37102412_437086326Atlas_of_Endovascular_Venous_Surgery_1E_2011__PDF__UnitedVRG

CHAPTER 29 Thrombolytic Therapy for Vascular Occlusive Disease

with heparin or low-molecular-weight heparin, followed On the basis of the limited data available, anticoagula-
by oral warfarin, has been the standard of care. tion remains the standard of care for treating most patients
who present with acute DVT. Patients with extensive ilio-
Despite the difference in thrombus burden between ilio- femoral DVT appear to benefit from thrombolytic therapy.
femoral and infrainguinal DVT on clinical presentation, Catheter-directed therapy represents an important ad-
many clinicians treat them as if they were identical prob- junctive therapy to anticoagulation.
lems. Patients with iliofemoral DVT are at much higher
risk for post-thrombotic morbidity, including venous hy- • With the lower rates of effective lysis, systemically ad-
pertension and chronic venous insufficiency. ministered thrombolytic therapy has largely been aban-
doned in favor of the catheter-directed approach
The use of percutaneous intervention for critical ve-
nous occlusive disease remains controversial. Numerous • Anticoagulation remains the standard of care for treat-
investigators have suggested that thrombus removal in ing most patients with acute DVT with mild or moder-
patients with acute DVT is not associated with improved ate symptoms and extent of thrombosis
outcome. Proponents of percutaneous intervention main-
tain that thrombolysis improves the structural and func- • Catheter-directed therapy represents an important ad-
tional integrity of the vein. The combination of venous junctive therapy to anticoagulation
obstruction and valve incompetence is associated with
increased severity of post-thrombotic symptoms. Histori- Questions
cally, systemic thrombolytic therapy produced significant
or complete lysis in 45% of cases. One study showed that 1. A 63-year-old man presents with right leg pain of 4
successful lysis of the clot was associated with significant hours’ duration. The patient has known coronary artery
decreases in post-thrombotic morbidity and, to some ex- disease and was discharged recently after being treated
tent, preservation of venous valve function. Systemically for an anterior myocardial infarction. On examination,
administered thrombolytic therapy has largely been aban- his right leg is cool and mottled below the knee. Strength
doned in favor of the catheter-directed approach. As with and sensation are diminished in the right foot. The left
intra-arterial therapy, catheter-directed thrombolysis in foot is warm with a palpable pulse. What is the optimal
the venous system allows for accelerated thrombolysis, treatment strategy?
which increases the likelihood of success and decreases a. Systemic thrombolysis
the risk of bleeding complications. b. Open embolectomy
c. Intravenous heparin, with a glycoprotein IIb/IIIa in-
Several reports have shown favorable outcomes after hibitor
catheter-directed thrombolysis of venous occlusions. The d. Primary below-knee amputation
majority (71%) of the 287 patients enrolled in the National
Venous Registry presented with iliofemoral DVT. Cath- 2. Which of the following predicts successful outcome
eter-directed thrombolysis was performed with UK. Of after catheter-directed thrombolysis of an occluded ar-
these 287 patients, 31% had 100% resolution of thrombus, terial bypass graft?
52% had 50% to 99% resolution, and 17% had less than a. Graft occlusion of <14 days
50% of the thrombus dissolved; overall, significant throm- b. Guidewire cannot traverse the occluded graft
bolysis was seen for 83% of the patients. c. One-vessel runoff
d. Inflow stenosis >60%
Survival data from the National Venous Registry
showed thrombosis-free survival in 65% of the patients 3. Which of the following factors increases the risk of
at 6 months and 60% of the patients at 12 months. Of the bleeding during catheter-directed thrombolysis?
89 patients with complete clot resolution, 78% had patent a. Use of mechanical thrombectomy device
veins at 1 year, compared with 37% of those with less than b. Low-dose heparin regimen (300 U/h)
50% of the clot resolved with thrombolysis. In addition to c. Short dwell time
sustained patency, early success of thrombolytic therapy d. Fibrinogen level <100 mg/dL
correlated directly with valve function at 6 months; 62%
of patients with less than 50% of the clot burden lysed had 4. Which of the following is the least likely sequela of
venous valvular incompetence, whereas 72% of those with revascularizing a non-viable limb?
complete lysis had normal valve function. a. Infection
b. Acute renal failure
A recent series used a combination of modalities, includ- c. Hyperkalemia
ing thrombolysis, mechanical thrombectomy, percutane- d. Alkalosis
ous venoplasty, and stent placement, to treat 25 patients
with critical venous thromboses or occlusions. Resolution
of symptoms was achieved in 18 patients (72%) and par-
tial resolution occurred in 4 patients (16%).

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Vascular Medicine and Endovascular Interventions

5. A 60-year-old woman presents with acute right lower Hess H, Mietaschk A, Bruckl R. Peripheral arterial occlusions: a
extremity arterial ischemia. The femoral pulse is palpa- 6-year experience with local low-dose thrombolytic therapy.
ble. Based on the results of the TOPAS trial, which of the Radiology. 1987;163:753-8.
following statements is correct?
a. Survival rates at 1 year are equivalent with surgery or Kessel DO, Berridge DC, Robertson I. Infusion techniques for
thrombolysis. peripheral arterial thrombolysis. Cochrane Database Syst Rev.
b. The major amputation rate at 1 year is higher with 2004; No. 1:CD000985.
surgery than with thrombolysis.
c. Ongoing ischemia is higher with thrombolysis than Laird JR, Dangas G, Jaff M, et al. Intra-arterial reteplase for
with surgery. the treatment of acute limb ischemia. J Invasive Cardiol.
d. The ankle-brachial index is increased more with 1999;11:757-62.
thrombolysis than with surgery.
McNamara TO, Bomberger RA. Factors affecting initial and 6
Suggested Readings month patency rates after intraarterial thrombolysis with high
dose urokinase. Am J Surg. 1986;152:709-12.
Akesson H, Brudin L, Dahlstrom JA, et al. Venous function as-
sessed during a 5-year period after acute ilio-femoral venous Mewissen MW, Seabrook GR, Meissner MH, et al. Catheter-di-
thrombosis treated with anticoagulation. Eur J Vasc Surg. rected thrombolysis for lower extremity deep venous throm-
1990;4:43-8. bosis: report of a national multicenter registry. Radiology.
1999;211:39-49. Erratum in: Radiology. 1999;213:930.
Allie DE, Hebert CJ, Lirtzman MD, et al. Novel simultaneous
combination chemical thrombolysis/rheolytic thrombectomy Ouriel K, Gray B, Clair DG, et al. Complications associated with
therapy for acute critical limb ischemia: the power-pulse spray the use of urokinase and recombinant tissue plasminogen
technique. Catheter Cardiovasc Interv. 2004;63:512-22. activator for catheter-directed peripheral arterial and venous
thrombolysis. J Vasc Interv Radiol. 2000;11:295-8.
Ansel GM, George BS, Botti CF, et al. Rheolytic thrombectomy in
the management of limb ischemia: 30-day results from a mul- Ouriel K, Katzen B, Mewissen M, et al. Reteplase in the treatment
ticenter registry. J Endovasc Ther. 2002;9:395-402. of peripheral arterial and venous occlusions: a pilot study. J
Vasc Interv Radiol. 2000;11:849-54.
Berridge DC, Gregson RH, Hopkinson BR, et al. Randomized
trial of intra-arterial recombinant tissue plasminogen activa- Ouriel K, Shortell CK, DeWeese JA, et al. A comparison of throm-
tor, intravenous recombinant tissue plasminogen activator and bolytic therapy with operative revascularization in the initial
intra-arterial streptokinase in peripheral arterial thrombolysis. treatment of acute peripheral arterial ischemia. J Vasc Surg.
Br J Surg. 1991;78:988-95. 1994;19:1021-30.

Comerota AJ, Aldridge SC. Thrombolytic therapy for acute deep Ouriel K, Veith FJ, Sasahara AA, TOPAS Investigators. Throm-
vein thrombosis. Semin Vasc Surg. 1992;5:76-81. bolysis or peripheral arterial surgery: phase I results. J Vasc
Surg. 1996;23:64-73.
Comerota AJ, Aldridge SC. Thrombolytic therapy for deep ve-
nous thrombosis: a clinical review. Can J Surg. 1993;36:359-64. Sarac TP, Hilleman D, Arko FR, et al. Clinical and economic
evaluation of the trellis thrombectomy device for arterial oc-
Dayal R, Bernheim J, Clair DG, et al. Multimodal percutaneous clusions: preliminary analysis. J Vasc Surg. 2004;39:556-9.
intervention for critical venous occlusive disease. Ann Vasc
Surg. 2005;19:235-40. Semba CP, Murphy TP, Bakal CW, et al, The Advisory Panel.
Thrombolytic therapy with use of alteplase (rt-PA) in periph-
Earnshaw JJ, Whitman B, Foy C. National Audit of Thrombolysis eral arterial occlusive disease: review of the clinical literature.
for Acute Leg Ischemia (NATALI): clinical factors associated J Vasc Interv Radiol. 2000;11:149-61.
with early outcome. J Vasc Surg. 2004;39:1018-25.
The STILE Investigators. Results of a prospective randomized
Gardiner GA Jr, Harrington DP, Koltun W, et al. Salvage of oc- trial evaluating surgery versus thrombolysis for ischemia of
cluded arterial bypass grafts by means of thrombolysis. J Vasc the lower extremity: the STILE trial. Ann Surg. 1994;220:251-
Surg. 1989;9:426-31. 66.

Hanover TM, Kalbaugh CA, Gray BH, et al. Safety and efficacy Sullivan KL, Gardiner GA Jr, Kandarpa K, et al. Efficacy of throm-
of reteplase for the treatment of acute arterial occlusion: com- bolysis in infrainguinal bypass grafts. Circulation. 1991;83
plexity of underlying lesion predicts outcome. Ann Vasc Surg. Suppl:I99-105.
2005;19:817-22.
Weaver FA, Comerota AJ, Youngblood M, et al, The STILE In-
Haskal ZJ. Mechanical thrombectomy devices for the treatment vestigators (Surgery versus Thrombolysis for Ischemia of the
of peripheral arterial occlusions. Rev Cardiovasc Med. 2002;3 Lower Extremity). Surgical revascularization versus throm-
Suppl 2:S45-52. bolysis for nonembolic lower extremity native artery occlu-
sions: results of a prospective randomized trial. J Vasc Surg.
1996;24:513-21.

Working Party on Thrombolysis in the Management of Limb
Ischemia. Thrombolysis in the management of lower limb
peripheral arterial occlusion: a consensus document. Am J
Cardiol. 1998;81:207-18.

292

30 Endovascular Treatment of Venous
Disease

Robert M. Schainfeld, DO

Venous Thromboembolism Goals of Therapy for DVT:

Venous thromboembolism (VTE), which includes deep • Decrease symptoms
vein thrombosis (DVT) and pulmonary embolism (PE), • Prevent PE
is a potentially fatal condition with an estimated annual • Minimize recurrence
incidence of 0.1% in white populations. About 400,000 • Prevent PTS and chronic thromboembolic pulmonary
new cases occur annually in the United States, and one-
third of patients have recurrent episodes within 10 years. hypertension
PE accounts for approximately 100,000 to 200,000 deaths
per year in the United States. The primary goals of ini- Prospective natural history studies have shown that pa-
tial treatment of VTE are to limit the extent of thrombus tients with DVT can have development of progressive val-
and the long-term sequelae of post-thrombotic syndrome vular incompetence over time (months to years), with PTS
(PTS) related to residual obstruction and valvular incom- occurring in two-thirds of patients. Manifestations of PTS
petence, which frequently results in disability. Clinicians include pain, edema, hyperpigmentation, or ulceration.
must not only accurately diagnose the disorder but also Trophic skin changes can be seen in 6 to 7 million people in
provide patients with the most appropriate and cost-ef- the United States; 400,000 to 500,000 patients have ulcera-
fective treatment options. Anticoagulation remains the tion, primarily due to chronic venous insufficiency. The
cornerstone of treatment for VTE. underlying pathophysiology of PTS is ambulatory venous
hypertension caused by residual venous obstruction and
• VTE includes DVT and PE valvular incompetence. The combination of venous ob-
• The annual incidence of VTE is 0.1% in white popula- struction and valvular insufficiency has been shown to be
particularly virulent. Valvular damage results in venous
tions reflux and hypertension, which leads to stasis and second-
• Anticoagulation is the mainstay of therapy ary skin changes, including ulceration. Patients with more
extensive DVT involving the proximal segments, includ-
The treatment goals for DVT include decreasing the sever- ing the iliac veins and inferior vena cava (IVC), are more
ity and duration of symptoms, preventing PE, minimiz- likely to have PTS.
ing the risk of recurrence, and preventing PTS and chronic
thromboembolic pulmonary hypertension. The complica- • PTS occurs in two-thirds of patients with antecedent
tions associated with proximal (iliofemoral) DVT include DVT
PE, which develops in 50% of untreated patients within
the first few days, and recurrent thrombosis, which com- • Trophic skin changes are observed in 6-7 million people
monly occurs early but also has some long-term risk. The in the United States
incidence of DVT recurrence is up to 10% in the first year
in patients with unprovoked (“idiopathic”) VTE. • 400,000-500,000 Americans have venous ulcerations

© 2007 Society for Vascular Medicine and Biology Catheter-Directed Pharmacologic Thrombolysis

Despite standard anticoagulation therapy, symptomatic
PTS develops in a substantial number of patients with
DVT. It has been proposed that the more rapid and com-

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Vascular Medicine and Endovascular Interventions

plete thrombus dissolution achieved with pharmacologic • Patient symptomatic despite therapeutic anticoagu-
thrombolytic therapy could potentially decrease the inci- lation
dence of this long-term complication. A recent systematic
review of thrombolytic therapy showed increased rates of Contraindications to thrombolytic therapy are stratified
early vein patency, but major hemorrhagic rates were in- into two categories, absolute and relative. Absolute con-
creased compared with unfractionated heparin treatment. traindications include stroke within 2 months, bleeding
Because of methodologic flaws in the reported trials, it diathesis, active or recent (within 10 days) gastrointesti-
is not possible to draw definitive conclusions about the nal tract bleeding, neurosurgery (intracranial or spinal;
effectiveness of thrombolytic therapy on the incidence of within 12 months), intracranial trauma within 3 months,
PTS. or neoplasm. Relative contraindications include cardio-
pulmonary resuscitation within 10 days, major non-vascu-
An alternative approach to systemic thrombolytic lar surgery or trauma within 10 days, uncontrolled hyper-
therapy is to administer lytic agents through a catheter tension (systolic >180 mm Hg or diastolic >110 mm Hg),
introduced into the femoral or popliteal vein—“catheter- puncture of non-compressible vessel, intracranial tumor,
directed thrombolysis” (CDT). In hopes of assessing the recent eye surgery, pregnancy, or bacterial endocarditis.
feasibility of CDT for iliofemoral DVT, a National Venous
Thrombolysis Registry was assembled in a prospective, Contraindications
multicenter study that enrolled 473 patients from 63 sites.
Complete lysis was seen in 31% and partial lysis in 52%. • Absolute:
The degree of lysis was a significant predictor of early • Stroke (<2 months)
and continued patency. Of the patients who had complete • Bleeding diathesis
clot dissolution, 78% had patent veins at 1 year, compared • Active or recent gastrointestinal tract bleeding (<10
with 37% of those with less than 50% clot resolution after days)
lytic therapy. In addition, early success of thrombolytic • Neurosurgery (intracranial, spinal; <12 months)
therapy directly correlated with 6-month valvular func- • Intracranial trauma (<3 months) or neoplasm
tion. Major bleeding was observed in 11%—39% of these
occurred at the access site, and 13% were retroperitoneal • Relative:
bleeds. Minor bleeding was reported in 16%. Major neu- • Cardiopulmonary resuscitation (<10 days)
rologic complications occurred in 0.4% of patients. PE oc- • Major non-vascular surgery or trauma (<10 days)
curred during treatment in 1% of patients, and 2 deaths • Uncontrolled hypertension (systolic >180 mm Hg or
were reported, for a mortality rate of 0.4% in the entire diastolic >110 mm Hg)
series. • Puncture of non-compressible vessel
• Intracranial tumor
At present, CDT most likely should be reserved for • Recent eye surgery
exceptional circumstances, such as in patients with limb- • Pregnancy
threatening ischemia caused by phlegmasia cerulea dolens • Bacterial endocarditis
and in young patients with extensive iliofemoral DVT (i.e.,
those with a favorable risk-benefit ratio). Other candidates Several thrombolytic agents are currently available in the
who may benefit from CDT are those with multisegment United States, although none are Food and Drug Admin-
DVT, those with expected long-term survival, and those istration (FDA)-approved for the treatment of DVT. Avail-
who remain symptomatic despite therapeutic anticoagu- able agents include streptokinase, urokinase, alteplase,
lation. Additional randomized trials are warranted to ad- reteplase, and tenecteplase. Each agent has different
dress these specific issues. characteristics with respect to fibrin affinity, specificity,
and selectivity, half-life, and average time to clot lysis.
• CDT for DVT achieves more rapid lysis, may decrease Despite the widespread availability and increasing use of
PTS, preserves valvular competence, and restores ves- these agents, no dosage regimens have been universally
sel patency compared with standard anticoagulation or validated to guide therapy; the most frequently reported
systemic thrombolytic therapy regimens are shown in Table 30.1.

• Access via common femoral or popliteal vein After thrombolytic therapy of iliofemoral DVT, an un-
• CDT is associated with an increased risk of hemorrhagic derlying residual stenosis may be identified in the iliac
vein, which must be corrected to avoid rethrombosis of
complications the venous segment. This condition, May-Thurner syn-
• Indications for CDT include: drome, results from compression of the left iliac vein by
the overlying right iliac artery. The response to percuta-
• Phlegmasia cerulea dolens neous transluminal angioplasty (PTA) alone is usually
• Young patients with iliofemoral DVT
• Multisegment DVT
• Expected long-term survival

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CHAPTER 30 Endovascular Treatment of Venous Disease

Table 30.1 Thrombolytic Agents and Regimens giography. Because outcomes are optimized for maximal
clot removal and because thrombolytic agents are less
Agent Infusion effective or ineffective on subacute or chronic thrombus,
mechanical thrombolysis has emerged as a useful adjunct
Alteplase 0.5-1.0 mg/h to pharmacologic therapy. In addition, some patients with
Reteplase 0.5-1.0 U/h absolute contraindications to pharmacologic thromboly-
Tenecteplase 0.25-0.5 mg/h sis may still be candidates for mechanical thrombectomy.
Urokinase 60,000-240,000 U/h PMT is also a possible alternative or adjunct to CDT for
the treatment of DVT. Other potential advantages of PMT
suboptimal; therefore, self-expanding nitinol stents are are that it has a shorter treatment time to patency, is more
preferred to avoid potential stent compression, but place- cost-effective, and is safer. Numerous devices are already
ment should be restricted to the suprainguinal portion FDA approved for other applications; however, none are
of the iliac vein. On the basis of current evidence, stent- currently approved for DVT management.
ing below the lesser trochanter or the inguinal ligament
should be avoided. Technique

• Adjunctive PTA and stenting are indicated for residual The extent of thrombosis is determined by imaging with
venous stenosis after lysis duplex ultrasonography and computed tomography
• Nitinol self-expanding stents are preferable in selected cases. Cross-sectional imaging can indicate
other pertinent anatomic factors such as May-Thurner
• Confine deployment to the above-inguinal segment of syndrome, osteophytes, tumors, masses, or the presence
iliac vein, and avoid stenting below the lesser trochan- of concomitant PE. Access is obtained peripheral to the
ter thrombosed segment, and an antegrade approach is used
with ultrasonographic guidance. The tibial or popliteal
• Duration of antiplatelet and anticoagulant therapy de- veins can be punctured with a single-wall technique, and
pends on the underlying substrate venography is performed to delineate the extent of throm-
bus. After traversal of the thrombosed vein, options in-
• Postprocedural clinical and non-invasive imaging are clude pharmacologic lysis to remove acute thrombus and
mandated preemptive use of a mechanical thrombectomy device,
which may provide more rapid partial decompression in
Warfarin anticoagulation, in addition to antiplatelet thera- the setting of phlegmasia cerulea dolens. If the thrombus
py, should be continued for at least 3 to 6 months, depend- is unresponsive to pharmacologic lysis, combined PMT
ing on the underlying cause, recurrence, or presence of a and lysis may be more effective than either therapy alone.
hypercoagulable state (which may justify indefinite anti- The role of retrievable IVC filters is yet to be defined; fur-
coagulation). Clinical and non-invasive imaging (duplex ther investigation is needed to assess their role in patients
ultrasonography) should be performed post procedure undergoing PMT for DVT.
as a baseline, at 6- and 12-month intervals, and annually
thereafter. The reported 1-year patency rate is 79% in se-
lected series.

Summary of CDT for DVT • Access for PMT is obtained via tibial or popliteal veins
under ultrasonographic guidance
• CDT is a promising therapy that has demonstrated
excellent angiographic lysis rates in highly selected pa- • Combined therapeutic modalities are the norm (e.g.,
tients lysis combined with PMT)

• Long-term follow-up data are not available • The role of retrievable IVC filters in PMT is yet to be
• There is a need for validation of concepts in controlled, defined

prospective, randomized studies The seventh American College of Chest Physicians Con-
sensus Committee concluded that “the use of thrombolytic
Percutaneous Mechanical Thrombectomy agents in the treatment of PE continues to be highly indi-
vidualized, and clinicians should have latitude in using
Indications these agents. In general, patients with hemodynamically
unstable PE” or massive iliofemoral thrombosis are the
Percutaneous mechanical thrombectomy (PMT) refers to best candidates. Although the authors of this consensus
a heterogeneous group of devices and techniques used statement recognized the potential benefits of thrombolyt-
to fragment, ablate, or extract intravascular thrombus in ic therapy, in the absence of Level I evidence they made no
an effort to produce more rapid lysis and limit repeat an- firm recommendations regarding thrombolytic therapy.

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Vascular Medicine and Endovascular Interventions

Endovascular Therapy for DVT sertion. The contraindications to IVC filter placement are
absence of access, IVC thrombosis, bleeding diathesis, and
• Lack of randomized, prospective, controlled data to septic emboli or positive blood cultures. All indications,
support it complications, and contraindications must be considered
for each patient before device insertion. Patients with IVC
• Some safety concerns vs standard anticoagulation filters should be followed up annually to evaluate the
• Introduction of device technology despite lack of prior mechanical stability of the filter and determine preserved
patency of the vena cava.
trials
• Lack of accepted reporting system and clinical benefit • IVC filters are important in the management of venous
thromboembolic disease
end points
• No FDA-approved lytic agent or device available • Indications, complications, and contraindications must
be contemplated before filter placement
IVC Filters
• Patients with IVC filters should undergo annual fol-
In the late 1960s, methods were developed that allowed low-up to evaluate mechanical stability of the filter and
caval interruption devices to be placed into the vena cava determine preserved patency of the IVC
percutaneously through the femoral or jugular veins. In
the ensuing years, intracaval devices have undergone Placement of Suprarenal IVC Filters
substantial modification with respect to efficacy, patency,
and ease of insertion, and are widely used as both treat- Certain circumstances preclude the placement of a filter
ment and prophylaxis for thromboembolic disease. in the infrarenal IVC. These include thrombus extending
into the infrarenal IVC, renal vein thrombosis, or preg-
IVC filters now have an important role in the manage- nancy. The safety of suprarenal filters has been well docu-
ment of venous thromboembolic disease. Indications mented, with no reported instances of renal dysfunction,
for IVC filter placement include: contraindications to or and when compared with infrarenal filters there are no
complications from anticoagulation; as prophylaxis for differences in the rates of filter migration, recurrent PE, or
patients without VTE or for patients with VTE and anti- caval thrombosis.
coagulation; to prevent PE after failure of a previous de-
vice; or in concert with thrombectomy, embolectomy, or Placement of Superior Vena Cava Filters
thrombolytic therapy. Possible indications include chronic
thromboembolic disease or large free-floating iliocaval The incidence of upper extremity DVT is increasing due to
thrombus. Types of IVC filters are shown in Table 30.2. the increased use of short- and long-term upper extremity
central venous catheters; because of this, 12% to 16% of
Complications from IVC filters are related to their inser- all PEs now originate in the upper extremities. In patients
tion, long-term consequences, and subsequent retrieval who have such a complication or a contraindication to
for cases in which a temporary, removable filter is used. anticoagulation, a filter can be safely placed immediately
The complications most frequently cited are venous access below the confluence of the innominate veins. The orien-
site thrombosis (2%-3%), filter thrombosis (0%-28%), and tation of the filter must be reversed to allow stabilization
recurrent PE (3%-4%). Other rare, albeit potential, compli- and thrombus trapping, and special attention must be
cations include filter penetration of the IVC, device frac- given to the size of the superior vena cava (SVC) relative
ture or migration, and arteriovenous fistula or guidewire to the filter.
entrapment during subsequent central venous catheter in-
Technique
Table 30.2 Types of Inferior Vena Cava Filters
The most common access site for IVC filter placement is
Product Indicated use FDA the right common femoral vein because it allows relative-
approval ly direct entry into the vena cava and thus less tilting of
the filter during placement compared with using the left
ALN Permanent/temporary No common femoral vein. Other access sites, in decreasing
Simon nitinol Permanent Yes frequency of use, include the left common femoral vein,
Recovery Optional Yes the right and left internal jugular veins, the right and left
Vena Tech Permanent Yes antecubital veins, and the right and left subclavian veins,
Greenfield (stainless steel/titanium) Permanent Yes in rare instances. Most of the available IVC filters are in-
Bird’s nest Permanent Yes dicated for use in IVCs with diameters of 28 mm or less.
Günther tulip Optional Yes
Trapease Permanent Yes
Optease Optional Yes

FDA, Food and Drug Administration.

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CHAPTER 30 Endovascular Treatment of Venous Disease

The filter is typically deployed below the level of the renal pain free after stent placement, and absence of limb swell-
veins. The left renal vein is traditionally lower than the ing was noted in 3% to 42%. In contrast, 26% to 59% of pa-
right, but this should be confirmed with contrast venog- tients with May-Thurner syndrome were pain free, with
raphy before filter placement. comparable rates of edema resolution in the PTS cohort.

Chronic Venous Insufficiency • Endovascular treatment of May-Thurner syndrome was
associated with excellent technical success, few compli-
Chronic venous insufficiency is an extremely common cations, and excellent primary-assisted and secondary
condition, with an estimated 27% of the US adult popu- patency rates
lation affected by some form of lower extremity venous
disease. Approximately 25 million Americans have vari- Endovascular Treatment of Varicose Veins
cose veins of varying degrees of severity, with advanced,
severe disease in 2 to 6 million adults; 500,000 have had Treatment of superficial venous disease has changed sub-
venous ulcers. The true prevalence of varicose veins in stantially in the past 5 years. Previously, elimination of
a general population is difficult to accurately discern, saphenous vein reflux was accomplished surgically (liga-
owing to the lack of uniformity in reporting standards tion and stripping) or chemically (sclerotherapy). Surgical
and to other confounding variables in data collection that ligation and stripping has been associated with complica-
compromise the integrity of current epidemiologic stud- tions, including hematoma, paresthesias, and recurrence.
ies. Chronic venous insufficiency therefore represents a Sclerotherapy is performed commonly throughout the
substantial health problem in terms of both expenditures world with minimal risk but with high failure rates. The
for care and patients’ quality of life. Annual health care currently available treatment options continue to evolve
costs for venous ulcerations in the United States are an rapidly with the adoption of the latest novel endovenous
estimated $1 billion. techniques for ablation of incompetent superficial veins
(greater and lesser saphenous); they include radiofre-
Endovascular Treatment of Chronic Iliac Vein quency ablation (RFA) and endovascular laser ablation
Obstruction (EVLA). The available options for surgical treatment of
varicose veins include ligation and stripping, ambulatory
Occlusive lesions of iliac veins can result from thrombosis phlebectomy, subfascial endoscopic perforator surgery,
or extrinsic compression of the vessel and are more com- valvuloplasty, valve transplantation, and percutaneous
mon on the left side. Surgical bypass to relieve iliofemoral valve bioprosthesis.
obstruction traditionally has been used to treat this condi-
tion. Several studies have recently reported the results of The latest innovations in minimally invasive therapies
endovascular management to recanalize obstructed iliac deliver thermal energy intraluminally to the vein wall to
vein segments. In one of the largest series to date, technical destroy the intima and denature collagen in the media.
success was achieved in 97%. The rate of stent thrombosis The result is fibrous occlusion of the vein. Thermal abla-
was only 8%, and 2-year primary, assisted, and second- tion for reflux of the saphenous veins can be achieved
ary patency rates were 52%, 88%, and 90%, respectively, by RFA or EVLA and is most commonly applied to the
in patients treated for PTS. greater and lesser saphenous veins. Patients not suitable
for endovascular therapy, including those with multiple
May-Thurner syndrome (iliocaval compression syn- comorbid conditions, allergy to lidocaine, thrombophilia,
drome) is diagnosed in 2% to 5% of patients undergoing prior DVT with incomplete recanalization, and active su-
evaluation for venous disorders of the lower extremities perficial thrombophlebitis, are best treated conservatively
and, if chronic, may result in intraluminal venous webs. with compression. Large superficial varicose veins (tribu-
Because of the mechanical nature of the obstruction (left taries of the greater and lesser saphenous) often are best
common iliac vein compression by the overlying artery), removed surgically; tortuous veins can be challenging
patients respond poorly to conservative therapy, and in because of difficult guidewire navigation. Experience and
the past, surgical reconstruction was the only available clinical judgment are essential.
treatment option. Recently, endovascular treatment (PTA
and/or stent placement) of this condition has shown • Endovascular treatment options for varicose veins in-
promising results. After endovascular therapy, patients clude RFA and EVLA
with May-Thurner syndrome had 60% primary patency
with 100% primary-assisted and secondary patency rates • RFA and EVLA result in fibrous occlusion of the vein
at 2-year follow-up. Between 6% and 60% of patients with after destruction of the intima and collagen within the
PTS (without documented May-Thurner syndrome) were media

• Poor candidates for endovascular or surgical treatment
should be managed conservatively

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Vascular Medicine and Endovascular Interventions

• Superficial and tortuous veins make endovascular ther- cess is obtained with duplex ultrasonographic guidance
apy undesirable using a 21-gauge needle for both RFA and EVLA proce-
dures. The laser fiber tips or radiofrequency electrodes are
RFA and EVLA positioned 1 cm distal to the common femoral vein. Com-
plications of RFA and EVLA include paresthesias (12% at
Percutaneous endovenous ablation procedures are per- 1 week and 2.6% at 5 years), phlebitis (2.9%), edema (2%),
formed using tumescent anesthesia, which avoids skin skin burn (1.2%), DVT (0.9%), and access site infection
burns and paresthesias (less than 2% incidence). RFA (0.2%).
consists of a bipolar heat generator and a catheter with
the capacity to close veins of 2 to 12 mm in diameter. The • RFA and EVLA are promising endovascular techniques
catheter is introduced percutaneously into the saphenous for treating varicose veins in appropriately selected pa-
vein under ultrasonographic guidance and navigated to tients
the saphenofemoral junction. Upon completion of RFA,
absence of flow is assessed with ultrasonography, and pat- • RFA has advantages over vein stripping, with less re-
ent segments are retreated. The clinical results for RFA in a covery time and postoperative pain, greater safety, and
registry study of 1,222 limbs were excellent, with a techni- superior quality-of-life scores
cal success rate of 98.5% and absence of reflux in 88.2% at
1-year follow-up. Maintenance of occlusion was seen in • RFA and EVLA have excellent rates of technical success
87.2% of veins at 5 years, along with an absence of reflux in and maintenance of greater saphenous vein closure
83.8% of limbs. The EVOLVeS (Endovenous Radiofrequen-
cy Obliteration [Closure] Versus Ligation and Vein Strip- • Neovascularization, common after vein stripping, has
ping) study was a multicenter, prospective, randomized not been observed with RFA in short-term follow-up
trial comparing quality-of-life factors between RFA and
vein stripping. RFA and vein stripping had identical treat- • Endovenous failure, which occurs in approximately
ment results: 91.2% versus 91.7% of limbs free of reflux at 2 10% of cases at 1 year, can be decreased by ablating all
years. However, in all outcome variables, patients treated perforating and refluxing veins
with RFA had faster recovery, less postoperative pain,
fewer adverse events, and superior quality-of-life scores Upper Extremity Venous Thrombosis
than did those treated with surgical stripping.
Upper extremity venous thrombosis accounts for 2% to
EVLA allows delivery of laser energy directly into the 4% of all cases of DVT. The axillary and subclavian veins
blood vessel using an 810-nm diode laser, which results in are most frequently involved, although in some cases
destruction of the vein endothelium by selective photo- thrombus propagates to involve more peripheral deep
thermolysis. Excellent clinical results, similar to those for veins. When thrombus propagates into collateral chan-
RFA, have been reported with EVLA. One study showed nels or distal superficial veins, symptoms can be further
technical success in 98% of 499 limbs treated. Greater exacerbated. Patients typically present with arm swelling,
saphenous vein closure was maintained in 93.4% of limbs venous engorgement, skin discoloration, and pain or dis-
at 2 years, with no recurrence in 40 limbs at 36 months. comfort involving the arm, shoulder, and neck regions. Ax-
illary-subclavian vein thrombosis (ASVT) can be classified
Venous stripping has been associated with postopera- as primary or secondary based on the presence or absence
tive hematomas, paresthesias, and wound complications, of associated conditions. Primary ASVT has no obvious
with high recurrence rates, presumably because of neovas- cause on initial examination. Paget-Schroetter syndrome,
cularization in the groin (approximately 60% at 38 years). or effort-related ASVT, is a potentially disabling condition
After RFA in 63 limbs, no neovascularity was identified that typically affects young, healthy persons. Secondary
at 24 months. The early literature reported failure rates ASVT is the result of various causative factors, which
with either RFA or EVLA of approximately 10%, which include central venous access catheters, pacemakers, im-
seemed to occur during the first year. The result appears to plantable cardioverter-defibrillator devices, malignancy,
be caused by leaving other larger tributaries or perforat- thrombophilia, and trauma.
ing veins untreated.
The risk of acute PE due to upper extremity thrombo-
Technique sis varies from 11% to 36% with a reported mean of ap-
proximately 12%. Long-term sequelae of upper extremity
The greater saphenous vein is accessed percutaneously thrombosis result primarily from venous hypertension
at the most distal segment of axial vein reflux. The lesser secondary to obstruction (as opposed to lower extremity
saphenous vein is accessed at the mid calf posteriorly, DVT, which is mainly a result of venous hypertension due
where the gastrocnemius muscle becomes prominent. Ac- to reflux with or without obstruction). Loss of future vas-
cular access is a concern. Severe cases have been reported
in approximately 13% of patients with PTS, owing to the

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CHAPTER 30 Endovascular Treatment of Venous Disease

robust venous collateral development of upper extremity nign conditions, and this distinction significantly affects
venous systems. the available treatment options and goals of therapy.

• ASVT accounts for 2%-4% of all venous thromboses Most often, SVC syndrome is seen in the context of tho-
• Clinical presentation includes swelling, pain, and dis- racic malignancy (80%-90%), with the obstruction caused
predominantly by tumor invasion and extrinsic SVC
comfort in the upper extremity and neck, with promi- compression, sometimes with a component of radiation
nent superficial chest veins or collaterals fibrosis or central venous catheter–related stenosis. The
• Primary ASVT, or Paget-Schroetter syndrome, is charac- most common benign causes of SVC syndrome are central
terized by the absence of associated disease or trauma; venous catheter–related or pacemaker-related stenosis,
secondary ASVT has a recognized cause fibrosing mediastinitis, granulomatous infection, thoracic
• PE occurs in approximately 12% of cases aortic aneurysm–related compression, and anastomotic
• PTS is seen in approximately 13% of cases stenosis associated with heart or heart-lung transplanta-
tion. Treatment options in SVC obstruction include anti-
Prompt and accurate diagnosis of ASVT is paramount for coagulation, head elevation, corticosteroids for laryngeal
guiding treatment. Although no multicenter, randomized edema, venous bypass, chemotherapy, external beam ra-
trials to date have studied different treatment regimens diotherapy, and endovascular therapy.
for upper extremity venous thrombosis, some recom-
mendations can be made. Whereas secondary ASVT is • Malignancy accounts for 80%-90% of patients with SVC
managed conservatively, primary (effort-related) ASVT syndrome
should be treated expeditiously with catheter-directed
fibrinolytic therapy. After successful lysis of the throm- • Benign causes:
bus and achievement of vein patency, immediate surgical • Central venous catheter
decompression of the vein by removal of the offending • Pacemaker
osseous structures (first or cervical ribs), hypertrophied • Fibrosing mediastinitis
anterior scalene muscle, or subclavius tendon should be • Granulomatous infection
performed to relieve persistent vein narrowing due to • Thoracic aortic aneurysm–related compression
extrinsic compression. The role of PTA and endovascular • Anastomotic stenosis associated with heart or heart-
stenting remains controversial. However, if a residual ste- lung transplantation
nosis persists after thrombolysis and definitive surgical
decompression, endovascular stenting may be indicated • Treatment options:
to avoid rethrombosis. Individualized treatment, using • Anticoagulation
the method with the most favorable risk-benefit ratio, is • Head elevation
necessary to optimize quality of life. • Corticosteroids
• Chemotherapy
• The optimal treatment strategy for ASVT is a matter of • External beam radiotherapy
debate • Endovascular therapy

• Prompt and accurate diagnosis is paramount Surgical results for benign SVC obstruction have indicated
• Early local thrombolysis is universally accepted primary patency rates of 53% to 81% at 5 years and 81% at
• Individualized treatment is necessary to optimize qual- 10 years in one study using spiral saphenous vein grafts.
The role of endovascular therapy for SVC recanalization
ity of life in patients with benign disease remains to be determined.
Technical success is excellent, with reported patency rates
Superior Vena Cava Syndrome at 1 year of 70% to 91% and secondary patency rates of
85% at 18 months. Longer-term results, however, are not
SVC obstruction produces upper body venous hyperten- yet known for endovascular therapy. Therefore, surgical
sion, which can be associated with clinical consequences therapy is an acceptable option in selected patients with
of varying severity. Because medical and surgical methods benign SVC syndrome.
of treating SVC occlusion have been only partially suc-
cessful, endovascular techniques were initially applied to Although randomized trials have not been performed,
the palliative treatment of these patients in the 80s. Mod- other evidence suggests that endovascular therapy is
ern combined endovascular therapy has been extremely reasonable as a first-line therapy for malignant SVC syn-
successful in relieving pain for patients with venous ob- drome. Those data show that endovascular SVC recanali-
struction of varying causes and in different locations. SVC zation for malignant obstruction has impressive technical
obstruction can be caused by malignancies or various be- success rates of 95% to 100%, achieves clinical relief within
days, and shows secondary patency rates of 93% to 100%
at 3 months. Given the poor prognosis of these patients,

299

Vascular Medicine and Endovascular Interventions

who usually have metastatic disease, no long-term follow- b. Systemic thrombolysis via peripheral intravenous
up data are available. line

After diagnosis of SVC syndrome, preprocedural cross- c. CDT via basilic vein followed by PTA and stenting of
sectional imaging of the chest is recommended, using con- residual subclavian vein stenosis
trast-enhanced computed tomography or magnetic reso-
nance imaging. Bilateral upper extremity venography via d. CDT followed by surgical decompression (first rib
the basilic veins is initially performed to assess patency resection) after restoring patency of veins
of the SVC and innominate and subclavian veins, the na-
ture of the occlusion, the length of the occluded segment, e. Anticoagulation therapy for 3 months, followed by
and the presence of acute thrombus. If acute thrombus first rib resection of persistently thrombosed axillary-
is present, catheter-directed therapy is usually the initial subclavian veins.
method of reestablishing flow in the involved veins. Ad-
junctive PMT can be used to macerate and remove the 2. Which method would be least effective in treating an
thrombus. acute DVT of the iliac vein?
a. Catheter-directed thrombolysis
In general, venous stenosis and residual thrombus are b. Systemic thrombolytic therapy
best treated with balloon angioplasty followed by endovas- c. Percutaneous mechanical thrombectomy
cular stent placement to facilitate maximal expansion and d. Surgical thrombectomy
to avoid restenosis due to recoil in these fibrotic and elas- e. Balloon maceration
tic venous lesions. Because of their high radial strength,
precise positioning, and lack of significant foreshortening, 3. Which of the following candidates would benefit most
balloon-expandable stents are preferred for focal stenosis. from CDT?
If the SVC is extremely capacious, larger-diameter self- a. A 60-year-old patient with acute iliofemoral DVT of 2
expanding nitinol stents may be used. The limitation of weeks’ duration
nitinol stents is that they do not resist radial compression b. Patient with subacute IVC thrombosis
to the same extent as balloon-expandable stents. Further c. Patient with chronic iliofemoral DVT
study is needed to determine long-term patency of SVC d. Patient with progression of thrombus despite thera-
stents in patients with long life expectancy. peutic anticoagulation
e. Patient with phlegmasia cerulea dolens

• Endovascular venous recanalization techniques are ex- 4. Which of the following statements is true regarding iliac
cellent options in treating malignant and benign SVC vein revascularization?
obstruction a. Thrombolysis is essential in all cases of recanaliza-
tion.
• Despite lack of available trials, evidence suggests that b. Balloon-expandable stents are preferred.
endovascular therapy is reasonable as first-line therapy c. Stand-alone balloon angioplasty has a primary role.
for malignant SVC syndrome d. Access is obtained via the ipsilateral common femoral
or popliteal vein.
• Short-term patency rates for endovascular recanaliza- e. IVC filters are mandated before endovascular inter-
tion in benign SVC syndrome compare favorably with vention.
those of modern surgical bypass methods
5. Which type of IVC filter is removable?
• Further study is needed to determine long-term patency a. Simon nitinol
of SVC stents in patients with long life expectancy b. Greenfield
c. Bird’s nest
Questions d. Trapease
e. Optease
1. A 21-year-old lobster fisherman from Maine presented
to the emergency department with a 3-day history of 6. A 43-year-old woman with a history of extensive left
left arm and hand swelling and discomfort, without any leg DVT, which occurred post partum involving the
obvious antecedent trauma. Duplex ultrasonography iliofemoral and popliteal veins, presents with a recur-
confirms acute ASVT extending into the basilic vein. rent venous ulcer at the medial malleolus. Despite me-
What would be the most appropriate management ticulous local wound care, compression, and a course of
strategy for an optimal clinical outcome? antibiotics, the ulcer was recalcitrant to healing. Non-
a. Commencement of anticoagulation with either low- invasive assessment of the deep and superficial venous
molecular-weight or unfractionated heparin with
concomitant warfarin

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CHAPTER 30 Endovascular Treatment of Venous Disease

system showed persistent thrombosis/occlusion of the Frisoli JK, Sze D. Mechanical thrombectomy for the treatment of
iliac vein and partial recanalization of the femoral and lower extremity deep vein thrombosis. Tech Vasc Interv Ra-
popliteal veins with reflux/incompetence throughout diol. 2003;6:49-52.
the deep system. The greater saphenous vein also was
shown to be incompetent throughout its course. What Girard P, Tardy B, Decousus H. Inferior vena cava interruption:
is the most appropriate initial course of management to how and when? Annu Rev Med. 2000;51:1-15.
facilitate healing of the ulcer?
a. CDT of the iliac, femoral, and popliteal veins Joffe HV, Goldhaber SZ. Upper-extremity deep vein thrombosis.
b. Endovenous ablation of the greater saphenous vein Circulation. 2002;106:1874-80.

only Lurie F, Creton D, Eklof B, et al. Prospective randomized study of
c. PTA and stenting of the left iliac vein endovenous radiofrequency obliteration (closure procedure)
d. Popliteal vein valvuloplasty or valve transplantation versus ligation and stripping in a selected patient population
e. Saphenous vein ablation followed by PTA/stenting (EVOLVeS Study). J Vasc Surg. 2003;38:207-14.

of the iliac vein if no ulcer healing after successful Mewissen MW, Seabrook GR, Meissner MH, et al. Catheter-di-
superficial vein intervention rected thrombolysis for lower extremity deep venous throm-
bosis: report of a national multicenter registry. Radiology.
Suggested Readings 1999;211:39-49. Erratum in: Radiology. 1999;213:930.

Büller HR, Agnelli G, Hull RD, et al. Antithrombotic therapy for Min RJ, Khilnani N, Zimmet SE. Endovenous laser treatment of
venous thromboembolic disease: the Seventh ACCP Confer- saphenous vein reflux: long-term results. J Vasc Interv Radiol.
ence on Antithrombotic and Thrombolytic Therapy. Chest. 2003;14:991-6.
2004;126 Suppl:401S-28S.
Semba CP, Razavi MK, Kee ST, et al. Thrombolysis for lower
Comerota AJ, Throm RC, Mathias SD, et al. Catheter-directed extremity deep venous thrombosis. Tech Vasc Interv Radiol.
thrombolysis for iliofemoral deep venous thrombosis improves 2004;7:68-78.
health-related quality of life. J Vasc Surg. 2000;32:130-7.
Sevestre MA, Kalka C, Irwin WT, et al. Paget-Schröetter syn-
drome: what to do? Catheter Cardiovasc Interv. 2003;59:71-6.

Urschel HC Jr, Razzuk MA. Paget-Schröetter syndrome: what is
the best management? Ann Thorac Surg. 2000;69:1663-8.

Vedantharn S. Endovascular strategies for superior vena cava
obstruction. Tech Vasc Interv Radiol. 2000;3:29-39.

301

31 Complications of Endovascular
Procedures

Alan B. Lumsden, MD, FACS
Imran Mohiuddin, MD
Michael Reardon, MD, FACS
Eric K. Peden, MD

With the number of endovascular procedures being per- • Peripheral vascular complications include (in descend-
formed increasing rapidly, complications of procedures ing order of frequency) hematomas, pseudoaneurysms,
are being encountered with increasing frequency. Indeed, arteriovenous fistulae, acute arterial occlusions, choles-
new and previously unimagined complications are being terol emboli, and infections
described in association with new procedures and devices.
Examples include ultrafiltration through the first-devel- Groin Hematoma
oped aortic endograft and occlusion of cerebral protection The complication of groin hematoma varies from trivial
devices. Nevertheless, some complications are common to to potentially life threatening (Fig. 31.1). Sudden onset of
all endovascular procedures. Endovascular complications massive bleeding can occur. Symptoms vary from mild
can be categorized generally as access site complications, groin discomfort to severe pain, swelling, and potential
complications related to passage of catheters and devices, necrosis of the overlying skin from the pressure of the he-
or intervention-specific complications. matoma. Initially, minimal ecchymosis occurs, but more
extensive discoloration subsequently develops over hours
Access Site Complications to days. As the patient ambulates, the ecchymosis may ex-
tend down the thigh, and patients should be cautioned
The frequency of groin complications after an endovascu-
lar procedure performed via femoral access depends on the Fig. 31.1 Massive groin hematoma after percutaneous coronary
type of procedure performed, the size of device inserted, angioplasty. A hematoma of this size is usually associated with immediate
and whether adjunctive antithrombotic therapy is used. hemodynamic instability, compromises skin integrity, and mandates urgent
Because of the large number of coronary interventions exploration and femoral artery repair.
performed compared with peripheral procedures, reports
of groin complications tend to be described predominant-
ly after coronary interventions. After cardiac catheteriza-
tion, the incidence of groin complications is 0.05% to 0.7%,
whereas after percutaneous transluminal angioplasty the
incidence is much higher (0.7%-9.0%). Peripheral vascular
complications include (in descending order of frequency)
hematomas, pseudoaneurysms, arteriovenous fistulae,
acute arterial occlusions, cholesterol emboli, and infec-
tions; these complications occur with an overall incidence
of 1.5% to 9%. As a result of the increasing use of groin
closure devices, the unusual complication of arterial infec-
tion has been reported increasingly. Acceptable threshold
incidences for these complications have been described by
the Society for Interventional Radiology.

© 2007 Society for Vascular Medicine and Biology

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CHAPTER 31 Complications of Endovascular Procedures

about these developments. Eventually, the discoloration Fig. 31.2 Postprocedural duplex ultrasonography of the groin shows
may extend into the leg below the knee and does not rep- arterialization of the femoral vein with an obvious fistulous communication
resent new bleeding. with the artery. PFA, profunda femoris artery; SFA, superficial femoral
artery.
Indications for groin exploration and hematoma evacu-
ation are severe pain, progressive enlargement of the he- not be used in the management of arteriovenous fistulae
matoma, skin compromise, or evidence of femoral nerve or pseudoaneurysms. Because the fistula occurs in the
compression. The incidence of wound infection after he- groin, stents would be subject to substantial movement
matoma evacuation is high. during hip flexion and extension; their durability at this
location has not been proven. Likewise, coil embolization
Typically, a vertical incision is made over the femoral also is not recommended. These fistulae are typically very
artery in the groin. Ideally, control of the common femo- short, and coil placement can result in venous or periph-
ral or distal external iliac artery is gained by dissecting eral arterial embolization.
down the inguinal ligament, perhaps dividing some of its
fibers. In some cases the groin hematoma is so large that • Fistulae usually do not close spontaneously and may
full exposure of the artery is not feasible; indeed, extensive progressively enlarge with time; therefore, operative
exposure and control may not be necessary if no attendant repair is indicated when they are detected
pseudoaneurysm is present inside the hematoma. How-
ever, the original puncture site may begin bleeding as the Pseudoaneurysm
artery is dissected. All puncture sites should be oversewn
with a single 5-0 prolene suture if groin exploration is war- Pseudoaneurysm after arterial puncture results from
ranted, to prevent rebleeding. Drains should be placed, failure of the arteriotomy site to close, with contained
because once the hematoma is evacuated a large potential bleeding into the soft tissue around the artery. Pseudoan-
space remains. Groin infection after hematoma evacua- eurysms can occur in any vessel, although most develop
tion is common (up to 20%), and the patient should be in the femoral artery. They can be difficult to detect if
cautioned about this risk. Antibiotics should be continued accompanied by a hematoma. However, the presence of
for several days. expansile pulsation and tenderness should raise suspicion
and lead to diagnosis by duplex scanning (Fig. 31.3). The
• Indications for groin exploration and hematoma evacu- duplex examination should note the size and likely source
ation are severe pain, progressive enlargement of the of the pseudoaneurysm. Some are complex and appear to
hematoma, skin compromise, or evidence of femoral have multiple lobes; others are a single, simple cavity. The
nerve compression neck of the pseudoaneurysm should be defined, whether
it is a single wide neck or a long, tortuous narrow neck
• The incidence of wound infection after hematoma evac- (the latter are easier to compress).
uation is high
Pseudoaneurysm can be treated in several ways. Surgi-
Arteriovenous Fistula cal repair previously was the mainstay of therapy but has
been replaced in up to 70% of cases by ultrasonography-
The most common cause of arteriovenous fistula is inad-
vertent puncture of the profunda femoris artery and the
vein, which crosses in the angle between the profunda
femoris and superficial femoral arteries. Fistulae are usu-
ally detected clinically by the presence of a palpable thrill
in the groin or by auscultating a continuous bruit. Duplex
ultrasonography confirms the presence of a fistula, show-
ing the characteristic systolic-diastolic flow pattern with
arterialization of the venous signal (Fig. 31.2). Fistulae
usually do not close spontaneously and may progressively
enlarge with time; therefore, operative repair is indicated
when they are detected.

Surgical repair is performed by dissection of the artery
until the defect is identified by brisk arterial bleeding. The
artery is then controlled either by clamping or digital pres-
sure. Once the defect in the artery is exposed, it is first re-
paired with interrupted prolene suture, followed by repair
of the vein. Usually only one or two horizontal mattress
sutures are required in each vessel. Covered stents should

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Vascular Medicine and Endovascular Interventions

Fig. 31.3 Duplex ultrasonography of a pseudoaneurysm with a long transducer. Pressure is increased until the jet is obliterated,
and compression is continued for 20-minute intervals until
narrow neck. It is unilocular and is ideal for thrombin injection. thrombosis is documented. Mean time to thrombosis is 22
minutes but can be as long as 120 minutes. The increased
guided thrombin injection. When surgery is needed to time, however, may be associated with considerable pa-
repair a pseudoaneurysm, the standard operation begins tient discomfort; therefore, sedation and analgesia may be
with exposure of the femoral artery through a groin in- required. This technique is quite labor intensive because it
cision by varying techniques. Some surgeons opt to gain requires a dedicated technician to apply pressure.
full control of the artery before exposing the puncture site.
Proximal control can be obtained by sliding down the ex- • Surgical repair has been replaced in up to 70% of cases
ternal oblique muscle and identifying the femoral artery by ultrasonography-guided thrombin injection
as it enters the thigh. Rolling the inguinal ligament supe-
riorly or dividing the external oblique fibers permits expo- • Most small pseudoaneurysms thrombose spontane-
sure of the external iliac artery. Gaining proximal control ously within 2 to 4 weeks
is particularly important with a large hematoma or pseu-
doaneurysm. Because the arterial defect is usually only a Ultrasonography-guided thrombin injection is an off-
2- to 3-mm puncture site, an alternate approach is to enter label use for thrombin, but it is very successful in induc-
the pseudoaneurysm directly, controlling the bleeding ing thrombosis of pseudoaneurysms, thereby avoiding
digitally and oversewing the puncture site. It is extremely operative intervention. Sterile gel is applied to the af-
important to ensure that the arterial wall is exposed before fected groin area and the pseudoaneurysm is identified
repair. A common error is to misidentify a hole in the fascia with the duplex probe. Lidocaine is injected superficial
as the arterial defect and place sutures within the fascia. to the pseudoaneurysm. Thrombin is reconstituted and
This can lead to recurrent pseudoaneurysm formation or drawn into a syringe with a change of needle to an echo-
persistent bleeding. Routine exploration of the posterior genic biopsy needle to reach appropriate depth of the
wall of the artery is not recommended. pseudoaneurysm. While an image of the pseudoaneu-
rysm is obtained on the monitor, the physician inserts
Observation is very reasonable management strategy for the echogenic needle through the skin and into the pseu-
small pseudoaneurysms (<2 cm in diameter). Most small doaneurysm, directed away from its neck. The syringe is
pseudoaneurysms thrombose spontaneously within 2 to aspirated to confirm appropriate positioning in the sac
4 weeks. However, concurrent anticoagulation decreases of the pseudoaneurysm. The aspiration syringe is then
the likelihood of spontaneous thrombosis. changed to a syringe containing thrombin. Small aliquots
of thrombin are injected, and constant observation by ul-
Ultrasonography-guided compression is another treat- trasonography is maintained during injection. The needle
ment possibility. The neck of the pseudoaneurysm, iden- tip is redirected as needed until color flow becomes ab-
tified as a high velocity jet, is localized with duplex ul- sent in the pseudoaneurysm and thrombus is seen in the
trasonography, and direct compression applied with the sac of the pseudoaneurysm. The needle is then removed
and the groin is rescanned to confirm thrombosis of the
pseudoaneurysm and patency of the surrounding arter-
ies and veins. The patient is maintained on bed rest, and
follow-up duplex ultrasonography is performed 6 to 12
hours later to confirm continued aneurysm thrombosis.

Retroperitoneal Hematoma

Retroperitoneal hematoma (RPH) after groin puncture
is an infrequent (0.15% incidence) but morbid complica-
tion. It is perhaps the most feared complication of groin
puncture. The term refers to blood contained within the
retroperitoneum, but several patterns occur. An iliopsoas
hematoma occurs when bleeding enters and is confined
within the fascia of the iliopsoas muscle. The psoas muscle
contains the lumbar plexus, and this pattern of hematoma
may be more likely to be associated with compression
neuropathy. In contrast, the space between the peritoneum
and retroperitoneal structures is potentially vast and can

304

CHAPTER 31 Complications of Endovascular Procedures

Fig. 31.4 Computed tomography showing a large hematoma extending • RPH can occur as a result of bleeding from the access
into and around the psoas muscle. This can result in femoral nerve site, as a complication of anticoagulation or lysis during
compression because the lumbar plexus is within the body of the psoas an endovascular procedure, or as a consequence of an
muscle. endovascular procedure

• Any patient who has had groin puncture and in whom
lower abdominal pain develops should be suspected of
having an RPH

• Postcatheterization anticoagulation and high arterial
puncture are the principal risk factors

The threshold for performing abdomino-pelvic CT (which
is diagnostic) in such patients should be low. Management
of RPH must be individualized: 1) patients with neuro-
logic deficits in the ipsilateral extremity require urgent de-
compression of the hematoma; 2) anticoagulation should
be stopped or minimized; and 3) hematoma progression
by serial CT necessitates surgical evacuation and repair of
the arterial puncture site.

contain huge quantities of blood, which may be difficult to Miscellaneous Complications of Femoral
detect clinically (Fig. 31.4). These hematomas can lead to Puncture
pronounced compression of the ipsilateral kidney.
Acute thrombosis of the femoral artery occurs infrequent-
RPH can occur as a result of bleeding from the access ly and manifests as lower extremity ischemia. Exploration
site, as a complication of anticoagulation or lysis during of the femoral artery usually shows disruption of a large
an endovascular procedure, or as a consequence of an en- posterior plaque by the needle, sheath, or catheter, with
dovascular procedure (puncture of the renal parenchyma thrombosis of the residual lumen. Femoral endarterec-
during renal angioplasty). By computed tomography tomy, patch angioplasty, and balloon-catheter embolec-
(CT), the source of an RPH complicating groin puncture tomy of the external iliac and superficial femoral arteries
typically can be traced directly to the punctured artery. is the most commonly required procedure. Acute occlu-
However, a high puncture above the inguinal ligament sion of the artery is occasionally observed after the use
can be associated with a normal groin examination. Full- of femoral artery closure devices. Numerous such devices
ness in the lower quadrant or tenderness should support now exist; broadly, they can be classified as suture closure
early CT. RPH occurring as a result of antithrombotic devices, which can directly injure the arterial wall. The
therapy can occur anywhere in the retroperitoneum, may Angio-Seal vascular closure device involves placement of
be bilateral, and usually responds to correction of the un- a biodegradable bar inside the artery, and the Duett sys-
derlying coagulopathy. RPH occurring as a consequence tem involves injection of thrombin down the access tract.
of an endovascular procedure (iliac artery rupture during Distal embolization is more commonly caused by passage
stenting, renal capsule perforation with a guidewire) is of catheters and the intervention performed than by groin
best treated with an intervention targeted at the bleeding puncture alone. Rarely, catheter or wire passage can result
site, often with an endovascular procedure. in arterial perforation and, more rarely, in pseudoaneu-
rysm (Fig. 31.5).
Any patient who has had groin puncture and in whom
lower abdominal pain develops should be suspected of Axillary and Brachial Artery Puncture
having an RPH. Abdominal examination usually shows
tenderness only. Occasionally, palpable fullness may be All of the complications described above for femoral
detected. Thigh pain, numbness, or quadriceps weak- puncture also have been described for axillary and brachial
ness should lead to suspicion of RPH and femoral nerve arterial puncture. However, the incidence of neurapraxia
compression and mandates urgent CT and possible de- involving the median nerve or other branches of the bra-
compression. Postcatheterization anticoagulation and chial plexus is higher than the incidence of complications
high arterial puncture are the principal risk factors. Early limited to the punctured artery. In a recent prospective
recognition is essential and should be prompted by a de- study of cardiac catheterization via the femoral artery,
creasing hematocrit, lower abdominal pain, or neurologic damage to the adjacent femoral nerve occurred in 20 of
changes in the lower extremity.

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Vascular Medicine and Endovascular Interventions

AB

Fig. 31.5 A mycotic iliac pseudoaneurysm,
which developed after iliac perforation and
retroperitoneal hematoma from passage of
a wire and catheter, is shown by computed
tomography (A) and angiography (B).
Fortunately, this occurrence is rare.

9,585 cases (0.2%) and, although initially disabling, was nerve damage can be caused by the needle, catheter, or
reported to be almost completely reversible. Frequency introducer sheath. Nerve damage due to nerve ischemia
of injury to nerves of the brachial plexus is between 0.4% can be caused by varying degrees of arterial thrombosis.
and 12.7%. The three potential mechanisms of nerve in-
jury are hematoma, direct damage to the nerve, and nerve • The three potential mechanisms of nerve injury are he-
damage due to ischemia. Hematoma formation is the matoma, direct damage to the nerve, and nerve damage
most common mechanism; the hematoma forms within due to ischemia
a fascial compartment containing the neurovascular bun-
dle, which results in nerve compression (Fig. 31.6). Direct • Pain at the puncture site is the most common symptom
• Muscle weakness accompanied by numbness indicates

more severe symptoms and mandates immediate inter-
vention

Fig. 31.6 Magnetic resonance image showing a small but strategically Symptom onset after nerve damage can occur immedi-
located hematoma (black arrow) which compressed the median nerve ately to 3 days later (mean, 12 hours). Pain at the puncture
(white arrow) after brachial artery puncture. (From Kennedy AM, site is the most common symptom and may radiate down
Grocott M, Schwartz MS, et al. Median nerve injury: an underrecognised the arm. Muscle weakness accompanied by numbness
complication of brachial artery cardiac catheterisation? J Neurol Neurosurg indicates more severe symptoms and mandates immedi-
Psychiatry. 1997;63:542-6. Used with permission.) ate intervention. Swelling from a hematoma is not always
obvious; even a small strategically placed hematoma can
306 result in nerve compression. The size of a hematoma or
presence of ecchymosis does not correlate with the sever-
ity of symptoms or degree of nerve damage.

The treatment principles consist of, first, awareness of
the possibility of nerve compression after axillary or bra-
chial artery puncture. Second, the hand should be evalu-
ated post procedure for pain or sensory or motor dysfunc-
tion. Third, early surgical decompression should be used
for pain in excess of that anticipated from arterial punc-
ture or for presence of a motor or sensory deficit.

The artery should be surgically exposed, any hemato-
ma evacuated, and the puncture site repaired. The fascia
of the neurovascular bundle is widely opened and any
perineural hematoma evacuated. The deep fascia of the
forearm is not closed—only the subcutaneous fat and skin
should be approximated.

The functional outcome after a nerve injury that is not
identified and treated is poor, and most patients, although
having some improvement, report persistent sensory or
motor impairment. Disabling pain syndromes can devel-
op in some patients.

CHAPTER 31 Complications of Endovascular Procedures

Complications Related to Passage of When wires are passed blindly, they can enter side branch-
Catheters and Devices es or even the supra-aortic trunks. Even at the femoral
access site, wires may deflect inferiorly down the super-
As a wire, catheter, or device is passed through a blood ficial femoral or profunda femoris artery or may deflect
vessel, it can injure the vessel wall directly. Glide wires superiorly up the circumflex iliac artery. Femoral arterial
are notorious for entering the vessel wall and continuing injury results from attempts at sheath introduction when
to track in an intramural position. Lack of blood return the wire is misplaced in these positions. Good technique
through a catheter should raise suspicion of dissection. includes imaging of the wire and control of the wire tip. It
Hand injection of 3 to 5 mL of contrast medium confirms is possible for inadvertent perforation of organs to occur,
the catheter position by the appearance of a spot of dye such as renal perforation if the wire enters a renal artery
that fails to wash out with arterial flow. The catheter and is not visualized. Wires entering the supra-aortic
should be pulled back until blood return is obtained and a trunks can lead to cerebrovascular accident. Perforation of
wire used to navigate the true lumen. These types of dis- the renal parenchyma by hydrophilic wires during renal
sections, when identified, are usually of no clinical con- angioplasty and stenting is a well-known complication.
sequence. Occasionally, however, large dissections can be It can result in severe RPH, subcapsular hematoma, and
created and may be flow limiting. The renal artery is par- compromise of renal function.
ticularly prone to this complication. The interventionalist
must make a judgment as to whether the dissection is he- When aortic stent grafts were first introduced, the
modynamically significant or likely to be self-limiting and incidence of iliac artery injury was high due to passage
consequently whether to repair the affected area. Possible of these large stiff devices through the iliac artery. This
complications in this category include perforation of the complication is becoming more frequent again as large
main artery, perforation of a side branch, intimal dissec- endografts are increasingly used to treat thoracic aortic
tion, atheromatous embolization, thrombus embolization aneurysms. The introducer sheath is up to 24F, and the
from catheter or wire, or air embolization. incidence of avulsion of the external iliac artery has been
notable. As interventionalists have become increasingly
Microembolization can occur after passage of any en- adept at inserting large-bore devices, the iliac artery in-
dovascular device (Fig. 31.7). It is particularly likely to jury typically is not manifest until the sheath is removed.
happen in patients with severe atheromatous disease. This results in an “iliac artery on the stick” phenomenon
Stroke from catheter manipulation in an atheromatous and can lead to exsanguinating hemorrhage. This compli-
aortic arch is well recognized. Catheters and wires should cation is best avoided by placing the stent graft through
be kept out of the arch unless access is necessary for the a Dacron graft placed on the iliac artery to avoid having
procedure, and manipulation should be minimized. to traverse a small, tortuous, or calcified external iliac
artery.
• Lack of blood return through a catheter should raise
suspicion of dissection Although catheters and wires are fairly thromboresis-
tant, clot can form on both in patients not treated with an-
• Microembolization is particularly likely to happen in ticoagulants. Clot forms particularly on guidewires when
patients with severe atheromatous disease outside of the patient and covered in blood. Meticulous
technique in catheter flushing and wiping of guidewires is
extremely important and should be practiced, regardless
of which vascular bed is being manipulated. However,
such care is of paramount importance when working in
the aortic arch or the supra-aortic trunks. Thrombus on a
guidewire is “snowplowed” off the end of the wire when
a catheter is inserted and can lead to stroke.

Similarly, meticulous removal of air bubbles from cath-
eters is fundamentally important in minimizing the risk
of stroke when working in the carotid circulation. An air
bubble in the cerebral circulation may result in stroke.

Fig. 31.7 Microembolization (atheroemboli) to the toes is usually Intervention-Specific Complications
associated with palpable pedal pulses because a continuous conduit is
usually necessary for such distal embolization to occur. Intervention-specific complications can be broadly clas-
sified as infection, bleeding, rupture, dissection, emboli-
zation, occlusion, or restenosis. They can occur with es-
sentially any intervention. However, the frequency and

307

Vascular Medicine and Endovascular Interventions

significance of each varies depending on the type of inter- ing of hematoma, retroperitoneal bleeding, or pseudoan-
vention being performed. eurysm. In most cases, these may be controlled by local
application of pressure. There should be a high index of
Device Infection suspicion of RPH in any patient receiving lytic therapy in
whom the hematocrit decreases with no obvious source of
Infection of endovascular devices is rare. Given the large blood loss. This can be confirmed easily with abdominal
number of coronary procedures performed, including CT. Development of an RPH usually requires discontinu-
stent implantation, reports of infection of these devices ation of fibrinolytic therapy.
are remarkably uncommon. Antibiotic prophylaxis has
been sporadic and its necessity questioned. However, the • History of a cerebrovascular accident within the pre-
advent of stent grafting clearly has been associated with ceding 2 months is an absolute contraindication to lytic
increasing reports of device infection. Two mechanisms therapy
exist: infection at the time of implantation and seeding
of an implanted graft via bacteremia. Unlike aortic graft • The National Institutes of Health Consensus Panel also
infections, which are indolent, slowly progressive, and recommends against the use of fibrinolytic therapy in
present years after implantation, infections of endografts patients with sustained systolic blood pressures >200
are rapidly progressive and result in rapid conformational mm Hg or diastolic pressures >110 mm Hg
changes and rupture of the aneurysm. Patients have the
classic signs of sepsis. The device must be removed and Bleeding from an anastomosis is usually a problem only
aortic reconstruction performed using standard tech- in recently implanted or infected grafts. Distal emboliza-
niques for aortic graft infection. tion is, in theory, more likely during graft lysis than lysis
of native vessels due to the more extensive thrombus
• The advent of stent grafting clearly has been associated formation. Transgraft bleeding is a concern only in re-
with increasing reports of device infection cently placed dacron grafts. Cerebrovascular accident is
an uncommon but serious complication of lytic therapy.
Reports of infection in bare stents also have been increas- No specific factors increase this risk, other than a history
ing. This is particularly likely to occur if stents are placed of cerebrovascular accident. History of a cerebrovascular
in patients with long catheter dwell times (such as for accident within the preceding 2 months is an absolute con-
lysis). Stent infection results in septic arteritis within the traindication to lytic therapy. The National Institutes of
wall of the host artery, pseudoaneurysm formation, and Health Consensus Panel also recommends against the use
rupture. of fibrinolytic therapy in patients with sustained systolic
blood pressures greater than 200 mm Hg or diastolic pres-
Another source of stent graft infection is a result of direct sures greater than 110 mm Hg.
erosion of the device into adjacent hollow viscera. Isolated
cases of aorto-esophageal and aorto-bronchial fistulae have Complications of Aortic Stent Grafts
been reported complicating thoracic aortic stent grafting.
In the abdomen, aorto-duodenal fistulae have also been Numerous complications have now been described which
reported from abdominal aortic stent grafting. are relatively specific for endovascular aortic aneurysm
repair. Iliac artery dissection and rupture can occur with
Another area of concern for device infection is after the device insertion. This is particularly likely in patients with
use of groin closure devices. Although this complication small, calcified iliac arteries, especially those with concur-
is rare, it has essentially introduced a surgical challenge, rent occlusive disease. Increasing awareness of this prob-
hitherto only seen in intravenous drug abusers who in- lem has led to the development of alternate approaches,
jected directly into the femoral artery. Mycotic femoral such as insertion of an iliac conduit using a retroperitoneal
arteritis is a particular challenge for the vascular surgeon, approach, to avoid such difficult iliac arteries. Misplace-
necessitating arterial resection, reconstruction with saphe- ment can result in coverage of the renal arteries and lead
nous vein routed around the infected field, and muscle to development of renal failure. Occlusion of the inferior
flap. It is a life- and limb-threatening problem. mesenteric artery or hypogastric arteries can lead to colon
ischemia.
Complications of Fibrinolysis
Embolization or coverage of the internal iliac arteries
Lytic agents activate plasminogen to form plasmin, which results in buttock claudication in 30% of cases. Pelvic
breaks fibrin into fibrin degradation products, resulting in ischemia syndromes, including cauda equina ischemia
clot lysis. In appropriately selected patient groups, com- and colon ischemia, can also occur.
plications of fibrinolysis are minor and most commonly
relate to local bleeding at the site of catheter entry, consist- Consequences and complications of endoleaks are
beyond the scope of this chapter. Graft migration, com-

308

CHAPTER 31 Complications of Endovascular Procedures

ponent separation, and loss of seal at the proximal and • Microembolization may account for the deterioration in
distal attachment sites can lead to re-pressurization of the renal function that occurs in some patients after renal
aneurysm sac, resulting in continued aneurysm enlarge- stenting
ment and rupture.
• Restenosis remains the major complication of renal
Complications of Renal Angioplasty and stenting, with rates reported as high as 20%
Stenting
Complications of Iliac Angioplasty and Stenting
Performance of renal angioplasty can be one of the more
technically challenging endovascular procedures. Gain- The most common problem encountered with iliac an-
ing atraumatic access to the renal artery and establishing gioplasty is subintimal passage of the guidewire. This
a stable platform for intervention are the keys to avoid- is prevented by observing the movement of the wire as
ing complications. Traumatic crossing of a renal stenosis it crosses the lesion. Suspicion of subintimal passage is
can result in dissection of the renal artery, a condition that raised by failure to aspirate blood from the catheter and
must be recognized and is usually successfully treated by hand injection of 2 to 3 mL of dye that forms a spot in the
renal stenting. aortic wall and fails to wash out. The catheter and wire
are retrieved and the lesions re-crossed. Failure to recog-
The procedure is set up with the tip of the guidewire nize that the wire is in a subintimal location can lead to
always visible in the peripheral image field. Inadvertent catastrophic problems if devices are then advanced over
advancement of the wire can result in perforation of the the wire.
renal parenchyma and perinephric hematoma (Fig. 31.8).
Most of these hematomas can be managed by anticoagu- Iliac rupture is remarkably uncommon but is a particu-
lation reversal and observation, but branch renal vessel lar risk in small or calcified iliac arteries, especially the
embolization may be required. external iliac artery (Fig. 31.9). In these high-risk patients,
a stent graft should be immediately available to seal off
Microembolization may account for the deterioration the rupture. Embolization is uncommon, but the risk is
in renal function that occurs in some patients after renal increased when recanalizing total occlusions.
stenting. This is usually implied rather than documented,
although cholesterol embolization has been documented • The most common problem encountered with iliac an-
on renal biopsy. gioplasty is subintimal passage of the guidewire

Renal artery occlusion occurs infrequently, usually as a Complications of Venous Interventions
result of dissection. However, this complication threatens
the viability of the kidney and mandates immediate inter- Venous angioplasty and stenting is performed for central
vention: thrombolysis, stenting, and occasionally surgical
bypass grafting. AB

Restenosis remains the major complication of renal
stenting, with rates reported as high as 20%. Restenosis
can result in return of hypertension or deterioration in
renal function. Repeat angioplasty is required. Surgical
bypass can be significantly more complicated if stents ex-
tend well beyond the ostia of the renal arteries.

Fig. 31.8 Computed tomography showing a subcapsular hematoma Fig. 31.9 Iliac artery angiography. A, Extravasation from the iliac artery
caused by a guidewire perforation during renal angioplasty. after balloon angioplasty and stenting. B, The perforation has been sealed
by judicious placement of a covered stent.

309

Vascular Medicine and Endovascular Interventions

venous stenoses such as occur with dialysis access or in the Filter obstruction due to embolization of a large portion
left common iliac vein in May-Thurner syndrome. Venous of atheroma appears as complete occlusion of the internal
lesions, especially those associated with dialysis access, carotid artery. A catheter should be used to aspirate debris
are notoriously difficult to dilate, often require very high from the filter before filter retrieval.
balloon pressures (up to 30 atm), and can result in venous
rupture. Most of these venous ruptures are self-limiting Filter separation from the delivery catheter, usually
and seal either spontaneously or with a few minutes of from entanglement of the filter in the stent, can be avoid-
balloon tamponade. ed by maintaining separation of these two devices at all
times. Detached filters have been compressed against the
Stent deployment in central veins is associated with a vessel wall using a balloon-expandable stent, but surgical
high incidence of device migration. Because of the highly conversion may be necessary.
compliant nature of the veins and their ability to change in
diameter substantially, stent migration can occur. Careful Balloon Angioplasty and Stenting
measurement, oversizing, and ensuring a secure proximal
anchor for the stent are important. Angioplasty of the carotid bifurcation can result in brady-
cardia, asystole, and hypotension. Coughing is usually
• Stent deployment in central veins is associated with a sufficient to restart the heart, but atropine (0.4 mg intra-
high incidence of device migration venously) may be necessary. Pressors should be available
should pressure support be necessary. These events can
Inferior vena cava filters are widely used. Specific filter occur with predilation, stent placement, or after dilation
complications include occlusion, caval penetration, filter of the stent.
migration, and improper deployment.
• Angioplasty of the carotid bifurcation can result in
Complications of Carotid Stenting bradycardia, asystole, and hypotension

Carotid artery stenting can be separated into several com- • Subacute thrombosis of the stent is more likely if clopid-
ponents, each of which has specific complications: 1) arch ogrel was not administered before the procedure, with
angiography and selective catheterization of the common inadequate intraprocedural anticoagulation, or with
carotid artery; 2) placement and retrieval of an embolic poor dilation of the stent
protection device; 3) balloon angioplasty and stenting of
the target lesion; and 4) stent thrombosis. Stent Thrombosis

Arch Angiography Subacute thrombosis of the stent is more likely if clopid-
ogrel was not administered before the procedure, with
The principal risk during arch angiography and selective inadequate intraprocedural anticoagulation, or with poor
catheterization of the common carotid artery is of em- dilation of the stent. This typically manifests as altered
bolization due to dislodgement of plaque during catheter mental status, agitation, or development of focal neuro-
insertion, re-forming reversed-curve catheters within the logic deficits.
aortic arch, or engaging the orifice of the target vessel. Pa-
tients at particular risk include those with a type III arch, Questions
for whom increased catheter manipulation is often re-
quired, and patients with extensive atherosclerosis within 1. What is the optimal treatment for a narrow-necked
the arch. pseudoaneurysm (2 cm in diameter) after femoral
puncture?
Embolic Protection Devices a. Surgical repair
b. Ultrasonography-guided compression
Certain unique problems can arise from use of embolic fil- c. Stent graft of the femoral artery
ters. Spasm of the internal carotid artery can occur around d. Ultrasonography-guided thrombin injection
the filter, usually due to filter movement stimulating the
arterial wall. Occasionally spasm is so severe as to com- 2. What is the most common severe complication of tho-
pletely collapse the filter. This is treated by intra-arterial racic aortic stent grafting?
administration of 100 μg of nitroglycerin. Angioplasty a. Femoral nerve injury
may be necessary in severe flow-limiting cases that do not b. Groin hematoma
respond to nitroglycerin. This is performed after the filter c. Iliac artery injury
has been removed. d. Ureteric injury

310

CHAPTER 31 Complications of Endovascular Procedures

3. Which of the following complications is(are) associated Suggested Readings
with renal artery stenting?
a. Renal artery rupture Baltacioglu F, Cimsit NC, Cil B, et al. Endovascular stent-graft ap-
b. Deterioration of renal function plications in iatrogenic vascular injuries. Cardiovasc Intervent
c. Renal artery dissection Radiol. 2003;26:434-9.
d. All of the above
Basche S, Eger C, Aschenbach R. Transbrachial angiography: an
4. Which statement is true regarding RPHs? effective and safe approach. Vasa. 2004;33:231-4.
a. All should be evacuated
b. All should be followed up with serial hemoglobin Chitwood RW, Shepard AD, Shetty PC, et al. Surgical complica-
and hematocrit measurements tions of transaxillary arteriography: a case-control study. J Vasc
c. All require surgical repair of the bleeding source Surg. 1996;23:844-9.
d. All are caused by excessive anticoagulation
Fransson SG, Nylander E. Vascular injury following cardiac cath-
5. Which of the following is associated with femoral neu- eterization, coronary angiography, and coronary angioplasty.
ropathy caused by an RPH? Eur Heart J. 1994;15:232-5.
a. Weak knee extension
b. Inability to dorsiflex the foot Lin PH, Dodson TF, Bush RL, et al. Surgical intervention for com-
c. Posterior thigh numbness plications caused by femoral artery catheterization in pediatric
d. Scrotal pain patients. J Vasc Surg. 2001;34:1071-8.

6. An arteriovenous fistula <2 mm in diameter will usu- Lumsden AB, Miller JM, Kosinski AS, et al. A prospective evalua-
ally: tion of surgically treated groin complications following percu-
a. Close spontaneously taneous cardiac procedures. Am Surg. 1994;60:132-7.
b. Result in a pseudoaneurysm
c. Progressively enlarge over time Parmer SS, Carpenter JP, Fairman RM, et al. Femoral neuropathy
d. Be easily treated with coil embolization following retroperitoneal hemorrhage: case series and review
of the literature. Ann Vasc Surg. 2006 Jul;20:536-40. Epub 2006
7. Which of the following symptoms would be an May 31.
indication(s) for surgical exploration of a large groin
hematoma? Perings SM, Kelm M, Jax T, et al. A prospective study on incidence
a. Severe pain and risk factors of arteriovenous fistulae following transfemo-
b. Skin compromise ral cardiac catheterization. Int J Cardiol. 2003;88:223-8.
c. Toe numbness
d. Hemodynamic instability Sreeram S, Lumsden AB, Miller JS, et al. Retroperitoneal hemato-
ma following femoral arterial catheterization: a serious and
often fatal complication. Am Surg. 1993;59:94-8.

Toursarkissian B, Allen BT, Petrinec D, et al. Spontaneous closure
of selected iatrogenic pseudoaneurysms and arteriovenous fis-
tulae. J Vasc Surg. 1997;25:803-8.

Watkinson AF, Hartnell GG. Complications of direct brachial ar-
tery puncture for arteriography: a comparison of techniques.
Clin Radiol. 1991;44:189-91.

311

Answers

Chapter 1 sclerotic plaque to preserve the lumen size. Over time
this process is thought to be overwhelmed and the
1. b. Vascular smooth muscle cells (not endothelial cells) lumen decreases in size. Negative remodeling refers to a
migrate into the intima during atherosclerosis initia- decrease in size of the whole artery segment; this tends
tion. Endothelin is primarily a vasoconstrictor via the to contribute to lumen narrowing and the development
endothelin A receptor on vascular smooth muscle. En- of stenoses. Metalloproteases are more often found in
dothelin can act on endothelin B receptors on endothe- positively remodeled arterial segments and are thought
lial cells to increase nitric oxide (a potent vasodilator), to contribute to the growth of the artery.
but the net effect of endothelin on arteries is dominated
by the vasoconstrictor effect on endothelin A receptors. Chapter 2
The smaller muscular arteries (rather than elastic arter-
ies) regulate resistance. The adventitia contains connec- 1. d
tive tissue, but the media contains abundant smooth 2. b
muscle and connective tissue. 3. c
4. b
2. e. HDL is considered the main transport lipoprotein for 5. b
reverse cholesterol transport, which removes choles-
terol from peripheral tissues. Chapter 3

3. c. Nitric oxide tends to prevent activation of NF-κB. 1. c
The selectins are most responsible for monocyte rolling, 2. a
whereas the CAMs are most responsible for monocyte 3. d
arrest and recruitment into the artery wall. MCP-1 en- 4. d
hances (not blocks) monocyte recruitment. 5. a
6. d
4. e. All are found in advanced plaques. 7. f
5. b and e. Monocytes and leukocytes are more character- 8. a

istic of atheroma than are neutrophils. Therapies that Chapter 4
lower LDL levels usually do not decrease plaque size.
Most human studies (intravascular ultrasonographic 1. c. The calf pump failure syndrome is caused by either
and angiographic) suggest intensive lipid lowering is retrograde flow through incompetent perforator veins
associated with small changes in plaque size (gener- during calf muscle contraction or ineffective muscle
ally less than 5%) compared with the large decrease in contraction, both of which result in secondary varicose
the risk of clinical events. Calcification is an active (not veins.
passive) process that in some cases mimics construction
and destruction processes seen in bone.
6. b. Compensatory enlargement refers to the enlarge-
ment of the whole artery to accommodate the athero-

© 2007 Society for Vascular Medicine and Biology

313

Answers

2. c. May-Thurner syndrome is caused by compression 5. e
of the left iliac vein by the right iliac artery as the vein 6. d
crosses over to the left leg. The term “May-Thurner syn-
drome” is only used when significant venous obstruction Chapter 7
is produced by the overlying artery. During pregnancy,
an otherwise normal woman may have symptoms of 1. c. Both PW and CW Doppler instruments can detect
this condition, due to increased intra-abdominal pres- forward and reverse flow, but CW Doppler instruments
sure. are less costly and simpler to use. The penetration of
ultrasound in tissue is primarily dependent on trans-
3. c. The Trendelenburg test is a simple bedside test that mitting frequency (with lower frequencies penetrating
can help distinguish primary from secondary varicose to deeper depths) and is the same for PW and CW Dop-
veins and should be performed before consideration of pler. Only PW Doppler can distinguish between flow at
sclerotherapy. She had no symptoms or history of DVT, different sites or depths in tissue.
and duplex ultrasonography would be the preferred
diagnostic test to exclude DVT rather than venography. 2. a. Compressibility (or stiffness) should not affect pneu-
The veins will decompress with elevation, but neither matic cuff pressure measurements in normal tibial and
bed rest nor analgesics will resolve her condition in the brachial arteries. However, if calcification or atheroscle-
long term. rotic occlusive disease is present in the tibial arteries, they
may be less compressible, which leads to erroneously
4. b. Reducing edema is the most important element of high cuff pressure measurements. The mean arterial
CVI treatment and decreases cutaneous complications. pressure decreases as the pulse moves distally, whereas
Diuretics only help edema minimally. Small ulcers the systolic pressure increases and the diastolic pressure
should be treated first with aggressive medical therapy decreases (so the pulse pressure widens). Because the
before consideration of skin grafting. In the SEPS pro- brachial artery site of pressure measurement is closer
cedure, ligation of perforator veins is performed under to the heart, this augmentation or increase in systolic
endoscopic guidance. pressure makes the normal ankle pressure greater than
the arm pressure and the ABI greater than 1.0. Cuff arti-
5. c. Filariasis is the most common cause of lymphedema facts should not be significant at the brachial and ankle
worldwide and is especially prominent in Africa, India, sites.
and South America. Lymphedema sometimes secondar-
ily complicates CVI. Milroy disease is a form of familial 3. b. The digital arteries are not affected by medial calci-
primary lymphedema. fication, even if the tibial arteries are heavily calcified.
Toe-brachial indices are in the range of 0.80 to 0.90 in
6. d. This patient has lymphedema praecox, which typi- normal persons. It is often difficult to obtain Doppler
cally presents during puberty. The patient has swelling flow signals from the toes, and PPG is easier to use for
that extends into the feet and toes with cutaneous fun- this purpose. Although patients with diabetes mellitus
gal infection, which are characteristics of lymphedema. are especially prone to medial calcification in the tibial
Stemmer sign is positive if the skin at the base of the toes arteries, the digital arteries are not involved, so toe pres-
cannot be pinched. Swelling from lymphedema usually sure measurements are not different in diabetic and
progresses slowly up the leg over time. non-diabetic patients.

Chapter 5 4. d. The normal segmental plethysmographic waveform
is characterized by a rapid steep upstroke, a sharp
1. e systolic peak, and a more prolonged downslope that
2. c bows toward the baseline. Changes in amplitude alone
3. a generally have little diagnostic significance. A promi-
4. d nent dicrotic wave is normally seen on the downslope
5. d of the waveform and represents the reverse-flow phase
6. b of the arterial flow pulse. Significant arterial occlusive
disease proximal to the recording cuff is excluded by the
Chapter 6 presence of a dicrotic wave.

1. e 5. c. The maximum change in ankle pressure after tread-
2. c mill exercise occurs immediately after walking, so it is
3. c important to measure pressures as quickly as possible. A
4. f slight increase in ankle pressure after treadmill exercise
is often seen in normal persons. Patients with signifi-

314

Answers

cant arterial occlusive disease typically have symptoms 3. d
within 5 minutes of walking at 2 mph up a 12% grade, 4. d
and more prolonged exercise times are rarely necessary. 5. c
Some mild-to-moderate arterial lesions are not hemo- 6. b
dynamically significant at resting flow rates, but they 7. a
become flow limiting when flow rates are increased by
exercise. Chapter 11

Chapter 8 1. e
2. d
1. b 3. d
2. e 4. e
3. d 5. d
4. a 6. e
5. d 7. b

Chapter 9 Chapter 12

1. c. This patient has intermediate risk factors and is 1. c
scheduled to undergo a high-risk vascular operation. 2. b
β-Blockers decrease the risk of adverse preoperative 3. d
cardiovascular events; this medical management in this 4. a
situation would result in an outcome similar to coro- 5. b
nary revascularization before vascular surgery.
Chapter 13
2. a. This patient has an impending rupture of an abdomi-
nal aortic aneurysm and requires urgent surgery. Per- 1. e. Although increased levels of LDL are associated with
formance of any cardiac tests would delay the opera- an increased incidence of lower extremity PAD, diabe-
tion. tes mellitus and cigarette smoking are more strongly as-
sociated with PAD. Obesity is not as strong a risk factor
3. d. This patient has a symptomatic carotid stenosis. Ca- for PAD as diabetes and cigarette smoking.
rotid endarterectomy, an intermediate-risk procedure,
should be performed. She has excellent functional 2. b. Patients with PAD have a 3.0- to 4.0-fold increased
capacity and minimal risk factors. She can proceed di- risk of cardiovascular disease mortality compared with
rectly to surgery with perioperative administration of patients without PAD.
β-blockers and aspirin because she is at low risk for an
adverse cardiovascular event. 3. c. Most epidemiologic studies show the sensitivity of
the intermittent claudication questionnaire for the di-
4. a. This patient likely has three-vessel coronary artery agnosis of PAD to be approximately 10% to 25%.
disease, left ventricular dysfunction, and angina. The
popliteal artery aneurysm repair is elective. Regardless 4. d. Cigarette smoking and diabetes mellitus are the two
of the popliteal artery aneurysm, he should be referred most important predictors of critical limb ischemia
for cardiac catheterization as a prelude to a coronary among PAD patients with intermittent claudication.
revascularization procedure.
5. b. Patients with PAD who have rest pain are less likely
5. a. According to the ACC/AHA practice guidelines, the to require amputation than those who have gangrene or
presence of symptomatic aortic valvular stenosis, even an ulcer.
in the absence of a critical stenosis (<1.0 cm2), indicates a
very high risk that should prompt aortic valve replace- Chapter 14
ment before planned elective vascular surgery.

Chapter 10 1. a
2. c
1. a 3. b
2. c 4. c

315

Answers

5. c 3. a. This is a type A IMH in the ascending aorta. The
6. c proper management is blood pressure control and rapid
7. a repair.

Chapter 15 4. c. The factors that most strongly predict need for aneu-
rysm repair are an aortic diameter ≥4.0 cm and a patent
1. b. Arterial emboli usually lodge at or proximal to ar- false lumen.
terial bifurcations and predominantly affect the lower
extremities. About three-fourths of all cases occur be- 5. d. For patients with a type A aortic dissection, pericar-
tween the aortic and popliteal bifurcation, with the rest diocentesis is associated with higher rates of mortality,
affecting the upper limbs and the cerebral and visceral and catheterization has not been shown to provide ben-
circulation. efit. β-Blockers would be contraindicated in a hypoten-
sive patient.
2. d. Most patients with clinical atheromatous embolism
are men aged 60 years or older. Whites are affected more Chapter 18
frequently than blacks.
1. a. Bilateral RAS is a volume-mediated form of hyper-
3. e tension. Thus, many of these patients have low renin
4. b. Acute compartment syndrome is especially common levels and are not angiotensin dependent for filtration.
If a diuretic was added, the blood pressure would prob-
in patients with combined arterial and venous injury, ably decrease but at the risk of acute renal failure devel-
due to the added venous hypertension. oping.

Chapter 16 2. b. Typical medial fibroplasia should be treated with PTA
alone. There is no reason for a stent. Branch involvement
1. b. The most common complication of a fusiform pop- does not contraindicate PTA. Although the blood pres-
liteal artery aneurysm is formation of a thrombus, which sure may be normalized with medications, the patient is
can embolize to distal vessels. Thrombotic occlusion of young and may not require any blood pressure medica-
the popliteal artery and emboli may cause acute limb tions after PTA.
ischemia.
3. d. The renal-aortic ratio is 5.5 on the right side, and the
2. b. Increased concentration of MMPs has been observed PSV is greater than 200 cm/s. This indicates a 60%-99%
in experimental models of aortic aneurysm and in tis- stenosis. The RRIs are normal.
sues excised from human aortic aneurysms.
4. c. Answers a, b, and d are not correct because patients
3. d. This aneurysm has expanded 1 cm over the course of with FMD do not require stenting; a creatinine value of
1 year and meets one criterion for repair. 3.5 mg/dL cannot be explained by unilateral RAS; and
40%-60% stenosis is not enough to cause severe hyper-
4. d. Of the factors listed, only diabetes mellitus is not as- tension.
sociated with aneurysm formation.
5. c. The patient has non-occlusive mesenteric ischemia.
5. a. The risk of rupture of TAA increases progressively This is due to hypoperfusion and not to a fixed obstruc-
with expansion, and most studies recommend repair tion. The diagnosis is made angiographically and the
of a descending TAA with a diameter of 6.5 to 7.0 cm. initial treatment is infusion of vasodilators. If peritoneal
Similar to AAAs, TAAs should be imaged every 6 to signs develop, exploration would be the next step, but
12 months to determine whether the size has increased only after vasodilator infusion.
considerably.
Chapter 19
Chapter 17
1. c. The most common cause of cerebral ischemia is
1. a. Because aortic dissection cannot be excluded, an im- atherosclerotic thrombosis, likely as a result of long-
aging test must be ordered. The carotid artery and aorta standing hypertension involving the lenticulostriate
may be imaged well with MRI but not with ultrasonog- arteries deep in the brain. CT will show classic abnor-
raphy. malities of a lacunar infarct. The erythrocyte sedimen-
tation rate is an acute-phase reactant used to identify
2. d. Pulse deficits are associated with a marked increase cerebral vasculitis, a rare cause of cerebral ischemia.
in the risk of death for patients with a type B dissec- Transcranial Doppler ultrasonography is useful for de-
tion.

316

Answers

termining intracranial collateral pathways in the brain who undergo CAS placement to prevent early stent
in a patient with extracranial carotid stenosis. Trans- thrombosis.
esophageal echocardiography is used to determine aor-
tic arch atherosclerosis, patent foramen ovale, valvular Chapter 20
heart disease, and cardiac chamber thrombi, which are
all sources of emboli. Hemoglobin A1c will only identify 1. a
diabetes mellitus and will not determine the cause of 2. b
cerebrovascular ischemia. 3. c
2. d. The most important clinical clue is clear evidence of 4. d
a symptom attributable to a moderate or severe carotid 5. b
artery stenosis. Cervical bruits are markers of atheroscle-
rosis but do not predict the severity of carotid stenosis Chapter 21
or indicate the need for revascularization. The absence
of a temporal artery pulse suggests clinically significant 1. c. This patient has right subclavian disease involving
disease at the carotid artery bifurcation but may repre- the ostium. The right subclavian typically projects pos-
sent stenosis of the external carotid artery only. Derma- teriorly, and the true ostium of the right subclavian ar-
tologic manifestations of familial hypercholesterolemia tery is frequently eclipsed by the carotid in the LAO and
suggest the need for aggressive lipid-lowering therapy; AP views. This anatomy varies depending on the tortu-
however, they do not suggest significant carotid ste- osity and redundancy of the great vessels, particularly
nosis or the need for carotid revascularization. Tobacco in elderly patients, but an RAO view usually provides
use is a risk factor for atherosclerosis, but it does not the best definition of the subclavian ostium.
define the severity of carotid stenosis or the need for
revascularization. 2. d. CH (Charriere) is synonymous with French size (F).
3. b. The basic diagnostic algorithm for carotid artery ste- 6F=0.33×6=1.98 mm. 1.98/2.54=0.78 in.
nosis is a thorough history and physical examination
followed by CDUS. If duplex ultrasonography shows 3. c. Shaping the Simmons sidewinder catheter in the
severe carotid stenosis in a patient who would benefit aortic arch can put the patient at risk for atheroemboli-
from revascularization, digital subtraction arteriogra- zation. Aggressive maneuvers to shape the catheter in
phy would be the next step. Digital subtraction arteri- the ascending aorta should be avoided. It is generally
ography should rarely, if ever, be the initial diagnostic recommended to first gently advance the catheter over
test. Diffusion-weighted magnetic resonance imaging is a wire into the left subclavian artery. The wire is then
used to evaluate the brain. MRA is an excellent test but retracted into the secondary curve to provide rigidity
requires use of a contrast agent. The two-dimensional at the point of the secondary bend, improving the ease
time-of-flight images cannot be used alone because the of prolapse as the catheter is advanced forward and as-
severity of carotid artery stenosis is often overestimated. sumes its preformed shape. The Simmons sidewinder
MRA and multidetector CTA are rarely used together is the carotid-selective catheter of choice for many op-
because of the cost. erators, but its use has a learning curve and aggressive
4. e. A systolic and diastolic cervical bruit caused by ex- manipulation in the aortic arch must be avoided.
tracranial carotid artery stenosis suggests critical bilat-
eral disease. The cardiac valvular pathology that could 4. e. The only incorrect answer is increasing the psi
result in a systolic/diastolic bruit is aortic insufficiency. threshold and proceeding with an injection. The typical
Impaired left ventricular function and jugular vein diagnostic catheter has a rated burst of 1,050 to 1,200
thrombosis are unrelated to this physical finding. psi. By simply increasing the psi threshold of the injec-
5. c. Carotid revascularization is indicated for patients tor, the catheter could rupture, and the risk is increased
with symptomatic and severe carotid artery stenosis. of dislodging a thrombus or occlusive material from the
CAS placement is recommended as an alternative to CEA catheter into the artery or vein of interest.
for patients with high-risk anatomic or medical comor-
bid conditions. This patient has a severe symptomatic 5. b. Typically, shaped catheters should be removed over a
carotid artery stenosis and an anatomic factor (contral- wire. However, advancing a wire into a diagnostic cath-
ateral internal carotid artery occlusion) that places him eter that has no blood return could result in embolization
at high risk with CEA. Combination antiplatelet therapy of the occlusive material through the tip of the catheter
has not been shown to offer benefit over aspirin alone as the wire is advanced. If blood cannot be withdrawn
as the primary medical therapy or after CEA. However, from a catheter stationed in a vessel, an attempt should
combination antiplatelet therapy is critical for patients first be made to reposition and make certain the catheter
tip is not against the vessel wall or in a small side branch
or plaque. After these maneuvers, if the catheter still will

317

Answers

not flush and there is no evidence of a kink, attempts to Chapter 24
clear the catheter while inside the body using a power
injection, forward flush, or guidewire are ill advised. 1. c
6. f. Typically, a 65-cm pigtail catheter has a maximal flow 2. d
rate of 33 mL/s. All of the choices listed would be ap- 3. c
propriate on the basis of Poiseuille’s law. 4. b
7. e. This is the most feared catastrophic complication of 5. b
simple abdominal angiography. The complication is 6. a
less common now that image quality has improved and 7. a
fewer end-hole catheters are being used for non-selec-
tive angiography. The complication occurs by inadvert- Chapter 25
ent injection of contrast into a thoracic branch that hap-
pens to provide circulation to the anterior spinal artery. 1. c
The rapid high-pressure injection of contrast is associ- 2. b
ated with barotrauma to the spinal cord and immediate 3. d
paralysis. There is some theoretical benefit from venting 4. a
of the spinal fluid immediately after this complication, 5. b
but no controlled studies have confirmed change in out-
come after venting. Chapter 26
8. d. This is a fairly common normal variant and would
not be considered a pathologic finding. If the right sub- 1. c
clavian artery originates distal to the left subclavian or 2. e
contiguous with the left subclavian, this is considered 3. a
an anomalous origin that can be associated with aneu- 4. c
rysmal change or the so-called Kommerell diverticulum 5. a
(marked by dysphagia and tracheal encroachment). 6. d
9. c. This case illustrates the importance of meticulous im-
aging and of preprocedural physical examination when Chapter 27
making decisions within the angiographic suite. Unilat-
eral absence of pedal pulses cannot be explained with 1. c. On the basis of the MRA, the patient most likely has
the “normal” angiographic findings reported. This pa- giant cell arteritis. Because she presented more than 6
tient had an occult popliteal stenosis that was eclipsed hours after symptom onset, immediate intervention with
by the prosthetic knee. This type of lesion is frequently local thrombolytic or angioplasty and stenting would
missed without appropriate image intensifier angula- increase the patient’s risk of hemorrhagic conversion.
tion. Lesions in patients with giant cell arteritis result from
inflammation, not atherosclerosis. Thus, atherectomy
Chapter 22 would not be beneficial. Treatment with corticosteroids
should be initiated. Aorta-to-carotid bypass in 5 to 7
1. c days would provide the best revascularization option
2. d (Figure).
3. b
4. b 2. a. In the vast majority of patients, occlusion of the sub-
5. c clavian artery does not lead to serious clinical conse-
quences. If the endograft procedure requires covering
Chapter 23 the left subclavian artery, preoperative imaging with
CTA, MRA, or 4-vessel cerebral angiography is war-
1. d ranted to verify patency of the innominate and right
2. b subclavian arteries, assess the size of the vertebral
3. b arteries, and determine whether the circle of Willis is
4. a intact.
5. a

318

Answers

3. c
4. a
5. c

Chapter 29

Figure for Answer 1. 1. b. The most common cause of acute limb ischemia is
thromboembolism (75% of cases). The most common
3. b. The right aortic arch with aberrant left subclavian source is the left atrial appendage in atrial fibrillation
artery is the most common form of right aortic arch. It is or the left ventricle after an anterior wall myocardial
one of the most common causes of symptom-producing infarction. In some cases, atheromatous material can
vascular ring. embolize from the aorta. Typically, patients with an em-
bolic etiology of ischemia have abrupt onset of pain, a
4. a. Based on results of the WASID study, patients with recent cardiac event, and no history of claudication. If
symptomatic intracranial stenosis should be treated the etiology is clearly embolic and the site of occlusion
with aspirin. Patients randomly assigned to aspirin (as can be identified (e.g., the popliteal artery), the patient
opposed to warfarin) tolerated the medication better, should undergo surgical embolectomy. Systemic throm-
had a lower incidence of hemorrhage, and had a lower bolysis is rarely used. Catheter-directed thrombolysis
mortality rate. would be appropriate for patients with thrombosis in
situ. Neither intravenous heparin nor a glycoprotein
5. a. CT shows dissection of the left vertebral artery. Most IIb/IIIa inhibitor will dissolve the clot, and amputation
vertebral artery dissections heal spontaneously. Antico- is reserved for non-viable limbs.
agulation is recommended to decrease the potential for
secondary thromboembolic complications. Catheter- 2. a. Several factors predict successful outcome, including
based intervention is reserved for patients with ongoing graft occlusion <14 days, ability to traverse the lesion
symptoms despite maximal anticoagulation or the pres- with a guidewire, and two- or three-vessel runoff. Cath-
ence of an aneurysm causing recurrent thromboembo- eter-directed thrombolysis can unmask the etiology un-
lism or with impending rupture. derlying the graft failure. Unless the underlying lesion
is treated (angioplasty, stenting, or surgical revision),
Chapter 28 the graft is likely to reocclude.

1. c 3. d. Adjunctive use of mechanical thrombectomy devices
2. e may avert the need for thrombolysis or permit lower
doses of thrombolytic drugs. Low-dose heparin and
shorter catheter dwell times decrease bleeding rates. Fi-
brinogen levels should be checked approximately every
6 hours because levels <100 mg/dL are associated with
systemic fibrinolysis.

4. d. In assessing patients with acute limb ischemia, the
degree of limb ischemia can be categorized as Category I
(viable), IIa (marginally threatened) or IIb (immediately
threatened), or III (irreversible). Revascularizing a non-
viable limb leads to profound metabolic acidosis, hyper-
kalemia, myoglobinuria, acute renal failure, and death.

5. a. The TOPAS study compared rUK with primary
surgery in patients with acute lower extremity arte-
rial ischemia. The increase in ankle-brachial index was
similar in the surgery and thrombolysis arms. There
was no difference in the rate of either major amputation
or death between the groups within 1 year of follow-
up. The TOPAS trial established equivalency of the two
treatment arms.

319

Answers Chapter 31

Chapter 30 1. d
2. c
1. d 3. d
2. b 4. b
3. e 5. a
4. d 6. c
5. e 7. a, b, and d
6. e

320

Index

AAAs see abdominal aortic aneurysms complications, 175–6 anatomic criteria, patient selection, 222–3
abdominal angiography, 228 CT, 174 anatomy
abdominal aorta intervention, aortoiliac diagnosis, initial, 174–5
differential diagnosis, 172 arteries, 1
intervention, 239–40 duplex ultrasonography, 174 brachiocephalic vessels, 267, 270–1
abdominal aortic aneurysms (AAAs), embolic vs. thrombotic cause, 171–2 CAS, 254–5
etiology, 170–2 aneurysmal disease, brachiocephalic
186–9, 245–8 extrinsic occlusions, 170, 171–2
CT, 188 future directions, 177 vessels, 270
diagnostic testing, 188 incidence, 169 aneurysms see named aneurysms
epidemiology, 187 intrinsic occlusions, 170–1 angiography
EVAR, 247–9 laboratory studies, 174
mortality, 245, 246–7 management, 174–5 abdominal, 228
natural history, 187–8 medications, 175–6 aortic arch, 228
presentation, 188 pathophysiology, 169–70 aortoiliac, 239
risk factors, 246 postoperative care, 175–6 arch angiography, 310
rupture, 245–7 thrombolysis, 175 brachiocephalic vessels, 271–2
therapy, 189 ultrasonography, 174 carotid, 217, 229–31
ultrasonography, 188 acute mesenteric ischemia, 208 carotid artery disease, 217
abdominal vascular trauma, 182 acute non-occlusive intestinal ischemia, contralateral lower extremity access,
ABI see ankle-brachial index
access site complications, 302–6 208 232
arteriovenous fistula, 303 acute venous occlusion CTA, 205, 263
axillary and brachial artery puncture, diagnostic, 226–33
see also deep vein thrombosis (DVT) extracranial carotid arteries, 230–1
305–6 thrombolytic therapy, 290–1 extracranial vertebral artery occlusive
femoral puncture, 305 adrenocortical carcinoma, 135
groin hematoma, 302–3 Adson test (scalene maneuver), TOS, 41 disease, 271–2
pseudoaneurysm, 303–4 advanced lesions lower extremity access, 232
RPH, 304–5 asymptomatic plaque rupture, 8 lymphangiography, 56
ACE inhibitors, Raynaud syndrome, 37 calcification, 8 MRA, 205, 217, 263
acrocyanosis, 127 lipid pool, 7–8 non-selective, 227–9
acupuncture, Raynaud syndrome, 38 thrombosis, 8 popliteal aneurysm, 287
acute arterial disorders, 169–85 adventitia layer, arteries, 1 pulmonary angiography, VTE, 79
acute arterial occlusion, 169–77 air plethysmography, CVI, 112–13 RAS, 204
arteriography, 174 allergic granulomatous angiitis, 16, 17 renal, 231
causes, 170–2 alpha-1 adrenergic receptor blockers, renal artery occlusive disease, 263
clinical categories, 173–4 selective, 229–32
clinical evaluation, 172–3 Raynaud syndrome, 36 thrombolytic therapy, 287
clinical presentation, 172–3 ANA see antinuclear antibodies upper extremity, 231
vertebral, 229–31
visceral, 231

321

Index

angioplasty iliac PTA vs. stent placement, 241–2 balloon angioplasty
see also carotid angioplasty and stents, 240–2 brachiocephalic vessels, 268–70
stenting (CAS); percutaneous arch angiography, complications, 310 complications, 310
transluminal angioplasty (PTA) arrhythmias, surgery, perioperative cutting balloon angioplasty, 280–1
balloon angioplasty, 268–70, 280–1, 310
brachiocephalic vessels, 268–70 management, 121 balloon-expandable stents, 236
cutting balloon angioplasty, 280–1 arterial occlusion, acute see acute arterial aortoiliac intervention, 240–2
lower extremity PAD, 280–1
occlusion balloons, endovascular techniques,
angiosarcomas, 132–3, 136–7 arterial occlusive disease, thrombolytic 235–6
ankle-brachial index (ABI)
therapy, 285–92 basilar artery occlusion, brachiocephalic
arterial testing, 97–8 arterial system evaluation, lower vessels, 274
lower extremity PAD, 157–8, 160
mortality, 160 extremity PAD, 279 BCS see Budd-Chiari syndrome
answers, 313–19 arterial testing, 92–108 Behçet syndrome, 17–18, 19
anticoagulation therapy, Raynaud beta-blocking drugs, Raynaud
ankle-brachial index (ABI), 97–8
syndrome, 37 cuff artifacts, 98 syndrome, 31
antinuclear antibodies (ANA), Raynaud digital plethysmography, 99–100 blood viscosity, Raynaud syndrome, 32
duplex ultrasonography, 95–6, 101–7 blue rubber bleb nevus syndrome,
syndrome, 29 error sources, 98
antiplatelet therapy, Raynaud syndrome, penile blood flow, 101 138–9
plethysmography, 96–7 brachiocephalic vessels
37 pulse volume recording, 99
aorta diseases, 244–50 reactive hyperemia, 100 anatomy, 267, 270–1
aortic aneurysms, 186–93, 245–9 segmental limb pressures, 98 aneurysmal disease, 270
stress testing, 100 angiography, 271–2
AAAs, 186–9, 245–8 TcPO2, 101 balloon angioplasty, 268–70
defining, 186 toe pressures, 99 basilar artery occlusion, 274
isolated iliac artery aneurysms, 248 treadmill exercise, 100 endovascular therapy, 267–76
pathophysiology, 186–7 ultrasonography, 92–6 etiology of occlusive disease, 267–8
popliteal artery aneurysm, 191 arterial thrombosis, thrombophilia, 67–8 extracranial vertebral artery occlusive
TAAs, 189–91, 248–9 arteries, anatomy, 1
aortic arch angiography, 228 arteriovenous fistula, access site disease, 271–2
aortic body tumors, 134–5 indications for intervention, 268
aortic dissection, 194–200, 244–5 complications, 303 intracranial vertebral artery occlusive
carotid artery dissection, 198 asymptomatic plaque rupture, advanced
classification, 194–5 disease, 273–4
DeBakey classification, 194–5 lesions, 8 patient assessment/treatment, 268–70
diagnosis, 196 atheromatous embolization, 177–81 stents, 268–70
dissection-like syndromes, 197–8 subclavian and innominate artery
Ehlers-Danlos syndrome, 195 causes, 177–8
epidemiology, 194 cholesterol embolization, 179 intervention, 267–70
follow-up, 197 clinical presentation, 178–9 vertebral and basilar artery
hypertension, 195 computed tomography (CT), 180
IMH, 197–8 diagnosis, 179–80 intervention, 270–4
management, 196–7 etiology, 177–8 vertebral artery dissection, 272–3
Marfan syndrome, 195 laboratory studies, 179 vertebral artery trauma, 273
pathogenesis, 194 management, 180–1 brachytherapy, lower extremity PAD,
PAU, 198 prevalence, 177
presentation, 195–6 atherosclerosis 282
risk factors, 195 Raynaud syndrome, 29–30 Budd-Chiari syndrome (BCS), VTE, 88–9
Stanford classification, 194–5 renal artery occlusive disease, 259–61 Buerger disease, 18–21
aortic stent grafts, complications, 308–9 atherosclerotic risk factors, 3–8
aortoiliac angiography, 239 lesion initiation, 4–7 CAD see coronary artery disease
aortoiliac intervention, 239–43 atrophie blanche, CVI, 47–8 calcification, advanced lesions, 8
abdominal aorta intervention, 239–40 axillary and brachial artery puncture, calcium-channel blockers, Raynaud
aortoiliac angiography, 239
iliac artery intervention, 240–2 access site complications, 305–6 syndrome, 36
CAMs see cellular adhesion molecules
B-mode ultrasonography, 95 captopril renography, RAS, 205–6
bacillary (epithelioid) angiomatosis, 132 cardiac myxomas, 134
cardiovascular disease, risk, 213–14
cardiovascular morbidity/mortality,

lower extremity PAD, 159–60
carotid angiography, 217, 229–31

322

Index

carotid angioplasty and stenting (CAS), carotid stenting, complications, 310 deep venous insufficiency, 44–6
251–8 CAS see carotid angioplasty and stenting; diagnostic testing, 49–50, 112–13
differential diagnosis, 49
see also angioplasty carotid artery stent drug therapy, 50
anatomy, 254–5 catheter-directed intra-arterial DVT, 44–6
CEA, 251–2 edema reduction, 50
cerebral protection, 255–6 thrombolysis, 285–8 endovascular treatment, 51, 297–8
complications, 256 catheter-directed pharmacologic examination, 47–9
contraindications, 252 history, 47
duplex follow-up, 253–4 thrombolysis (CDT) leg ulcers, 44, 50–1
future directions, 256 contraindications, 294–5 lipodermatosclerosis, 47–50
indications, 252 VTE, 293–5 May-Thurner syndrome, 45
pharmacologic adjuncts, 256 catheters natural history, 44
restenosis, 253–4 characteristics, 226–7 obstruction, 44–5
results, 253–4 complications, 307 pathophysiology, 44–7
short-term results, 253 construction, 227 PPG, 112
stent implantation, 253–4 definitions, 226–7 skin care, 50
technical aspects, 254–6 design, 227 superficial venous insufficiency, 46–7
carotid artery endovascular techniques, 226–33 surgical/endovascular treatment, 51
dissection, 215 materials, 227 treatment, 50–1
dissection, aortic, 198 terms, 226–7 ulcer treatment, 50–1
FMD, 215 cavernous hemangiomas, 132 ultrasonography, 113
carotid artery disease, 212–20 CDT see catheter-directed pharmacologic valvular incompetence, 45–6
angiography, 217 Churg-Strauss syndrome, 16, 17
carotid bruits, 213–14 thrombolysis Cogan syndrome, 13, 14
CAS, 218–19 CEA see carotid endarterectomy color-flow imaging, ultrasonography, 96
CEA, 218 CEAP (Clinical-Etiology-Anatomy- comorbid conditions, surgery,
cerebral ischemia, 214–15, 217–19
diagnostic testing, 216–17 Pathophysiology) classification, perioperative management, 120–1
differential diagnosis, 214–15 CVI, 48 compartment syndrome, vascular
duplex ultrasonography, 216 cellular adhesion molecules (CAMs),
extracranial, 212, 230–1 lesion initiation, 5 trauma, 184
history, 213 cerebral ischemia complications
invasive arteriography, 217 carotid artery disease, 214–15, 217–19
MRA, 217 differential diagnosis, 214–15 access site, 302–6
multidetector CTA, 217 stroke, 214–15 acute arterial occlusion, 175–6
percutaneous therapy, 218–19 cerebral venous sinus thrombosis aortic stent grafts, 308–9
physical examination, 213 (CVST), VTE, 86–7 arch angiography, 310
progression, 213 cerebrovascular disease, lower extremity arteriovenous fistula, 303
risk factors, 215–16 PAD, 159 axillary and brachial artery puncture,
stroke, 214–15 cerebrovascular FMD, 128–9
surgical therapy, 218 chemodectoma, 134 305–6
treatment, 217–19 chemotherapy agents, Raynaud balloon angioplasty, 310
carotid artery injuries, vascular trauma, syndrome, 31 carotid stenting, 310
CHF see congestive heart failure CAS, 256
182 chilblain, 39, 125–6 catheters, 307
carotid artery stent (CAS), carotid artery cholesterol embolization, atheromatous device infection, 308
embolization, 179 devices, 307
disease, 218–19 chronic iliac vein obstruction, embolic protection devices, 310
carotid body tumors, 134 endovascular treatment, 297 endovascular procedures, 302–11
carotid bruits, 213–14 chronic intestinal ischemia, 208–9 femoral puncture, 305
carotid duplex ultrasonography, 101–3 chronic limb dependence, vs. lymphatic fibrinolysis, 308
carotid endarterectomy (CEA) disease, 55 groin hematoma, 302–3
chronic venous insufficiency (CVI), 44–51 iliac angioplasty and stenting, 309
carotid artery disease, 218 air plethysmography, 112–13 intervention-specific, 307–10
CAS, 251–2 atrophie blanche, 47–8 lymphatic disease, 54
without arteriography, duplex causes, 44–6 pseudoaneurysm, 303–4
CEAP (Clinical-Etiology-Anatomy- renal angioplasty and stenting, 309
ultrasonography, 103 Pathophysiology) classification, 48

323

Index

complications (continued) see also acute venous occlusion; venous dissection, vertebral artery, 272–3
RPH, 304–5 thromboembolism (VTE) dobutamine stress echocardiography,
stent thrombosis, 310
venous interventions, 309–10 CDT, 293–5 perioperative management, 119
wires, 307 combined approaches to diagnosis, Doppler, laser, Raynaud syndrome, 34
Doppler ultrasonography, 92–5
compression stockings, VTE, 86 111–12
compression ultrasonography, VTE, 78–9 diagnosis, 109–12 CW (continuous-wave) Doppler, 93
computed tomography angiography endovascular therapy, 296 Fourier analysis, 93–4
goals, therapy, 293 PW (pulsed-wave) Doppler, 93–5
(CTA) impedance plethysmography, 109 spectral waveform analysis, 93–5
RAS, 205 PMT, 295 drug-eluting stents, 237, 281–2
renal artery occlusive disease, 263 risk factors, 62–3 drug-induced Raynaud syndrome, 31–2
computed tomography (CT) thrombolytic therapy, 290–1 duplex ultrasonography
AAAs, 188 trends, 75–6 see also ultrasonography
acute arterial occlusion, 174 ultrasonography, 109–12 acute arterial occlusion, 174
atheromatous embolization, 180 VTE, 62–4 arterial testing, 95–6, 101–7
VTE, 79 deep venous insufficiency, 44–6 carotid, 101–3
congestive heart failure (CHF) device infection, complications, 308 carotid artery disease, 216
vs. lymphatic disease, 55 devices, complications, 307 carotid endarterectomy without
RAS, revascularization, 208 diabetes mellitus, PAD, 165
surgery, perioperative management, diagnosis arteriography, 103
see also differential diagnosis CAS follow-up, 253–4
120 acute arterial occlusion, 174–5 CVI, 113
connective tissue diseases (CTDs), 21–4 aortic dissection, 196 lower extremity artery, 105–7
atheromatous embolization, 179–80 pseudoaneurysm, 303–4
CREST syndrome, 21–2, 29 DVT, 109–12 RAS, 204–5
Raynaud syndrome, 29 leg ulcerations, 141–2 renal artery, 104–5
scleroderma, 21–3 PE, 112 transcranial Doppler/duplex
Continuous-wave (CW) Doppler, 93 RAS, 203–4
coronary artery disease (CAD), lower scleroderma, 22–3 ultrasonography, 103
SLE, 24 venous testing, 113
extremity PAD, 159–60 TO, 20 visceral artery, 103–4
Costoclavicular maneuver (military TOS, 41–2 DVT see deep vein thrombosis
diagnostic angiography, 226–33
position), TOS, 41 diagnostic assessment, patient selection, echocardiography
covered stents, 237, 282 dobutamine stress echocardiography,
CREST syndrome 224–5 119
diagnostic testing surgery, perioperative management,
CTDs, 21–2 118, 119
Raynaud syndrome, 29 carotid artery disease, 216–17
critical limb ischemia, lower extremity CVI, 49–50, 112–13 edema reduction
lymphatic disease, 55–6 CVI, 50
PAD, 161 surgery, perioperative management, lymphatic disease, 56
cryoplasty, lower extremity PAD, 280
CT see computed tomography 119–20 EDHF see endothelium-derived
CTA see computed tomography thrombophilia, 64–71 hyperpolarizing factor
differential diagnosis
angiography see also diagnosis Ehlers-Danlos syndrome
CTDs see connective tissue diseases acute arterial occlusion, 172 aortic dissection, 195
cuff artifacts, arterial testing, 98 carotid artery disease, 214–15 TAAs, 189–90
cutting balloon angioplasty, lower cerebral ischemia, 214–15
CVI, 49 embolic protection devices,
extremity PAD, 280–1 lower extremity PAD, 154–5 complications, 310
CVI see chronic venous insufficiency lymphatic disease, 54–5
CVST see cerebral venous sinus stroke, 214–15 endocrine diseases, Raynaud syndrome,
digital plethysmography, arterial testing, 32
thrombosis
CW (continuous-wave) Doppler, 93 99–100 endothelial cell activation, lesion
cystic adventitial disease, 129–30 dissection, aortic see aortic dissection initiation, 5
cytokines, lesion initiation, 6
endothelial dysfunction, lesion initiation,
DeBakey classification, aortic dissection, 4
194–5
endothelial function, 1–3
deep vein thrombosis (DVT), 44–6, 109–12 inflammation regulation, 3

324

Index

thrombosis regulation, 3 femoral puncture, access site hyperbaric oxygen
endothelium-derived hyperpolarizing complications, 305 leg ulcerations, 146
Raynaud syndrome, 38
factor (EDHF), vasodilator, 3 fibrin D-dimer testing, VTE, 79–80
endothelium-derived vasoconstrictors, 3 fibrinolysis, complications, 308 hypercoagulable states, PAD, 165
endothelium-derived vasodilators, 2–3 fibrinolytic therapy, VTE, 85–6 hyperhomocysteinemia
endovascular aortic aneurysm repair fibromuscular dysplasia (FMD), 128–9
lower extremity PAD, 158
(EVAR), AAAs, 247–9 carotid artery, 215 PAD, 165
endovascular laser ablation (EVLA), classification, 204 hyperlipidemia, PAD, 164
RAS, 203, 204 hypersensitivity vasculitides, 16–17
varicose veins, 297–8 renal artery occlusive disease, 259–61 hypertension
endovascular procedures fibroproliferative atheroma, lesion aortic dissection, 195
PAD, 164
complications, 302–11 initiation, 6 surgery, perioperative management,
patient selection, 221–5 finger systolic blood pressures, Raynaud
endovascular techniques, 226–38 120
balloons, 235–6 syndrome, 33 hypertension pathogenesis, RAS, 201–2
catheters, 226–33 fingers, blood flow, Raynaud syndrome, hypothenar hammer syndrome,
stents, 236–7
wires, 234–5 27 Raynaud syndrome, 30
endovascular therapy fingertip thermography, Raynaud
brachiocephalic vessels, 267–76 iliac angioplasty and stenting,
DVT, 296 syndrome, 33 complications, 309
endovascular treatment flash pulmonary edema, RAS,
chronic iliac vein obstruction, 297 iliac artery intervention, aortoiliac
CVI, 51, 297–8 revascularization, 208 intervention, 240–2
lower extremity PAD, 277–84 FMD see fibromuscular dysplasia
mesenteric arterial occlusive disease, fondaparinux, VTE, 83 imaging
Fontaine Classification, lower extremity lymphatic disease, 56
264–5 mesenteric arteries, 264–5
renal artery occlusive disease, 262–3 PAD, 278 renal arteries, 263
upper extremity venous thrombosis, food supplements, Raynaud syndrome,
imaging studies
298–9 37–8 Raynaud syndrome, 34
varicose veins, 297–8 Fourier analysis, Doppler TO, 20–1
venous disease, 293–301
environmental disorders, 124–8 ultrasonography, 93–4 IMH see intramural hematoma
epidemiology frostbite, 126–7 impedance plethysmography, DVT, 109
AAAs, 187 future directions in-stent restenosis, patient selection,
aortic dissection, 194
leg ulcerations, 141 acute arterial occlusion, 177 223
lower extremity PAD, 156 carotid angioplasty and stenting inferior vena cava (IVC) filters, VTE, 85,
mesenteric arterial occlusive disease,
(CAS), 256 296–7
263 inflammation, PAD, 159, 165
renal artery occlusive disease, 259 glomus tumors, 132 inflammation regulation
TO, 18 groin hematoma, access site
VTE, 75–6 endothelial function, 3
erythema ab igne, 127–8 complications, 302–3 nitric oxide, 3, 4
erythermalgia, 38–9, 124–5 inflammatory bowel disease, VTE, 77
erythromelalgia, 38–9, 124–5 HDL see high-density lipoprotein injuries see trauma
EVAR see endovascular aortic aneurysm hemangioendothelioma, 133–4 intervention-specific complications,
hemangiomas, 130–2
repair hemodynamic monitoring, surgery, 307–10
EVLA see endovascular laser ablation intestinal ischemia, chronic, 208–9
exercise abduction stress test, TOS, 41–2 perioperative management, 121 intima layer, arteries, 1
extremities, vascular trauma, 183 heparin intimal sarcomas, 133
intracranial vertebral artery occlusive
Fabry disease, 138 fondaparinux, 83
factor V Leiden, VTE, 64–5 LMWH, 82–3 disease, brachiocephalic vessels,
fatty streak, lesion initiation, 5–6 unfractionated heparin, 81–2 273–4
VTE, 81–3 intramural hematoma (IMH), aortic
hereditary hemorrhagic telangiectasia dissection, 197–8
intravascular angiomatosis, 132
(HHT), 138 intravascular papillary endothelial
high-density lipoprotein (HDL), reverse hyperplasia, 132

cholesterol transport, 4–5
hyperabduction test (Wright test), TOS,

41

325

Index

invasive testing, patient selection, 224 vascular remodeling, 6–7 prognosis, 160
ischemic nephropathy, RAS, 202 lesions, advanced, 7–8 progression, 151–2
IVC filters see inferior vena cava filters lipedema, vs. lymphatic disease, 55 renal disease, 158–9
lipid pool, advanced lesions, 7–8 risk factors, 158
Kaposi sarcoma, 135–6 lipodermatosclerosis, CVI, 47–50 Rutherford classification, 278–9
Kasabach-Merritt syndrome, 138 livedo reticularis, 39 significance, 277
Kawasaki disease, 15 LMWH see low-molecular-weight stenting, 281–2
Klippel-Trénaunay syndrome, 137–8 symptoms, 157
heparin symptoms location, 151
large vessel vasculitis, 11–14 low-density lipoprotein (LDL) TASC classification, 279
laser Doppler, Raynaud syndrome, 34 therapeutic options, 279–82
lasers, lower extremity PAD, 281 oxidative modification, 4 lymphangiography, lymphatic disease,
LDL see low-density lipoprotein retention, 4
left atrial myxoma, 134 risk factor modification, 8 55, 56
leg ulcerations, 141–8 low-molecular-weight heparin (LMWH), lymphangiosarcomas, 136–7
lymphatic disease, 52–7
causes, 141, 142 VTE, 82–3
chronic, 142–4 lower extremity artery duplex appearance, 53–4
CVI, 44, 50–1 bacterial infection, 52–3
debridement, 145–6 ultrasonography, 105–7 causes, 52–3
diagnosis, 141–2 lower extremity PAD vs. CHF, 55
diagnostic testing, 142, 144 vs. chronic limb dependence, 55
dressings, 146 see also peripheral arterial disease complications, 54
epidemiology, 141 (PAD) diagnostic testing, 55–6
etiology, 141, 142 differential diagnosis, 54–5
growth factors, 146–7 ABI, 157–8, 160 distribution, 53
history, 141 angioplasty, 280–1 edema reduction, 56
hyperbaric oxygen, 146 arterial system evaluation, 279 history, 53–4
infections, 145 brachytherapy, 282 imaging, 56
management, 144–7 CAD, 159–60 inflammatory disease, 53
pain management, 147 cardiovascular morbidity/mortality, vs. lipedema, 55
pathogenesis, 142–4 lymphangiography, 55, 56
physical examination, 141–2, 143 159–60 lymphoscintigraphy, 55–6
prognostic indices, 145 causes, 149 maintenance therapy, 56
skin grafts, 146 cerebrovascular disease, 159 malignancy, 53, 54
therapy, 144–7 claudication differential diagnosis, vs. myxedema, 55
topical negative pressure therapy, 146 natural history, 52
vacuum-assisted closure, 146 154–5 parasitic infection, 53
wound care centers, 147 claudication, intermittent, 156–7 pathophysiology, 52–3
leiomyomatosis of the uterus, 135 clinical evaluation, 149–55 physical examination, 53–4
leiomyosarcomas, 132–3 clinical presentation, 278–9 preventive measures, 57
lesion initiation critical limb ischemia, 161 primary (congenital) lymphedema,
atherosclerotic risk factors, 4–7 cryoplasty, 280
CAMs, 5 cutting balloon angioplasty, 280–1 52
cytokines, 6 differential diagnosis, 154–5 progression, 53
endothelial cell activation, 5 endovascular treatment, 277–84 secondary (acquired) lymphedema,
endothelial dysfunction, 4 epidemiology, 156
fatty streak, 5–6 etiology, 277 52–3
fibroproliferative atheroma, 6 Fontaine classification, 278 surgical procedures, 57
HDL, 4–5 functional decline, 160–1 tissue damage, 53
LDL, 4 hyperhomocysteinemia, 158 trauma, 53
neovascularization, 6, 7 inflammation, 159 treatment, 56
proteases, 6–7 intermittent claudication, 156–7 ultrasonography, 56
signal amplification, 6 lasers, 281 vs. venous disease, 54–5
T cell entry, 6 measuring, 157–8 lymphedema-associated angiosarcoma,
mechanical atherectomy, 281
mortality, 159–60 136–7
natural history, 160, 277–8 lymphoscintigraphy, lymphatic disease,
pain, 149–50
patient history, 149–52 55–6
physical examination, 152–4
prevalence, 157–8, 277

326

Index

Maffucci syndrome, 138 non-invasive testing diabetes mellitus, 165
magnetic resonance angiography (MRA) patient selection, 224 drug therapy, claudication, 166
surgery, perioperative management, exercise rehabilitation, 166
carotid artery disease, 217 118–19 hypercoagulable states, 165
RAS, 205 hyperhomocysteinemia, 165
renal artery occlusive disease, 263 non-selective angiography, 227–9 hyperlipidemia, 164
malignancy novel drug therapies, Raynaud hypertension, 164
lymphatic disease, 53, 54 inflammation, 165
Raynaud syndrome, 32 syndrome, 37 medical treatment, 163–8
venous obstruction, 45 nuclear myocardial perfusion imaging, revascularization, 166–7
VTE, 78 risk factors, 163–6
Marfan syndrome surgery, perioperative management, smoking cessation, 163–4
aortic dissection, 195 118 systemic therapy, 165–6
TAAs, 189–90 pernio, 39, 125–6
Masson pseudoangiosarcoma, 132 ovarian vein thrombosis (OVT), VTE, 90 PHACES syndrome, 137
May-Thurner syndrome, 45 photoplethysmography (PPG), CVI, 112
mechanical atherectomy, lower extremity PAD see peripheral arterial disease plethysmography
PAES see popliteal artery entrapment air plethysmography, 112–13
PAD, 281 arterial testing, 96–7
media layer, arteries, 1 syndrome CVI, 112–13
mediastinal paragangliomas, 134–5 Paget-Schroetter syndrome, TOS, 41 digital, arterial testing, 99–100
medium vessel vasculitis, 14–15 pain, lower extremity PAD, 149–50 impedance plethysmography, 109
mesenteric arterial occlusive disease, pain management, leg ulcerations, 147 PPG, 112
papillary endothelial hyperplasia, 132 venous testing, 109, 112–13
263–5 paragangliomas, 134 PMT see percutaneous mechanical
causes, 263–4 patient selection
endovascular treatment, 264–5 thrombectomy
epidemiology, 263 anatomic criteria, 222–3 pneumatic vascular pump, Raynaud
etiology, 263 contraindications, 223
natural history, 263–4 diagnostic assessment, 224–5 syndrome, 38
mesenteric artery disease, 208–9 endovascular procedures, 221–5 POEMS syndrome, 139
mesenteric vein thrombosis (MVT), VTE, evaluation, 221–2 polyarteritis nodosa, 14–15
functional criteria, 223–4 popliteal aneurysm, angiography, 287
89 in-stent restenosis, 223 popliteal artery aneurysm, 191
military position (costoclavicular invasive testing, 224 popliteal artery entrapment syndrome
non-invasive testing, 224
maneuver), TOS, 41 thrombolytic therapy, 285–6 (PAES), 129
mortality vascular access, 223 port-wine stain, 132
PAU see penetrating atherosclerotic ulcer PPG see photoplethysmography
AAAs, 245, 246–7 PE see pulmonary embolism prostacyclin, vasodilator, 2–3
ABI, 160 penetrating atherosclerotic ulcer (PAU), prostaglandins, Raynaud syndrome, 37
lower extremity PAD, 159–60 proteases, lesion initiation, 6–7
MRA see magnetic resonance aortic dissection, 198 pseudoaneurysm
penile blood flow, arterial testing, 101
angiography percutaneous mechanical thrombectomy access site complications, 303–4
mucocutaneous lymph node syndrome, 15 duplex ultrasonography, 303–4
MVT see mesenteric vein thrombosis (PMT), DVT, 295 PTA see percutaneous transluminal
mycotic aneurysms, TAAs, 190 percutaneous therapy, carotid artery
myocardial infarction, postoperative angioplasty
disease, 218–19 pulmonary angiography, VTE, 79
monitoring, 121 percutaneous transluminal angioplasty pulmonary embolism (PE)
myxedema, vs. lymphatic disease, 55
(PTA) diagnosis, 112
nailfold capillary microscopy, Raynaud see also angioplasty risk factors, 62–3
syndrome, 34 aortoiliac intervention, 241–2 ultrasonography, 112
iliac PTA vs. stent placement, 241–2 VTE, 62–4
neovascularization, lesion initiation, 6, 7 RAS, 206–7 pulse volume recording, arterial testing,
nephrotic syndrome, VTE, 78 perfusion imaging, nuclear myocardial,
nitrates, Raynaud syndrome, 36–7 99
nitric oxide 118 pulsed-wave (PW) Doppler, 93–5
peripheral arterial disease (PAD) PW (pulsed-wave) Doppler, 93–5
inflammation regulation, 3, 4
vasodilator, 2 see also lower extremity PAD
non-invasive imaging, stents, 237 claudication treatment, 166
clinical evaluation, 149–55

327

Index

radiofrequency ablation (RFA), varicose Raynaud syndrome (Continued) renal FMD, 128
veins, 297–8 terminology, 26–7 renal salvage revascularization, RAS,
thermoregulation, 27
RAS see renal artery stenosis thromboembolism, 30 207–8
Raynaud syndrome, 26–38 thrombolysis, 37 renal vein thrombosis (RVT), VTE, 87–8
TO, 30 restenosis, CAS, 253–4
ACE inhibitors, 37 TOS, 31 retinal vein thrombosis (RtVT), VTE,
acupuncture, 38 toxins, 31–2
alpha-1 adrenergic receptor blockers, transcutaneous nerve stimulation, 38 89–90
treatment, 34–8 retroperitoneal hematoma (RPH), access
36 vasospasm mechanism, 28
ANA, 29 vibration-induced, 30–1 site complications, 304–5
anticoagulation therapy, 37 revascularization
antiplatelet therapy, 37 reactive hyperemia, arterial testing, 100
associated conditions, 28–32 renal angiography, 231 PAD, 166–7
atherosclerosis, 29–30 renal angioplasty and stenting, pharmacologic issues, 166–7
behavioral therapy, 34–5 RAS, 207–8
beta-blocking drugs, 31 complications, 309 RFA see radiofrequency ablation
blood viscosity, 32 renal artery duplex ultrasonography, risk
calcium-channel blockers, 36 cardiovascular disease, carotid bruits,
chemotherapy agents, 31 104–5
cold recovery time, 33, 34 renal artery occlusive disease 213–14
CREST syndrome, 29 stroke, 212
critical ischemia, 38 atherosclerosis, 259–61 surgery, adverse cardiovascular
CTDs, 29 causes, 259–61
defining, 26 CTA, 263 events, 115–18
drug-induced, 31–2 endovascular treatment, 262–3 risk factors
drug therapy, 35–7 epidemiology, 259
endocrine diseases, 32 etiology, 259–61 AAAs, 246
finger systolic blood pressures, 33 FMD, 259–61 aortic dissection, 195
fingers, blood flow, 27 imaging studies, 263 atherosclerotic, 3–8
fingertip thermography, 33 MRA, 263 carotid artery disease, 215–16
food supplements, 37–8 natural history, 261–2 DVT, 62–3
hyperbaric oxygen, 38 renal artery stenosis (RAS), 201–8 lower extremity PAD, 158
hypothenar hammer syndrome, 30 angiography, 204 modification, 8
imaging studies, 34 captopril renography, 205–6 PAD, 158, 163–6
incidence, 27–8 CHF control, revascularization, 208 PE, 62–3
infections, 32 clinical manifestations, 202–3 stroke, 215–16
laboratory evaluation, 32–4 CTA, 205 VTE, 76–8
laser Doppler, 34 diagnosis, 203–4 RPH see retroperitoneal hematoma
malignancy, 32 duplex ultrasonography, 204–5 RtVT see retinal vein thrombosis
nailfold capillary microscopy, 34 flash pulmonary edema, Rutherford classification, lower
nitrates, 36–7
novel drug therapies, 37 revascularization, 208 extremity PAD, 278–9
pharmacologic therapy, 35–7 FMD, 203 RVT see renal vein thrombosis
physical examination, 32 hypertension pathogenesis, 201–2
pneumatic vascular pump, 38 ischemic nephropathy, 202 sarcomas, 132–3
primary, 26–8 management, 206–7 scalene maneuver (Adson test), TOS, 41
prostaglandins, 37 MRA, 205 scleroderma, 21–3
scleroderma, 29 natural history, 203
secondary, 26–7, 28–32 prevalence, 202–3 clinical manifestations, 22
segmental blood pressure PTA, 206–7 diagnosis, 22–3
renal salvage revascularization, 207–8 pathophysiology, 22
measurements, 33 revascularization, 207–8 Raynaud syndrome, 29
SLE, 29 stenting, 206–7 treatment, 23
small vessel vasculitis, 29 surgical revascularization, 207–8 segmental limb pressures, arterial
spinal cord stimulation, 38 renal cell carcinoma, 135
sympathectomy, 38 renal disease, lower extremity PAD, testing, 98
selective angiography, 229–32
158–9 self-expanding stents, 236–7
signal amplification, lesion initiation, 6
SLE see systemic lupus erythematosus
small vessel vasculitis, 16–18, 29
smoking cessation, PAD, 163–4

328

Index

spectral waveform analysis, Doppler non-invasive testing, 118–19 Paget-Schroetter syndrome, 41
ultrasonography, 93–5 nuclear myocardial perfusion Raynaud syndrome, 31
types, 40–1
spinal cord stimulation, Raynaud imaging, 118 venous TOS, 41
syndrome, 38 physical examination, 115–16 Wright test (hyperabduction test), 41
risk, adverse cardiovascular events, thoracic vascular trauma, 181–2
spondyloarthropathies, TAAs, 190 thromboangiitis obliterans (TO), 18–21
Stanford classification, aortic dissection, 115–18 clinical evaluation, 20
treadmill exercise tolerance testing, diagnosis, 20
194–5 diagnostic criteria, 21
stent implantation, CAS, 253–4 118 epidemiology, 18
stent thrombosis, complications, 310 treatment, additional, 119–20 history, 18–20
stents/stenting valvular heart disease, 120–1 imaging studies, 20–1
surgical revascularization, RAS, 207–8 laboratory tests, 20
aortic stent grafts, 308–9 SVC syndrome see superior vena cava pathology, 20
aortoiliac intervention, 240–2 presentation, 18–20
balloon-expandable, 236, 240–2 syndrome Raynaud syndrome, 30
brachiocephalic vessels, 268–70 sympathectomy, Raynaud syndrome, 38 treatment, 21
carotid stenting, 310 systemic lupus erythematosus (SLE), thromboembolism, Raynaud syndrome,
CAS, 251–8
covered, 237, 282 23–4 30
drug-eluting, 237, 281–2 clinical manifestations, 24 thrombolysis
endovascular techniques, 236–7 diagnosis, 24
iliac angioplasty and stenting, 309 pathophysiology, 23–4 acute arterial occlusion, 175
lower extremity PAD, 281–2 Raynaud syndrome, 29 catheter-directed intra-arterial, 285–8
non-invasive imaging, 237 treatment, 24 catheter-directed pharmacologic,
RAS, 206–7
renal angioplasty and stenting, 309 T cell entry, lesion initiation, 6 293–5
self-expanding, 236–7 TAAs see thoracic aortic aneurysms Raynaud syndrome, 37
stress testing, arterial testing, 100 Takayasu arteritis, 13, 14 thrombolytic therapy, 285–92
stroke, 212–20 angiography, 287
carotid artery disease, 214–15 TAAs, 190 arterial occlusive disease, 285–92
cerebral ischemia, 214–15 TASC classification, lower extremity catheter-directed intra-arterial
differential diagnosis, 214–15
incidence, 212 PAD, 279 thrombolysis, 285–8
prevention, 217–19 TcPO2 see transcutaneous oxygen DVT, 290–1
risk, 212 techniques, endovascular see indications, 285–6
risk factors, 215–16 mechanical adjuvants, 290
Sturge-Weber syndrome, 138 endovascular techniques patency, 287–8
superficial (capillary) hemangiomas, 131 temporal arteritis, 11–14 patient selection, 285–6
superficial venous insufficiency, CVI, testicular neoplasms, 135 popliteal aneurysm, 287
thermal disorders, 124–8 thrombolytic agents, 286
46–7 thermoregulation, fingers, blood flow, 27 venous occlusive disease, 285–92
superior vena cava (SVC) syndrome, thoracic aortic aneurysms (TAAs), thrombophilia, 59–74
see also venous thromboembolism
endovascular treatment, 299–300 189–91, 248–9
surgery, perioperative management, causes, 189–90 (VTE)
Ehlers-Danlos syndrome, 189–90 acquired, 59–60, 65
115–23 etiology, 189–90 acute therapy, 69–70
arrhythmias, 121 Marfan syndrome, 189–90 arterial thrombosis, 67–8
CHF, 120 mycotic aneurysms, 190 causes, 59–60
clinical predictors, 116–18 prognosis, 191 counseling, 61–2
comorbid conditions, 120–1 spondyloarthropathies, 190 diagnostic testing, 64–71
diagnostic testing, additional, 119–20 Takayasu arteritis, 190 familial, 59–60, 65
dobutamine stress echocardiography, thoracic outlet syndrome (TOS), 39–42 family members, 61–2
Adson test (scalene maneuver), 41 hereditary, 60
119 anatomy, 39–40 laboratory evaluation, 66–7
echocardiography, 118, 119 arterial TOS, 40–1 manifestations, 60
hemodynamic monitoring, 121 costoclavicular maneuver (military primary, 60
history, 115–16
myocardial infarction, postoperative position), 41
diagnosis, 41–2
monitoring, 121 exercise abduction stress test, 41–2
neurogenic TOS, 40

329

Index

thrombophilia (continued) venous, 109–12 nitric oxide, 2
primary prophylaxis, 69 VTE, 78–9 prostacyclin, 2–3
screening, 61–2 unfractionated heparin, VTE, 81–2 vegetant intravascular
secondary, 59–60 unusual vascular diseases, 124–40
secondary prophylaxis, 70–1 upper extremity angiography, 231 hemangioendothelioma, 132
testing, 60–4 upper extremity arterial disease, 26–43 venous disease
testing, diagnostic, 64–71 upper extremity venous thrombosis
trends, 61–2 endovascular treatment, 298–9 endovascular treatment, 293–301
VTE, 60, 61–6 VTE, 90–1 vs. lymphatic disease, 54–5
venous injury, 183
thrombosis, advanced lesions, 8 valvular heart disease, surgery, venous interventions, complications,
thrombosis regulation, endothelial perioperative management, 120–1
309–10
function, 3 valvular incompetence, CVI, 45–6 venous occlusive disease, thrombolytic
TO see thromboangiitis obliterans varicose veins
toe pressures, arterial testing, 99 therapy, 285–92
TOS see thoracic outlet syndrome endovascular treatment, 297–8 venous testing, 109–14
toxins, Raynaud syndrome, 31–2 EVLA, 297–8
transcranial Doppler/duplex RFA, 297–8 DVT, 109–12
vascular access, patient selection, 223 venous thromboembolism (VTE), 75–91,
ultrasonography, 103 vascular anomalies, 130–2
transcutaneous nerve stimulation, associated syndromes, 137–9 293–7
vascular biology, 1–10 see also deep vein thrombosis (DVT);
Raynaud syndrome, 38 abnormal, 3–8
transcutaneous oxygen (TcPO2), arterial normal, 1–3 thrombophilia
vascular malformations, 130, 132 BCS, 88–9
testing, 101 vascular remodeling, lesion initiation, CDT, 293–5
trauma clinical history, 78
6–7 clinical presentation, 75
lymphatic disease, 53 vascular trauma, 181–4 compression stockings, 86
vascular, 181–4 compression ultrasonography, 78–9
vertebral artery trauma, 273 abdominal, 182 CT, 79
treadmill exercise, arterial testing, 100 carotid artery injuries, 182 CVST, 86–7
treadmill exercise tolerance testing, compartment syndrome, 184 DVT, 62–4
extremities, 183 epidemiology, 75–6
surgery, perioperative management, minimal, 183 evaluation, 78–80
118 thoracic, 181–2 factor V Leiden, 64–5
trench foot, 127 venous injury, 183 fibrin D-dimer testing, 79–80
trends vertebral artery injuries, 182–3 fibrinolytic therapy, 85–6
DVT, 75–6 vascular tumors, 130–7 fondaparinux, 83
thrombophilia, 61–2 vasculitis, 11–18 heparin, 81–3
tumors, vascular, 130–7 Behçet syndrome, 17–18, 19 hormones, 77
Churg-Strauss syndrome, 16, 17 hospitalized patients, risk factors,
ulcers, leg see leg ulcerations Cogan syndrome, 13, 14
ultrasonography hypersensitivity vasculitides, 16–17 76–7
Kawasaki disease, 15 inflammatory bowel disease, 77
see also duplex ultrasonography large vessel, 11–14 IVC filters, 85, 296–7
AAAs, 188 medium vessel, 14–15 LMWH, 82–3
accuracy, 110 polyarteritis nodosa, 14–15 malignancy, 78
acute arterial occlusion, 174 small vessel, 16–18, 29 MVT, 89
arterial testing, 92–6 Takayasu arteritis, 13, 14 nephrotic syndrome, 78
B-mode ultrasonography, 95 temporal arteritis, 11–14 OVT, 90
color-flow imaging, 96 Wegener granulomatosis, 17, 18 PE, 62–4
compression ultrasonography, 78–9 vasoconstrictors, endothelium-derived, 3 physical examination, 78
CVI, 113 vasodilators PMT, 295
Doppler ultrasonography, 92–5 EDHF, 3 pregnancy, 77
DVT, 109–12 endothelium-derived, 2–3 prevention, 80
limitations, 110–11 primary prevention, 62–3
lymphatic disease, 56 pulmonary angiography, 79
negative studies, 111 recurrent, 63–4, 65
PE, 112 risk factors, 76–8

330

Index

RtVT, 89–90 ventilation perfusion scanning, VTE, visceral artery duplex ultrasonography,
RVT, 87–8 79 103–4
secondary prevention, 63–4
surgical risk factors, 77–8 vertebral and basilar artery intervention, von Hippel-Lindau disease, 138
thrombophilia, 60, 61–6 brachiocephalic vessels, 270–4 VTE see venous thromboembolism
treatment, 80–6
ultrasonography, 78–9 vertebral angiography, 229–31 warfarin, VTE, 83–5
unusual sites, 86–91 vertebral artery dissection, Wegener granulomatosis, 17, 18
upper extremity venous thrombosis, wires
brachiocephalic vessels, 272–3
90–1 vertebral artery injuries, vascular complications, 307
ventilation perfusion scanning, 79 endovascular techniques, 234–5
warfarin, 83–5 trauma, 182–3 Wright test (hyperabduction test), TOS,
vibration-induced Raynaud syndrome,
41
30–1
visceral angiography, 231

331