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Thrombotic Lesions in the Lower Extremity Peripheral Arteries: Diagnosis and Management Chapter | 32 467
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[25] Diener HC, Aisenberg J, Ansell J, et al. Choosing a particular oral anticoagulant and dose for stroke prevention in individual patients with
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[31] Weaver FA, Comerota AJ, Youngblood M, Froehlich J, Hosking JD, Papanicolaou G. Surgical revascularization versus thrombolysis for non-
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for Ischemia of the Lower Extremity. J Vasc Surg 1996;24:513e21.
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especially with concomitant endovascular treatment. Ann Vasc Dis 2017;10:125e31.
[34] Shammas NW, Weissman NJ, Coiner D, et al. Dethrombosis of lower extremity thrombus by local delivery of thrombolysis using ClearWay
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[35] Lurie F, Vaidya V, Comerota A. Clinical outcomes and cost-effectiveness of initial treatment strategies for nonembolic acute limb ischemia in real-
life clinical settings. J Vasc Surg 2015;61:138e46.
[36] McNamara T, Parikh S, Motarjeme A, et al. Ultrasound accelerated thrombolysis in peripheral arterial occlusion: complete lysis rates using the
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[37] Wissgott C, Richter A, Kamusella P, Steinkamp HJ. Treatment of critical limb ischemia using ultrasound-enhanced thrombolysis (PARES Trial):
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[38] Schrijver AM, van Leersum M, Fioole B, et al. Dutch randomized trial comparing standard catheter-directed thrombolysis and ultrasound-
accelerated thrombolysis for arterial thromboembolic infrainguinal disease (DUET). J Endovasc Ther 2015;22:87e95.
[39] Schleder S, Diekmann M, Manke C, et al. Percutaneous aspiration thrombectomy for the treatment of arterial thromboembolic occlusions following
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[42] Ansel GM, George BS, Botti CF, et al. Rheolytic thrombectomy in the management of limb ischemia: 30-day results from a multicenter registry.
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extremity peripheral arteries with the excimer laser: a feasibility study. Cardiovasc Revasc Med 2012;13:211e4.
[44] Topaz O. Plaque removal and thrombus dissolution with the photoacoustic energy of pulsed-wave lasers-biotissue interactions and their clinical
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[45] Topaz O, Minisi AJ, Bernardo NL, et al. Alterations of platelet aggregation kinetics with ultraviolet laser emission: the “stunned platelet”
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[46] Shammas NW, Shammas GA, Jerin M. Differences in patient selection and outcomes between SilverHawk atherectomy and laser ablation in the
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[47] Dahm JB, Topaz O, Woenckhaus C, et al. Laser-facilitated thrombectomy: a new therapeutic option for treatment of thrombus-laden coronary
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[49] Shammas NW. Bivalirudin: pharmacology and clinical applications. Cardiovasc Drug Rev Winter 2005;23(4):345e60.
[50] Shammas NW. Complications in peripheral vascular interventions: emerging role of direct thrombin inhibitors. J Vasc Interv Radiol 2005;16(2 Pt
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e52.
Chapter 33
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Thrombosis of the Venous Vasculature:
Diagnosis and Management
David A. Hirschl and Richard L. Zampolin
Montefiore Medical Center, Albert Einstein School of Medicine, Bronx, NY, USA
INTRODUCTION
The spectrum of thrombosis in the venous vasculature is of major clinical importance. Venous thrombosis and
thromboembolism encompass a broad spectrum of disease involving multiple organ systems. Clinical presentation will
depend upon the location of the thrombus or may be the consequence of embolization of a clot from another location.
Venous thromboembolism has an annual incidence of 1 per 1000 and is a major cause of morbidity and mortality in the
United States, resulting in over 250,000 hospital admissions per year [1,2]. The majority of these cases are deep venous
thrombosis (DVT) of the lower extremities with or without pulmonary embolism (PE). Venous thrombus in other parts of
the body, such as extension from the lower extremities into the inferior vena cava (IVC), renal veins, upper extremity veins,
portal vein, and cerebral dural sinuses, is also associated with significant morbidity and mortality. After diagnosing the
presence of venous thrombosis, it is important to consider the potential causes to treat the disease and prevent additional
sequelae.
Virchow’s triad refers to three of the most common factors that contribute to the formation of venous thrombus. The
triad includes venous stasis, endothelial injury, and hypercoagulable state. Stasis may be caused by immobility such as
postsurgical state or prolonged travel. Stasis may also be caused by venous obstruction due to external compression,
stenosis, or vascular webs. Endothelial injury results in a breakdown of the naturally antithrombotic nature of the normal
endothelium and exposes the blood to subendothelial tissue factors and collagen. This promotes platelet binding,
activation, and aggregation, leading to clot formation. Sources of endothelial injury include trauma, surgery, venipuncture,
and long-term indwelling intravascular devices such as catheters and pacemaker leads. Finally, many disease states can
result in hypercoagulability, including but not limited to malignancy, pregnancy, oral contraceptive (OCP) use, and protein
C/S deficiency.
The incidence of venous thrombosis increases with age. Before the fourth decade of life, venous thrombosis occurs in
approximately 1 per 10,000 annually. This rate increases after age 45 and is seen in 5e6 per 1000 by 80 years of age [2].
The morbidity and mortality of venous thrombosis also increases with age, with higher rates of PE seen in older patients.
Significant adverse clinical outcomes related to venous thrombosis include recurrence, postthrombotic syndrome, major
bleeding due to anticoagulation, and death [2]. When controlled for reproductive risk factors, equal rates of DVT can be
seen in men and women [3]. Among ethnic groups in the United States, the highest rates of venous thrombosis is observed
in African Americans, with significantly lower rates in Asian and Pacific Islander populations [2,4].
After an initial diagnosis of venous thrombosis, patients have a 20%e30% chance of recurrence within the next decade.
Higher recurrence rates are observed in men (10% per year vs. 2%e5% per year in women). Higher recurrence rates are
also associated with idiopathic DVT compared with provoked events [3,5]. This chapter presents the pathophysiology and
clinical features of venous thrombosis, demonstrates related imaging modalities and describes updated management
options.
Cardiovascular Thrombus. https://doi.org/10.1016/B978-0-12-812615-8.00033-8
Copyright © 2018 Elsevier Inc. All rights reserved.
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DEEP VENOUS THROMBOSIS OF THE LOWER EXTREMITY
Patients with DVT of the lower extremity classically present with pain and swelling of the leg. Other findings on physical
exam include erythema and cyanosis. These signs are not specific for DVT and can also be seen in other conditions such as
cellulitis, superficial thrombophlebitis, and lymphatic obstructi on. If DVT is suspected, further assessment with imaging
will help to confirm the diagnosis and determine the extent of involvement. The Wells score is a clinical assessment scale
ranging from 2 to 9 and is designed to assign a pretest probability for the presence of DVT (Table 33.1) [6]. With scores
less than 2, a negative D-dimer assay is sufficient to rule out DVT. Other patients with higher pretest probability should go
on for further testing.
Duplex ultrasonography is quick, inexpensive, and readily available. Sonography has a high sensitivity and specificity
for the detection of thrombus in the femoropopliteal system and tibial veins due to the relatively superficial location of
these structures. Imaging of the pelvic veins is more difficult, and visualization of the vessels will be affected by patient
body habitus as well as the experience level of the sonographer. Deep veins of the lower extremity should be visualized
using gray-scale ultrasound. Once visualized, veins should be assessed for compressibility and flow. Hemodynamics can
be assessed with color and spectral Doppler to determine the direction and velocity of flow. DVT is diagnosed when the
vein is incompletely compressible or not compressible at all. Complete thrombosis of the vessel will make the vein
incompressible. Gray-scale imaging may show internal echoes within the vessel lumen. Doppler will show an absence of
flow (Fig. 33.1). Partial compressibility with preserved flow may indicate nonocclusive thrombus or maybe the sequela of
TABLE 33.1 Wells Criteria for Deep Venous Thrombosis (DVT) of the Lower Extremities [6]
Criteria Score
Active cancer or cancer treated within 6 months þ1
Recently bedridden (>3 days) or major surgery within past 4 weeks þ1
Calf swelling >3 cm (measured 10 cm below tibial tuberosity) þ1
Collateral superficial veins present þ1
Entire leg swollen þ1
Localized tenderness along the deep venous system þ1
Pitting edema þ1
Recent paresis, paralysis, or plaster immobilization of the lower extremity þ1
Previously documented DVT þ1
Alternate diagnosis more likely than DVT 2
FIGURE 33.1 Right superficial femoral vein DVT. (A) Noncompression (left) and compression (right) ultrasound images of the right superficial femoral
vein (V) show internal echoes within the vessel and noncompressibility. (B) Color and spectral Doppler of the right superficial femoral vein demonstrates a
lack of flow within the vessel indicating the presence of DVT. Flow is, however, present in the adjacent artery (asterisk). DVT, deep venous thrombosis.
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prior DVT. When DVT is diagnosed, the extent of the clot burden must be described as it will guide further management. If
iliofemoral thrombus is suspected but not confirmed with ultrasound, consideration can be given to adjunctive imaging
modalities such as computed tomography (CT), magnetic resonance imaging (MRI), or contrast venography.
Traditionally the anatomic division of lower extremity venous thrombosis is defined by proximal and distal DVT.
Proximal DVT includes the popliteal vein and above, while distal DVT typically involves only the calf veins [1]. When
describing proximal DVT, it is important to determine if the iliofemoral system is involved. Occlusion of the iliofemoral
veins prevents outflow of blood from the lower extremity, from both primary and collateral pathways, leading to increased
clinical symptoms. Prognosis is improved if the iliac veins are not involved. Patients with proximal DVT are at higher risk
for PE and worse outcomes related to postthrombotic syndrome.
DVT can have significant acute and chronic consequences. Phlegmasia cerulea dolans (PCD) occurs when both
superficial and deep veins are thrombosed, leading to venous congestions with or without capillary involvement. This can
lead to arterial ischemia, necrosis of the soft tissues, and threatened limb. PCD is associated with high rates of compartment
syndrome, venous gangrene, and limb amputation [7]. A less severe form is phlegmasia alba dolans, in which there is
severe swelling of the limb with discoloration, but no threat of ischemia due to a lack of involvement of the superficial
veins of the leg. Another feared complication of DVT is embolization. The clot can migrate with the direction of blood
flow, leading to impaired drainage of the contralateral lower extremity and kidneys in cases of IVC thrombus. More
commonly the clot burden is not large enough to occlude the IVC, and flows into the pulmonary artery, resulting in PE. PE
can cause a spectrum of clinical presentations from mild chest pain to sudden cardiovascular collapse.
Even when appropriately diagnosed and treated, DVT can lead to chronic clinical sequelae known as postthrombotic
syndrome. After an episode of DVT, the valves of the lower extremity veins may become damaged, leading to chronic
reflux, venous hypertension, and varices. This hemodynamic state can lead to stasis, recurrent DVT, venous claudication,
hyperpigmentation, and nonhealing ulcers, which can lead to a significant impairment in the quality of life.
Treatment of acute DVT is aimed at relieving the acute symptoms and preventing long-term complications. Systemic
anticoagulation is the initial approach applied both to patients with proximal DVT and to those with extension into the
iliofemoral system. Choices for anticoagulation include unfractionated heparin (UFH ), low-molecular-weight heparin
(LMWH), factor Xa inhibitors, and thrombin inhibitors. Anticoagulation alone will help prevent progression of DVT but is
not effective in reducing the clot burden already present. Systemic thrombolysis for iliofemoral DVT is discouraged by the
Society for Vascular Surgery because of low rates of thrombus reduction and risk of bleeding complications [8]. Early clot
removal should be performed in patients with the following characteristics: image-proven IVC, iliac, common femoral, or
femoral DVT; fewer than 14e28 days of symptoms; low risk of bleeding; and ambulatory with good functional capacity
and an acceptable life expectancy. Early thrombus removal strategies should also be performed in patients with
limb-threatening venous ischemia due to iliofemoral DVT with or without associated femoropopliteal thrombosis. Patients
with isolated popliteal and/or tibial DVT can be managed with anticoagulation.
Catheter-directed therapy is an image-guided treatment with the intention of directly reducing the clot burden. The
devices and their mechanism of thrombus reduction can be divided into three categories: pharmacologic, mechanical, and
pharmacomechanical. Pharmacologic techniques can be flow directed or catheter directed. Flow-directed thrombolysis
refers to the placement of an intravenous ca theter into a vein of the affected limb. In the setting of lower extremity DVT,
this would be a pedal vein. Thrombolytic drugs are then delivered with or without the use of a tourniquet . Catheter-directed
pharmacologic devices allow for the delivery of thrombolytic agents via an infusion catheter and/or wire placed directly
within the thrombus. By infusing medication directly into the thrombus, the local affect is maximized and potentially
harmful systemic effects are reduced. In lower extremity cases, vascular access is established via the popliteal vein. A
vascular sheath is inserted, and a venogram is performed. Venography will demonstrate a filling defect in the vessel.
Depending on the clot burden, there may be stasis of contrast (Fig. 33.2) or collateral flow. After confirming the extent of
thrombosis, a lysis catheter is coaxially inserted. The American Heart Association (AHA) recommended dosage for tissue
plasminogen activator (tPA) in catheter-directed thrombolysis is 0.01 mg/kg/h, and for urokinase is 120,000e180,000 U/h
[1]. Protocols regarding bolus and infusion time vary by institution but typically range from 12 to 36 h. During infusion
patients require close monitoring, often in an intensive care unit.
Ultrasound-assisted devices such as the EkoSonic endovascular system (BTG International) contain multiple ultrasound
transducers along the length of a wire, which is inserted into a catheter within the thrombus. The transducers emit a
high-frequency, low ultrasound energy, which loosens the fibrin lattice within the clot. This enhances the penetration of the
thrombolytic agent and exposes more plasminogen receptor sites. During infusion, arterial punctures should be avoided.
Fibrinogen and partial thromboplastin time (PTT) should be monitored every 6 h. If fibrinogen levels fall below 150, the
tPA dose should be halved. If below 100, tPA should be discontinued. After completing the infusion, the patient will return
for a venogram and treatment of underlying stenosis with angioplasty with or without stent placement.
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FIGURE 33.2 Prone venogram performed via popliteal access demonstrates filling defects and stasis of contrast in the left superficial femoral and
common femoral vein.
Mechanical techniques also require percutaneous vascular access to physically disrupt thrombus. The simplest form of
maceration can be performed with an angioplasty balloon. Other rotational devices such as the Cleaner (Argon Medical)
and Arrow-Trerotola (Teleflex) utilize a high-velocity rotating helix to macerate thrombus.
The AngioJet system (Boston Scientific) utilizes a percutaneously inserted catheter, which is connected to a proprietary
pump console. Catheters for venous use are available in 6- and 8-Fr sizes. The device uses pressurized saline jets to create a
low-pressure zone at the catheter tip causing a vacuum effect. Thrombus is fragmented and evacuated through the same
catheter. This is known as rheolytic thrombectomy. The device can also be used in power-pulse mode, allowing the
catheter to forcibly deliver a thrombolytic drug into the thrombus. The drug is allowed to dwell for approximately 30 min,
which softens the clot. After the dwell time is completed, the same catheter is used in aspiration mode, and the softened
thrombus is evacuated. The use of power-pulse mode can reduce the total amount of thrombolytic drug delivered compared
with standard infusion therapy. The short dwell time relative to a standard infusion catheter will also reduce the total
procedure time and may eliminate the need for intensive care monitoring.
Absolute contraindications to pharmacologic and pharmacomechanical thrombolysis include intracranial
hemorrhage, active internal bleeding or disseminated intravascular coagulation, and recent cerebrovascular event. Relative
contraindications include recent surgery, intracranial or spinal mass, obstetrical delivery, septic thrombus, uncontrolled
hypertension, recent gastrointestinal bleed, severe thrombocytopenia, known right-to-left cardiac shunt, left-heart
thrombus, hemorrhagic retinopathy, pregnancy, lactation, and renal failure.
When pharmacologic thrombolysis or pharmacomechanical thrombolysis is absolutely contraindicated, direct clot
aspiration can be performed with devices such as the Indigo (Penumbra) and AngioVac (AngioDynamics) systems. The
Penumbra Indigo system uses a percutaneously inserted end-hole catheter ranging in size from 3.4 to 8 Fr, and with straight
or angled tip configurations. The catheter is connected to a vacuum pump, and continuous suction is applied once the
catheter has been positioned within the thrombus under fluoroscopic control. The Indigo separator can be used in
conjunction with the catheter to maintain end-hole patency during aspiration.
The AngioVac system uses a 22-Fr coil-reinforced, aspiration cannula. The cannula has a balloon-actuated, expandable
funnel-shaped distal tip. This tip design enhances venous drainage flow when the balloon is inflated, helps to prevent
clogging of the cannula, and facilitates en bloc removal of fresh, soft thrombi or emboli. The system is designed for use in
the venous system in the setting of large thrombus burden. Because of the size of the catheter and volume of blood that is
aspirated, the patient is placed on extracorporeal bypass, with an additional venous access site necessary for blood return.
Use of this system requires a perfusionist to operate the pump circuit, which aspirates, filters, and reinfuses blood.
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To avoid procedure-related symptomatic PE, patients should be adequately anticoagulated before, during, and after the
thrombolysis procedure. The incidence of symptomatic PE in patients undergoing catheter-directed infusion therapy does
not exceed that of patients receiving anticoagulation alone; therefore the routine use of IVC filters during infusion-only
catheter-directed therapy is not recommended [7]. The role of IVC filters in pharmacomechanical therapy is less clear
and may be considered in patients at high risk of symptomatic PE, such as those with poor cardiopulmonary reserve [7].
When chronic stenosis or occlusion is the underlying cause of DVT, placem ent of a stent may be necessary to prevent
recurrence and provide symptomatic relief. The predilection of left lower extremity compared with the right is well
described [9e12]. This fact is attributed to compression of the left iliac vein between the right common iliac artery and the
fifth lumbar vertebra. Chronic compression leads to venous webs, stenosis, and ultimately occlusion. While some degree of
venous compression is normal and does not affect most patients, those who become symptomatic are more likely to have
formed membranous disease. Symptomatic anatomic compression of the left common iliac vein is known by several
names, including MayeThurner syndrome, Cockett’s syndrome, and iliac compression syndrome.
Standard contrast venography is suboptimal in diagnosing left common iliac vein compression. Most iliac venograms
are acquired in an anteroposterior projection. Because the vascular compression is parallel to the imaging plane it may
not be appreciated on a two-dimensional image unless the venogram was acquired in an orthogonal plane. Similarly,
intravascular membranous lesions are also easily missed. CT and MRI can demonstrate compression of the vessel;
however, these findings may be observed in asymptomatic patients. Intravascular ultrasound (IVUS) is an intraluminal
imaging modality, which is becoming increasingly available and has been shown to be superior to venography in detecting
common iliac vein compression. In one study, IVUS had a 90% sensitivity compared with 66% for venography. IVUS is
also superior at demonstrating the length and severity of disease by analyzing the luminal area of the vein. The use of IVUS
prior to stent placement is also useful to determine the optimal landing zone and stent diameter. IVUS can also assess the
adequacy of venoplasty and quantify the presence of residual thrombus within the treated segment of vein. In a comparison
of IVUS with venography during stent placement, the lesion was missed by venography in 25% of patients and the site of
maximum stenosis was incorrect in 67%. The degree of stenosis was also underestimated by venography in 69% [9]
(Fig. 33.3).
The goal of treatment of iliac compression syndrome in the setting of iliofemoral DVT is to prevent postthrombotic
syndrome and the consequences of venous stasis, including pain, claudication, and ulceration. Restoration of venous flow
can be accomplished by lysing the thrombus using one of the methods described previously. The degree of lysis has been
found to be a major predictor of early and long-term patency. More complete clearance of thrombus yields venous patency
rates in excess of 75% in most studies, whereas incomplete lysis (>50% residual clot) leads to poor (<40%) patency rates
[10]. Adjuvant balloon venoplasty and stenting relieves the mechanical obstruction in the common iliac vein and improves
long-term vessel patency. A large self-expanding stent (12e16 mm in diameter) is deployed across the stenosis and
extended into the IVC. The stent is oversized slightly relative to the diameter of the common iliac vein and is allowed to
extend into the IVC, just above the iliocaval junction. Several studies have demonstrated improved outcomes in patients
who received iliac vein stents compared with those who did not. Stented patients have a greater venous patency rate at
1 year, and have a decreased incidence of recurrent thrombosis [1]. Complications of stent placement include access site
infections and bleeding. Stent fracture, migration, erosion, and embolization are exceedingly rare. Primary 2-year stent
patency rates for iliac vein compression approach 95%e100% [11,12].
Following initial management and treatment strategies, patients with proximal lower extremity DVT and/or PE are
treated with anticoagulation. In most cases, long-term anticoagulation (3 months) is initiated. Extended anticoagulation is
treatment beyond 3 months and is used in cases requiring indefinite therapy. The duration of treatment is based on
thrombus recurrence risk stratification as well as the patient’s risk of significant bleeding. Patients with thrombus related to
surgery or nonsurgical transient risk factor such as estrogen therapy, pregnancy, or a long flight have a lower risk of
recurrence than patients with a malignancy or unprovoked venous thrombus. Therefore those patients with unprovoked
proximal DVT or cancer and low risk of bleeding should receive extended therapy. Patients without cancer should be
treated with 3 months of anticoagulant therapy using a factor Xa inhibitor or direct thrombin inhibitor. If use of a novel
anticoagulant is contraindicated because of renal insufficiency, treatment with a vitamin K antagonist is recommended. In
patients with DVT and malignancy, anticoagulant therapy with LMWH is preferred [13].
UPPER EXTREMITY THROMBOSIS
Upper extremity DVT (UEDVT) accounts for approximately 10% of DVT cases. With the increased use of central venous
access devices and percutaneously inserted central catheters, the incidence of UEDVT is on the rise. UEDVT is classified
as primary or secondary. It is further divided anatomically as proximal or distal, with proximal UEDVT involving the
axillary or subclavian veins and distal involving the brachial vein or more peripheral veins.
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(A) (B)
(C) (D)
FIGURE 33.3 Left common iliac vein compression. (A) Intravascular ultrasound catheter is in the inferior vena cava (IVC). Vessel is patent and adjacent
aorta (Ao) is seen. Echogenic-appearing vein wall is due to IVC stent. (B) Left common iliac vein (LCIV) is compressed (arrowheads) by adjacent right
common iliac artery (RCIA). (C) Common iliac vein (V) caudal to compression, and adjacent iliac artery (A). (D) Left iliac venogram showing
corresponding area of compression (arrowheads). Note that on the venogram the vessel appears patent. Thrombus is present in the left external iliac vein
(arrow).
The incidence of primary UEDVT is approximately 2 per 100,000 per year. It may be idiopathic or effort related
(PageteSchroetter syndrome). Patients with PageteSchroetter syndrome usually present with pain and swelling in their
dominant arm after strenuous repetitive activity such as weightlifting, rowing, or pitching. This type of exercise can cause
microtrauma to the intima of the axillary and subclavian veins, thereby activating the coagulation cascade, thrombosis, and
eventual fibrosis. These patients are also more likely to have underlying venous compre ssion related to thoracic outlet
syndrome. Due to an anatomic anomaly, the subclavian vein is compressed in the anterior part of the thoracic outlet
triangle formed by the intersection of the following structures: the clavicle and the first rib with the subclavius muscle and
costoclavicular ligament anteromedially and the anterior scalene muscle posterolaterally. Patients with idiopathic UEDVT
have no risk factors or underlying thoracic outlet compression. A hypercoagulability workup in patients with UEDVT is
more likely to be negative than in patients with idiopathic lower extremity DVT.
The majority of UEDVT is caused by the secondary form, largely due to central venous access devices and less
frequently due to cardiac device leads. Other risk factors include malignancy, history of thrombosis, thrombophilia,
thoracic radiation, chemotherapy, surgery, trauma, and parenteral nutrition. Malignancy can cause thrombosis via the mass
effect, through vascular invasion, or by inducing a prothrombotic state.
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The clinical presentation includes extremity heaviness, pain, and swelling with or without paresthesia. On physical
exam there may be edema, redness, cyanosis, visible collateral veins, or fever. Patients with thrombosis related to central
catheters may present only with a nonfunctioning catheter or any of the symptoms mentioned previously.
Pretest probability diagnostic strategies are not well validated for UEDVT compared with lower extremities. While
venography remains the gold standard, ultrasound should be used first to evaluate suspected upper extremity thrombus.
Compression ultrasonography has 97% sensitivity and 96% specificity. Ultrasound should be performed using both color
and spectral analysis with attention to respiratory variation particularly in the proximal veins, where compression is not
possible because of overlying bony structures. Contrast-enhanced computed tomographic venography (CTV) may be
helpful in determining the extent of thrombosis and potential extension into the superior vena cava (SVC). CT may also
elicit an associated diagnosis, including undiagnosed primary thoracic malignancy or metastatic disease.
Goals of treatment are to alleviate symptoms, prevent propagation of thrombus, prevent PE, and prevent postthrombotic
syndrome. Anticoagulation therapy with LMWH should be initiated for at least 5 days, followed by vitamin K antagonists
for 3 months. Extension of anticoagulation therapy beyond 3 months in idiopathic UEDVT is not recommended. In those
patients with secondary UEDVT related to malignancy LMWH is preferred over vitamin K antagonists, and treatment
should be continued as long as there is active malignant disease, provided thrombosis was not related to a central venous
catheter. In cases of catheter-associated thrombosis, anticoagulation therapy can be discontinued after 3 months if the
catheter has been removed. If the catheter remains in place, anticoagulation should be continued as long as it remains
[14,15].
Catheter-directed therapy should be considered in patients with proximal UEDVT, severe symptoms, good functional
status, and low risk of bleeding. These strategies include both pharmacologic and pharmacomechanical percutaneous
interventions (Fig. 33.4). Devices, techniques, and complications are similar to those of lower extremity DVT therapy
previously discussed. If there is residual stenosis, angioplasty can be considered; however, stenting of the subclavian vein
is not advised because of high rates of stent compression, fracture, and reocclusion. Surgical intervention in the absence of
thoracic outlet syndrome, including open thrombectomy or venous bypass, is reserved for refractory cases due to potential
complications, including phreni c nerve or brachial plexus injury, hemothorax, and lymphatic fistula [14]. Patients with
thoracic outlet syndrome as the underlying cause of DVT will require surgical correction of the underlying anatomic
anomaly to prevent recurrent thrombosis. Resection of the first rib and costoclavicular ligament, anterior scalenectomy, and
venolysis is the preferred surgical approach and is the current standard of care [14].
SUPERIOR VENA CAVA THROMBOSIS
The SVC returns approximately 33% of the venous return to the heart. Obstruction of the SVC is most often associated
with malignancy. Thrombosis secondary to intravascular devices such as pacemakers and catheters has become
increasingly prevalent since the late 1990s, accounting for up to 28% of SVC syndrome cases. Patients with SVC
syndrome typically present with edema of the face, neck, and upper extremities. Other symptoms can include hoarseness,
dyspnea, stridor, cough, and chest pain. In addition, physical exam may reveal collateral veins on the neck and chest wall.
Severe cases of SVC syndrome may result in intracranial hypertension. These patients may develop cerebral edema and
present with headache, dizziness, altered mental status, hemorrhage, and obtundation [16].
Imaging of the chest is necessary to elicit the etiology of SVC obstruction. Chest X-ray may show widening of the
superior mediastinum with or without pleural effusion; however, these findings are not specific. Ultrasound with Doppler
can be useful in the evaluation of the upper extremities and assessing the direction of flow in the veins of the neck. Its
utility for evaluating the SVC is anatomically restricted by the overlying ribs and lungs. A contrast-enhanced CT venogram
is the preferred diagnostic imaging modality. CT can demonstrate the extent of thrombosis and presence of collateral veins
with or without involvement of thrombus (Fig. 33.5A). Quality CT imaging with multiplanar reconstruction is also helpful
in preprocedural planning for stent placement.
Percutaneous stent placement is a potential first-line therapy in selected patients and can provide rapid relief of
symptoms. The Kishi scoring system (Table 33.2) was developed to assist with the decision to place a stent. A score of 4 or
more indicates the need for a stent. In patients with SVC syndrome related to neoplasm, treatment options include stenting
followed by radiotherapy. In such patients, radiotherapy alone as a first-line treatment does provide symptom relief as
quickly as stent placement. If SVC occlusion is purely thrombotic, anticoagulation should be initiated as first-line therapy.
Anticoagulation alone can be effective in up to 88% of patients if started within 5 days of thrombus development [17].
Infectious etiologies with associated lymphadenopathy should be treated with an appropriate course of antibiotics.
Prompt treatment is necessary in cases of cerebral or laryngeal edema. Percutaneous stent placement can be performed
with local anesthesia with or without conscious sedation. A contrast venogram of the SVC is performed. Once the diseased/
476 Cardiovascular Thrombus
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(A) (B)
(C)
FIGURE 33.4 Left upper extremity thrombosis. (A) Filling defect in left brachial vein. (B) EKOS catheter in thrombosed vein. Note the multiple
transducers along the length of the treatment zone (arrows). (C) Posttreatment venogram shows opacification of the vein without filling defects.
thrombosed segment of the SVC is crossed with a wire, and an appropriate landing zone selected, a stent can be deployed
(Fig. 33.5C). Headache is often immediately relieved, while facial and upper extremity edema tends to subside within 72 h.
Covered stents have a 94% 12-month patency rate versus 48% for noncovered stents. Careful consideration and planning
must be given before placing a covered stent, as it may occlude other veins such as the azygous and brachiocephalic veins
[16].
Minor complications of SVC stent placement include access site hematoma and infection. Majo r complications include
stent migration, PE, cardiac injury, cardiac tamponade, and pulmonary edema.
PORTAL VEIN THROMBOSIS
Portal vein thrombosis (PVT) refers to thrombus formation within the extrahepatic trunk of the portal vein. Thrombus
may also extend into the mesenteric and splenic veins as well as into the intrahepatic portal veins. While cirrhosis and
malignancy are the most common causes of PVT, other causes include hypercoagulable states and intraabdominal inflammatory conditions such as colitis, pancreatitis, cholecystitis, and cholangitis, as well as trauma and iatrogenic injury.
PVT occurs in 0.6%e16% of patients with compensated cirrhosis and 35% of patients with decompensated cirrhosis and
hepatocellular carcinoma (HCC) [18].
The portal vein supplies approximately 66%e75% of the blood flow to the liver. In the acute phase of PVT there is an
initial arterial vasodilation, which compensates for the diminished portal flow to preserve hepatic function. Within a few
days, collateral venous channels form, which ultimately results in cavernous transformation within several weeks. Clinical
presentations of portal thrombosis may be acute or chronic. Acute partial or complete occlusion of the portal vein may be
Thrombosis of the Venous Vasculature: Diagnosis and Management Chapter | 33 477
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(A) (B) (C)
FIGURE 33.5 Superior vena cava (SVC) thrombosis. (A) Coronal contrast-enhanced CT shows a low-density filling defect surrounding a port catheter
in the SVC (arrows). (B) Contrast venogram demonstrates severe stenosis of the SVC with filling defect (arrow) and reflux into the azygous vein and
jugular veins (asterisk). (C) Contrast venogram after stent placement demonstrating flow into the right atrium and minimal reflux into the right jugular
vein.
TABLE 33.2 Kishi Scoring System
Clinical Signs Score
Neurologic Signs
Awareness disorders or coma 4
Visual disorders, headache, vertigo, or memory disorders 3
Mental disorders 2
Malaise 1
Thoracic or PharyngealeLaryngeal Signs
Orthopnea or laryngeal edema 3
Stridor, dysphagia, or dyspnea 2
Coughing or pleurisy 1
Facial Signs
Lip edema 2
Facial edema 1
Vessel Dilation
Neck, face, or arms 1
A score of 4 or higher indicates the need for superior vena cava stent placement [16].
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