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134
A. F. Derakhshani et al.
of the affected limb, which is typically circumferentially larger than the contralateral side. Although thrombi can form in the upper extremities or spontaneously in the right ventri­cle, the majority of pulmonary emboli are believed to origi­nate from DVT in the lower extremities. As thrombi in the calf veins extend to the deep veins of the thigh, they can break, dislodge, and travel to the right heart and pulmonary arteries. PE can present with the sudden onset of dyspnea, pleuritic chest pain, cough, wheezing, tachycardia, tachy­pnea, hemoptysis, or cardiovascular collapse and shock. These symptoms are non-specic such that further diagnos­tic testing is needed [8, 9].
Compression ultrasound is the noninvasive test of choice for diagnosis of DVT.It is highly sensitive for the detection of femoropopliteal DVT but less sensitive for calf and ilioca­val thrombosis. The diagnosis of lower extremity DVT is made by evaluation of the common femoral to popliteal veins using a 5–10-MHz transducer. Upper extremity DVT is diagnosed by ultrasound of the upper arm, axilla, neck, and subclavian veins during quiet respiration using a 7.5-MHz imaging transducer coupled to a 5-MHz pulsed Doppler transducer. Criteria for a positive exam include (1) vessel non-compressibility, (2) absent Doppler signal, (3) absence of respiratory phasicity or augmentation, and/or (4) visible thrombus, typically a hypo-echoic or hyper-echoic intralu­minal mass. Respiratory phasicity suggests patency between the imaged vein and the heart. Normal augmentation sug­gests patency between the imaged vein and the site of man­ual venous compression. In patients with suspected thrombosis and a negative compression ultrasound, the test should be repeated in 7days [6, 8].
Key Point
Compression US is the noninvasive test of choice for diagnosis of DVT.Diagnostic criteria include:
• Non-compressible vessel
• Absent Doppler signal
• Absence of respiratory phasicity or augmentation
• Visible thrombus
CT (computed tomography) angiography is the most commonly used imaging test to evaluate for PE.It is more reliable than ventilation-perfusion (V/Q) scanning using technetium DTPA (ditriaminopentaric acid), historically, a more popular method for PE evaluation, and less invasive than pulmonary angiography, the previous gold standard [8,
9]. CT angiography has the added benet of visualizing pul-
monary arterial anatomy over V/Q scanning. Filling defects in the pulmonary arteries during the appropriate phase of contrast injection conrms the diagnosis (Fig. 10.1a). CT
angiography has limited sensitivity for more peripheral emboli in smaller vessels [8, 9]. The use of brin D-dimer is also used to add to the diagnostic accuracy of noninvasive tests. In one study, the sensitivity of D-dimer concentrations over 500μg for the presence of PE was 98% with a negative predictive value of 98% [8].
Key Point
PE is most commonly diagnosed with CTPA although V/Q scan and pulmonary angiography can also be used.
Findings of PE on chest radiograph (CXR) are neither sensitive nor specic. The Westermark sign (hyperlucency surrounding oligemia), Fleischner sign (prominent central artery), and Hampton hump (pleural opacication indicating pulmonary infarct) have all been described as radiographic signs of PE.The role of the CXR in the setting of suspected PE is to rule out other causes, such as pneumonia, as most CXRs in the setting of PE are normal. The same is often true of the electrocardiogram (ECG), although there are charac­teristic ECG ndings of right heart strain in the setting of PE.ECG can also diagnose left bundle branch block (LBBB), which is of signicance if the patient undergoes pulmonary artery catheterization. The interventionist must be aware of preexisting LBBB because complete heart block can be induced during catheterization of the right heart [9].
Anticoagulation is the standard of care in the treatment of most patients with VTE; however, a small number of patients with DVT present with acute limb-threatening venous hyper­tension known as phlegmasia. In its early phase, the condi­tion presents as phlegmasia alba dolens, characterized by a painful, swollen, and pale extremity. With subsequent pro­gression and occlusion of venous collaterals, the condition progresses to phlegmasia cerulea dolens, characterized by blue discoloration of the extremity (Fig.10.2a). This condi­tion can rapidly progress to arterial compromise, venous gangrene, and limb loss. Most experts agree that in the absence of high bleeding risk, these patients will benet from active thrombus removal techniques, including catheter­directed thrombolysis (CDT) [10]. In addition, some experts support the escalation of therapy and use of CDT in patients with progressive IVC thrombosis or progression of DVT symptoms despite adequate anticoagulation [11].
Key Point
Anticoagulation for a minimum of 3 months is the
standard of care for treatment of VTE.CDT may help
in high-risk patients (i.e., massive PE).
10 Venous Thromboembolism: Deep Venous Thrombosis andPulmonary Embolism
135
Fig. 10.1 A 51-year-old female who presents with acute shortness of
breath after prolonged car ride. CT pulmonary angiogram (CTPA) (a) demonstrates saddle embolus extending across the bifurcation of the main pulmonary artery, with a large clot within the right main pulmo-
Fig. 10.2 A 62-year-old
female with history of ovarian cancer and right pelvic lymph node mass presents with severe right leg pain and swelling. Right leg photograph (a) demonstrates painful blue discoloration characteristic of phlegmasia cerulea dolens. Prone venogram (b) demonstrates signicant lling defects (arrows) within the entirety of the right femoral vein and lack of patent collaterals. Follow-up prone venogram (c) after CDT demonstrates restored patency of the right femoral vein. Right leg photograph (d) 10days after CDT demonstrates improvement in appearance of right leg. Courtesy of Brooke Spencer, MD
nary artery and (b) a markedly abnormal RV:LV ratio. Frontal radio­graph (c) demonstrates lysis catheters extending intothe bilateral lower lobe pulmonary arteries
136
Key Point
Acute limb-threatening venous hypertension due to DVT:
Phlegmasia alba dolens = painful, swollen, pale
extremity
Phlegmasia cerulea dolens=blue discoloration of the
extremity
Patients with PE are stratied into high-, intermediate-, and low-risk categories. Patients with high-risk (massive) PE present with hemodynamic instability (tachycardia, hypoten­sion) and are at high risk of mortality. In addition to antico­agulation, these patients may require treatments such as thrombolytic therapy or embolectomy. Patients with intermediate- risk (sub-massive) PE present with hemody­namic stability but demonstrate signs of right ventricular dysfunction, which have been associated with early clinical deterioration and mortality. Presence of right heart dilation on echocardiography or CT pulmonary angiogram (right ventricle/left ventricle ratio>0.9, Fig.10.1b) and/or elevated serum troponin or brain natriuretic peptide (BNP) supports the diagnosis of intermediate-risk PE.Use of catheter-based therapies in addition to anticoagulation, remains controver­sial [12]. All other patients have low-risk PE and may poten­tially be managed as outpatients [5, 12].
Key Point
Signs of right heart strain:
• RV:LV ratio>0.9
• Elevated troponin or BNP

Conventional Therapy

As mentioned, anticoagulants are the mainstay of therapy for VTE [12]. Anticoagulants, such as heparin, warfarin, low­molecular- weight heparins (enoxaparin, dalteparin), direct factor Xa inhibitors (apixaban, rivaroxaban, edoxaban), and direct thrombin inhibitors (dabigatran), mainly function to inhibit clot propagation [12]. In general, anticoagulation for a minimum of 3months is the standard of care for the major­ity of patients with PE, with some patients requiring pro­longed or indenite anticoagulation [12, 13].
Systemic thrombolytics and surgical embolectomy are typically reserved for patients with massive PE. Thrombolytics, such as recombinant tissue plasminogen
A. F. Derakhshani et al.
activator (rTPA), actively lyse clot by interacting with plas­minogen to form plasmin, a proteolytic enzyme that degrades brin strands. Absolute contraindications to the use of thrombolytics and anticoagulants include active bleeding or cerebrovascular accident within 2months, intracranial neo­plasm, or recent head trauma. Major bleeding is a known complication of thrombolytics and anticoagulation; the risks and benets of therapy must be carefully weighed in each individual clinical scenario. Relative major and minor con­traindications also exist. In the case of an absolute contrain­dication to anticoagulation, an IVC lter may be placed to provide a physical barrier to clot migration to the lungs, though their efcacy has not been well documented and their long-term deleterious consequences are well known (refer to Chap. 11 for more information) [5, 14].
Key Point
Absolute contraindications to thrombolytics and anticoagulation:
• Active bleeding
• Cerebrovascular accident within 2months
• Intracranial neoplasm
• Recent head trauma
Similar to PE, anticoagulation for a minimum of 3months is the standard of care for treating the vast majority of patients with DVT [12]. One of the main goals in medical therapy of DVT is to preserve function of the venous valves. When these valves become damaged, normal venous blood ow becomes compromised leading to venous hypertension and venous stasis, subsequently causing further problems [10, 15]. Most patients with DVT can be treated as outpa­tients, except in cases of signicant comorbidity such as chronic kidney disease or limb-threatening venous hyperten­sion. Furthermore, anticoagulation is not routinely recom­mended for distal calf vein thrombosis, unless the patient is symptomatic, has risk factors for proximal extension, or the thrombus shows extension at 2-week follow-up imaging [5].

Interventional Therapy

Many institutions use a pulmonary embolism response team (PERT) to standardize and expedite the treatment of patients with PE [16]. This multidisciplinary team includes medical, surgical, and interventional specialists interested in treating PE.Convening at the time of PE diagnosis in a virtual space, such as a phone or video conference, the PERT allows rapid
10 Venous Thromboembolism: Deep Venous Thrombosis andPulmonary Embolism
evaluation and formulation of a treatment plan. In general, endovascular intervention is reserved for the most severe situations, specically patients with high-risk (massive) and
Key Point
Absolute contraindications for CDT:
intermediate-risk (sub-massive) PE. The Pulmonary Embolism Severity Index (PESI) was developed to help identify patients at risk of complication from PE and guide initial treatment [17]. Using 11 patient characteristics, the PESI straties a patient with PE into 5 classes of increasing risk of mortality and adverse outcome.
• Active bleeding
• Recent stroke
• Intracranial mass
• Intracranial aneurysm
• Recent GI bleeding
• Spinal surgery
Key Point
PESI score clinical criteria:
• Age
• Sex
• History of cancer
• History of heart failure
• History of chronic lung disease
In most cases, lysis catheter placement is relatively pain­less for both DVT and PE treatment. However, patients may require moderate sedation for positioning and/or anxiety. Pre-procedure imaging includes CT pulmonary angiogram and echocardiography. BMP and troponin can also be useful tools for assessing organ function.
• HR 110
• SBP <100mmHg
• RR 30
• Temp <36
• Altered mental status
• O2 saturation<90%
The How to: PE
1. Access is achieved via either internal jugular or common femoral approach. Ultrasound-guided access is recommended since inadvertent arterial puncture increases bleeding risk when thrombolyt­ics are being given.
In these high-risk patients, prompt improvement of right ventricular function may be necessary to avoid cardiogenic shock and death [18]. The effects of heparin on right ven­tricular function are minimal in the rst 28–48 h [19]. Options for transcatheter therapy include fragmentation of the thrombus into smaller pieces that are less obstructive to ow or removing the thrombus using a thrombectomy device. Several devices exist which use rotation, aspiration, or rheolysis to mechanically break and remove the thrombus from the pulmonary circulation. These methods will quickly improve right ventricular function compared to CDT, which will slowly improve function over time as thrombolysis occurs. As such, CDT is more often appropriate for treating patients with intermediate-risk PE given their hemodynamic
2. A catheter is directed through the superior vena cava (SVC) or IVC, right atrium, tricuspid valve, right ventricle, pulmonic valve, and into the main pulmonary artery. To avoid induction of ventricular ectopy from wire manipulation in the heart and avoid traversing chordae tendineae with the cathe­ter, a pigtail catheter is used when traversing the heart.
3. Pulmonary angiography may be performed, but is not always necessary. If angiography is performed, it is usually recommended to perform unilateral studies for best visualization. Additionally, pulmo­nary arterial pressures are usually obtained.
4. A lysis catheter or thrombectomy device is then
stability.
Prior to CDT, patients must be evaluated for contraindica­tions to thrombolytic therapy. Absolute contraindications include active bleeding, recent stroke, intracranial lesion (mass or aneurysm), recent gastrointestinal bleeding, and spinal surgery. Relative contraindications include recent major abdominal surgery, pregnancy, or coagulopathy. In patients who cannot receive anticoagulation and thrombo-
5. If a mechanical thrombectomy device is being used (hemodynamically unstable patients), the thrombus is fragmented and removed with the device. If thrombolysis alone is being performed (more hemo­dynamically stable patients), rTPA is infused for
lytic medications, mechanical thrombectomy may be the favored treatment.
137
10.1c).
(continued)
138
A. F. Derakhshani et al.

References

divided if bilateral infusion is necessary. While pro­tocols vary at each institution, if bleeding develops,
at a lower infusion if safe to do so. Fibrinogen and
ogen level is below 100, the infusion is reduced. If it is below 50, the infusion is stopped and labs are
6. Some institutions will remove the catheters at bedside following the completion of the infusion protocol. Others will have the patient return for angiography and repeat pressure measurement. Manual compression is used to achieve hemostasis.
The How to: DVT
1. Access is achieved via the common femoral vein for pelvic DVT and via the popliteal or posterior tibial vein for all other DVTs, depending on the extent of the thrombus. Ultrasound-guided access is recommended since inadvertent arterial puncture increases bleeding risk when thrombolytics are being given.
2. A catheter is directed through the clot and into a
venography.
3. Based on the length of the clot, an appropriate
10.2b). Some phar-
macomechanical devices and published tech­niques allow same-session thrombectomy and thrombolysis, avoiding prolonged thrombolytic exposure [20, 21].
4.
divided for bilateral infusion.
5. The patient returns for venography at the comple-
10.2c). Additional throm-
bus removal (pharmacomechanical or infusion) is performed if there is residual thrombosis. Underlying causative stenoses are treated with stenting. Fibrinogen and CBCs are checked and acted upon as above.
1. Goodman LR.Search of venous thromboembolism: the rst 2913 years. AJR Am JRoentgenol. 2013;201(4):W576–81.
2. Hume M. Pulmonary embolism. Historical aspects. Arch Surg. 1963;87:709–14.
3. Virchow R. Weitere Untersuchungen ueber die Verstopfung der
-
Lungenarterien und ihre Folge. Traube’ s Beitraege exp Path u. Physiol. 1846;2:21–31.
4. Galanaud JP, Laroche JP, Righini M. The history and histori­cal treatments of deep vein thrombosis. J Thromb Haemost. 2013;11(3):402–11.
5. Wilbur J, Shian B.Deep venous thrombosis and pulmonary embo­lism: current therapy. Am Fam Physician. 2017;95(5):295–302.
6. Savader SJ, Gomez-Jorge J.Peripheral and central deep venous thrombosis. In: Savader SJ, etal., editors. Venous interventional radiology with clinical perspectives. 2nd ed. NewYork: Thieme;
2000.
7. Kroegel C, Reissig A. Principle mechanisms underlying venous thromboembolism: epidemiology, risk factors, pathophysiology and pathogenesis. Respiration. 2003;70(1):7–30.
8. Turpie AG, Chin BS, Lip GY. Venous thromboembolism: pathophysiology, clinical features, and prevention. BMJ. 2002;325(7369):887–90.
9. Johnson M. Pulmonary embolism: diagnosis and interventional options for treatment. In: Savader SJ, etal., editors. Venous inter­ventional radiology with clinical perspectives. 2nd ed. NewYork: Thieme; 2000.
10. Vedantham S. Interventional approaches to deep vein thrombosis. Am JHematol. 2012;87(Suppl 1):S113–8.
11. Bates SM, Ginsberg JS.Clinical practice. Treatment of deep-vein thrombosis. N Engl JMed. 2004;351(3):268–77.
12. Kearon C, Akl EA, Ornelas J, Blaivas A, Jimenez D, Bounameaux H, et al. Antithrombotic therapy for VTE disease. Chest. 2016;149(2):315–52.
13. Lee AY, Levine MN, Baker RI, Bowden C, Kakkar AK, Prins M, etal. Low-molecular-weight heparin versus a coumarin for the pre­vention of recurrent venous thromboembolism in patients with can­cer. N Engl JMed. 2003;349(2):146–53.
14. Group PS. Eight-year follow-up of patients with permanent vena cava lters in the prevention of pulmonary embolism: the PREPIC (prevention du Risque d’Embolie Pulmonaire par interruption cave) randomized study. Circulation. 2005;112(3):416–22.
15. Vedantham S.Treating infrainguinal deep venous thrombosis. Tech Vasc Interv Radiol. 2014;17(2):103–8.
16. Dudzinski DM, Piazza G.Multidisciplinary pulmonary embolism response teams. Circulation. 2016;133(1):98–103.
17. Aujesky D, Obrosky DS, Stone RA, Auble TE, Perrier A, Cornuz J, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am JRespir Crit Care Med. 2005;172(8):1041–6.
18. Konstantinides SV, Torbicki A, Agnelli G, Danchin N, Fitzmaurice D, Galie N, etal. ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J.2014;35(43):3033–69. 69a-69k
19. Konstantinides S, Tiede N, Geibel A, Olschewski M.Just H, Kasper W.Comparison of alteplase versus heparin for resolution of major pulmonary embolism. Am JCardiol. 1998;82(8):966–70.
10 Venous Thromboembolism: Deep Venous Thrombosis andPulmonary Embolism
139
20. Amin VB, Lookstein RA. Catheter-directed interventions for acute iliocaval deep vein thrombosis. Tech Vasc Interv Radiol. 2014;17(2):96–102.
21. Garcia MJ, Lookstein R, Malhotra R, Amin A, Blitz LR, Leung DA, et al. Endovascular Management of Deep Vein Thrombosis
with Rheolytic Thrombectomy: nal report of the prospec­tive multicenter PEARL (peripheral use of AngioJet Rheolytic Thrombectomy with a variety of catheter lengths) registry. J Vasc Interv Radiol. 2015 June;26(6):777–85.

IVC Filters

JamesChen andS.WilliamStavropoulos

Pathophysiology

Venothromboembolism (VTE) is a spectrum of conditions resulting from dysregulation of clot formation and break­down, including deep venous thrombosis (DVT) and pul­monary embolism (PE). VTE has an annual incidence of 1–1.8 per 1000 person-years [1], and despite advances in therapy, VTE continues to convey signicant morbidity and mortality. This results in approximately 100,000 deaths annually in the United States, where associated treatment costs total more than $10 billion yearly [2]. The prevalence of VTE has been increasing due to increased risk factors but also secondary to increased utilization of diagnostic imaging. This increase in identication highlights the need for effective tools and management algorithms for preven­tion and treatment. Various risk factors have been identied for development of VTE including older age, obesity, malignancy, trauma, major surgery, immobility, smoking, increased estrogen, inherited coagulopathy, and prior his­tory of VTE.
DVT most commonly develops in the lower extremities, where local thrombus and resultant disruption of venous out­ow manifest acutely with leg swelling, erythema, and pain. In rare cases with massive clot burden, the degree of venous outow obstruction is severe enough to result in arterial com­promise, manifesting with a pale limb (phlegmasia alba), with subsequent progression to massive limb swelling and cyanosis (phlegmasia cerulea dolens) followed by venous gangrene, which can be limb- and life-threatening. The majority of DVTs do not have this degree of acute morbidity, but in the chronic setting, many DVT patients can experience debilitating symptoms from postthrombotic syndrome (PTS), which range from pain, skin pigmentation, chronic swelling,
J. Chen · S. W. Stavropoulos (*) Division of Interventional Radiology, Perelman School of Medicine at the University of Pennsylvania, Department of Radiology, Philadelphia, PA, USA
11
and venous stasis ulcers. Lower extremity DVT is also the most common cause of PE, which induces hypoxia from dis­ruption of gas exchange, increases pulmonary artery and right heart pressures, and in severe cases can result in cardiopul­monary collapse or death. This pathophysiological connec­tion between PE and DVT was the impetus for the development of inferior vena cava (IVC) lters to prevent embolization of lower extremity clot to the pulmonary arteries.

Clinical Indication

Clinical, laboratory, and imaging evaluations are used in conjunction to diagnose VTE.Symptoms of DVT include leg edema, tenderness, and palpable cords, but these symp­toms can be relatively nonspecic. Lower extremity venous duplex ultrasound is the rst-line imaging modality and can diagnose DVT by lack of luminal color Doppler signal and loss of compressibility of the venous lumen (Fig. 11.1). Pulmonary emboli frequently manifest with a nonspecic clinical presentation with dyspnea, hypoxia, cough, pleu­ritic chest pain, and occasionally hemoptysis. EKG may reveal ndings of right ventricular strain. Imaging diagno­sis is primarily made with pulmonary CT angiography, which has largely supplanted ventilation/perfusion (V/Q) scans which are predominantly reserved for patients with poor renal function. For both DVT and PE, D-dimer can be a useful laboratory test in patients with low pretest proba­bility – a negative D-dimer effectively rules out VTE in these cases.
The mainstay of VTE therapy is systemic anticoagulation (AC), which prevents clot propagation and allows endoge­nous thrombolysis to break down existing clot. AC is indi­cated for almost all cases of acute PE, for which studies have shown decreased mortality and PE recurrence rates. The only scenario in which AC does not demonstrate benet is subsegmental emboli in patients with no DVT and low risk of VTE recurrence [3].
© Springer International Publishing AG, part of Springer Nature 2018 N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_11
141
142
J. Chen and S. W. Stavropoulos
Fig. 11.1 A 57-year-old man with gastric carcinoma presented with acute
right leg swelling and pain. Lower extremity venous ultrasound demon­strated loss of compressibility and color Doppler signal in the (a) right

Conventional Therapy

Key Point
Pharmacologic anticoagulation should be the rst-line therapy in patients with VTE, in the absence of a contraindication.
There is a strong evidence base supporting the efcacy and safety of pharmacologic AC as the rst-line treatment for VTE [3]. In the acute setting, the most commonly used agents are unfractionated heparin and low-molecular-weight heparins (LMWH, e.g., enoxaparin). Heparin must be moni­tored using PTT or Xa; refer to Chap. 5 for further informa­tion. LMWH has more convenient dosing and does not require serial blood assays; however it has an associated higher cost. Long-term AC has typically been maintained with LMWH or Coumadin (warfarin). Newer agents includ­ing factor Xa inhibitors (subcutaneous: fondaparinux; oral: rivaroxaban, apixaban, edoxaban) and direct thrombin inhib­itors (dabigatran) are emerging as effective long-term AC alternatives. An important consideration for the newer agents in the setting of acute bleed or trauma is that they do not cur­rently have a reversal agent.
Not all patients can receive systemic AC due to contrain­dications, related to high-bleeding risk (see Key Point). Systemic AC can also be ineffective in some cases, necessi­tating alternative management strategies. Surgical methods of ligating or constricting the infrarenal IVC were developed
external iliac vein and (b) right femoral vein, diagnostic of acute occlusive iliofemoral DVT.For comparison, the patent (c) left external iliac vein and (d) left femoral vein demonstrated normal color Doppler signal
Key Point
Contraindications to systemic anticoagulation
• Active gastrointestinal bleed
• Recent intracranial hemorrhage
• Vascular brain tumor/metastases
• Recent central nervous systemic hemorrhage or trauma
prior to the 1960s as a means of preventing DVT-related emboli from reaching the pulmonary circulation. These tech­niques were not widely adopted due to their high morbidity and mortality rates.

Interventional Therapy

Genesis ofIR Procedure: Development ofIVC Filters
The poor outcomes of surgical IVC interruption techniques motivated the development of endovascular means of IVC ltration. The rst IVC lter was the Mobin-Uddin umbrella, which was introduced in 1967 [4]. This lter was made of a perforated plastic cone supported by six metal ribs and was implanted into the IVC with apex pointing caudally, from an internal jugular (IJ) vein approach via a surgical cutdown. Although the lter demonstrated efcacy in thrombus ltra­tion, outcome studies showed high rates of associated IVC thrombosis [5]. The Greeneld IVC lter [6], which is the
11 IVC Filters
considered the archetype for many contemporary lters, was developed in 1968 by Lazar Greeneld, a vascular sur­geon, and Garman Kimmell, an oil industry engineer. Kimmell adapted the idea from sludge valve baskets used underground in the oil eld and applied the same technol­ogy to design a delicate wire umbrella-type device to block blood clots attempting to embolize from the lower extremi­ties. The original stainless steel model was a conical device consisting of six legs with hooks for wall adherence that converged on an apical cap. The lter was delivered from a 24-French system, apex pointing cephalad, into the IVC, via a surgical cutdown IJ approach. Subsequent iterations of the Greeneld lter have had lower-prole delivery systems, which no longer require a surgical cutdown, but maintain the familiar lter geometry (Fig.11.2). In the decades since the development of the rst lters, evolving technologies have allowed for improvements in lter design resulting in delivery systems with lower proles and reduced complica­tions. Burgeoning interest in lter utilization during the past two decades has fueled the development of the wide array of devices available today [713] (Table 11.1). Current IVC lters are divided into two classes: permanent versus optional lters, the latter describing lters which are suit­able to act as permanent devices but can also be retrieved when no longer needed [7, 911, 13]. The latest develop­ment in optional lter technology is convertible lters [8] which allow in situ conversion from a ltration congura­tion to a nonltration, stent-like conguration once IVC l­tration is no longer needed.
143
Fig. 11.2 An abdominal radiograph demonstrates a titanium green-
eld lter, a permanent IVC lter with 6 struts converging on a small apical cap
Indications forIVC Filter Placement
Several professional societies have issued guidelines based on current evidence to guide the appropriate utilization of IVC lters. The American College of Chest Physicians
Table 11.1 Inferior vena cava lter models
Filter model Permanent Gianturco-Roehm
Bird’s Nest Greeneld (titanium) Greeneld (over the wire) Simon Nitinol 1990 Bard Nitinol 9 Fr 28mm Jugular, femoral,
TrapEase 2000 Cordis Elgiloy 6 Fr 30mm Jugular, femoral,
Vena Tech LGM 1989 B.Braun Phynox 12 Fr 28mm Jugular, femoral Vena Tech LP 2001 B.Braun Phynox 9 Fr 28mm (the United
Optional ALN (with hook) 2013 ALN
Celect 2008 Cook Conichrome 7 Fr, 8.5 Fr 30mm Jugular, femoral Denali 2013 Bard Nitinol 8.4 Fr 28mm Jugular, femoral Gunther Tulip 2000/2003 Cook Conichrome 8.5 Fr 30mm Jugular, femoral OptEase 2002 Cordis Elgiloy 6 Fr 30mm Jugular, femoral,
Option 2009 Argon Medical Nitinol 6.5 Fr 30mm Jugular, femoral
Year introduced Manufacturer Material
1982 Cook Stainless
1989 Boston
Scientic
1995 Boston
Scientic
International
steel Titanium 12 Fr 28mm Jugular, femoral
Stainless steel
Stainless steel
Sheath size (outer diameter) Maximum IVC diameter Insertion site
12 Fr 40mm Jugular, femoral
12 Fr 28mm Jugular, femoral
subclavian, antecubital
antecubital
Jugular, femoral
States), 35mm (Europe)
7 Fr 32mm Jugular, femoral,
brachial
antecubital
144
J. Chen and S. W. Stavropoulos
(ACCP) guidelines state that IVC lters should only be used in (1) patients with a contraindication to AC in the setting of acute proximal DVT or PE and (2) patients with chronic thromboembolic pulmonary hypertension (CTEPH) prior to pulmonary thromboendarterectomy [3]. The Society of Interventional Radiology (SIR) guidelines [14] include those same indications but also extend indications to encompass additional clinical scenarios (Table11.2).
The differences between the respective society guidelines remain a topic of debate, but the importance of judiciously utilizing IVC lters has become well acknowledged. The more than ten fold rise in IVC lter placement in the past three decades [15] has been met with reports of lter­associated complications, further described below [16, 17].
Results andData
IVC Filter Placement
The technical success rate for placement of modern IVC l­ters is nearly 100% [79, 1113]. The small minority of cases
Table 11.2 SIR guidelines for IVC lter placement
Indications Contraindications
Absolute Contraindication to AC
Recurrent VTE despite adequate AC Complication of AC Inability to achieve therapeutic AC
Relative Iliocaval DVT
Large free-oating thrombus in the iliac vein or IVC Massive PE treated with thrombolysis, embolectomy Difculty establishing therapeutic AC/noncompliance with AC VTE in patient with limited cardiopulmonary reserve Recurrent PE with IVC lter in situ High risk of bleeding complications on AC (i.e., frequent falls)
Prophylactic Trauma with high VTE risk
Surgery patient with high risk for VTE (i.e., bariatric population) Medical condition with high VTE risk (i.e., critically ill, history of VTE)
in which lter placement is unsuccessful are usually due to extensive caval thrombosis resulting in IVC occlusion.
VTE Prevention
IVC lters have demonstrated efcacy in their primary purpose of PE prevention across various lter models, with cumulative short-term recurrent PE rates in modern lter trials of 1.3% [16]. The utility of IVC lters in patients receiving AC was evaluated in the Prevention du Risque d’Embolie Pulmonaire par Interruption Cave (PREPIC) prospective randomized controlled trials (Table11.3). The PREPIC study [18] and eight-year fol­low-up data on the PREPIC patients [19] demonstrated signicantly lower PE risk in patients treated with a per­manent IVC lter and AC compared to those treated with only AC (see Table 11.3). However, the subsequent PREPIC2 prospective RCT was conducted using a newer optional IVC lter model and demonstrated no signicant difference in rates of recurrent PE, symptomatic PE, or mortality in patients who received a lter and AC com­pared to those treated with only AC [20](see Table11.3).
Inability to gain venous access Complete thrombosis of IVC IVC caliber too large or small
Severe coagulopathy (note: most current 6- and 7- French delivery systems have relatively low-bleeding risk even in the setting of coagulopathy) Sepsis (controversial)
Table 11.3 PREPIC prospective randomized controlled trial results
Study Patient population Treatment arms Results PREPIC (1998) 400 patients with acute
PREPIC 8yr follow-up (2005)
PREPIC 2 (2015) 399 patients with PE and lower
Abbreviations: PREPIC Prevention du Risque d’Embolie Pulmonaire par Interruption Cave, AC anticoagulation, DVT deep venous thrombosis, PE pulmonary embolism
proximal lower extremity DVT
400 patients with acute proximal lower extremity DVT
extremity DVT or supercial venous thrombosis
Filter: AC+permanent IVC lter
Control: AC alone
Filter: AC+permanent
IVC lter
Control: AC alone
Filter: AC+optional IVC
lter Control: AC alone
Signicantly lower PE risk in lter + AC arm: 4% absolute risk reduction in PE after 12days compared to AC only arm Signicantly higher risk of DVT in lter + AC arm: 21% of patients in the lter arm had DVT at 2-year follow-up, which was double the rate of the AC only arm Signicantly lower risk of symptomatic PE in the lter + AC arm: 6% in lter + AC arm, compared to 15% in AC only arm Signicantly higher risk of DVT: 36% in lter + AC arm, compared to 28% in AC only arm No signicant difference in rate of PE: 3% in lter + AC arm, 1.5% in AC only arm at 3-month follow-up No signicant difference in rate of DVT or mortality between arms at 6-month follow-up