date: April 11, 2016 Expiration Date: April 10, 2017 From the a Division of Cardiovascular Disease, University of Rochester Medical Center, Rochester, New York; b Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania; c Department of Surgery, Section of Vascular Surgery, Uni- versity of Rochester Medical Center, Rochester, New York; and the d Division of Cardiovascular Disease, Temple University Hospital, Philadelphia, Pennsylvania. The authors have reported that they have no relationships relevant to the contents of this paper to disclose. Manuscript received September 8, 2015; revised manuscript received November 22, 2015, accepted December 17, 2015. JACC: CARDIOVASCULAR INTERVENTIONS VOL. 9, NO. 7, 2016 ª 2016 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 1936-8798/$36.00 PUBLISHED BY ELSEVIER http://dx.doi.org/10.1016/j.jcin.2015.12.268
Transcript

J A C C : C A R D I O V A S C U L A R I N T E R V E N T I O N S V O L . 9 , N O . 7 , 2 0 1 6

ª 2 0 1 6 B Y T H E AM E R I C A N C O L L E G E O F C A R D I O L O G Y F O UN DA T I O N I S S N 1 9 3 6 - 8 7 9 8 / $ 3 6 . 0 0

P U B L I S H E D B Y E L S E V I E R h t t p : / / d x . d o i . o r g / 1 0 . 1 0 1 6 / j . j c i n . 2 0 1 5 . 1 2 . 2 6 8

STATE-OF-THE-ART REVIEW

Inferior Vena Cava Thrombosis

Mohamad Alkhouli, MD,a Mohammad Morad, MD,b Craig R. Narins, MD,a,c Farhan Raza, MD,d

Riyaz Bashir, MBBSd

JACC: CARDIOVASCULAR INTERVENTIONS CME

This article has been selected as this issue’s CME activity, available online

at http://www.acc.org/jacc-journals-cme by selecting the CME tab on the

top navigation bar.

Accreditation and Designation Statement

The American College of Cardiology Foundation (ACCF) is accredited by

the Accreditation Council for Continuing Medical Education (ACCME) to

provide continuing medical education for physicians.

The ACCF designates this Journal-based CME activity for a maximum

of 1 AMA PRA Category 1 Credit(s)�. Physicians should only claim credit

commensurate with the extent of their participation in the activity.

Method of Participation and Receipt of CME Certificate

To obtain credit for this CME activity, you must:

1. Be an ACC member or JACC: Cardiovascular Interventions subscriber.

2. Carefully read the CME-designated article available online and in this

issue of the journal.

3. Answer the post-test questions. At least 2 out of the 3 questions

provided must be answered correctly to obtain CME credit.

4. Complete a brief evaluation.

From the aDivision of Cardiovascular Disease, University of Rochester Med

Medicine, Temple University Hospital, Philadelphia, Pennsylvania; cDepart

versity of Rochester Medical Center, Rochester, New York; and the dDivi

Hospital, Philadelphia, Pennsylvania. The authors have reported that they h

paper to disclose.

Manuscript received September 8, 2015; revised manuscript received Novem

5. Claim your CME credit and receive your certificate electronically by

following the instructions given at the conclusion of the activity.

CME Objective for This Article: 1) Identify the clinical context in which

inferior vena cava thrombosis should be suspected. 2) Describe the

diagnostic tests for inferior vena cava thrombosis. 3) Differentiate the

various treatment modalities of inferior vena cava thrombosis with

respect to the indications, risks versus benefits, technical aspects and

patient selection.

CME Editor Disclosure: JACC: Cardiovascular Interventions CME Editor

Bill Gogas, MD, PhD, has received research grant support from NIH T32,

Gilead Sciences, and Medtronic Inc.

Author Disclosures: The authors have reported that they have no re-

lationships relevant to the contents of this paper to disclose.

Medium of Participation: Print (article only); online (article and quiz).

CME Term of Approval

Issue Date: April 11, 2016

Expiration Date: April 10, 2017

ical Center, Rochester, New York; bDepartment of

ment of Surgery, Section of Vascular Surgery, Uni-

sion of Cardiovascular Disease, Temple University

ave no relationships relevant to the contents of this

ber 22, 2015, accepted December 17, 2015.

Alkhouli et al. J A C C : C A R D I O V A S C U L A R I N T E R V E N T I O N S V O L . 9 , N O . 7 , 2 0 1 6

IVC Thrombosis A P R I L 1 1 , 2 0 1 6 : 6 2 9 – 4 3

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Inferior Vena Cava Thromb

osis

ABSTRACT

Thrombosis of the inferior vena cava (IVC) is an under-recognized entity that is associated with significant short- and

long-term morbidity and mortality. In absence of a congenital anomaly, the most common cause of IVC thrombosis is the

presence of an unretrieved IVC filter. Due to the substantial increase in the number of IVC filters placed in the United

States and the very low filter retrieval rates, clinicians are faced with a very large population of patients at risk for

developing IVC thrombosis. Nevertheless, there is a paucity of data and societal guidelines with regards to the diagnosis

and management of IVC thrombosis. This paper aims to enhance the awareness of this uncommon, but morbid, condition

by providing a concise, yet comprehensive, review of the etiology, diagnostic approaches, and treatment strategies in

patients with IVC thrombosis. (J Am Coll Cardiol Intv 2016;9:629–43) © 2016 by the American College of Cardiology

Foundation.

I nferior vena cava (IVC) thrombosis is anunder-recognized entity that is associated withsignificant morbidity and mortality (1). It is esti-

mated that 2.6% to 4.0% of patients with lower ex-tremity deep vein thrombosis (DVT) have IVCthrombosis (2–5). However, the true incidence ofIVC thrombosis may be underestimated due to thelack of standardized methods of its detection andreporting, as well as the exponential increase in thenumber of unretrieved IVC filters in the UnitedStates, a major predisposing factor to IVC thrombosis(5,6). The mortality rate of IVC thrombosis is twice ashigh as that of DVT confined to the lower extremities(2). If untreated, patients with IVC thrombosis willalso suffer from significant morbidities: post-thrombotic syndrome (PTS) in up to 90%, disablingvenous claudication in 45%, pulmonary embolism(PE) in 30%, and venous ulceration in 15% (1,3,4).Phlegmasia cerulea dolens and renal vein thrombosisare rare, but well-described, limb and life-threateningcomplications of IVC thrombosis (7).

In this review, we aim to enhance the awarenessof this uncommon, but morbid, condition, and pro-vide readers with a guide detailing the diagnosisand management of IVC thrombosis with specialemphasis on contemporary endovascular treatmentmodalities.

ETIOLOGY

CONGENITALLY ABNORMAL IVC. IVC thrombosisis prevalent (60% to 80%) among patients withcongenital IVC anomalies (8–10). These anomaliesoccur in 0.5% to 1% of the general population, and in2% to 3% of patients with congenital cardiac defects(9,11). Congenital IVC anomalies can be classified into3 anatomic categories (12) (Figure 1):

1. Infrarenal: duplicate IVC, persistent left-sided IVC,pre-aortic IVC, and absence of the infrarenal IVC

2. Renal: accessory left renal vein, retroaortic andcircumaortic left renal vein

3. Suprarenal: absence of the hepatic IVC with azygoscontinuation, congenital caval stenosis or atresia,and IVC membranes

Most IVC anomalies are subclinical for many yearsdue to well-developed collaterals. They are oftendiscovered incidentally on abdominal imaging (10).However, thrombosis of the collateral channels or oftheir feeding vessel (often the common iliac vein) canlead to acute or subacute proximal DVT or findings ofchronic venous insufficiency.

CONGENITALLY NORMAL IVC. Thrombosis of theIVC in the absence of congenital abnormalitiesis rare, and is usually a result of a predisposing hy-percoagulable state along with an acquired pathologyin the IVC or one of its adjacent structures (1,7,13,14).

1. Prothrombotic factors: thrombophilia, malignancy,oral contraceptives, smoking, obesity, pregnancy,hormonal replacement therapy, and nephroticsyndrome.

2. Abdominal pathology: renal cell tumor, abdominalmasses producing extrinsic compression such as avery large uterine fibroid, Budd-Chiari syndrome,abdominal trauma/surgery, May-Thurner syn-drome, and thrombotic occlusion of an IVC filter.

Thrombotic occlusion of IVC filters is of particularimportance in the United States, where presumedoverutilization of IVC filters and low retrieval rateshave drawn recent attention. It is estimated that IVCfilter placement rates in the United States in 2012were 25 times that of an equivalent population inEurope (224,700 vs. 9,070) (6). Although the majority

AB BR E V I A T I O N S

AND ACRONYM S

ACCP = American College of

Chest Physicians

CDT = catheter-directed

thrombolysis

CT = computed tomography

DVT = deep vein thrombosis

GCS = graduated compression

stockings

IVC = inferior vena cava

MR = magnetic resonance

J A C C : C A R D I O V A S C U L A R I N T E R V E N T I O N S V O L . 9 , N O . 7 , 2 0 1 6 Alkhouli et al.A P R I L 1 1 , 2 0 1 6 : 6 2 9 – 4 3 IVC Thrombosis

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of implanted filters are retrievable in design andplaced in patients without clinical indications forpermanent caval interruption, the highest retrievalrate reported in the United States is only 34%, andsome series have reported retrieval rates of <10%(6,15,16). Because late filter thrombosis has been re-ported in up to 33% of patients (4,6,17), we are facedwith a large population of patients who are at risk forIVC thrombosis and its clinical sequelae. A systematicreview by Fox and Kahn (18) suggested a significantincrease in PTS and venous ulcers in patients withunretrieved IVC filters.

SEE PAGE 644 PE = pulmonary embolism

PMCT = pharmacomechanical

catheter-directed thrombolysis

PTA = percutaneous

transluminal angioplasty

PTS = post-thrombotic

ome

CLINICAL PRESENTATION

The clinical presentation of IVC thrombosis is oftenambiguous and varies significantly according to theacuity, the level, and the extent of thrombosis.Similar to those with lower extremity DVT, patientswith IVC thrombosis commonly complain of legheaviness, pain, swelling, and cramping. Nonspecificback and abdominal/pelvic pain along with scrotalswelling frequently precede leg symptoms (19).Because of its insidious onset, the diagnosis of IVCthrombosis is often made when signs and symptomsof clot migration and/or venous hypertensionbecome apparent. Clot migration or embolizationinto the lungs and renal veins can manifest withdyspnea and oliguria, respectively (7,17,19). If leftuntreated, the majority of patients with IVC throm-bosis will develop variable degrees of PTS, rangingfrom leg cramping and skin pigmentation todisabling claudication and or venous ulceration. Onrare occasions, the development of large paraspinalcollateral channels in chronic IVC occlusion canresult in severe lumbar radicular pain, sciatica, andeven cauda equina syndrome due to externalcompression of the spinal cord/peripheral nerves bythese dilated veins.

DIAGNOSTIC APPROACH

The diagnosis of IVC thrombosis is challenging forseveral reasons. First, thrombosis of the IVC usuallyhas an insidious onset and presents with nonspecificsymptoms. Second, physicians are often not familiarwith IVC thrombosis and may not entertain this diag-nosis unless the patient has a proximal lower extremityDVT. Third, the majority of patients with lower ex-tremities DVT do not have IVC thrombosis. Hence,screening all DVT patients for IVC thrombosis can betedious, low-yield, and cost-ineffective. Fourth, nospecific societal guidelines are currently available to

aid with the diagnosis andmanagement of IVCthrombosis.

Despite the paucity of data on the bestdiagnostic approach for IVC thrombosis, theliterature suggest that screening for IVCthrombosis is reasonable among patientswith a lower extremity DVT with high-riskfeatures (Figure 2) (1,8,9,14,17,19,20).

Once the diagnosis of IVC thrombosis issuspected, a careful review of the lower ex-tremity duplex ultrasound is warranted. Thisstudy may offer clues about an upstream oc-clusion (loss of respirophasic variation,waveform blunting in the femoral vein, etc.)even when there is no evidence of infrain-guinal DVT. A dedicated IVC duplex ultra-sound is usually the modality of choice forinitial screening. However, ultrasound isoperator-dependent, and visualization of the

IVC is frequently hampered due to bowel gas orobesity. Therefore, appropriately timed computedtomography (CT) and magnetic resonance (MR) im-aging are essential for the diagnosis (13,21). There isno standard CT protocol for imaging of the IVC. TheIVC is typically evaluated in the portal venous phase(60 to 70 s after contrast injection), but longer delays(90 to 180 s) should be considered if occlusivethrombus or low cardiac output are suspected (21).Magnetic resonance imaging is the most reliabletechnique for depicting the presence and extent oftumor thrombus, although limited availability andcost considerations prohibit its routine use. Famil-iarity with certain pitfalls in imaging of the IVC iscritical to avoid missed or overdiagnoses. These pit-falls are primarily related to a flow-related phenom-enon at the level of the renal veins, manifesting as apseudo-filling defect because of the confluence ofthe enhanced blood in the renal veins and the unen-hanced venous return from the lower body (21). Itshould be noted that MR venography in the presenceof an existing IVC filter could be associated withferromagnetic artifact, which may limit the reader’sability to assess IVC patency. In these patients, CTvenography may be the preferred diagnostic modal-ity. Direct catheter venogram is the definitive diag-nostic method. However, this more invasive methodcan be challenging if occlusive thrombus is present inthe femoral and or popliteal access site. Figure 3illustrates the utility of various diagnostic modal-ities in the diagnosis of IVC thrombosis.

Dedicated imaging for complications of IVCthrombosis should be considered in the appropriateclinical context. These could include: 1) CT an-giogram of the thorax to rule out PE may be

syndr

FIGURE 1 Graphic Illustration of the Most Common IVC Congenital Anomalies

IVC ¼ inferior vena cava; L ¼ left; R ¼ right. Adapted with permission from Truty et al. Congenital Anomalies of the Inferior Vena Cava and Left

Renal Vein: Implications During Open Abdominal Aortic Aneurysm Reconstruction. Ann Vasc Surg 2007;21(2):186-97.

Alkhouli et al. J A C C : C A R D I O V A S C U L A R I N T E R V E N T I O N S V O L . 9 , N O . 7 , 2 0 1 6

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considered in symptomatic patients. However, theoverall management in not likely to change as anti-coagulation is a key component in the treatment ofIVC thrombosis; 2) nuclear renal scanning to rule outrenal vascular compromise if renal vein thrombosis issuspected (Figure 3D); and 3) lumbar spine CT/MR torule out spinal cord compression if symptoms ofcompressive neuropathy are present; and 4) finally,suprarenal IVC thrombus can be occasionally visibleon echocardiography when detailed subcostal imagesare recorded (22)

TREATMENT OF IVC THROMBOSIS

Anticoagulation is the mainstay of treatment for pa-tients with IVC thrombosis. Adjunctive therapeuticmodalities are useful in selected patients, dependingon the acuity of their presentation (CentralIllustration). Patients with acute (<14 days), and sub-acute (15 to 28 days) presentation who are not at highrisk for bleeding might benefit from catheter-directedthrombolysis (CDT)/pharmacomechanical catheter-directed thrombolysis (PMCT) � percutaneous

transluminal angioplasty (PTA)/stenting, whereasthose with chronic presentation (>28 days) mightbenefit from PTA/stenting alone with a limited role forCDT/PMCT (Figure 4).ANTICOAGULATION AND COMPRESSIVE STOCKINGS.

The American College of Chest Physicians (ACCP)guidelines on proximal DVT (23), recommend the useof parental anticoagulation in the acute phase, fol-lowed by 3 to 6 months of oral anticoagulation forprovoked DVT and an extended period of anti-coagulation (>12 months) for unprovoked DVT (23).Patients with IVC thrombosis have a large thrombusburden, are at significant risk of thrombosis-relatedmorbidity and mortality, and often have uncorrect-able risk factor for rethrombosis (congenital anomaly,remote unretrieved filter, and so on). There are nospecific recommendations to guide anticoagulationmanagement in patients with IVC thrombosis. In ourpractice, we initiate intravenous unfractionatedheparin as soon as the diagnosis is suspected. If thepatient is not a candidate for additional CDT/PMCT,we also start warfarin at the time of diagnosis andswitch unfractionated heparin to enoxaparin upon

CENTRAL ILLUSTRATION Diagnosis and Management of Inferior Vena Cava Thrombosis

J A C C : C A R D I O V A S C U L A R I N T E R V E N T I O N S V O L . 9 , N O . 7 , 2 0 1 6 Alkhouli et al.A P R I L 1 1 , 2 0 1 6 : 6 2 9 – 4 3 IVC Thrombosis

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discharge if the international normalized ratio is nottherapeutic. Anticoagulation management of patientswho undergo CDT/PMCT is summarized in Table 1.

The routine use of compression stockings inpatients with proximal DVT has been an area ofdebate. The ACCP guidelines recommend the use ofgraduated compression stockings (GCS) to reduce theincidence of PTS after acute proximal DVT (grade 2B),and a trial of GCS in patients with an establisheddiagnosis of PTS (23). A recent randomized trial ofGCS in patients with proximal DVT (SOX trial) foundthat compression stockings do not reduce the risk ofPTS, and hence recommended against their use (24).However, several limitations of the study precludeits generalizability. In addition, patients with IVCthrombosis have massive thrombus burden and are

at significant risk of developing disabling PTS (25).We therefore treat these patients with GCS, applyingan ankle pressure of 30 to 40 mm Hg and a lowerpressure higher up the leg. In the acute phase, ban-dages may be used to provide initial compressivetherapy if GCS could not be fitted or if a rapiddecrease in leg swelling and subsequent refitting ofthe GCS is expected.SURGICAL THROMBECTOMY AND SYSTEMIC

THROMBOLYSIS. A large percentage of patients withproximal DVT treated with anticoagulation alonedevelop disabling PTS. Therefore, surgical throm-bectomy and systemic thrombolysis have beeninvestigated as complementary treatment to anti-coagulation in those patients (26,27). Most publishedseries of surgical thrombectomy studied patients with

FIGURE 2 A Suggested Algorithm for the Diagnosis of IVC Thrombosis

*A minority of patients with IVC thrombosis do not have a proximal iliofemoral DVT. **CT venography may require physician supervision due to

the need of individual protocol modification for optimal delayed venous phase imaging. ¶MRI venography is contraindicated in patients with an

indwelling IVC filter. AKI ¼ acute kidney injury; CT ¼ computed tomography; DVT ¼ deep vein thrombosis; IJ ¼ internal jugular vein; IVC ¼inferior vena cava; IVUS ¼ intravascular ultrasound; MRI ¼ magnetic resonance imaging.

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acute iliofemoral DVT, and reported high successrates and low operative mortality (28,29). However,iliofemoral thrombectomy is a minimally invasivesurgery performed by advancing a Fogarty catheterthrough a femoral venotomy and removing the distalclots with massaging maneuvers. Inferior vena cavathrombectomy is a much more invasive surgery thatrequires direct caval venotomy � temporary groinarteriovenous fistula creation and does not allow aconcomitant treatment of residual stenosis afterthrombectomy (30,31). Therefore, this modality hasfallen out of favor and is now limited to patients withtumor-associated thrombus (1,32).

The use of systemic thrombolysis in proximal ilio-femoral and iliocaval DVT has been assessed inseveral randomized trials (28,29,33,34). In these tri-als, streptokinase led to a complete clot lysis in 45%and partial lysis in 65% of patients, comparedwith <5% complete lysis and 20% partial lysis foranticoagulant therapy alone. Thrombolytic therapyalso led to significant reduction in the rates of PTS.However, this benefit was outweighed by the high

frequency of major bleeding complications (14% forstreptokinase vs. 4% for heparin alone), which pre-vented systemic thrombolytic agents from gainingwidespread adoption.

ENDOVASCULAR TREATMENT OF IVC THROMBOSIS.

Localized delivery of thrombolytic agents directlyinto the thrombus, also known as CDT, was consid-ered as a potentially safer and more effective alter-native to systemic thrombolysis (35). This modalityhas demonstrated safety and efficacy in multiplevascular beds, and has been increasingly utilized inthe treatment of patients with acute IVC thrombosis(36–38). Disadvantages of CDT include the need formultiple treatment sessions in the angiography suite,lengthy infusion times (often up to 48 to 72 h) withattendant patient discomfort, need for meticulousmonitoring for bleeding complications and longerintensive care stay. In addition, many patients withvenous thrombosis present few days after the onset oftheir symptoms, making CDT alone less effective dueto the rapid organization and fibrosis of the clot. Most

FIGURE 3 Diagnostic Modalities for IVC Thrombosis

(A to C) Catheter venography (A) and CT venography (B) in a patient with massive compressive leiomyoma (inset). Note the decompression of the IVC after hysterectomy

showing re-expansion of the IVC filter along with resolution of the thrombus (C). Dashed arrow indicates the IVC filter. Asterisk indicates a leiomyoma. (D) A renal (99m-

technetium diethylene triamine pentaacetic acid [DPTA]) scan suggestive of renal vascular compromise due to severely reduced uptake of DPTA bilaterally. A0 shows a

sudden drop in perfusion at the level of the kidneys (circled) compared with normal perfusion in the spleen (arrow). B0 illustrates a 60-s time activity curve with

markedly delayed tracer uptake in the right and left renal arteries indicative of renal vascular compromise. C0 shows delayed (0 to 30 min) static images at 2-min intervals

with persistent tracer uptake is seen in both kidneys at 30 min, suggestive of renal vascular obstruction. (E) Catheter venography in a patient with chronic IVC thrombosis

and a prior IVC filter. Dashed arrow indicates the IVC filter. Double asterisks indicate significant collateral formation below the site of IVC occlusion. (F) CT venography in

a patient with IVC thrombosis extending to the IVC/RA junction. White arrow indicates the IVC thrombus; dashed arrow indicates the IVC filter. LT ¼ left; RT ¼ right;

other abbreviations as in Figure 2.

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of these issues have been addressed by adding me-chanical thrombectomy techniques to CDT, which isreferred to as PMCT. PMCT reduces the dose ofthrombolytic used, critical care unit days as well astotal hospital stay and charges (39–44). These deviceswork by adding low-energy high-frequency ultra-sound waves to enhance thrombolysis (EKOS,Bothell, Washington), or by mechanically fragmen-tation the clot through PMCT via rotating sinusoidaldispersion wires (Trellis-8, Bacchus Vascular, SantaClara, California) or pulsatile saline jets (AngioJet,Possis Medical, Minneapolis, Minnesota). Most

recently, suction thrombectomy with the AngioVacveno-venous bypass system (Vortex Medical, Nor-well, Massachusetts) was introduced to treat patientswith massive clot burden (45).

Thrombus removal with PMCT in patients withproximal DVT has been shown in several observationalstudies to significantly reduce the incidence of PTSand improve quality of life (46–50). However, thesestudies were inconclusive with regards to thecomparative safety outcomes of PMCT versus stan-dard anticoagulation due to the small number of pa-tients enrolled. This had led to conflicting guideline

FIGURE 4 Treatment Algorithm for Patients With IVC Thrombosis

CDT ¼ catheter-directed thrombolysis; PMCT ¼ pharmacomechanical catheter-directed thrombectomy; PTA ¼ percutaneous transluminal

angioplasty; Tx ¼ treatment; other abbreviations as in Figure 2.

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recommendations from the American Heart Asso-ciation and ACCP on the use of PMCT in patientswith proximal DVT (23,51). The more definitiveNIH-sponsored trial ATTRACT (Acute Venous Throm-bosis: Thrombus Removal With Adjunctive Catheter-Directed Thrombolysis) investigating the efficacy ofPMCT versus standard anticoagulation therapy fortreatment proximal DVT has recently completedenrollment, and may shed more light on the efficacy ofcontemporary PMCT techniques in these patients (52).Nevertheless, even though IVC thrombosis is classi-fied under the category of proximal DVT, the afore-mentioned studies rarely include patients with IVCthrombosis. Therefore, the assumed benefit of PMCTin this subgroup of patients is largely extrapolative.

Despite the current lack of robust data or unifiedrecommendations, the utilization rate of adjunctivemechanical modalities in the treatment of IVCthrombosis in the United States has increased from16% in 2005 to 35% in 2011 (Figure 5) (38). This trend islikely due to the increasing recognition of themorbidity associated with IVC thrombosis and the

limited effectiveness of traditional anticoagulation inits treatment. In the following text, we describe somecommonly available options for percutaneous treat-ment of IVC thrombosis (Table 2).

PERCUTANEOUS TREATMENT MODALITIES. Per iphera linfus ion catheter -d i rected thrombolys i s . In-fusion catheters have side holes for uniform slowdispersion of therapeutic agents within the clottedsegment. Typically, after the thrombus is crossedwith a 0.035-inch wire (angled glide wire, Terumo,Tokyo, Japan), and an infusion catheter is advancedinto the clotted segment. Our agent of choice alte-plase (10 mg mixed in 1,000 ml of 0.9% NaCl), infusedat a rate of 0.01 mg/kg/h to a maximum of 24 mg in24 h (53). During infusion, hemoglobin, Partialthromboplastin time and fibrinogen levels are moni-tored every 4 to 6 h to minimize bleeding complica-tions. A fibrinogen level of <150 mg/dl is associatedwith significantly higher risk of major bleeding duringthrombolytic infusion (54). Therefore, it is our prac-tice is to stop/decrease the infusion rate when the

TABLE 1 Periprocedural Management of Anticoagulation and Antiplatelet Therapy in

Patients With IVC Thrombosis

Pre-procedural

IV UFH (PTT target 2–2.5 times UL) or SC LMWH (stop 8 h before CDT/PMCT)*

Argatroban if HIT (PTT target 2–2.5 times UL)

Intraprocedural

IV UFH (PTT target 1.5–2 times UL) or bivalirudin

Argatroban (PTT target 1.5–2 times UL) if or bilvalirudin if HIT

Post-procedural

IV heparin (start 1 h after sheath removal), or argatroban (PTT target 2–2.5 times UL) if HIT

Start warfarin or fondaparinux the evening after the procedure†

If PTA/stenting performed: ASA 325 mg and clopidogrel 300–600 mg

Long-term therapy:

1st Year

If no PTA/stenting: ASA 81 mg and warfarin daily

If PTA/stenting: ASA 81 mg, clopidogrel 75 mg daily and warfarin for 1 month, then ASA 81mg and warfarin daily‡

After 1 year

Repeat venogram

If no restenosis, continue daily ASA 81 mg indefinitely

If restenosis/nonocclusive thrombus, continue daily ASA 81 mg and warfarin indefinitely

*Stop heparin 1 h and LMWH 8 h before CDT/PMCT. †Use IV UFH instead if repeat CDT/PMCT sessions areplanned or expected. ‡Can substitute warfarin with a NOAC after one month, but higher failure rates have beenobserved in our experience.

ASA ¼ aspirin; CDT ¼ catheter-directed thrombolysis; HIT ¼ heparin-induced thrombocytopenia; IV ¼ intra-venous; IVC ¼ inferior vena cava; LMWH ¼ low-molecular-weight heparin; NOAC ¼ novel anticoagulant agent;PMCT ¼ pharmacomechanical catheter-directed thrombectomy; PTA ¼ percutaneous transluminal angioplasty;PTT ¼ partial thromboplastin time; SC ¼ subcutaneous; UFH ¼ unfractionated heparin; UL ¼ upper limit ofnormal.

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fibrinogen level drops below 100 mg/dl. Repeatvenography is performed every 12 to 24 h to assessclot resolution. If the angiographic results are unsat-isfactory (<50% of clot lysis), thrombolytic therapycan be repeated, but for a maximum durationof <96 h.Ultrasound-enhanced CDT. This system comprises a5.2-F multilumen drug delivery catheter, an ultra-sound core wire, and a controller (Figure 6A). Thecatheter is advanced over a guidewire to traversethe length of the thrombus, and the guidewire isexchanged for the ultrasound core wire. The throm-bolytic agent is infused and ultrasound energy isturned on simultaneously. Ultrasound waves accel-erate the thrombolysis process by disturbing thefibrin matrix within the thrombus, which exposesmore binding sites for the thrombolytic agent,causing acoustic streaming, thus driving the throm-bolytic deep into the thrombus. EKOS showed similarefficacy in thrombolysis, but possibly shorter treat-ment duration, compared with standard infusioncatheters (35). Given the lack of evidence to suggestsignificant additional benefit over standard cathetersand the added cost, the role of the EKOS catheter as afirst-line device in patients with IVC thrombosisremains questionable. A prospective multicenterregistry, ACCESS PTS (Accelerated Thrombolysis forPost Thrombotic Syndrome Using the EKOS System)study, is ongoing to further assess the safety and ef-ficacy of the EKOS system combined with CDT amongindividuals with proximal chronic DVT and PTS.

AngioJet rheolyt i c thrombectomy. This systemis a combined PMCT system, which consists of 3 com-ponents: a single-use dual-lumen catheter, pump set,and a pump drive unit (Figure 6B). The catheter con-sists of one lumen supplying pressurized saline to thedistal catheter tip, and a second lumen incorporatingthe first lumen, guidewire, and thrombus particulatedebris. The drive unit/pump generates high-pressure(10,000 psi) pulsatile saline flow that exits the cath-eter tip through multiple retrograde-directed jets.These jets create a localized low-pressure zone (Ber-noulli effect) for thrombus aspiration and maceration,and provide the driving force for evacuation ofthrombus debris through the catheter (55). The systemalso has a PowerPulse Spray feature that allows directinfusion of thrombolytic drugs into the clot. In a typicalcase, the IVC clot is traversed with the AngioJet cath-eter over a 0.035-inch wire. The catheter outflowlumen is occluded and up to 10 mg of Alteplase dilutedin 50 ml of saline is injected into the clot in a pulsespray fashion during catheter withdrawal. Thethrombolytic agent is allowed 15 to 30 min to work

before thrombectomy is performed with the outflowlumen reopened. The major advantage of the AngioJetsystem is its ability to reduce the duration and the doseof thrombolytic therapy. We have found the new Zel-lante AngioJet device to be particularly helpful in cavalthrombosis patients.The Tre l l i s per iphera l infus ion system ( iso latedPMCT) . The Trellis has 2 occluding balloons, druginfusion holes, and mechanical fluid dispersion ca-pabilities (Figure 6C). This catheter is placed in theclotted segment, and the 2 balloons are inflated toisolate the thrombus. Once the drug is dispersedthrough the catheter side holes, the catheter oscil-lates, mixing the thrombolytic drug into the bloodclot. After 10 min, the remaining thrombolytic agentand the dissolved portion of the clot are aspirated. Apotential advantage of this system is that it isolatesthe thrombus and provides targeted therapy. Utilizingthe Trellis device for the treatment of iliofemoral andIVC thrombosis has been shown to decrease theduration and dose of thrombolytic therapy, and ach-ieve a higher lytic success rate (41,56,57). Certaintechnical limitations of this device should be noted:First, the device is designed to treat short (10 to 30 cm)thrombotic segments. However, treating longer seg-ments with sequential sessions or kissing balloon

FIGURE 5 Temporal Trends of CDT Utilization in The Treatment of IVC Thrombosis in

the United States, 2005–2011

1 indicates catheter-directed thrombolysis (CDT). IVC ¼ inferior vena cava thrombosis.

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techniques has been reported (58). Second, the Trellisballoons may not expand enough to occlude a largeIVC. Third, in case of IVC-filter thrombosis, the pres-ence of the filter in the treatment zone may affect therotational efficacy of the Trellis catheter. Finally, theTrellis device was recently subject to a Class I recall bythe Food and Drug Administration due to mislabelingerror of the balloon inflation ports, and is thereforetemporarily off the market.Suct ion thrombectomy: AngioVac veno-venousbypass . The AngioVac circuit is an extracorporealveno-venous bypass system that is designed toremove large clots in an en-bloc fashion from largevasculature such as the IVC (Figures 6D and 6E),right heart, or proximal pulmonary artery. Thesystem includes a 22-F coil-reinforced suctioncannula with a balloon-expandable funnel-shaped

TABLE 2 Comparison of Endovascular Treatment Modalities for Patie

Device/Treatment Method Access Treatment Length

Infusion catheters CDT 4-F, 5-F 5–50 cm Simple, loInexpensi

EKOSUltrasound-enhanced CDT

6-F 6–50 cm Simple, loShorter th

TrellisPMCT

6-F, 8-F 10–30 cm Single-seIsolation

AngioJet rheolytic catheterPMCT

6-F, 7-F Flexible User frienCould pre

AngioVacAspiration thrombectomy

17-F & 22-F Flexible Useful inCan be us

Abbreviations as in Table 1.

distal tip and a 17-F reinfusion cannula. The suctioncannula can be advanced to the clot via a femoral orinternal jugular vein access. The venous bloodalong with the thrombus is drained via the tipof the suction cannula by a centrifugal pumpand passed through a filter, which removes thethrombus and then reinfuses the venous blood intoa central vein via a reinfusion cannula (Figure 7D).Several small series suggested a role for AngioVacin the treatment of IVC thrombosis (59–61). Thismodality is particularly useful in patients withacute IVC thrombosis and a contraindication tothrombolysis.

In contemporary practice, operators view thesedevices as complementary rather than alternativetools that can be often be used in conjunction withCDT in selected patients (Figure 7).

ADJUNCTIVE IMAGING AND INTERVENTIONS

ANGIOPLASTY/STENT. Fibrotic transformation ofthe thrombus occurs within 2 weeks of clot formation(4). Because patients with IVC thrombosis often pre-sent late, they usually have a combination of acutesoft thrombus and a chronic fibrotic thrombus.Although the acute thrombus can effectively betreated with PMCT, the fibrotic component is lessamenable to these therapies, resulting in high fre-quency of residual luminal stenosis after PMCT(Figure 8). Untreated residual stenosis followingthrombectomy is associated with high rates of recur-rent DVT. In a large series of iliocaval thrombosispatients treated with surgical thrombectomy, the rateof recurrent DVT was 73% in those with untreatedresidual outflow stenosis versus 13% in those who hadvenoplasty/stenting of residual stenosis (p < 0.01)(62). Adjunctive balloon angioplasty and stentingto restore venous patency in patients with iliocaval

nts With IVC Thrombosis

Advantages Disadvantages

w profileve

Multiple treatment session needed

w profilerombolysis duration

Multiple treatment session neededExpensive, limited data

ssion treatmentof the thrombus

Shorter treatment lengths

dlyvent distal embolization

Single session rarely sufficientCould lead to proximal embolization

large clot burdened without thrombolytic agents

Large bore, 2 access sites neededLimited data and experienceGeneral anesthesia may be necessary

FIGURE 6 Illustration of Endovascular Treatment Modalities for Patients

With IVC Thrombosis

(A) The EKOS ultrasound-enhanced CDT system. (B) The AngioJet CDT þ PMT rheolytic system. (C) The Trellis CDT þ PMT system. (D) The AngioVac extracorporeal

bypass aspiration system. (E) The AngioVac suction cannula. PMT ¼ pharmacomechanical thrombolysis; other abbreviations as in Figures 2 and 4.

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DVT is also effective in preventing the recurrenceof thrombosis, reducing PTS, enabling healing ofvenous ulcers, and improving quality-of-life mea-sures (63–66). In contemporary U.S. practice, 60% ofpatients who undergo PMCT for IVC thrombosisreceived balloon venoplasty � stenting (38). Severaltechnical considerations should be emphasized whenIVC stenting is entertained:

1. Choice of IVC stent: one limitation of stenting inthe IVC is the limited choice of stents suitable foruse in the IVC. Only 2 stainless steel stents, theWallstent (Boston Scientific Corporation, Natick,Massachusetts), the Z-stent (Cook, Bloomington,Indiana) are available in large enough sizes forIVC stenting (up to 24 mm and 35 mm, respec-tively). The Wallstent offers strength and flexi-bility but suffers from foreshortening, which makeprecise placement challenging. The Z-stent offers afew advantages over the Wallstent, due to itsminimal foreshortening, more radial force, and its

larger interstices; however, it has large fixingspines and therefore carries a higher risk of cavalperforation (67).

2. Stenting across IVC filters: in cases of IVC filter-related thrombosis, the residual stenosis afterPMCT is frequently located within the filter.Stenting across the filter might, therefore, benecessary to ensure patency of the caval outflow.Many operators have expressed reluctance todilate the filter-bearing segment for fear of tearingthe IVC, fracturing or displacing filters, orincreasing the risk for subsequent PE. However, ina large series of patients undergoing IVC stentingfor chronically occluded IVC, stenting across thefilter was safe and did not result in an increasedmorbidity or mortality (64).

3. Stenting across the iliocaval bifurcation: In themajority of cases of IVC thrombosis, the thrombusextends into the iliocaval confluence. Stentingacross the iliocaval confluence may also be

FIGURE 7 Combine

(A) Suction thrombec

residual thrombus in

performed via left fe

pharmacomechanical

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necessary if significant lesions are present afterPMCT. Although multiple techniques have beendescribed for stenting of the iliocaval bifurcation,the kissing stents technique seems to yield the bestlong-term patency rates (63,65).

4. External compression: If clinically indicated,removal of external compressive masses may leadto spontaneous decompression of the IVC(Figures 3A to 3C). However, if surgical relief of theexternal compression is not possible, stenting ofthe IVC is appropriate and technically feasible.

Finally, it should be noted that the iliocavalsystem is a low pressure system and routine follow-up with duplex ultrasonography, CT, or cathetervenography is necessary to maintain primary assistedpatency.

INTRAVASCULAR ULTRASOUND. Intravascular ul-trasound can help provide very useful complemen-tary information on the underlying pathology behindclot formation and help guide therapy (e.g., inpatients with suspected renal vein thrombosis orMay-Thurner syndrome). It can also be used to

d Suction Thrombectomy and CDT/PMCT in a Patient With Massive IVC Th

tomy with the AngioVac aspiration catheter (arrow). (B) Catheter venography

the IVC and the iliac veins. Inset (B0) shows the filtered clot during suction

moral vein access (asterisk), revealing near complete resolution of the ilioca

catheter-directed thrombolysis; other abbreviations as in Figures 2 and 4.

evaluate thrombus burden, degree of stenosis, andadjacent structures (Figure 9). Occasionally, intra-vascular ultrasound can detect fibrous bands, webs,spurs, and trabeculations seen in recanalized DVT,which may be missed on traditional venography.

PROPHYLACTIC IVC FILTERS. A major concernrelated to PMCT in the IVC has been development ofPE; however, the data on the use of IVC filters as anadjunct to PMCT remain controversial. In contempo-rary U.S. practice, w20% of patients received a pro-phylactic IVC filter before or at the time of PMCT (38).Although it is intuitive to assume that the use ofmechanical thrombectomy devices will increase therisk of distal embolization, a study of 40 patients whohad retrievable filters placed before CDT and removedafter the procedure found no correlation between theuse of these devices and the detection of embolizedclot in the filters (68). Most operators opt to place aretrievable IVC filter in the infrarenal or suprarenalsegments of IVC only in high-risk patients such asthose with large floating thrombus and those withdiminished lung reserve (68,69). Given the significant

rombosis

performed via left femoral vein access (asterisk), revealing significant

thrombectomy with the AngioVac system. (C) Catheter venography

val thrombosis after CDT/PMCT with the AngioJet system. PMCT ¼

FIGURE 8 Adjunctive Balloon Angioplasty and Stenting in Patients with IVC Thrombosis

(A) Cavogram in a patient with chronic IVC thrombosis and severe PTS following CDT with EKOS. Significant residual IVC stenosis is seen due to the chronicity of

the thrombosis. Arrow indicates the IVC filter. B shows restoration of flow in the IVC after adjunction balloon angioplasty and stenting (dashed arrow) with 2

self-expanding stents. (C) Cavogram in a patient with acute IVC thrombosis. Complete occlusion of the IVC is seen at the level of the filter (arrow). D shows acceptable

results (>50% clot lysis) following 1 treatment session with AngioJet and 12-h tissue-type plasminogen activator infusion via a fountain catheter. PTS ¼ post-thrombotic

syndrome; other abbreviations as in Figures 2 and 4.

FIGURE 9 Illustration of IVUS Utility in the Treatment of IVC Thrombosis

(A) Invasive venography of a patient presenting with IVC thrombosis. Large residual thrombus is seen at and above the level of the IVC filter after PMCT with AngioJet.

Severe IVC stenosis is seen near the IVC/right atrial junction and is confirmed with IVUS imaging (inset). (B and C) IVUS guided stenting of the IVC below (B) and

above (C) the IVC filter. The IVC stenosis at the IVC/RA junction was hemodynamically significant (gradient >10 mm Hg), and was therefore stented to prevent recurrent

IVC thrombosis. Abbreviations as in Figures 2, 4, and 7.

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morbidity associated with IVC filter thrombosis,removal of these filters as soon as possible should beplanned at the outset.

CONCLUSIONS

IVC thrombosis is an under-recognized entity that isassociated with significant short- and long-termmorbidity. The diagnosis of IVC thrombosis is chal-lenging, and a high index of suspicion is required.Knowledge of the pitfalls of noninvasive IVC imagingis essential to select the appropriate and the highestyield modality. Once the diagnosis is confirmed, im-mediate treatment is warranted to avoid the acuteand chronic complications of this disease. The limited

effectiveness of anticoagulation alone, and the unfa-vorable risk/benefit ratio of systemic thrombolysisand surgical thrombectomy, led to the developmentand the widespread utilization of CDT � PMCT in thetreatment of IVC thrombosis. In the absence of ran-domized trials or societal guidelines, careful caseselection and technical expertise in CDT � PMCT areessential for successful endovascular management ofIVC thrombosis.

REPRINT REQUESTS AND CORRESPONDENCE: Dr.Mohamad Alkhouli, Division of Cardiovascular Dis-ease, University of Rochester Medical Center, 601Elmwood Avenue, Rochester, New York 14642.E-mail: [email protected].

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KEY WORDS catheter-directedthrombolysis, deep venous thrombosis,inferior vena cava, pharmacomechanicalcatheter-directed thrombolysis, post-thrombotic syndrome

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