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324
T. C. Huber et al.
Prostate Cancer/Hematuria
Prostate cancer is one of the most common cancers to affect
men worldwide with an estimated 1.6 million cases and
360,000 deaths annually [11]. Prostate artery embolization is
not approved for the treatment of prostate cancer. However,
prostate carcinoma can be associated with hemorrhage, both
spontaneous and after treatment. Prostate artery embolization for control of hematuria associated with prostate carcinoma was rst described in the 1970s using Gelfoam as an
embolic agent, typically administered in the anterior division
of the internal iliac artery without selection of prostatic
branches [12]. Today, the armamentarium for embolization
for prostate cancer hemorrhage includes particles (such as
polyvinyl alcohol or PVA particles). The advent of microcatheters and microwires has allowed the reduction in the
risk of nontarget embolization to other branches of the anterior division.
Clinical Indication
The initial evaluation of a patient with BPH is intended to
assess the severity of the patient’s LUTS, which can be quantied using the metrics dened in Table29.2. A digital rectal
exam, urinalysis, and serum prostate-specic antigen (PSA)
should be performed [14]. It should be noted, however, that
as of 2012, the US Preventive Services Task Force recommends against PSA screening for prostate cancer [15]. If the
initial evaluation is concerning for prostate cancer or intrinsic bladder dysfunction, the patient should be referred to an
urologist prior to intervention, if not already being followed
by one.
For patients with LUTS and evidence of bladder outlet
obstruction (BOO), who have failed medical therapy and are
signicantly distressed by their symptoms, interventional
therapies are an option. The type of intervention varies
depending on the experience and resources of the treating
interventionalist.
Pre-procedural imaging may include MRI or
CTA. Multiparametric MRI may demonstrate a diffusely
enlarged central zone or discrete BPH nodules (see Fig.29.2)
[9]; however, MRI is not routinely used in the evaluation of
BPH.MRI plays a larger role in the evaluation of prostatic
carcinoma. CTA may be obtained prior to PAE to better
dene the highly variable pelvic vascular anatomy (Figs.29.3
and 29.4) [13, 16].
The internal iliac artery can terminate in four distinct
branching patterns (Fig.29.5) [17]. The prostatic artery can
be single or multiple, with up to three branches supplying the
prostate gland on each side; it can arise from the inferior vesical artery, internal pudendal artery, umbilical artery, obturator
artery, inferior gluteal artery, or internal iliac artery [16].
Embolization of the pelvic vessels can additionally be
used to treat hematuria related to bladder or prostate carcinoma [18]. Patients with radiation cystitis, chemotherapyinduced cystitis, or advanced prostate cancer can develop
persistent hematuria, which can be a signicant source of
morbidity [19]. In such cases, embolization with a variety of
embolic agents including Gelfoam, coils, or polyvinyl alcohol (PVA) may be performed to tamponade bleeding [12, 19].
Table 29.2 Key elements of the evaluation of LUTS prior to PAE [13]
Denitions
IPSS International prostate symptom score. Seven symptom-
related questions and one quality-of-life question
QOL Quality of life score. Questionnaires exist to try to quantify
IIEF International index of erectile function. Questionnaire used
to assess erectile dysfunction
PV Prostate volume (<30cc is normal)
PSA Prostate-specic antigen (normal range<4ng/ml)
Qmax Peak urinary ow rate. 12–15ml/s suggests bladder outlet
obstruction
Fig. 29.2 Post-contrast T1 magnetic resonance image of the prostate
after successful bilateral prostate embolization. The non-enhancing
infarcted central gland (white arrowhead) can be seen, surrounded by
enhancing capsular tissue (white arrow)
29 Prostate Artery Embolization
Fig. 29.3 Internal iliac artery anatomy, type A branching pattern. CT
angiogram of the pelvis. Superior gluteal artery (white arrowhead) constituting the posterior division of the internal iliac artery. The inferior
gluteal artery (black arrowhead) arises from the anterior division, as the
gluteo-pudendal trunk, which branches into the inferior gluteal artery,
the internal pudendal artery (black arrow)
Conventional Therapy
Medical therapy is indicated for patients with mild to moderate LUTS.Since the 1980s, the mainstay of therapy has been
two classes of drugs, 5-α-reductase inhibitors and α-1 blocking agents [20]. 5-α-Reductase inhibitors (e.g., nasteride)
block the conversion of testosterone to DHT, a more potent
androgen. Selective α-1 blockers (e.g., doxazosin and terazosin) block the binding of norepinephrine and result in
decreased smooth muscle tone, which can improve
LUTS.The α-1 blocking agents are typically started as rstline therapy for LUTS, while 5-α-reductase inhibitors are
more effective at treating symptoms caused by enlarged
prostates [20]. The combination of these two therapies has
been shown to be effective at reducing the progression of
LUTS, especially for men with high baseline PSA [21].
Surgical and interventional therapies are reserved for
patients with moderate to severe LUTS or those who have
325
Fig. 29.4 Internal iliac artery anatomy, type A branching pattern.
Digital subtraction angiogram after injection of the left internal iliac
artery. Superior gluteal artery (white arrowhead) constituting the posterior division of the internal iliac artery. The inferior gluteal artery (black
arrowhead) arises from the anterior division, as the gluteo-pudendal
trunk, which branches into the inferior gluteal artery, the internal pudendal artery (black arrow), and the superior vesical artery (white arrow)
failed medical therapy. Several different surgical options are
available for the treatment of BPH [14]. Transurethral resection of the prostate (TURP) remains the gold standard for
treatment of BPH [1]. This technique utilizes a resectoscope
with a cautery loop to surgically resect and aspirate tissue via
retrograde urethral access. TURP has the potential complication of hemorrhage, and PAE may be performed in the setting of post-TURP hemorrhage. Open surgical resection is
reserved for patients with prostates greater than 100g or with
anatomy precluding transurethral approach. Other methods
include laser prostatectomy, transurethral incision of the
prostate, transurethral microwave therapy, and transurethral
needle ablation [14].
326
AT
Inferior
Inferior
Superior
iliac artery
iliac artery
gluteal artery
gluteal artery
Superior
Type C
Type D
T. C. Huber et al.
Internal
Anterior
division
gluteal artery
AP AP
Type
Superior
gluteal artery
gluteal artery
Internal
pudendal artery
Inferior
gluteal artery
Internal iliac
artery
Anterior
division
gluteal artery
ype B
gluteal artery
Internal
pudendal artery
AP AP
Internal
Internal
pudendal artery
Fig. 29.5 Branching patterns described by Yamaki etal. [17]
Interventional Therapy
Prostatic artery embolization was originally used for treatment of
hematuria of prostatic origin. Post-procedurally it was noted that
the prostatic volume was reduced [22]. This gave rise to the idea
that BPH could be treated with transcatheter embolization.
Subsequent studies have demonstrated that prostate vol-
ume can be reduced with embolization of the prostatic ves-
Internal
iliac artery
Superior
Inferior
Anterior
division
Internal
pudendal
artery
sels, with resultant improvement in LUTS. A recent
meta-analysis demonstrated statistically signicant reductions in prostate volume and post-void residual volume, signicant increase in maximum urinary ow rate, and no
change in erectile function at 12months post-embolization
[23]. These ndings are supported by similar earlier analyses [24, 25], indicating that PAE is an effective means of
treating LUTS.
Prostatic artery:
Superior vesical
29 Prostate Artery Embolization
The How To
Prior to the procedure, imaging with CTA or MRA is
performed to evaluate anatomy and prostate volume as
described above. Procedural steps are as follows:
1. Access is obtained via the common femoral artery
or radial artery using the Seldinger technique. This
may be either unilateral or bilateral, although a
unilateral approach is more commonly used.
2. A pelvic angiogram may be performed, although
this is not necessary if a pre-procedure CTA has
been obtained.
3. A 5F catheter is advanced through a vascular sheath.
The catheter is used to select the contralateral internal iliac artery and then the prostatovesical artery.
A pre- procedure CTA can aid in delineating complex anatomical variants. A 2.7F microcatheter
(or smaller) is then used to select the main trunk
giving rise to the individual prostatic vessels
29.6 and 29.7).
4. Cone beam CT scans can be obtained during the
procedure in most modern angiography sites allowing precise characterization of the tissue being
embolized.
5.
an embolic agent such as PVA or microspheres is
injected until stasis.
6. The previously described method is then repeated
on the side ipsilateral to the access, if only one vascular access was obtained.
327
Fig. 29.6 Digital subtraction angiogram of the left prostaticovesicular
artery after embolization. There is absence of lling in the distal
branches, with lling of the more proximal vesicular branches supplying the bladder (black arrow). Prostatic parenchymal contrast staining
related to prior injections is seen
PAE can be performed in the outpatient setting, though
some centers prefer that patients be admitted overnight
for observation. Intravenous antibiotics are continued for
1 week post-procedurally, and nonsteroidal anti-inammatory medications can be used for pain control. Other
medications including phenazopyridine and belladonnaopium suppositories can help control bladder spasms and
pelvic discomfort. Routine followup should be performed
at 1 and 6 months, at a minimum. This should include
assessment of symptoms with IPSS, QoL, and IIEF. While
complications following PAE are uncommon, they can
occur with rectalgia and dysuria being the most common
(Table 29.3).
Internal iliac
artery
artery
Prostatovesical
artery
Inferior vesical
artery
Fig. 29.7 Pelvic vascular anatomy
Urinary bladder
Seminal vesicle
Prostate gland
Anterior branch
posterolateral
branch
328
T. C. Huber et al.
Table 29.3 Most common complications after PAE [23]
Rectalgia or dysuria 10%
Transient acute urinary retention 8%
Transient hematuria 4%
Hematospermia 4%
Mild UTI 3%
UTI Urinary tract infection
References
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12. Bischoff W, Goerttler U.Successful intra-arterial embolization of
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13. Bilhim T, Pereira JA, Fernandes L, Tinto HR, Pisco JM.
Angiographic anatomy of the male pelvic arteries. Am JRoentgenol.
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14. McVary KT, Roehrborn CG, Avins AL, Barry MJ, Bruskewitz RC,
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Part VII
Lower Extremity Interventions
Aortoiliac Disease
AlokB.Bhatt andJamesF.Benenati
Pathophysiology
The worldwide prevalence of peripheral artery disease
(PAD) is estimated at between 3 and 12 percent with nearly
202 million people around the world and 10 million in the
USA alone affected [1]. The incidence of PAD is rising, and
as the US population continues to age, the incidence of PAD
will continue to rise. Its clinical importance is not only
related to the symptoms it causes but also because it is a
coronary artery disease (CAD) equivalent. Even asymptomatic patients with PAD have a signicantly increased risk of
cardiovascular events like myocardial infarction and stroke
[2]. Similar to CAD, its risk factors include smoking, age,
hypertension, chronic kidney disease, hyperlipidemia, male
gender, diabetes mellitus, obesity, family history, and physical inactivity. As is expected, the morbidity and mortality in
patients with PAD are often due to cardiac disease and stroke.
Peripheral arterial disease can be broadly compartmentalized into aortoiliac disease, also known as “inow” disease,
and infrainguinal disease, or “outow” disease. Infrainguinal
disease refers to the common femoral and more peripheral
arteries of the lower extremities. In general, the clinical
severity of peripheral arterial disease can be assessed by the
Rutherford classication, which straties patients into six
categories (Table30.1). Inow disease may involve isolated
segments or a combination of the abdominal aorta, common
iliac, external iliac, and internal iliac (hypogastric) arteries.
In general, patients with aortoiliac disease have a worse
prognosis than patients with infrainguinal disease with
respect to cardiovascular events such as MI and stroke as
well as overall mortality [3].
The presentation of aortoiliac occlusive disease varies
depending on severity of stenosis, distribution of disease, and
A. B. Bhatt • J. F. Benenati (*)
Miami Cardiac and Vascular Institute, Baptist Hospital of Miami,
Department of Interventional Radiology, Miami, FL, USA
e-mail: JamesB@baptisthealth.net
30
Table 30.1 Rutherford classication. Grades 0 and I refer to asymp-
tomatic patients and claudicants, respectively. Grade II and III refers to
patients that have critical limb ischemia. The Rutherford category further subcategorizes patients by the severity of their claudication or critical limb ischemia
Grade Category Clinical Objective criteria
0 0 Asymptomatic Normal treadmill or reactive
I 1 Mild
claudication
I 2 Moderate
claudication
I 3 Severe
claudication
II 4 Ischemic rest
pain
III 5 Minor tissue
loss
III 6 Major tissue
loss
the presence of other sites of disease such as concurrent
infrainguinal disease. Commonly, patients with inow disease present with chronic symptoms. A classic presentation is
intermittent claudication in which patients describe pain as
cramping, which worsens with activity and is quickly relieved
with rest. In this setting, symptoms are often located in the
buttock or thigh (Table30.2). Although intermittent claudication is the “classic” symptom of inow disease, patients will
also commonly present with “atypical” leg pain including
vague leg achiness, heaviness, and joint pain among other
symptoms. It is important to remember that patients with
PAD often have other comorbid conditions such as arthritis,
peripheral neuropathy, and concurrent venous disease which
may confound the diagnosis. In 1 study of 460 PAD patients,
only about 40% of patients with PAD presented with classic
claudication [4]. For this reason, the threshold to evaluate a
hyperemia test
Completes treadmill test; AP
after exercise >50mmHg but at
least 20mmHg lower than
resting value
Between categories 1 and 3
Cannot complete standard
treadmill exercise, and AP after
exercise <50mmHg
Resting AP <40mmHg, at or
barely pulsatile ankle or
metatarsal PVR; TP<30mmHg
Resting AP <60mmHg, ankle
or metatarsal PVR at or barely
pulsatile; TP<40mmHg
Same as category 5
© Springer International Publishing AG, part of Springer Nature 2018
N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_30
331
332
A. B. Bhatt and J. F. Benenati
Table 30.2 Localization of diseased vessel based on symptomology
Location of symptoms Diseased artery
Hip/buttock
claudication
Impotence Aorta, bilateral common iliac, bilateral
Thigh claudication Aortoiliac, common femoral
Calf claudication Aortoiliac, supercial femoral, popliteal
Table 30.3 Ankle-brachial index
>1.3 Non-compressible
0.9–1.3 Normal
0.4–0.9 Mild to moderate PAD
<0.4 Severe PAD
Aorta, common iliac, internal iliac
internal iliac
patient for PAD should be low, even if the symptoms are not
completely typical. First-line evaluation includes obtaining
an ankle-brachial index (ABI) which is a measure of lower
extremity arterial stenosis (Table30.3).
Critical limb ischemia (CLI) is another manifestation of
peripheral arterial disease and refers to chronically and severely
diminished blood ow to an extremity with an ABI less than
0.4. These patients are Rutherford class 4–6 and typically have
multi-segment disease, meaning there is usually a combination
of aortoiliac, femoral, popliteal, and tibial arterial disease. CLI
patients have high morbidity and mortality related to their vascular disease. One meta-analysis found that during a median
follow-up of 12months, all- cause mortality in CLI patients was
22%, and major amputation rate was 22% [5].
Acute aortoiliac occlusive disease is usually the result of
embolization from a central source such as the heart, more
proximal aortic plaque, or in situ thrombosis due to plaque
rupture. Symptoms related to acute occlusions vary based on
which segment of artery is affected and can range from acute
limb ischemia with profound motor and sensory decits to
renal failure, rhabdomyolysis, limb loss, and death [6].
Blue Toe Syndrome
“Blue toe” syndrome refers to ischemic changes within a
digit due to microembolism from more central atherosclerotic disease. Although the source of the cholesterol embolus
may be anywhere within the arterial tree, it will often arise
from plaque within the aorta or iliac arteries. Emboli from
the iliac arteries result in unilateral symptoms, whereas
emboli from the aorta may be unilateral or bilateral.
the classic triad of buttock claudication, impotence, and
absent or diminished femoral pulses.
Fibromuscular Dysplasia
Fibromuscular dysplasia (FMD) is a non-atherosclerotic,
noninammatory condition that is characterized by abnormal
cell development within the arterial wall. Two types of FMD
exist: focal and diffuse. The most common is the multifocal
type which is associated with the typical “string of pearls”
appearance. In FMD, collagen is deposited within the arterial
wall resulting in thick bromuscular ridges, which in turn
causes luminal stenosis. Its clinical manifestations are varied,
and patients with FMD may present with dissection, distal
embolism, lifestyle-limiting claudication, or occlusion [7].
Clinical Indication
As previously mentioned, patients with chronic aortoiliac
occlusive disease classically present with symptoms of
claudication, distal embolization, or critical limb ischemia
(rest pain or non-healing wounds). Even in the absence of
classic symptoms, in patients with leg pain, there should be a
low threshold to evaluate for PAD.
In addition to performing a good history and physical
exam, the best initial steps for evaluating a patient for PAD are
with duplex sonography, ankle-brachial index (ABI), and
pulse volume recordings. The ABI is an excellent way to
detect the presence of PAD as well as determine its severity
(see Table 30.3). Used in conjunction with pulse volume
recordings and duplex sonography, the segment of arterial disease and physiologic signicance of a particular lesion can be
ascertained (Fig.30.1). Once a noninvasive evaluation is completed, CT and MR angiography can help better delineate
important anatomic details prior to proceeding with an intervention. Although both CT and MRI provide valuable information, CT may be more useful in evaluating aortoiliac disease
because it has better spatial resolution than MRI.MRI can be
more valuable in evaluating tibial disease than CT as CT evaluation of small vessels is limited by arterial calcications.
CT and MR have largely replaced the need for diagnostic
arteriography because in aggregate, noninvasive tests can
typically delineate exact location of disease, physiologic
signicance, and anatomic information required to plan
treatment.
Leriche Syndrome
Leriche syndrome is characterized by occlusion of the infrarenal abdominal aorta and both common iliac arteries. It is
typically related to a chronic occlusion and manifests with
Conventional Therapy
Treatment of patients with aortoiliac occlusive disease varies
based on symptomology, comorbidities, and anatomic
distribution of disease. For patients that present with
30 Aortoiliac Disease
333
Fig. 30.1 (a) Patient with a normal ABI and normal pulse volume
recordings suggesting no signicant arterial occlusive disease. If
asymmetrically dampening of the high-thigh waveforms was seen,
this would suggest ipsilateral inow disease. If inow disease is suspected by segmental pressures or pulse volume recordings, then the
common femoral arterial (CFA) Doppler ultrasound waveform
should be reviewed for a monophasic waveform suggesting hemodynamically signicant inow disease. (b) Normal triphasic left CFA
waveform. (c) Monophasic right CFA waveform suggests iliac stenosis or occlusion
334
A. B. Bhatt and J. F. Benenati
Fig. 30.1 (continued)
intermittent claudication, they may initially be managed with
conservative therapy. Modiable risk factors should be
addressed. Smoking cessation programs, strict hemoglobin
A1C control, blood pressure management, and statin therapy
all play a vital role in medically optimizing patients with
PAD. Exercise programs are a mainstay of therapy, and in
fact, supervised exercise training programs improve both
morbidity and mortality in PAD [2]. Revascularization
procedures combined with a supervised exercise program
lead to better outcomes than each do individually [2].
Medications may also help relieve symptoms. Cilostazol is
an oral phosphodiesterase 3 inhibitor that promotes blood
ow and has been shown to increase walking distance in
claudicants [8].
Ever since Charles Dotter rst described angioplasty in
1964, there has been debate regarding when to treat
patients using open surgical versus endovascular techniques. For lesions involving the abdominal aorta and
iliac arteries, conventional surgical options involve various types of relatively morbid arterial bypasses. Types of