Key Points: Schwartz's Principles of Surgery Chapter 23. Arterial Disease

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KEY POINTS
1. Carotid intervention as a preventive strategy should be performed in patients with 50% or greater symptomatic
internal carotid artery stenosis, and those with 80% or greater asymptomatic internal carotid artery stenosis. Carotid
intervention for asymptomatic stenosis between 60% and 79% remains controversial, and is a function of an operator's
stroke rate. The choice of intervention—carotid endarterectomy vs. carotid stenting—remains controversial; currently,
carotid endarterectomy appears to be associated with lower stroke rate, whereas carotid stenting is more suitable under
certain anatomic or physiologic conditions.
2. Abdominal aortic aneurysms should be repaired when the risk of rupture, determined mainly by aneurysm size,
exceeds the risk of death due to perioperative complications or concurrent illness. Endovascular repair is associated with
less perioperative morbidity and mortality compared to open reconstruction, and is preferred for high-risk patients who
meet specific anatomic criteria.
3. Symptomatic mesenteric ischemia should be treated to improve quality of life and prevent bowel infarction. Operative
treatment—bypass—is superior to endovascular intervention, although changes in wire and stent technology have
improved the results of mesenteric stenting in recent series.
4. Aortoiliac occlusive disease can be treated with either endovascular means or open reconstruction, depending on
patient risk stratification, occlusion characteristics, and symptomatology.
5. Claudication is a marker of extensive atherosclerosis, and is mainly managed with risk factor modification and
pharmacotherapy. Only 5% of claudicants will need intervention because of disabling extremity pain. The five-year
mortality of a patient with claudication approaches 30%. Patients with rest pain or tissue loss need expeditious
evaluation and vascular reconstruction to ameliorate the severe extremity pain and prevent limb loss.
6. For infrainguinal occlusive disease, open revascularization is more durable than endovascular treatment. The latter,
however, is associated with significantly less morbidity, may represent the procedure of choice in high-risk patients, and
can provide adequate inflow to treat limited areas of tissue loss.
GENERAL APPROACH TO THE VASCULAR PATIENT

Because the vascular system involves every organ system in our body, the symptoms of vascular disease are as varied
as those encountered in any medical specialty. Lack of adequate blood supply to target organs typically presents with
pain; for example, calf pain with lower extremity (LE) claudication, postprandial abdominal pain from mesenteric
ischemia, and arm pain with axillosubclavian arterial occlusion. In contrast, stroke and transient ischemic attack (TIA)
are the presenting symptoms from middle cerebral embolization as a consequence of a stenosed internal carotid artery
(ICA). The pain syndrome of arterial disease usually is divided clinically into acute and chronic types, with all shades of
severity between the two extremes. Sudden onset of pain can indicate complete occlusion of a critical vessel, leading to
more severe pain and critical ischemia in the target organ, resulting in lower limb gangrene or intestinal infarction.
Chronic pain results from a slower, more progressive atherosclerotic occlusion, which can be totally or partially
compensated by developing collateral vessels. Acute on chronic is another pain pattern in which a patient most likely
has an underlying arterial stenosis that suddenly occludes; for example, the patient with a history of calf claudication
who now presents with sudden, severe acute limb-threatening ischemia. The clinician should always try to understand
and relate the clinical manifestations to the underlying pathologic process.
Vascular History
Appropriate history should be focused on the presenting symptoms related to the vascular system (Table 23-1). Of
particular importance in the previous medical history is noting prior vascular interventions (endovascular or open
surgical), and all vascular patients should have inquiry made about their prior cardiac history and current cardiac
symptoms. Approximately 30% of vascular patients will be diabetic. A history of prior and current smoking status should
be noted.
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Table 23-1 Pertinent Elements in Vascular History
History of stroke or transient ischemic attack
History of coronary artery disease, including previous myocardial infarction and angina
History of peripheral arterial disease
History of diabetes
History of hypertension
History of tobacco use
History of hyperlipidemia
The patient with carotid disease in most cases is completely asymptomatic, having been referred based on the finding of
a cervical bruit or duplex finding of stenosis. Symptoms of carotid territory TIAs include transient monocular blindness
(amaurosis), contralateral weakness or numbness, and dysphasia. Symptoms persisting longer than 24 hours constitute
a stroke. In contrast, the patient with chronic mesenteric ischemia is likely to present with postprandial abdominal pain
and weight loss. The patient fears eating because of the pain, avoids food, and loses weight. It is very unlikely that a
patient with abdominal pain who has not lost weight has chronic mesenteric ischemia.
The patient with LE pain on ambulation has intermittent claudication that occurs in certain muscle groups; for example,
calf pain upon exercise usually reflects superficial femoral artery (SFA) disease, while pain in the buttocks reflects iliac
disease. In most cases, the pain manifests in one muscle group below the level of the affected artery, occurs only with
exercise, and is relieved with rest only to recur at the same location, hence the term window gazers disease. Rest pain
(a manifestation of severe underlying occlusive disease) is constant and occurs in the foot (not the muscle groups),
typically at the metatarsophalangeal junction, and is relieved by dependency. Often, the patient is prompted to sleep
with their foot hanging off one side of the bed to increase the hydrostatic pressure.
Vascular Physical Examination

Specific vascular examination should include abdominal aortic palpation, carotid artery examination, and pulse
examination of the LE (femoral, popliteal, posterior tibial, and dorsalis pedis arteries). The abdomen should be palpated
for an abdominal aortic aneurysm (AAA), detected as an expansile pulse above the level of the umbilicus. It also should
be examined for the presence of bruits. Because the aorta typically divides at the level of the umbilicus, an aortic
aneurysm is most frequently palpable in the epigastrium. In thin individuals, a normal aortic pulsation is palpable, while
in obese patients even large aortic aneurysms may not be detectable. Suspicion of a clinically enlarged aorta should lead
to the performance of an ultrasound scan for a more accurate definition of aortic diameter.
The carotids should be auscultated for the presence of bruits, although there is a higher correlation with coronary artery
disease (CAD) than underlying carotid stenosis. A bruit at the angle of the mandible is a significant finding, leading to
follow-up duplex scanning. The differential diagnosis is a transmitted murmur from a sclerotic or stenotic aortic valve.
The carotid is palpable deep to the sternocleidomastoid muscle in the neck. Palpation, however, should be gentle and
rarely yields clinically useful information.
Upper extremity examination is necessary when an arteriovenous graft is to be inserted in patients who have symptoms
of arm pain with exercise. Thoracic outlet syndrome can result in occlusion or aneurysm formation of the subclavian
artery. Distal embolization is a manifestation of thoracic outlet syndrome; consequently, the fingers should be examined
for signs of ischemia and ulceration. The axillary artery enters the limb below the middle of the clavicle, where it can be
palpated in thin patients. It usually is easily palpable in the axilla and medial upper arm. The brachial artery is most
easily located at the antecubital fossa immediately medial to the biceps tendon. The radial artery is palpable at the wrist
anterior to the radius.
For LE vascular examination, the femoral pulse usually is palpable midway between the anterior superior iliac spine and
the pubic tubercle. The popliteal artery is palpated in the popliteal fossa with the knee flexed to 45° and the foot
supported on the examination table to relax the calf muscles. Palpation of the popliteal artery is a bimanual technique.
Both thumbs are placed on the tibial tuberosity anteriorly and the fingers are placed into the popliteal fossa between the
two heads of the gastrocnemius muscle. The popliteal artery is palpated by compressing it against the posterior aspect
of the tibia just below the knee. The posterior tibial pulse is detected by palpation 2 cm posterior to the medial
malleolus. The dorsalis pedis is detected 1 cm lateral to the hallucis longus extensor tendon, which dorsiflexes the great
toe and is clearly visible on the dorsum of the foot. Pulses can be graded using either the traditional four-point scale or
the basic two-point scale system (Table 23-2). The foot also should be carefully examined for pallor on elevation and
rubor on dependency, as these findings are indicative of chronic ischemia. Note should also be made of nail changes and
loss of hair. Ulceration and other findings specific to disease states are described in relevant sections below.
Table 23-2 Grading Scales for Peripheral Pulses
Traditional Scale Basic Scale

4+ Normal 2+ Normal
3+ Slightly reduced 1+ Diminished
2+ Markedly reduced 0 Absent
1+ Barely palpable — —
0 Absent — —
After reconstructive vascular surgery, the graft may be available for examination, depending on its type and course. The
in situ LE graft runs in the subcutaneous fat and can be palpated along most of its length. A change in pulse quality,
aneurysmal enlargement, or a new bruit should be carefully noted. Axillofemoral grafts, femoral-to-femoral grafts, and
arteriovenous access grafts usually can be easily palpated as well.
Noninvasive Diagnostic Evaluation of the Vascular Patient

ANKLE-BRACHIAL INDEX
There is increasing interest in the use of the ankle-brachial index (ABI) to evaluate patients at risk for cardiovascular
events. An ABI <0.9 correlates with increased risk of myocardial infarction and indicates significant, although perhaps
asymptomatic, underlying peripheral vascular disease. The ABI is determined in the following ways. Blood pressure (BP)
is measured in both upper extremities using the highest systolic BP as the denominator for the ABI. The ankle pressure
is determined by placing a BP cuff above the ankle and measuring the return to flow of the posterior tibial and dorsalis
pedis arteries using a pencil Doppler probe over each artery. The ratio of the systolic pressure in each vessel divided by
the highest arm systolic pressure can be used to express the ABI in both the posterior tibial and dorsalis pedis arteries
(Fig. 23-1). Normal is more than 1. Patients with claudication typically have an ABI in the 0.5 to 0.7 range, and those
with rest pain are in the 0.3 to 0.5 range. Those with gangrene have an ABI of <0.3. These ranges can vary depending
on the degree of compressibility of the vessel. The test is less reliable in patients with heavily calcified vessels. Due to
noncompressibility, some patients such as diabetics and those with end-stage renal disease may have an ABI of 1.40 or
greater and require additional noninvasive diagnostic testing to evaluate for peripheral arterial disease (PAD).
Alternative tests include toe-brachial pressures, pulse volume recordings, transcutaneous oxygen measurements, or
vascular imaging (duplex ultrasound).
Fig. 23-1.
Calculating the ankle-brachial index.
SEGMENTAL LIMB PRESSURES

By placing serial BP cuffs down the LE and then measuring the pressure with a Doppler probe as flow returns to the
artery below the cuff, it is possible to determine segmental pressures down the leg. These data can then be used to infer
the level of the occlusion. The systolic pressure at each level is expressed as a ratio, with the highest systolic pressure in
the upper extremities as the denominator. Normal segmental pressures commonly show high thigh pressures 20 mmHg
or greater in comparison to the brachial artery pressures. The low thigh pressure should be equivalent to brachial
pressures. Subsequent pressures should fall by no more than 10 mmHg at each level. A pressure gradient of 20 mmHg
between two subsequent levels is usually indicative of occlusive disease at that level. The most frequently used index is
the ratio of the ankle pressure to the brachial pressure, the ABI. Normally the ABI is >1.0, and a value <0.9 indicates
some degree of arterial obstruction and has been shown to be correlated with an increased risk of coronary heart
disease.1 Limitations of relying on segmental limb pressures include: (a) missing isolated moderate stenoses (usually
iliac) that produce little or no pressure gradient at rest; (b) falsely elevated pressures in patients with diabetes and end-
stage renal disease; and (c) the inability to differentiate between stenosis and occlusion.2 Patients with diabetes and
end-stage renal disease have calcified vessels that are difficult to compress, thus rendering this method inaccurate, due
to recording of falsely elevated pressure readings. Noncompressible arteries yield ankle systolic pressures of 250 mmHg
or greater and an ABI of >1.40. In this situation, absolute toe and ankle pressures can be measured to gauge critical
limb ischemia. Ankle pressures <50 mmHg or toe pressures <30 mmHg are indicative of critical limb ischemia. The toe
pressure is normally 30 mmHg less than the ankle pressure, and a toe-brachial index of <0.70 is abnormal. False-
positive results with the toe-brachial index are unusual. The main limitation of this technique is that it may be
impossible to measure pressures in the first and second toes due to pre-existing ulceration.
PULSE VOLUME RECORDING

In patients with noncompressible vessels, segmental plethysmography can be used to determine underlying arterial
occlusive disease. Cuffs placed at different levels on the leg detect changes in leg volume and produce a pulse volume
recording (PVR) when connected to a plethysmograph (Fig. 23-2). To obtain accurate PVR waveforms the cuff is inflated
to 60 to 65 mmHg to detect volume changes without causing arterial occlusion. Pulse volume tracings are suggestive of
proximal disease if the upstroke of the pulse is not brisk, the peak of the wave tracing is rounded, and there is
disappearance of the dicrotic notch.
Fig. 23-2.
A. Pulse volume recording is done by connecting blood pressure cuffs and plethysmograph to various levels of the leg. B. Typical
report of peripheral vascular study with arterial segmental pressure measurement plus Doppler evaluation of the lower extremity.
Although isolated segmental limb pressures and PVR measurements are 85% accurate when compared with angiography
in detecting and localizing significant atherosclerotic lesions, when used in combination, accuracy approaches 95%.3 For
this reason, it is suggested that these two diagnostic modalities be used in combination when evaluating PAD.
Radiological Evaluation of the Vascular Patient

ULTRASOUND
Ultrasound examinations are relatively time consuming, require experienced technicians, and may not visualize all
arterial segments. Doppler waveform analysis can suggest atherosclerotic occlusive disease if the waveforms in the
insonated arteries are biphasic, monophasic, or asymmetrical. B-mode ultrasonography provides black and white, real-
time images. B-mode ultrasonography does not evaluate blood flow; thus, it cannot differentiate between fresh
thrombus and flowing blood, which have the same echogenicity. Calcification in atherosclerotic plaques will cause
acoustic shadowing. B-mode ultrasound probes cannot be sterilized. Use of the B-mode probe intraoperatively requires a
sterile covering and gel to maintain an acoustic interface. Experience is needed to obtain and interpret images
accurately. Duplex ultrasonography entails performance of B-mode imaging, spectral Doppler scanning, and color flow
duplex scanning. The caveat to performance of duplex ultrasonography is meticulous technique by a certified vascular
ultrasound technician, so that the appropriate 60° Doppler angle is maintained during insonation with the ultrasound
probe. Alteration of this angle can markedly alter waveform appearance and subsequent interpretation of velocity
measurements. Direct imaging of intra-abdominal vessels with duplex ultrasound is less reliable because of the difficulty
in visualizing the vessels through overlying bowel. These disadvantages currently limit the applicability of duplex
scanning in the evaluation of aortoiliac and infrapopliteal disease. In a recent study, duplex ultrasonography had lower
sensitivity in the calculation of infrapopliteal vessel stenosis in comparison to conventional digital subtraction or
computer tomography angiography.4 Few surgeons rely solely on duplex ultrasonography for preoperative planning in LE
revascularizations. However, in the hands of experienced ultrasonographers, LE arteries can be assessed accurately by
determining the significance of velocity criteria across the arterial stenosis. Duplex scanning is unable to evaluate
recently implanted polytetrafluoroethylene (PTFE) and polyester (Dacron) grafts because they contain air, which
prevents ultrasound penetration.
COMPUTED TOMOGRAPHY ANGIOGRAPHY

Computed tomography angiography (CTA) is a noninvasive, contrast-dependent method for imaging the arterial system.
It depends on IV infusion of iodine-based contrast agents. The patient is advanced through a rotating gantry, which
images serial transverse slices. The contrast-filled vessels can be extracted from the slices and rendered in three-
dimensional format (Fig. 23-3). The extracted images can also be rotated and viewed from several different directions
during postacquisition image processing. This technology has been advanced as a consequence of aortic endografting.
CTA provides images for postprocessing that can be used to display the aneurysm in a format that demonstrates
thrombus, calcium, lumen, and the outer wall, and allows "fitting" of a proposed endograft into the aneurysm (Fig. 23-
4). CTA is increasingly being used to image the carotid bifurcation, and as computing power increases, the speed of
image acquisition and resolution will continue to increase. The major limitations of multidetector CTA are use of contrast
and presence of artifacts caused by calcification and stents. CTA can overestimate the degree of instent stenosis, while
heavy calcification can limit the diagnostic accuracy of the method by causing a ''blooming artifact."5 The artifacts can
be overcome with alteration in image acquisition technique. There are no randomized trials to document the superiority
of multidetector CTA over traditional angiography, but there is emerging evidence to support the claim that
multidetector CTA has sensitivity, specificity, and accuracy that rival invasive angiography.5
Fig. 23-3.
two patients with lower leg claudication. A. A 50-year-old man with an occluded right superficial femoral artery (single long
arrow) with reconstituted superficial femoral artery at the level of midthigh. Arterial calcifications (short arrows) in the bilateral
distal superficial femoral arteries. B. A 53-year-old man with occluded right common iliac artery (double arrows).
Fig. 23-4.
Three-dimensional computed tomographic angiogram of an abdominal aortic aneurysm that displays various aneurysm
components, including thrombus, aortic calcification, blood circulation, and aneurysm wall.
MAGNETIC RESONANCE ANGIOGRAPHY

Magnetic resonance angiography (MRA) has the advantage of not requiring iodinated contrast agents to provide vessel
opacification (Fig. 23-5). Gadolinium is used as a contrast agent for MRA studies, and as it is generally not nephrotoxic,
it can be used in patients with elevated creatinine. MRA is contraindicated in patients with pacemakers, defibrillators,
spinal cord stimulators, intracerebral shunts, cochlear implants, and cranial clips. Patients with claustrophobia may
require sedation to be able to complete the test. The presence of metallic stents causes artifacts and signal dropout;
however, these can be dealt with using alternations in image acquisition and processing. Nitinol stents produce minimal
artifact.6 Compared to other modalities, MRA is relatively slow and expensive. However, due to its noninvasive nature
and decreased nephrotoxicity, MRA is being used more frequently for imaging vasculature in various anatomic
distributions.
Fig. 23-5.
Magnetic resonance angiogram of aortic arch and carotid arteries. This study can provide a three-dimensional analysis of vascular
structures such as aortic arch branches, as well as carotid and vertebral arteries.
DIAGNOSTIC ANGIOGRAPHY
Diagnostic angiography is considered the gold standard in vascular imaging. In many centers, its use is rapidly
decreasing due to the development of noninvasive imaging modalities such as duplex arterial mapping, CTA, and MRA.
Nevertheless, contrast angiography still remains in widespread use. The essential aspects of angiography are vascular
access and catheter placement in the vascular bed that requires examination. The imaging system and the contrast
agent are used to opacify the target vessel. Although in the past this function has largely been delegated to the
interventional radiology service, an increasing number of surgeons are performing this procedure and following the
diagnostic imaging with immediate surgical or endovascular intervention. There are several considerations when relying
on angiography for imaging.
Approximately 70% of atherosclerotic plaques occur in an eccentric location within the blood vessel; therefore, images
can be misleading when trying to evaluate stenoses because angiography is limited to a uniplanar "lumenogram." With
increased use of intravascular stent deployment, it has been also noted that assessment of stent apposition and stent
position in relation to surrounding branches may be inaccurate. Furthermore, angiography exposes the patient to the
risks of both ionizing radiation and intravascular contrast. Nevertheless, contrast angiography remains the most
common invasive method of vascular investigation for both diagnostic and therapeutic intervention. The angiogram
usually provides the final information needed to decide whether or not to proceed with operation or endovascular
interventions.
Digital subtraction angiography (DSA) offers some advantages over conventional cut-film angiography, such as excellent
visualization despite use of lower volumes of contrast media. In particular when multilevel occlusive lesions limit the
amount of contrast reaching distal vessels, supplemental use of digital subtraction angiographic techniques may
enhance visualization and definition of anatomy. Intra-arterial DSA uses a portable, axially rotatable imaging device that
can obtain views from different angles. DSA also allows for real-time video replay (Fig. 23-6). An entire extremity can be
filmed with DSA, using repeated injections of small amounts of contrast agent to obtain sequential angiographic images,
the so-called pulse-chase technique.
Fig. 23-6.
Digital subtraction angiography provides excellent visualization of intravascular circulation with intra-arterial contrast
administration. As depicted in this digital subtraction angiography study, multilevel lesions are demonstrated that include a focal
left iliac artery stenosis (large arrow), right superficial femoral occlusion (curved arrows), left superficial femoral stenosis (small
arrow), and multiple tibial artery stenoses (arrowheads).
PREOPERATIVE CARDIAC EVALUATION

The most important and controversial aspect of preoperative evaluation in patients with atherosclerotic disease requiring
surgical intervention is the detection and subsequent management of associated CAD.7 Several studies have
documented the existence of significant CAD in 40 to 50% or more of patients requiring peripheral vascular
reconstructive procedures, 10 to 20% of whom may be relatively asymptomatic largely because of their inability to
exercise.8 Myocardial infarction is responsible for the majority of both early and late postoperative deaths. Most
available screening methods lack sensitivity and specificity to predict postoperative cardiac complications. There have
been conflicting reports regarding the utility of preoperative dipyridamole-thallium nuclear imaging or dobutamine-
echocardiography to stratify vascular patients in terms of perioperative cardiac morbidity and mortality. In nearly one
half of patients, thallium imaging proves to be unnecessary because cardiac risk can be predicted by clinical information
alone.7 Even with coronary angiography, it is difficult to relate anatomic findings to functional significance, and hence,
surgical risk. There are no data confirming that percutaneous coronary interventions or surgical revascularization before
vascular surgical procedures impacts mortality or incidence of myocardial infarctions. In fact, coronary angiography is
associated with its own inherent risks, and patients undergoing coronary artery bypass grafting or coronary
percutaneous transluminal angioplasty (PTA) before needed aortoiliac reconstructions are subjected to the risks and
complications of both procedures.
The Coronary Artery Revascularization Prophylaxis trial showed that coronary revascularization in patients with
peripheral vascular disease and significant CAD, who are considered high risk for perioperative complications, did not
reduce overall mortality or perioperative myocardial infarction.9 Additionally, patients who underwent prophylactic
coronary revascularization had significant delays before undergoing their vascular procedure and increased limb
morbidity compared to patients who did not. Studies do support improvement in cardiovascular and overall prognosis
with medical optimization of patients. Therefore, use of perioperative beta blockade, as well as use of antiplatelet
medication, statins, and angiotensin-converting enzyme (ACE) inhibitors is encouraged in vascular patients.10,11
BASIC PRINCIPLES OF ENDOVASCULAR THERAPY

Cardiovascular disease remains a major cause of mortality in the developed world since the beginning of the twenty-first
century. Although surgical revascularization has played a predominant role in the management of patients with vascular
disease, the modern treatment paradigms have evolved significantly with increased emphasis of catheter-based
percutaneous interventions over the past two decades. The increasing role of this minimally invasive vascular
intervention is fueled by various factors, including rapid advances in imaging technology and reduced morbidity and
mortality in endovascular interventions, as well as faster convalescence following percutaneous therapy when compared
to traditional operations. There is little doubt that, with continued device development and refined image-guided
technology, endovascular intervention will provide improved clinical outcomes and play an even greater role in the
treatment of vascular disease.
The technique of percutaneous access for both the diagnostic and therapeutic management of vascular disease has
resulted in tremendous changes in the practice of several subspecialties, including interventional radiology, invasive
cardiology, and vascular surgery. The development of catheter and endoscopic instrumentation allows the vascular
surgeon to operate via an intra- or extraluminal route. Endovascular techniques are now able to treat the full spectrum
of vascular pathology, including stenoses and occlusions resulting from several etiologies, aneurysmal pathology, and
traumatic lesions. Many of these procedures have only recently been developed, and, as such, have not been
investigated in a manner that would enable an accurate comparison with the more traditional methods of open surgical
intervention. Long-term follow-up for these procedures is frequently lacking. However, because of the potential to treat
patients with decreased mortality and morbidity, endovascular skills and techniques are being adopted into mainstream
vascular surgery.
Needles and Access

Needles are used to achieve percutaneous vascular access. The size of the needle will be dictated by the diameter of the
guidewire used. Most often, an 18-gauge needle is used, as it will accept a 0.035-in guidewire. A 21-gauge
micropuncture needle will accept a 0.018-in guidewire. The most popular access needle is the Seldinger needle, which
can be used for single- and double-wall puncture techniques.
Femoral arterial puncture is the most common site for access. The common femoral artery (CFA) is punctured over the
medial third of the femoral head, which is landmarked using fluoroscopy. The single-wall puncture technique requires a
sharp, beveled needle tip and no central stylet. The anterior wall of the vessel is punctured with the bevel of the needle
pointing up and pulsatile back-bleeding indicates an intraluminal position. This method is most useful for graft
punctures, patients with abnormal clotting profiles, or if thrombolytic therapy is anticipated. Once the needle assumes
an intraluminal position, verified by pulsatile back-bleeding, the guidewire may be advanced. This is always passed
gently and under fluoroscopic guidance to avoid subintimal dissection or plaque disruption. Double-wall puncture
techniques are performed with a blunt needle that has a removable inner cannula. The introducer needle punctures both
walls of the artery and is withdrawn until bleeding is obtained to confirm intraluminal position before advancing a
guidewire. There can be troublesome bleeding from the posterior arterial wall puncture; therefore, single puncture
techniques are preferred.
Retrograde femoral access is the most common arterial access technique (Fig. 23-7). The advantages of this technique
include the size and fixed position of the CFA, as well as the relative ease of compression against the femoral head at
the end of the procedure. Care should be taken to avoid puncturing the external iliac artery (EIA) above the inguinal
ligament because this can result in retroperitoneal hemorrhage secondary to ineffective compression of the puncture
site. Likewise, puncturing too low, at or below the CFA bifurcation can result in thrombosis or pseudoaneurysm
formation of the SFA or profunda femoris artery (PFA). Antegrade femoral access is more difficult than retrograde
femoral access and there is a greater tendency to puncture the SFA, but it is invaluable when the aortic bifurcation
cannot be traversed or when devices are not long enough to reach a lesion from a contralateral femoral access
approach. Occasionally, when the distal aorta or bilateral iliac arteries are inaccessible because of the extent of
atherosclerotic lesions, scarring, or presence of bypass conduits, the brachial artery must be used to obtain access for
diagnostic and therapeutic interventions. The left brachial artery is punctured, as this avoids the origin of the carotid
artery and thus decreases the risk of catheter-related emboli to the brain. The artery is accessed with a micropuncture
needle just proximal to the antecubital crease. The use of brachial access is associated with a higher risk of thrombosis
and nerve injuries than femoral access.
Fig. 23-7.
A. Antegrade femoral artery access. The needle is inserted just below the inguinal ligament in the common femoral artery
whereby the guidewire is inserted in the ipsilateral superficial femoral artery. B. Brachial artery approach. The needle is inserted
in a retrograde fashion in the brachial artery just above the antecubital fossa, whereby the guidewire is next inserted in the
brachial artery.
Guidewires
Guidewires are used to introduce, position, and exchange catheters. A guidewire generally has a flexible and stiff end. In
general, only the flexible end of the guidewire is placed in the vessel. All guidewires are composed of a stiff inner core
and an outer tightly coiled spring that allows a catheter to track over the guidewire. There are five essential
characteristics of guidewires: size, length, stiffness, coating, and tip configuration.
Guidewires come in different maximum transverse diameters ranging from 0.011 to 0.038 in. For most aortoiliac
procedures, a 0.03-in wire is most commonly used while the smaller diameter 0.018-in guidewires are reserved for
selective small vessel angiography, such as infrageniculate or carotid lesions. In addition to diameter size, guidewires
come in varying lengths usually ranging from 180 to 260 cm in length. Increasing the length of the wire always makes it
more difficult to handle and increases the risk of contamination. While performing a procedure, it is important to
maintain the guidewire across the lesion until the completion arteriogram has been satisfactorily completed.
The stiffness of the guidewire is also an important characteristic. Stiff wires allow for passage of large aortic stent graft
devices without kinking. They are also useful when trying to perform sheath or catheter exchanges around a tortuous
artery. An example of a stiff guidewire is the Amplatz wire. Hydrophilic coated guidewires, such as the Glidewire, have
become invaluable tools for assisting in difficult catheterizations. The coating is primed by bathing the guidewire in
saline solution. The slippery nature of this guidewire along with its torque capability significantly facilitates passage of
this guidewire in difficult catheterizations. Guidewires also come in various tip configurations. Angled tip wires like the
angled Glidewire can be steered to manipulate a catheter across a tight stenosis or to select a specific branch of a
vessel. The Rosen wire has a soft curled end that makes it ideal for renal artery stenting. The soft curl of this wire
prevents it from perforating small renal branch vessels.
Hemostatic Sheaths
The hemostatic sheath is a device through which endovascular procedures are performed. The sheath acts to protect the
vessel from injury as wires and catheters are introduced (Fig. 23-8). A one-way valve prevents bleeding through the
sheath, and a side port allows contrast or heparin flushes to be administered during the procedure. Sheaths are sized by
their inner diameter. The most commonly used sheaths for percutaneous access have a 5Fr to 9Fr inner diameter, but
with open surgical exposure of the CFA, sheaths as large as 26Fr can be introduced. Sheaths also vary in length and
long sheaths are available so that interventions remote from the site of arterial access can be performed.
Fig. 23-8.
All percutaneous endovascular procedures are performed through an introducer sheath (large arrow), which provides an access
conduit from skin to intravascular compartment. The sheath also acts to protect the vessel from injury as guidewires (small
arrows) and catheters are introduced.
Catheters
A wide variety of catheters exist that differ primarily in the configuration of the tip. The multiple shapes permit access to
vessels of varying dimensions and angulations. Catheters are used to perform angiography, protect the passage of
balloons and stents, and can be used to direct the guidewire through tight stenoses or tortuous vessels.
Angioplasty Balloons
Angioplasty balloons differ primarily in their length and diameter, as well as the length of the catheter shaft. As balloon
technology has advanced, lower profiles have been manufactured (i.e., the size that the balloon assumes upon
deflation). Balloons are used to perform angioplasty on vascular stenoses, to deploy stents, and to assist with additional
expansion after insertion of self-expanding stents (Fig. 23-9). Besides length and diameter, operators need to be
familiar with several other balloon characteristics. Noncompliant and low-compliance balloons tend to be inflated to their
preset diameter and offer greater dilating force at the site of stenosis. Low-compliance balloons are the mainstay for
peripheral intervention. Lower profile balloons are less likely to get caught during passage through stents and are easier
to pull out of sheaths. Under fluoroscopic guidance, balloon inflation is performed until the waist of the atherosclerotic
lesion disappears and the balloon is at the full profile. The duration of balloon inflation and pressures used for the
angioplasty depend on the indication for the intervention as well as the location and characteristics of the lesion being
treated. Frequently, several inflations are required to achieve a full profile of the balloon. Occasionally, a lower profile
balloon is needed to predilate the tight stenosis so that the selected balloon catheter can cross the lesion. After inflation,
most balloons do not regain their preinflation diameter and assume a larger profile. Trackability, pushability, and
crossability of the balloon should all be considered when choosing a particular balloon. Lastly, shoulder length is an
important characteristic to consider when selecting a balloon because of the potential to cause injury during
performance of PTA in adjacent arterial segments. There is always risk of causing dissection or rupture during PTA, thus
a completion angiogram is performed while the wire is still in place. Leaving the wire in place provides access for
repeating the procedure, or placing a stent or stent graft if warranted.
Fig. 23-9.
A. An artery with luminal narrowing caused by plaque. B. A balloon angioplasty catheter is positioned within the diseased artery,
which is inflated to enlarge the intravascular channel. C. The plaque is compressed with widened flow lumen as the result of
balloon angioplasty.
Stents
Vascular stents are commonly used after an inadequate angioplasty with dissection or elastic recoil of an arterial
stenosis. They serve to buttress collapsible vessels and help prevent atherosclerotic restenosis. Appropriate indications
for primary stenting of a lesion without an initial trial of angioplasty alone are evolving in manners that are dependent
on the extent and site of the lesion. Stents are manufactured from a variety of metals, including stainless steel,
tantalum, cobalt-based alloy, and nitinol. Vascular stents are classified into two basic categories: balloon-expandable
stents and self-expanding stents.
Self-expanding stents (Fig. 23-10) are deployed by retracting a restraining sheath. They usually consist of Elgiloy (a
cobalt, chromium, nickel alloy) or nitinol (a shape memory alloy composed of nickel and titanium), the latter of which
will contract and assume a heat-treated shape above a transition temperature that depends upon the composition of the
alloy. Self-expanding stents will expand to a final diameter that is determined by stent geometry, hoop strength, and
vessel size. The self-expanding stent is mounted on a central shaft and is placed inside an outer sheath. It relies on a
mechanical spring-like action to achieve expansion. With deployment of these stents, there is some degree of
foreshortening that has to be taken into account when choosing the area of deployment. In this way, self-expanding
stents are more difficult to place with absolute precision. There are several advantages related to self-expanding stents.
Self-expanding stents generally come in longer lengths than balloon-expandable stents and are therefore used to treat
long and tortuous lesions. Their ability to continually expand after delivery allows them to accommodate adjacent
vessels of different size. This makes these stents ideal for placement in the ICA. These stents are always oversized by 1
to 2 mm relative to the largest diameter of normal vessel adjacent to the lesion to prevent immediate migration.
Fig. 23-10.
Self-expanding stents are made of tempered stainless steel or nitinol, an alloy of nickel and titanium, and are restrained when
folded inside a delivery catheter. After release from the restraining catheter, the self-expanding stents will expand to a final
diameter that is determined by stent geometry, hoop strength, and vessel size.
Balloon-expandable stents are usually composed of stainless steel, mounted on an angioplasty balloon, and deployed by
balloon inflation (Fig. 23-11). They can be manually placed on a chosen balloon catheter or obtained premounted on a
balloon catheter. The capacity of a balloon-expandable stent to shorten in length during deployment depends on both
stent geometry and the final diameter to which the balloon is expanded. These stents are more rigid and are associated
with a shorter time to complete endothelialization. They are often of limited flexibility and have a higher degree of crush
resistance when compared to self-expanding. This makes them ideal for short-segment lesions, especially those that
involve the ostia, such as proximal common iliac or renal artery stenosis.
Fig. 23-11.
In a balloon-expandable stent, the stent is premounted on a balloon catheter. The balloon stretches the stent members beyond
their elastic limit. The stent is deployed by full balloon expansion. This type of stent has a higher degree of crush resistance when
compared to self-expanding. This makes them ideal for short-segment calcified ostial lesions.
The most exciting area of development in stents is the evolution of drug-eluting stents (DES). These stents are usually
composed of nitinol and have various anti-inflammatory drugs bonded to them. Over time, the stents release the drug
into the surrounding arterial wall and help prevent restenosis. Numerous randomized controlled trials have proven their
benefit in coronary arteries.12 Clinical studies have similarly proved early efficacy of DES in the treatment of PAD.
Stent Grafts
The combination of a metal stent covered with fabric gave birth to the first stent grafts. Covered stents have been
designed with either a surrounding PTFE or polyester fabric and have been used predominantly for treatment of
traumatic vascular lesions, including arterial disruption and arteriovenous fistulas (Fig. 23-12). However, these devices
may well find a growing role in treatment of iliac or femoral arterial occlusive disease as well as popliteal aneurysms.
Fig. 23-12.
A stent graft is a combination of a metal stent covered with fabric that is commonly used for aneurysm exclusion.
Endovascular aneurysm repair using the concept of stent grafts was initiated by Parodi in 1991.13 Since that time, a
large number of endografts have been inserted under the auspices of clinical trials at first and now as Food and Drug
Administration (FDA)-approved devices. Current FDA-approved devices include (a) AneuRx device (Medtronic/AVE,
Santa Rosa, Calif), (b) Gore Excluder device (WL Gore & Associates, Flagstaff, Ariz), (c) Endologix Powerlink device
(Endologix Inc., Irvine, Calif), (d) Zenith device (Cook Inc., Bloomington, Ind), and (e) Talent device (Medtronic/AVE,
Santa Rosa, Calif). All of these devices require that patients have an infrarenal aneurysm with at least a 15-mm
proximal aortic neck below the renal arteries, and not >60° of angulation. For those patients with associated common
iliac artery (CIA) aneurysmal disease, endovascular treatment can be achieved by initial coil embolization of the
ipsilateral hypogastric artery with extension of the endovascular device into the EIA. Clinical trials are underway with
devices that will expand indications to aneurysms involving the visceral segment of the abdominal aorta. The FDA has
similarly approved several thoracic endografts for the treatment of descending thoracic aortic aneurysm. Early studies
have demonstrated short-term efficacy of thoracic aortic devices in the treatment of traumatic aortic transections, and
aortic dissections.14–16 A larger experience with these devices exists in both Europe and Asia, and trials are underway in
the United States with several devices.
CAROTID ARTERY DISEASE

Atherosclerotic occlusive plaque is by far the most common pathology seen in the carotid artery bifurcation. Thirty to
60% of all ischemic strokes are related to atherosclerotic carotid bifurcation occlusive disease. In the following section,
discussion will be focused on clinical presentation, diagnosis, and management, including medical therapy, surgical
carotid endarterectomy, and stenting of atherosclerotic carotid occlusive disease. In the second part of the section, a
brief review will be focused on other less common non-atherosclerotic diseases involving the extracranial carotid artery,
including kink and coil, fibromuscular dysplasia (FMD), arterial dissection, aneurysm, radiation arteritis, Takayasu's
arteritis, and carotid body tumor.
Epidemiology and Etiology of Carotid Occlusive Disease

Approximately 700,000 Americans suffer a new or recurrent stroke each year.17 Eighty-five percent of all strokes are
ischemic and 15% are hemorrhagic. Hemorrhagic strokes are caused by head trauma or spontaneous disruption of
intracerebral blood vessels. Ischemic strokes are due to hypoperfusion from arterial occlusion, or less commonly due to
decreased flow resulting from proximal arterial stenosis and poor collateral network. Common causes of ischemic
strokes are cardiogenic emboli (35%), carotid artery disease (30%), lacunar (10%), miscellaneous (10%), and
idiopathic (15%).17 The term cerebrovascular accident (CVA) often is used interchangeably to refer to an ischemic
stroke. A transient ischemic attack (TIA) is defined as a temporary focal cerebral or retinal hypoperfusion state that
resolves spontaneously within 24 hours after its onset. However, the majority of TIAs resolve within minutes, and longer
lasting neurologic deficits more likely represent a stroke. Recently, the term brain attack has been coined to refer to an
acute stroke or TIA, denoting the condition as a medical emergency requiring immediate attention, similar to a heart
attack.
Stroke due to carotid bifurcation occlusive disease usually is caused by atheroemboli (Fig. 23-13). The carotid
bifurcation is an area of low-flow velocity and low-shear stress. As the blood circulates through the carotid bifurcation,
there is separation of flow into the low-resistance ICA, and the high-resistance external carotid artery. Characteristically,
atherosclerotic plaque forms in the outer wall opposite to the flow divider (Fig. 23-14). Atherosclerotic plaque formation
is complex, beginning with intimal injury, platelet deposition, smooth muscle cell proliferation, and fibroplasia, and
leading to subsequent luminal narrowing. With increasing degree of stenosis in the ICA, flow becomes more turbulent,
and the risk of atheroembolization escalates. The severity of stenosis is commonly divided into three categories
according to the luminal diameter reduction: mild (less than 50%), moderate (50 to 69%), and severe (70 to 99%).
Severe carotid stenosis is a strong predictor for stroke.18 In turn, a prior history of neurologic symptoms (TIA or stroke)
is an important determinant for recurrent ipsilateral stroke. The risk factors for the development of carotid artery
bifurcation disease are similar to those causing atherosclerotic occlusive disease in other vascular beds. Increasing age,
male gender, hypertension, tobacco smoking, diabetes mellitus, homocysteinemia, and hyperlipidemia are well-known
predisposing factors for the development of atherosclerotic occlusive disease.
Fig. 23-13.
Stroke due to carotid bifurcation occlusive disease is usually caused by atheroemboli arising from the internal carotid artery,
which provides the majority of blood flow to the cerebral hemisphere. With increasing degree of stenosis in the carotid artery,
flow becomes more turbulent, and the risk of atheroembolization escalates.
Fig. 23-14.
A. The carotid bifurcation is an area of low-flow velocity and low-shear stress. As the blood circulates through the carotid
bifurcation, there is separation of flow into the low-resistance internal carotid artery and the high-resistance external carotid
artery. B. The carotid atherosclerotic plaque typically forms in the outer wall opposite to the flow divider due in part to the effect
of the low-shear stress region, which also creates a transient reversal of flow during cardiac cycle.
Clinical Manifestations of Cerebral Ischemia

TIA is a focal loss of neurologic function, lasting for <24 hours. Crescendo TIAs refer to a syndrome comprising repeated
TIAs within a short period of time that is characterized by complete neurologic recovery in between. At a minimum the
term should probably be reserved either for those with daily events or multiple resolving attacks within 24 hours.
Hemodynamic TIAs represent focal cerebral events that are aggravated by exercise or hemodynamic stress and typically
occur after short bursts of physical activity, postprandially or after getting out of a hot bath. It is implied that these are
due to severe extracranial disease and poor intracranial collateral recruitment. Reversible ischemic neurologic deficits
refer to ischemic focal neurologic symptoms lasting longer than 24 hours but resolving within 3 weeks. When a
neurologic deficit lasts longer than 3 weeks, it is considered a completed stroke. Stroke in evolution refers to
progressive worsening of the neurologic deficit, either linearly over a 24-hour period, or interspersed with transient
periods of stabilization and/or partial clinical improvement.
The patients who suffer CVAs typically present with three categories of symptoms, including ocular symptoms,
sensory/motor deficit, and/or higher cortical dysfunction. The common ocular symptoms associated with extracranial
carotid artery occlusive disease include amaurosis fugax and presence of Hollenhorst plaques. Amaurosis fugax,
commonly referred to as transient monocular blindness, is a temporary loss of vision in one eye that patients typically
describe as a window shutter coming down or gray shedding of the vision. This partial blindness usually lasts for a few
minutes and then resolves. Most of these phenomena (>90%) are due to embolic occlusion of the main artery or the
upper or lower divisions. Monocular blindness progressing over a 20-minute period suggests a migrainous etiology.
Occasionally, the patient will recall no visual symptoms while the optician notes a yellowish plaque within the retinal
vessels, which is also known as the Hollenhorst plaque. These are frequently derived from cholesterol embolization from
the carotid bifurcation and warrant further investigation. Additionally, several ocular symptoms may be caused by
microembolization from the extracranial carotid diseases, including monocular vision loss due to retinal artery or optic
nerve ischemia, the ocular ischemia syndrome, and visual field deficits secondary to cortical infarction and ischemia of
the optic tracts. Typical motor and/or sensory symptoms associated with CVAs are located in either an ipsilateral or
contralateral neurologic deficit. Ischemic events tend to have an abrupt onset, with the severity of the insult being
apparent from the onset and not usually associated with seizures or paraesthesia. In contrast, they represent loss or
diminution of neurologic function. Furthermore, motor or sensory deficits can be unilateral or bilateral, with the upper
and lower limbs being variably affected depending on the site of the cerebral lesion.
The combination of a motor and sensory deficit in the same body territory is suggestive of a cortical thromboembolic
event as opposed to lacunar lesions secondary to small vessel disease of the penetrating arterioles. However, a small
proportion of the latter may present with a sensorimotor stroke secondary to small vessel occlusion within the posterior
limb of the internal capsule. Pure sensory and pure motor strokes and those strokes where the weakness affects one
limb only or does not involve the face are more typically seen with lacunar as opposed to cortical infarction. A number of
higher cortical functions, including speech and language disturbances, can be affected by thromboembolic phenomena
from the carotid artery with the most important clinical example for the dominant hemisphere being dysphasia or
aphasia, and visuospatial neglect being an example of nondominant hemisphere injury.
Diagnostic Evaluation
Duplex ultrasonography is the most widely used screening tool to evaluate for atherosclerotic plaque and stenosis of the
extracranial carotid artery. It is also commonly used to monitor patients serially for progression of disease, or after
intervention (carotid endarterectomy or angioplasty). Duplex ultrasound of the carotid artery combines B-mode gray-
scale imaging and Doppler waveform analysis. Characterization of the carotid plaque on gray-scale imaging provides
useful information about its composition. However, there are currently no universal recommendations that can be made
based solely on the sonographic appearance of the plaque. On the other hand, criteria have been developed and well
refined for grading the degree of carotid stenosis based primarily on Doppler-derived velocity waveforms.
The external carotid artery has a high-resistance flow pattern with a sharp systolic peak and a small amount of flow in
diastole. In contrast, a normal ICA will have a low-resistance flow pattern with a broad systolic peak and a large amount
of flow during diastole. The flow pattern in the common carotid artery (CCA) resembles that in the ICA, as 80% of the
flow is directed to the ICA, with waveforms that have broad systolic peaks and a moderate amount of flow during
diastole. Conventionally, velocity measurements are recorded in the common, external carotid bulb, and the proximal,
mid-, and distal portions of the ICA. Characteristically, the peak systolic velocity is increased at the site of the vessel
stenosis. The end-diastolic velocity is increased with a greater degree of stenosis. In addition, stenosis of the ICA can
lead to color shifts with color mosaics indicating a poststenotic turbulence. Dampening of the Doppler velocity
waveforms are typically seen in areas distal to severe carotid stenosis where blood flow is reduced. It is well known that
occlusion of the ipsilateral ICA can lead to a "falsely" elevated velocity on the contralateral side due to an increase in
compensatory blood flow. In the presence of a high-grade stenosis or occlusion of the ICA, the ipsilateral CCA displays
high flow resistance waveforms, similar to that seen in the external carotid artery. If there is a significant stenosis in the
proximal CCA, its waveforms may be dampened with low velocities.
The Doppler grading systems of carotid stenosis were initially established by comparison to angiographic findings of
disease. Studies have shown variability in the measurements of the duplex properties by different laboratories, as well
as heterogeneity in the patient population, study design, and techniques. One of the most commonly used classifications
was established at the University of Washington School of Medicine in Seattle. Diameter reduction of 50 to 79% is
defined by peak systolic velocity >125 cm/sec with extensive spectral broadening. For stenosis in the range of 80 to
99%, the peak systolic velocity is >125 cm/sec and peak diastolic velocity is >140 cm/sec. The ratio of internal carotid
to common carotid artery (ICA/CCA) peak systolic velocity has also been part of various ultrasound diagnostic
classifications. A ratio >4 is a great predictor of angiographic stenosis of 70 to 99%. A multispecialty consensus panel
has developed a set of criteria for grading carotid stenosis by duplex examination (Table 23-3).19
Table 23-3 Carotid Duplex Ultrasound Criteria for Grading Internal Carotid Artery Stenosis
Degree of Stenosis (%) ICA PSV (cm/s) ICA/CCA PSV ICA EDV Plaque Estimate (%)
Ratio (cm/s) a
Normal <125 <2.0 <40 None

<50 <125 <2.0 <40 <50
50–69 125–230 2.0–4.0 40–100 ≥50

≥70 to less than near >230 >4.0 >100 ≥50
occlusion
Near occlusion High, low, or not Variable Variable Visible
detected
Total occlusion Not detected Not applicable Not detected Visible, no lumen
a
Plaque estimate (diameter reduction) with gray-scale and color Doppler ultrasound. ICA = internal carotid artery; CCA
= common carotid artery; PSV = peak systolic velocity; EDV = end-diastolic velocity.
MRA is increasingly being used to evaluate for atherosclerotic carotid occlusive disease and intracranial circulation. MRA
is noninvasive and does not require iodinated contrast agents. MRA uses phase contrast or time-of-flight, with either
two-dimensional or three-dimensional data sets for greater accuracy. Three-dimensional, contrast-enhanced MRA allows
data to be obtained in coronal and sagittal planes with improved image qualities due to shorter study time. In addition,
the new MRA techniques allow for better reformation of images in various planes to allow better grading of stenosis.
There have been numerous studies comparing the sensitivity and specificity of MRA imaging for carotid disease to
duplex and selective contrast angiography.20 Magnetic resonance imaging (MRI) of the brain is essential in the
assessment of acute stroke patients. MRI with diffusion-weighted imaging can differentiate areas of acute ischemia,
areas still at risk for ischemia (penumbra), and chronic cerebral ischemic changes. However, computed tomographic
(CT) imaging remains the most expeditious test in the evaluation of acute stroke patients to rule out intracerebral
hemorrhage. Recently, multidetector CTA has gained increasing popularity in the evaluation of carotid disease.21 This
imaging modality can provide volume rendering, which allows rotation of the object with accurate anatomic structures
from all angles (Fig. 23-15). The advantages of CTA over MRA include faster data acquisition time and better spatial
resolution. However, grading of carotid stenosis by CTA requires further validation at the time of this writing before it
can be widely applied.
Fig. 23-15.
A. Carotid computed tomography angiography is a valuable imaging modality that can provide a three-dimensional image
reconstruction with high image resolution. A carotid artery occlusion is noted in the internal carotid artery. B. The entire segment
of extracranial carotid artery is visualized from the thoracic compartment to the base of skull.
Historically, DSA has been the gold standard test to evaluate the extra- and intracranial circulation (Fig. 23-16). This is
an invasive procedure, typically performed via a transfemoral puncture, and involves selective imaging of the carotid
and vertebral arteries using iodinated contrast. The risk of stroke during cerebral angiography is generally reported at
approximately 1%, and is typically due to atheroembolization related to wire and catheter manipulation in the arch aorta
or proximal branch vessels. Over the past decades, however, the incidence of neurologic complications following
angiography has been reduced, due to the use of improved guidewires and catheters, better resolution digital imaging,
and increased experience. Local access complications of angiography are infrequent and include development of
hematoma, pseudoaneurysm, distal embolization, or acute vessel thrombosis. Currently, selective angiography is
particularly used for patients with suspected intracranial disease and for patients in whom percutaneous
revascularization is considered. The techniques of carotid angioplasty and stenting for carotid bifurcation occlusive
disease are described in the "Techniques of Carotid Angioplasty and Stenting" section. Preoperative CTA or MRA is
routinely utilized to get information about the aortic arch anatomy and presence of concomitant intracranial disease and
collateral pathway in planning our strategy for carotid stenting or endarterectomy.
Fig. 23-16.
A carotid angiogram reveals an ulcerated carotid plaque (arrow) in the proximal internal carotid artery, which also resulted in a
high-grade, internal, carotid artery stenosis.
Treatment of Carotid Occlusive Disease

Conventionally, patients with carotid bifurcation occlusive disease are divided into two broad categories: patients
without prior history of ipsilateral stroke or TIA (asymptomatic) and those with prior or current ipsilateral neurologic
symptoms (symptomatic). It is estimated that 15% of all strokes are preceded by a TIA. The 90-day risk of a stroke in a
patient presenting with a TIA is 3 to 17%.17 According to the Cardiovascular Health Study, a longitudinal, population-
based study of CAD and stroke in men and women, the prevalence of TIA in men was 2.7% between the ages of 65 to
69 and 3.6% for ages 75 to 79; the prevalence in women was 1.4% and 4.1%, respectively.22 There have been several
studies reporting on the effectiveness of stroke prevention with medical treatment and carotid endarterectomy for
symptomatic patients with moderate to severe carotid stenosis. Early and chronic aspirin therapy has been shown to
reduce stroke recurrence rate in several large clinical trials.23
Symptomatic Carotid Stenosis

Currently, most stroke neurologists prescribe both aspirin and clopidogrel for secondary stroke prevention in patients
who had experienced a TIA or stroke.17 In patients with symptomatic carotid stenosis, the degree of stenosis appears to
be the most important predictor in determining risk for an ipsilateral stroke. The risk of a recurrent ipsilateral stroke in
patients with severe carotid stenosis approaches 40%. Two large multicenter randomized clinical trials, the European
Carotid Surgery Trial and the North American Symptomatic Carotid Endarterectomy Trial, have both shown a significant
risk reduction in stroke for patients with symptomatic high-grade stenosis (70 to 99%) undergoing carotid
endarterectomy when compared to medical therapy alone.24,25 There has been much discussion regarding the different
methodology used in the measurement of carotid stenosis and calculation of the life-table data between the two studies,
which still led to similar results.26 Findings of these two landmark trials have also been reanalyzed in many subsequent
publications. The main conclusions of the trials remain validated and widely acknowledged. Briefly, the North American
Symptomatic Carotid Endarterectomy Trial study showed that, for high-grade carotid stenosis, the cumulative risk of
ipsilateral stroke was 26% in the medically treated group and 9% in the surgically treated group at 2 years. For patients
with moderate carotid artery stenosis (50 to 69%), the benefit of carotid endarterectomy is less but still favorable when
compared to medical treatment alone; the 5-year fatal or nonfatal ipsilateral stroke rate was 16% in the surgically
treated group vs. 22% in the medically treated group.27 The risk of stroke was similar for the remaining group of
symptomatic patients with less than 50% carotid stenosis, whether they had endarterectomy or medical treatment
alone. The European Carotid Surgery Trial reported similar stroke risk reduction for patients with severe symptomatic
carotid stenosis and no benefit in patients with mild stenosis, when carotid endarterectomy was performed vs. medical
therapy.25
The optimal timing of carotid intervention after acute stroke, however, remains debatable. Earlier studies showed an
increased rate of postoperative stroke exacerbation and conversion of a bland to hemorrhagic infarction when carotid
endarterectomy was carried out within 5 to 6 weeks after acute stroke. The dismal outcome reported in the early
experience was likely related to poor patient selection. The rate of stroke recurrence is not insignificant during the
interval period and may be reduced with early intervention for symptomatic carotid stenosis. Contemporary series have
demonstrated acceptable low rates of perioperative complications in patients undergoing carotid endarterectomy within
4 weeks after acute stroke.27 In a recent retrospective series, carotid artery stenting, when performed early (<2 weeks)
after the acute stroke, was associated with higher mortality than when delayed (>2 weeks).28
ASYMPTOMATIC CAROTID STENOSIS

Whereas there is universal agreement that carotid revascularization (endarterectomy or stenting) is effective in
secondary stroke prevention for patients with symptomatic moderate and severe carotid stenosis, the management of
asymptomatic patients remains an important controversy to be resolved. Generally, the detection of carotid stenosis in
asymptomatic patients is related to the presence of a cervical bruit or based on screening duplex ultrasound findings. In
one of the earlier observational studies, the authors showed that the annual rate of occurrence of neurologic symptoms
was 4% in a cohort of 167 patients with asymptomatic cervical bruits followed prospectively by serial carotid duplex
scan.29 The mean annual rate of carotid stenosis progression to a greater than 50% stenosis was 8%. The presence of
or progression to a greater than 80% stenosis correlated highly with either the development of a total occlusion of the
ICA or new symptoms. The major risk factors associated with disease progression were cigarette smoking, diabetes
mellitus, and age. This study supported the contention that it is prudent to follow a conservative course in the
management of asymptomatic patients presenting with a cervical bruit.
One of the first randomized clinical trials on the treatment of asymptomatic carotid artery stenosis was the
Asymptomatic Carotid Atherosclerosis Study, which evaluated the benefits of medical management with antiplatelet
therapy vs. carotid endarterectomy.30 Over a 5-year period, the risk of ipsilateral stroke in individuals with a carotid
artery stenosis greater than 60% was 5.1% in the surgical arm. On the other hand, the risk of ipsilateral stroke in
patients treated with medical management was 11%. Carotid endarterectomy produced a relative risk reduction of 53%
over medical management alone. The results of a larger randomized trial from Europe, The Asymptomatic Carotid
Surgery Trial, confirmed similar beneficial stroke risk reduction for patients with asymptomatic greater than 70% carotid
stenosis undergoing endarterectomy compared to medical therapy.31 An important point derived from this latter trial
was that even with improved medical therapy, including the addition of statin drugs and clopidogrel, medical therapy
was still inferior to endarterectomy in the primary stroke prevention for patients with high-grade carotid artery stenosis.
It is generally agreed that asymptomatic patients with severe carotid stenosis (80 to 99%) are at significantly increased
risk for stroke and stand to benefit from either surgical or endovascular revascularization. However, revascularization for
asymptomatic patients with a less severe degree of stenosis (60 to 79%) remains controversial.
Carotid Endarterectomy vs. Angioplasty and Stenting

Currently, the argument is no longer that medical therapy alone is inferior to surgical endarterectomy in stroke
prevention for severe carotid stenosis. Rather, the debate now revolves around whether carotid angioplasty and stenting
produces the same benefit that has been demonstrated by carotid endarterectomy. Since carotid artery stenting was
approved by the FDA in 2004 for clinical application, this percutaneous procedure has become a treatment alternative in
patients who are deemed "high-risk" for endarterectomy (Table 23-4). In contrast to many endovascular peripheral
arterial interventions, percutaneous carotid stenting represents a much greater challenging procedure, because it
requires complex, catheter-based skills using the 0.014-in guidewire system and distal protection device. Moreover,
current carotid stent devices predominantly use the monorail guidewire system that requires more technical agility, in
contrast to the over-the-wire catheter system that is routinely used in peripheral interventions. This percutaneous
intervention often requires balloon angioplasty and stent placement through a long carotid guiding sheath via a groin
approach. Poor technical skills can result in devastating treatment complications such as stroke, which can occur due in
part to plaque embolization during the balloon angioplasty and stenting of the carotid artery. Because of these various
procedural components that require high technical proficiency, many early clinical investigations of carotid artery
stenting, which included physicians with little or no carotid stenting experience, resulted in alarmingly poor clinical
outcomes. A recent Cochrane review noted that, before 2006, a total of 1269 patients had been studied in five
randomized controlled trials comparing percutaneous carotid intervention and surgical carotid reconstruction.32 Taken
together, these trials revealed that carotid artery stenting had a greater procedural risk of stroke and death when
compared to carotid endarterectomy (odds ratio 1.33; 95% CI 0.86–2.04). Additionally, greater incidence of carotid
restenosis was noted in the stenting group than the endarterectomy cohorts. However, the constant improvement of
endovascular devices, procedural techniques, and adjunctive pharmacologic therapy will likely improve the treatment
success of percutaneous carotid intervention. Critical appraisals of these trials comparing the efficacy of carotid stenting
vs. endarterectomy are available for review.33 Several ongoing clinical trials will undoubtedly provide more insights on
the efficacy of carotid stenting in the near future.
Table 23-4 Conditions Qualifying Patients as "High Surgical Risk" for Carotid
Endarterectomy
Anatomical Factors Physiological Factors

High carotid bifurcation (above C2 Age ≥80 y
vertebral body)
Left ventricular ejection fraction ≤30%
Low common carotid artery (below
clavicle)
New York Heart Association Class III/IV congestive heart failure
Contralateral carotid occlusion
Restenosis of ipsilateral prior carotid Unstable angina: Canadian Cardiovascular Society Class III/IV angina pectoris
endarterectomy
Previous neck irradiation
Prior radical neck dissection Recent myocardial infarction
Contralateral laryngeal nerve palsy Clinically significant cardiac disease (congestive heart failure, abnormal stress
Presence of tracheostomy test, or need for coronary revascularization)
Severe chronic obstructive pulmonary disease
End-stage renal disease on dialysis
Surgical Techniques of Carotid Endarterectomy

Although carotid endarterectomy is one of the earliest vascular operations ever described and its techniques have been
perfected in the last two decades, surgeons continue to debate many aspects of this procedure. For instance, there is no
universal agreement with regard to the best anesthetic of choice, the best intraoperative cerebral monitoring, whether
to "routinely" shunt, open vs. eversion endarterectomy, and patch vs. primary closure. Various anesthetic options are
available for a patient undergoing carotid endarterectomy including general, local, and regional anesthesia. Typically,
the anesthesia of choice depends on the preference of the surgeon, anesthesiologist, and patient. However, depending
on the anesthetic given, the surgeon must decide whether intraoperative cerebral monitoring is necessary or intra-
arterial carotid shunting will be used. In general, if the patient is awake, then his or her abilities to respond to
commands during carotid clamp period determine the adequacy of collateral flow to the ipsilateral hemisphere. On the
other hand, intraoperative electroencephalogram or transcranial power Doppler (TCD) has been used to monitor for
adequacy of cerebral perfusion during the clamp period for patients undergoing surgery under general anesthesia. Focal
ipsilateral decreases in amplitudes and slowing of electroencephalogram waves are indicative of cerebral ischemia.
Similarly, a decrease to less than 50% of baseline velocity in the ipsilateral middle cerebral artery is a sign of cerebral
ischemia. For patients with poor collateral flow exhibiting signs of cerebral ischemia, intra-arterial carotid shunting with
removal of the clamp will restore cerebral flow for the remaining part of the surgery. Stump pressures have been used
to determine the need for intra-arterial carotid shunting. Some surgeons prefer to shunt all patients on a routine basis
and do not use intraoperative cerebral monitoring.
The patient's neck is slightly hyperextended and turned to the contralateral side, with a roll placed between the shoulder
blades. An oblique incision is made along the anterior border of the sternocleidomastoid muscle centered on top of the
carotid bifurcation (Fig. 23-17). The platysma is divided completely. Typically, tributaries of the anterior jugular vein are
ligated and divided. The dissection is carried medial to the sternocleidomastoid. The superior belly of the omohyoid
muscle is usually encountered just anterior to the CCA. This muscle can be divided. The carotid fascia is incised and the
CCA is exposed. The CCA is mobilized cephalad toward the bifurcation. The dissection of the carotid bifurcation can
cause reactive bradycardia related to stimulation of the carotid body. This reflex can be blunted with injection of
lidocaine 1% into the carotid body or reversed with administration of IV atropine. A useful landmark in the dissection of
the carotid bifurcation is the common facial vein. This vein can be ligated and divided. Frequently, the twelfth cranial
nerve (hypoglossal nerve) traverses the carotid bifurcation just behind the common facial vein. The external carotid
artery is mobilized just enough to get a clamp across. Often, a branch of the external carotid artery crossing to the
sternocleidomastoid can be divided to allow further cephalad mobilization of the ICA. For high bifurcation, division of the
posterior belly of the digastric muscle is helpful in establishing distal exposure of the ICA.
Fig. 23-17.
To perform carotid endarterectomy, the patient's neck is slightly hyperextended and turned to the contralateral side. An oblique
incision is made along the anterior border of the sternocleidomastoid muscle centered on top of the carotid bifurcation.
IV heparin sulfate (1 mg/kg) is routinely administered just before carotid clamping. The ICA is clamped first using a soft,
noncrushing vascular clamp to prevent distal embolization. The external and common carotid arteries are clamped
subsequently. A longitudinal arteriotomy is made in the distal CCA and extended into the bulb and past the occlusive
plaque into the normal part of the ICA. Endarterectomy is carried out to remove the occlusive plaque (Fig. 23-18). If
necessary, a temporary shunt can be inserted from the CCA to the ICA to maintain continuous antegrade cerebral blood
flow (Fig. 23-19). Typically, a plane is teased out from the vessel wall, and the entire plaque is elevated and removed.
The distal transition line in the ICA where the plaque had been removed must be examined carefully and should be
smooth. Tacking sutures are placed when an intimal flap remains in this transition to ensure no obstruction to flow (Fig.
23-20). The occlusive plaque is usually removed from the origin of the external carotid artery using the eversion
technique. The endarterectomized surface is then irrigated and any debris removed. A patch (autogenous saphenous
vein, synthetic such as polyester, PTFE, or biologic material) is sewn to close the arteriotomy (Fig. 23-21). Whether
patch closure is necessary in all patients and which patch is the best remain controversial. However, most surgeons
agree that patch closure is indicated particularly for the small vessel (<7 mm). The eversion technique also has been
advocated for removing the plaque from the ICA. In the eversion technique, the ICA is transected at the bulb, the edges
of the divided vessel are everted, and the occluding plaque is "peeled" off the vessel wall. The purported advantages of
the eversion technique are no need for patch closure and a clear visualization of the distal transition area. Reported
series have not shown a clear superiority of one technique over the others.34 Surgeons will likely continue to use the
technique of their choice. Just before completion of the anastomosis to close the arteriotomy, it is prudent to flush the
vessels of any potential debris. When the arteriotomy is closed, flow is restored to the external carotid artery first and to
the ICA second. IV protamine sulfate can be given to reverse the effect of heparin anticoagulation following carotid
endarterectomy. The wound is closed in layers. After surgery, the patient's neurologic condition is assessed in the
operating room (OR) before transfer to the recovery area.
Fig. 23-18.
A. During carotid endarterectomy, vascular clamps are applied in common carotid, external carotid, and internal carotid arteries.
Carotid plaque is elevated from the carotid lumen. B. Carotid plaque is removed and the arteriotomy is closed either primarily or
with a patch angioplasty.
Fig. 23-19.
A temporary carotid shunt is inserted from the common carotid artery (long arrow) to the internal carotid artery (short arrow)

during carotid endarterectomy to provide continuous antegrade cerebral blood flow.
Fig. 23-20.
The distal transition line (left side of the picture) in the internal carotid artery where the plaque had been removed must be
examined carefully and should be smooth. Tacking sutures (arrows) are placed when an intimal flap remains in this transition to
ensure no obstruction to flow.
Fig. 23-21.
A. An autologous or synthetic patch can be used to close the carotid arteriotomy incision, which maintains the luminal patency. B.
A completion closure of carotid endarterectomy incision using a synthetic patch.
COMPLICATIONS OF CAROTID ENDARTERECTOMY

Most patients tolerate carotid endarterectomy very well and typically are discharged home within 24 hours after surgery.
Complications after endarterectomy are infrequent but can be potentially life threatening or disabling. Acute ipsilateral
stroke is a dreaded complication following carotid endarterectomy. Cerebral ischemia can be due to either intraoperative
or postoperative events. Embolizations from the occlusive plaque or prolonged cerebral ischemia are potential causes of
intraoperative stroke. The most common cause of postoperative stroke is due to embolization. Less frequently, acute
carotid artery occlusion can cause acute postoperative stroke. This is usually due to carotid artery thrombosis related to
closure of the arteriotomy, an occluding intimal flap, or distal carotid dissection. When patients experience acute
symptoms of neurologic ischemia after endarterectomy, immediate intervention may be indicated. Carotid duplex scan
can be done expeditiously to assess patency of the extracranial ICA. Re-exploration is mandated for acute carotid artery
occlusion. Cerebral angiography can be useful if intracranial revascularization is considered.
Local complications related to surgery include excessive bleeding and cranial nerve palsies. Postoperative hematoma in
the neck after carotid endarterectomy can lead to devastating airway compromise. Any expanding hematoma should be
evacuated and active bleeding stopped. Securing an airway is critical and can be extremely difficult in patients with large
postoperative neck hematomas. The reported incidence of postoperative cranial nerve palsies after carotid
endarterectomy varies from 1 to 30%.35 Well-recognized injuries involve the marginal mandibular, vagus, hypoglossal,
superior laryngeal, and recurrent laryngeal nerves. Often these are traction injuries but can also be due to severance of
the respective nerves.
Techniques of Carotid Angioplasty and Stenting

Percutaneous carotid artery stenting has become an accepted alternative treatment in the management of patients with
carotid bifurcation disease (Fig. 23-22). The perceived advantages of percutaneous carotid revascularization are related
to the minimal invasiveness of the procedure compared to surgery. There are anatomical conditions based on
angiographic evaluation in which carotid artery stenting should be avoided due to increased procedural-related risks
(Table 23-5). In preparation for carotid stenting, the patient should be given oral clopidogrel 3 days before the
intervention if the patient was not already taking the drug. The procedure is done in either the OR with angiographic
capabilities or in a dedicated angiography room. The patient is placed in the supine position. The patient's BP and
cardiac rhythm are closely monitored.
Fig. 23-22.
A. Carotid angiogram demonstrated a high-grade stenosis of the left internal carotid artery. B. Completion angiogram
demonstrating a satisfactory result following a carotid stent placement.
Table 23-5 Unfavorable Carotid Angiographic Appearance in Which Carotid Stenting Should
Be Avoided
Extensive carotid calcification
Polypoid or globular carotid lesions
Severe tortuosity of the common carotid artery
Long segment stenoses (>2 cm in length)
Carotid artery occlusion
Severe intraluminal thrombus (angiographic defects)
Extensive middle cerebral artery atherosclerosis
To gain access to the carotid artery, a retrograde transfemoral approach is most commonly used as the access site for
carotid intervention. Using the Seldinger technique, a diagnostic 5F or 6F sheath is inserted in the CFA. A diagnostic arch
aortogram is obtained. The carotid artery to be treated is then selected using a 5F diagnostic catheter, and contrast is
injected to show the carotid anatomy. It is important to assess the contralateral carotid artery, vertebrobasilar, and
intracranial circulation if these are not known based on the preoperative, noninvasive studies. Once the decision is made
to proceed with carotid artery stenting, with the tip of the diagnostic catheter still in the CCA, a 0.035-in, 260-cm long
stiff glide wire is placed in the ipsilateral external carotid artery. Anticoagulation with IV bivalirudin bolus (0.75mg/kg)
followed by an infusion rate of 2.5 mg/kg per hour for the remainder of the procedure is routinely administered. Next,
the diagnostic catheter is withdrawn and a 90-cm 6F guiding sheath is advanced into the CCA over the stiff glide wire. It
is critical not to advance the sheath beyond the occlusive plaque in the carotid bulb. The stiff wire is then removed and
preparation is made to deploy the distal embolic protection device (EPD). Several distal EPDs are available (Table 23-6).
The EPD device is carefully deployed beyond the target lesion. With regard to the carotid stents, there are several stents
that have received approval from the FDA and are commercially available for carotid revascularization (Table 23-7). All
current carotid stents use the rapid-exchange monorail 0.014-in platform. The size selection is typically based on the
size of CCA. Predilatation using a 4-mm balloon may be necessary to allow passage of the stent delivery catheter. Once
the stent is deployed across the occlusive plaque, postdilatation is usually performed using a 5.5-mm or less balloon. It's
noteworthy that balloon dilation of the carotid bulb may lead to immediate bradycardia due to stimulation of the
glossopharyngeal nerve. The EPD is then retrieved and the procedure is completed with removal of the sheath from the
femoral artery. The puncture site is closed using an available closure device or with manual compression. Throughout
the procedure, the patient's neurologic function is closely monitored. The bivalirudin infusion is stopped, and the patient
is kept on clopidogrel (75 mg daily) for at least 1 month and aspirin indefinitely.
Table 23-6 Commonly Used Embolic Protection Devices (EPDs)
Mechanism Name of EPD Pore Size (micrometers)

Distal balloon occlusion PercuSurge Guard Wire, Export catheter (Medtronic) N/A
Distal filter Angioguard (Cordis) 100
Accunet (Abbott) 150
Emboshield (Abbott) 140
FilterWire (Boston Scientific) 110
SpiderRx (EV3) <100
Flow reversala Parodi Neuro Protection (Gore) N/A
N/A = not applicable.
a
Currently in clinical trial (EMPIRE) in United States.
Table 23-7 Currently Approved Carotid Stents in the United States
Name of Stent Manufacturer Cell Design Tapered Stent Delivery System Size (F)
Acculink Abbott Open Yes 6
Exact Abbott Closed Yes 6
NexStent Boston Scientific Closed Self-tapering 5
Protégé RX EV3 Open Yes 6
Precise RX Cordis Open No 6
Exponent Medtronic Open No 6
COMPLICATIONS OF CAROTID STENTING

Although there have been no randomized trials comparing carotid stenting with and without EPD, the availability of EPDs
appears to have reduced the risk of distal embolization and stroke. The results of the various clinical trials and registries
of carotid stenting have been reported and compared. It is well known that distal embolization as detected by TCD is
much more frequent with carotid stenting, even with EPD, when compared to carotid endarterectomy. However, the
clinical significance of the distal embolization detected by TCD is not clear, as most are asymptomatic. Acute carotid
stent thrombosis is rare. The incidence of instent carotid restenosis is not well known but is estimated at 10 to 30%.
Duplex surveillance shows elevated peak systolic velocities within the stent after carotid stenting can occur frequently.
However, velocity criteria are being formulated to determine the severity of instent restenosis after carotid stenting by
ultrasound duplex.36 It appears that systolic velocities exceeding 300 to 400 cm/s would represent greater than 70 to
80% restenosis. Bradycardia and hypotension occurs in up to 20% of patients undergoing carotid stenting.37 Systemic
administration of atropine is usually effective in reversing the bradycardia. Other technical complications of carotid
stenting are infrequent and include carotid artery dissection, and access site complications such as groin hematoma,
femoral artery pseudoaneurysm, distal embolization, and acute femoral artery thrombosis.
Non-Atherosclerotic Disease of the Carotid Artery

CAROTID COIL AND KINK
A carotid coil consists of an excessive elongation of the ICA producing tortuosity of the vessel (Fig. 23-23).
Embryologically, the carotid artery is derived from the third aortic arch and dorsal aortic root, and is uncoiled as the
heart and great vessels descend into the mediastinum. In children, carotid coils appear to be congenital in origin. In
contrast, elongation and kinking of the carotid artery in adults is associated with the loss of elasticity and an abrupt
angulation of the vessel. Kinking is more common in women than men. Cerebral ischemic symptoms caused by kinks of
the carotid artery are similar to those from atherosclerotic carotid lesions, but are more likely due to cerebral
hypoperfusion than embolic episodes. Classically, sudden head rotation, flexion, or extension can accentuate the kink
and provoke ischemic symptoms. Most carotid kinks and coils are found incidentally on carotid duplex scan. However,
interpretation of the Doppler frequency shifts and spectral analysis in tortuous carotid arteries can be difficult because of
the uncertain angle of insonation. Cerebral angiography, with multiple views taken in neck flexion, extension, and
rotation, is useful in the determination of the clinical significance of kinks and coils.
Fig. 23-23.
Excessive elongation of the carotid artery can result in carotid kinking (arrow), which can compromise cerebral blood flow and
lead to cerebral ischemia.
FIBROMUSCULAR DYSPLASIA
FMD usually involves medium-sized arteries that are long and have few branches (Fig. 23-24). Women in the fourth or
fifth decade of life are more commonly affected than men. Hormonal effects on the vessel wall are thought to play a role
in the pathogenesis of FMD. FMD of the carotid artery is commonly bilateral, and in about 20% of patients, the vertebral
artery also is involved.38 An intracranial saccular aneurysm of the carotid siphon or middle cerebral artery can be
identified in up to 50% of the patients with FMD. Four histological types of FMD have been described in the literature.
The most common type is medial fibroplasia, which may present as a focal stenosis or multiple lesions with intervening
aneurysmal outpouchings. The disease involves the media with the smooth muscle being replaced by fibrous connective
tissue. Commonly, mural dilations and microaneurysms can be seen with this type of FMD. Medial hyperplasia is a rare
type of FMD, with the media demonstrating excessive amounts of smooth muscle. Intimal fibroplasia accounts for 5% of
all cases and occurs equally in both sexes. The media and adventitia remain normal, and there is accumulation of
subendothelial mesenchymal cells with a loose matrix of connective tissue causing a focal stenosis in adults. Finally,
premedial dysplasia represents a type of FMD with elastic tissue accumulating between the media and adventitia. FMD
also can involve the renal and the external iliac arteries. It is estimated that approximately 40% of patients with FMD
present with a TIA due to embolization of platelet aggregates.38 DSA demonstrates the characteristic "string of beads"
pattern, which represents alternating segments of stenosis and dilatation. The string of beads can also be shown
noninvasively by CTA or MRA. FMD should be suspected when an increased velocity is detected across a stenotic
segment without associated atherosclerotic changes on carotid duplex ultrasound. Antiplatelet medication is the
generally accepted therapy for asymptomatic lesions. Endovascular treatment is recommended for patients with
documented lateralizing symptoms. Surgical correction is rarely indicated.
Fig. 23-24.
A carotid fibromuscular dysplasia with typical characteristics of multiple stenosis with intervening aneurysmal outpouching
dilatations. The disease involves the media, with the smooth muscle being replaced by fibrous connective tissue.
CAROTID ARTERY DISSECTION

Dissection of the carotid artery accounts for approximately 20% of strokes in patients younger than 45 years of age.
The etiology and pathogenesis of spontaneous carotid artery dissection remains incompletely understood. Arterial
dissection involves hemorrhage within the media, which can extend into the subadventitial and subintimal layers. When
the dissection extends into the subadventitial space, there is an increased risk of aneurysm formation. Subintimal
dissections can lead to intramural clot or thrombosis. Traumatic dissection is typically a result of hyperextension of the
neck during blunt trauma, neck manipulation, strangulation, or penetrating injuries to the neck. Even in supposedly
spontaneous cases, a history of preceding unrecognized minor neck trauma is not uncommon. Connective disorders such
as Ehlers-Danlos syndrome, Marfan syndrome, alpha1-antitrypsin deficiency, or FMD may predispose to carotid artery
dissection. Iatrogenic dissections also can occur due to catheter manipulation or balloon angioplasty.
Typical clinical features of carotid artery dissection include unilateral neck pain, headache, and ipsilateral Horner's
syndrome in up to 50% of patients, followed by manifestations of the cerebral or ocular ischemia and cranial nerve
palsies. Neurologic deficits can result either because of hemodynamic failure (caused by luminal stenosis) or by an
artery to artery thromboembolism. The ischemia may cause TIAs or infarctions, or both. Catheter angiography has been
the method of choice to diagnose arterial dissections, but with the advent of duplex ultrasonography, MRI/MRA, and
CTA, most dissections can now be diagnosed using noninvasive imaging modalities (Fig. 23-25). The dissection typically
starts in the ICA distal to the bulb. Uncommonly, the dissection can start in the CCA, or is an extension of a more
proximal aortic dissection. Medical therapy has been the accepted primary treatment of symptomatic carotid artery
dissection. Anticoagulation (heparin and warfarin) and antiplatelet therapy have been commonly used, although there
have not been any randomized studies to evaluate their effectiveness. The prognosis depends on the severity of
neurologic deficit but is generally good in extracranial dissections. The recurrence rate is low. Therapeutic interventions
have been reserved for recurrent TIAs or strokes, or failure of medical treatment. Endovascular options include intra-
arterial stenting, coiling of associated pseudoaneurysms, or more recently, deployment of covered stents.
Fig. 23-25.
Carotid ultrasound reveals a patient with a carotid artery dissection in which carotid flow is separated in the true flow lumen (long
arrow) from the false lumen (short arrow).
CAROTID ARTERY ANEURYSMS

Carotid artery aneurysms are rare, encountered in less than 1% of all carotid operations (Fig. 23-26). The true carotid
artery aneurysm generally is due to atherosclerosis or medial degeneration. The carotid bulb is involved in most carotid
aneurysms, and bilaterality is present in 12% of the patients. Patients typically present with a pulsatile neck mass. The
available data suggest that, untreated, these aneurysms lead to neurologic symptoms from embolization. Thrombosis
and rupture of the carotid aneurysm is rare. Pseudoaneurysms of the carotid artery can result from injury or infection.
Mycotic aneurysms often involve syphilis in the past, but are now more commonly associated with peritonsillar
abscesses caused by Staphylococcus aureus infection. FMD and spontaneous dissection of the carotid artery can lead to
the formation of true aneurysms or pseudoaneurysms. Whereas conventional surgery has been the primary mode of
treatment in the past, carotid aneurysms are currently being treated more commonly using endovascular approaches.39
Fig. 23-26.
A. An anteroposterior angiogram of the neck revealing a carotid artery aneurysm. B. A lateral projection of the carotid artery
aneurysm. C. Following endovascular placement, the carotid artery aneurysm is successfully excluded.
CAROTID BODY TUMOR

The carotid body originates from the third branchial arch and from neuroectodermal-derived neural crest lineage. The
normal carotid body is located in the adventitia or periadventitial tissue at the bifurcation of the CCA (Fig. 23-27). The
gland is innervated by the glossopharyngeal nerve. Its blood supply is derived predominantly from the external carotid
artery, but also can come from the vertebral artery. Carotid body tumor is a rare lesion of the neuroendocrine system.
Other glands of neural crest origin are seen in the neck, parapharyngeal spaces, mediastinum, retroperitoneum, and
adrenal medulla. Tumors involving these structures have been referred to as paraganglioma, glomus tumor, or
chemodectoma. Approximately 5 to 7% of carotid body tumors are malignant. Although chronic hypoxemia has been
invoked as a stimulus for hyperplasia of carotid body, approximately 35% of carotid body tumors are hereditary. The
risk of malignancy is greatest in young patients with familial tumors.
Fig. 23-27.
tumor is removed.
Symptoms related to the endocrine products of the carotid body tumor are rare. Patients usually present between the
fifth and seventh decade of life with an asymptomatic lateral neck mass. The diagnosis of carotid body tumor requires
confirmation on imaging studies. Carotid duplex scan can localize the tumor to the carotid bifurcation, but CT or MR
imaging usually is required to further delineate the relationship of the tumor to the adjacent structures. Classically, a
carotid body tumor will widen the carotid bifurcation. The Shamblin classification describes the tumor extent: I. tumor is
<5 cm and relatively free of vessel involvement; II. tumor is intimately involved but does not encase the vessel wall;
and III. tumor is intramural and encases the carotid vessels and adjacent nerves.40 With good resolution CT and MR
imaging, arteriography usually is not required. However, arteriography can provide an assessment of the vessel invasion
and intracranial circulation, and allows for preoperative embolization of the feeder vessels, which has been reported to
reduce intraoperative blood loss. Surgical resection is the recommended treatment for suspected carotid body tumor.
CAROTID TRAUMA
Blunt or penetrating trauma to the neck can cause injury to the carotid artery. Notwithstanding the massive bleeding
from carotid artery transection, injury to the carotid artery can result in carotid dissection, thrombosis, or
pseudoaneurysm formation. Carotid duplex ultrasound can be useful to locate the site of injury in the cervical segment
of the carotid artery. Spiral CTA has become the modality of choice to detect extracranial carotid artery injury.
Confirmation of carotid injury by contrast cerebral angiography remains the gold standard diagnostic test. Injuries to the
cervical segment of the common and internal carotid arteries can be repaired surgically. Acute carotid artery thrombosis
usually is treated medically with anticoagulation if the patient is asymptomatic. Revascularization should be considered
for patients presenting with ongoing cerebral ischemia related to carotid artery thrombosis. Traumatic carotid artery
dissection can cause cerebral ischemia due to thromboembolization, decreased flow, or thrombosis. Commonly, the
dissection involves the distal portion of the cervical and petrous segment of the ICA. Medical management with
antiplatelet or anticoagulation usually is adequate for uncomplicated traumatic carotid dissection. In patients with
pseudoaneurysms of the carotid artery that are located in a segment that is out of surgical reach, the use of selective
coil embolization of the pseudoaneurysm or exclusion of the pseudoaneurysm by a covered stent graft has been
reported. Bare metal stent has been used with success in the treatment of traumatic carotid artery dissection.
ABDOMINAL AORTIC ANEURYSM

In spite of more than 50,000 patients undergoing elective repair of abdominal aortic aneurysm (AAA) each year in the
United States, approximately 15,000 patients die annually as a result of ruptured aneurysm, making it the tenth leading
cause of death in men in this country.41 The incidence appears to be increasing, and this is due in part to improvements
in diagnostic imaging and, more importantly, is a result of a growing elderly population. With early diagnosis and timely
intervention, aneurysm rupture–related death is largely preventable. Conventional treatment of an AAA involves
replacing the aneurysmal segment of the aorta with a prosthetic graft, with the operation performed through a large
abdominal incision. Techniques for this open abdominal surgery have been refined, adapted, and extensively studied by
vascular surgeons over the past four decades. Despite a well-documented, low perioperative mortality rate of 2 to 3% in
large academic institutions, the thought of undergoing an open abdominal aortic operation often provokes a sense of
anxiety in many patients due in part to the postoperative pain associated with the large abdominal incision as well as
the long recovery time needed before the patient can return to normal physical activity.
The most common location of aortic aneurysms is the infrarenal aorta. Endovascular stent graft placement represents a
revolutionary and minimally invasive treatment for infrarenal AAAs that only requires 1 to 2 days of hospitalization, and
the patient can return to normal physical activity within 1 week. The concept of using an endoluminal device in the
management of vascular disease was first proposed by Dotter and colleagues, who successfully treated a patient with
iliac occlusion using transluminal angioplasty in 1964.42 Nearly three decades later, Parodi and colleagues reported the
first successful endovascular repair of AAA using a stent graft device.13 Since then, a variety of stent graft technologies
have been developed to treat the AAA. The rapid innovation of this new treatment modality has undoubtedly captured
the attention of patients with aortic aneurysms as well as physicians who practice endovascular therapy. Physicians in
general should be knowledgeable regarding available treatment options to provide adequate evaluation and education to
patients and their families. The following discussion is to outline the treatment options for AAAs, including conventional
repair and endovascular approach. Advantages and potential complications of these treatments also will be addressed.
Natural History of Aortic Aneurysm
The natural history of an AAA is to expand and rupture. AAA exhibits a "staccato" pattern of growth, where periods of
relative quiescence may alternate with expansion. Therefore, although an individual pattern of growth cannot be
predicted, average aggregate growth is approximately 3 to 4 mm/y. There is some evidence to suggest that larger
aneurysms may expand faster than smaller aneurysms, but there is significant overlap between the ranges of growth
rates at each strata of size.
Rupture risk appears to be directly related to aneurysm size as predicted by Laplace's law. Although more sophisticated
methods of assessing rupture risk based on finite element analysis of wall stress is under active investigation, maximum
transverse diameter remains the standard method of risk assessment for aneurysm rupture. In the past, AAA rupture
risk has been overestimated. More recently, two landmark studies have served to better define the natural history of
AAA.43,44 Based on best available evidence, the annualized risk of rupture is given in Table 23-8. The rupture risk is
quite low for aneurysms <5.5 cm and begins to rise exponentially thereafter. This size can serve as an appropriate
threshold for recommending elective repair provided one's surgical mortality is below 5%. For each size strata, however,
women appear to be at higher risk for rupture than men, and a lower threshold of 4.5 to 5.0 cm may be reasonable in
good-risk patients. Although data are less compelling, a pattern of rapid expansion of >0.5 cm within 6 months can be
considered a relative indication for elective repair. Aneurysms that fall below these indications may safely be followed
with CT or ultrasound at 6-month intervals, with long-term outcomes equivalent to earlier surgical repair. Interestingly,
in the ADAM study, 80% of all patients with AAA who were followed in this manner eventually came to repair within 5
years.44
Table 23-8 Annualized Risk of Rupture of Abdominal Aortic Aneurysm (AAA) Based on Size
Description Diameter of Aorta Estimated Annual Risk of Rupture Estimated 5-y Risk of Rupture
(cm) (%) (%)a
Normal aorta 2–3 0 0 (unless AAA develops)

Small AAA 4–5 1 5–10
Moderate AAA 5–6 2–5 30–40
Large AAA 6–7 3–10 >50
Very large >7 >10 Approaching 100
AAA
a
The estimated 5-y risk is more than five times the estimated annual risk because over that 5 y, the AAA, if left
untreated, will continue to grow in size.
Unless symptomatic or ruptured, AAA repair is a prophylactic repair. The rationale for recommending repair is predicated
on the assumption that the risk of aneurysm rupture exceeds the combined risk of death from all other causes such as
cardiopulmonary disease and cancer. On the other hand, our limitation in predicting timing and cause of death is
underscored by the observation that over 25% of patients who were deemed unfit for surgical repair because of their
comorbidities died from rupture of their aneurysms within 5 years.
Clinical Manifestations
Most AAAs are asymptomatic, and they are usually found incidentally during work-up for chronic back pain or kidney
stones. Physical examination is neither sensitive nor specific except in thin patients. Large aneurysms may be missed in
the obese, while normal aortic pulsations may be mistaken for an aneurysm in thin individuals. Rarely, patients present
with back pain and/or abdominal pain with a tender pulsatile mass. Patients with these symptoms must be treated as if
they had a rupture until proven otherwise. If the patient is hemodynamically stable and the aneurysm is intact on a CT
scan, the patient is admitted for BP control with IV antihypertensive agents and repaired usually within 12 to 24 hours
or at least during the same hospitalization. In contrast, patients who are hemodynamically unstable with a history of
acute back pain and/or syncope, and a known unrepaired AAA or a pulsatile abdominal mass should be immediately
taken to the OR with a presumed diagnosis of a ruptured AAA.
Overall mortality of AAA rupture is 71 to 77%, which includes all out-of-hospital and inhospital deaths, as compared to 2
to 6% for elective open surgical repair.45 Nearly one half of all patients with ruptured AAA will die before reaching the
hospital. For the remainder, surgical mortality is 45 to 50% and has not substantially changed in the last 30 years.
Relevant Anatomy
An AAA is defined as a pathologic focal dilation of the aorta that is >30 mm or 1.5 times the adjacent diameter of the
normal aorta (Fig. 23-28). Male aortas tend to be larger than female, and there is generalized growth of the aortic
diameter with each decade of life. Ninety percent of AAA are infrarenal in location and have a fusiform morphology.
There is a higher predilection for juxtarenal and suprarenal AAA in women as compared to men. Concomitant common
iliac and/or hypogastric artery aneurysms can be found in 20 to 25% of patients. Although the etiology of most aortic
aneurysms is atherosclerotic, clinically significant peripheral occlusive disease is unusual and present in less than 10% of
all cases.
Fig. 23-28.
An operative view of an infrarenal aortic aneurysm.
Although extravascular anatomy is important for open surgical repair of AAA, intravascular anatomy and aortoiliac
morphology are important for endovascular repair. Pertinent anatomic dimensions include the diameter of the proximal,
nondilated, infrarenal aortic neck, which can range from 18 to 30 mm, CIA, from 8 to 16 mm, and external iliac arteries,
6 to 10 mm. Morphologically, the aortic neck can manifest complex angulation above and below the renal arteries due to
a combination of elongation and anterolateral displacement by the posterior bulge of the aneurysmal aorta.
Furthermore, the shape of the proximal neck is rarely tubular, but often is conical, reverse conical, or barrel shaped.
Distally, the iliac arteries can have severe tortuosity with multiple compound turns. Although not significant from a
hemodynamic standpoint, severe iliac calcifications combined with extreme tortuosity can pose a formidable challenge
during endovascular repair.
Preoperative evaluation should include routine history and physical examination with particular attention to (a) any
symptoms referable to the aneurysm, which may impact the timing of repair, (b) a history of pelvic surgery or radiation,
in the event retroperitoneal exposure is required or interruption of hypogastric circulation is planned, (c) claudication
suggestive of significant iliac occlusive disease, (d) LE bypass or other femoral reconstructive procedures, and (e)
chronic renal insufficiency or contrast allergy.
Cross-sectional imaging is required for definitive evaluation of AAA. Although ultrasound is safe, widely available,
relatively accurate, and inexpensive, and, therefore, is the screening modality of choice, the CT scan remains the gold
standard for determination of anatomic eligibility for endovascular repair. Size of AAA may differ up to 1 cm between CT
and ultrasound, and, during longitudinal follow-up, comparisons should be made between identical modalities. With
modern multirow detector scanners, a timed-bolus IV contrast enhanced, 2.5 to 3.0-mm slice spiral CT of the chest,
abdomen, and pelvis can be performed in <30 seconds with a single breath hold. Extremely high-resolution images are
obtained with submillimeter spatial resolution (Fig. 23-29). Proper window level and width (brightness and contrast) is
important for discrimination among aortic wall, calcific plaque, thrombus, and lumen. The only major drawback to CT is
the risk of contrast nephropathy in diabetics and in patients with renal insufficiency.
Fig. 23-29.
High resolution of image displaying an aortic aneurysm (arrow) can be achieved with multidetector computed tomographic
angiography.
The spiral technique further affords the ability for three-dimensional reconstruction. Three-dimensional reconstructions
can yield important morphologic information that is critical to endovascular therapy. Using third-party software, these
images can be viewed and manipulated on a desktop computer and so-called "center-line" (transverse slices
perpendicular to the central flow-lumen of the aorta) diameter and length measurements obtained. Conventional
angiography has a minimal role in the current management of AAA. Angiography is invasive with an increased risk of
complications. Indications for angiography are isolated to concomitant iliac occlusive disease (present in less than 10%
of patients with AAA) and unusual renovascular anatomy.
Surgical Repair of Abdominal Aortic Aneurysm

General anesthesia is necessary when performing a conventional open AAA repair. Although a retroperitoneal incision is
a well-accepted surgical approach, a midline transabdominal incision remains the more common approach for open
aortic aneurysm operation. Because the abdominal incision can lead to significant pain and discomfort, an epidural
catheter can be placed before the operation for postoperative analgesic infusion to provide pain control. Once the
abdominal cavity is opened, the small intestines and transverse colon are retracted to expose the retroperitoneum
overlying the AAA. The retroperitoneum is next divided, followed by isolation of both proximal and distal segments of
the AAA. IV heparin (100 IU/kg) is given, followed by clamping of the proximal and distal segments of the aneurysm.
The aneurysm sac is opened next, and a prosthetic graft is used to reconstruct the aorta. If the aneurysm only involved
the abdominal aorta, a tube graft can be used to replace the aorta (Fig. 23-30). If the aneurysm extends distally to the
iliac arteries, a prosthetic bifurcated graft is used for either an aortobi-iliac or aortobifemoral bypass reconstruction (Fig.
23-31). The overlying aneurysm sac and the retroperitoneum are closed to cover the prosthetic bypass graft to minimize
potential bowel contact to the graft. Small and large intestines are returned to the abdominal cavity followed by the
closure of the abdominal fascia and skin.
Fig. 23-30.
A. Schematic depiction of an aortic tube graft used to repair an aortic aneurysm. B. Intraoperative image of an aortic tube graft
reconstruction.
Fig. 23-31.
Intraoperative view of a bifurcated graft used to repair an aortic aneurysm.
ADVANTAGES AND RISKS OF OPEN ABDOMINAL AORTIC ANEURYSM REPAIR

The main advantage of a conventional open repair is that the AAA is permanently eliminated because it is entirely
replaced by a prosthetic aortic graft. The risk of aneurysm recurrence or delayed rupture no longer exists. As a result,
long-term imaging surveillance is not needed with these patients. In contrast, the long-term efficacy of endovascular
repair remains unclear. Consequently, long-term imaging surveillance is critical to ensure that the aortic aneurysm
remains properly sealed by the stent graft. Other potential advantages of open repair include direct assessment of the
circulatory integrity of the colon. If signs of colonic ischemia become evident after aortic bypass grafting, a concomitant
mesenteric artery bypass can be performed to revascularize the colonic circulation. In addition, open repair permits the
surgeons to explore for other abdominal pathologies such as GI tumors, liver mass, or cholelithiasis.
As for the risks associated with open repair, cardiac complications, in the form of either myocardial infarction or
arrhythmias, remain the most common morbidity, with an incidence between 2 and 6%.46 Another significant
complication is renal failure or transient renal insufficiency as a result of perioperative hypotension, atheromatous
embolization, inadvertent injury to the ureter, preoperative contrast-induced nephropathy, or suprarenal aortic
clamping. Although the incidence of renal failure is less than 2% in elective aneurysm repair, it can occur in more than
20% of patients after repair of a ruptured AAA.46
Ischemic colitis is a devastating potential complication after open repair. The likelihood of such a complication is highest
in those who had a prior colon resection and undergo repair of a ruptured AAA, due to the loss of collateral blood supply
to the rectosigmoid colon. It is estimated that 5% of patients who undergo elective aneurysm repair will develop partial-
thickness ischemic colitis but without significant clinical sequelae.47 However, if the partial-thickness ischemia
progresses to full-thickness gangrene and peritonitis, mortality can be as high as 90%.47
The incidence of prosthetic graft infection ranges between 1 and 4% after open repair.47 It is more common in those
who undergo repair of a ruptured AAA. If the prosthetic graft is not fully covered by the aneurysm sac or
retroperitoneum, intestinal adhesion with subsequent bowel erosion may occur, resulting in an aortoenteric fistula. The
predominant sign of such a complication is massive hematemesis, and it typically occurs years after the operation.
Despite these potential complications, however, the majority of patients who undergo successful elective open repair
have an uneventful recovery.
Endovascular Repair of Abdominal Aortic Aneurysm

More than a decade has passed since the first report of human implantation of a homemade stent graft for endovascular
repair of an AAA by Parodi in 1991.3 Several prospective clinical trials across different devices and analysis of large
Medicare administrative databases and meta-analyses of published literature have consistently demonstrated
significantly decreased operative time, blood loss, hospital length of stay, and overall perioperative morbidity and
mortality of endovascular repair as compared to open surgical repair. For patients who are at increased risk for surgery
because of age or comorbidity, endovascular repair is a superior, minimally invasive alternative.
The principle of endovascular repair of AAA involves the implantation of an aortic stent graft that is fixed proximally and
distally to the nonaneurysmal aortoiliac segment, and thereby endoluminally excludes the aneurysm from the aortic
circulation (Fig. 23-32). Unlike open surgical repair, endovascular treatment does not remove or eliminate the aneurysm
sac, which therefore is subjected to potential aneurysm expansion or even rupture as persistent aneurysm sac
pressurization may occur following endograft implantation. Importantly, aortic branches such as lumbar arteries or the
inferior mesenteric artery (IMA) are ligated, which can lead to persistent aneurysm pressurization and aneurysm
expansion. Currently, five devices are available for elective repair of intact infrarenal AAA: (a) AneuRx device
(Medtronic/AVE, Santa Rosa, Calif), (b) Gore Excluder device (WL Gore & Associates, Flagstaff, Ariz), (c) Endologix
Powerlink device (Endologix Inc., Irvine, Calif), (d) Zenith device (Cook Inc., Bloomington, Ind), and (e) Talent device
(Medtronic/AVE, Santa Rosa, Calif). Despite some differences in physical appearance, mechanical properties, and
materials, they will be discussed collectively in this chapter. They are all modular devices consisting of a primary device
or main body and one or two iliac limbs that insert into the main body to complete the repair. Depending on the device,
there are varying degrees of flexibility in the choice of iliac limbs that can be matched to the main body, which can
impact the customizability for a particular anatomy.
Fig. 23-32.
A. An aortogram demonstrating a large, infrarenal, abdominal aortic aneurysm. B. Following endovascular stent graft
implantation, the aortic aneurysm is successfully excluded.
PATIENT SELECTION FOR ENDOVASCULAR AORTIC ANEURYSM REPAIR

Anatomic eligibility for endovascular repair is mainly based on three areas: the proximal aortic neck, CIAs, and the
external iliac and common femoral arteries, which relate to the proximal and distal landing zones or fixation sites and
the access vessels, respectively. The requirements for the proximal aortic neck are a diameter of 18 to 28 mm and a
minimum length of 15 mm (Table 23-9). Usually, multiple measurements of the diameter are taken along the length of
the neck to assess its shape. All diameter measurements are midwall to midwall of the vessel. Secondary considerations
include mural calcifications (<50% circumference), luminal thrombus (<50% circumference), and angulation (<45°).
Presence of a significant amount of any one of these secondary features in combination with a relatively short proximal
neck may compromise successful short- and long-term fixation of the stent graft and exclusion of the aneurysm. The
usual distal landing zone is the CIA. The EIA may serve as an alternate site when the ipsilateral CIA is aneurysmal or
ectatic. The treatable diameters of CIAs range from 8 to 20 mm, and there should be at least 20 mm of patent artery of
uniform diameter to allow adequate fixation. And finally, at least one of two common femoral and external iliac arteries
must be at least 7 mm in diameter to safely introduce the main delivery sheath. Slightly smaller iliac diameters may be
tolerated depending on the specific device and in the absence of severe tortuosity and calcific disease. Difficult access is
one of the main causes of increased procedural times and intraoperative complications. Using these criteria,
approximately 60% of all AAA are anatomic candidates for endovascular repair.
Table 23-9 Ideal Characteristics of an Aneurysm for Endovascular Abdominal Aortic

Aneurysm Repair
Neck length (mm) >15
Neck diameter (mm) >18, <32
Aortic neck angle (°) <60
Neck mural calcification (% circumference) <50
Neck luminal thrombus (% circumference) <50
Common iliac artery diameter (mm) between 8–20
Common iliac artery length (mm) >20
External iliac artery diameter (mm) >7
The next step in the preoperative planning is device selection. Typically, the proximal diameter of the main device is
oversized by 10 to 20% of the nominal diameter of the aortic neck. Distally, the iliac limbs are oversized by 1 to 4 mm
depending on the individual device's instructions for use. The biggest challenge to proper device selection remains
determining the optimal length from the renal arteries to the hypogastric arteries. Despite availability of sophisticated
three-dimensional reconstructions, the exact path that a device will take from the proximal aortic neck to the distal iliac
arteries is difficult to predict. It is dependent on a host of factors related to the mechanical properties of the stent graft
and the morphology of the aortoiliac flow lumen. "Plumb-line" measurements of axial CT images can be quite inaccurate,
typically grossly underestimating the length, while center-line measurements usually overestimate the length.
Angiographic measurements using a marker catheter are invasive, require contrast and radiation exposure, and also are
inaccurate because the marker catheter fails to take into account the stiffness of the stent graft. The consequences of
not choosing the correct length of the device include inadvertent coverage of the hypogastric artery if too long and the
need for additional devices if too short.
ADVANTAGES AND RISKS OF ENDOVASCULAR REPAIR

The obvious advantage of an endovascular AAA repair is its minimally invasive nature. Typically, patients who undergo
this procedure stay in the hospital for only 1 to 3 days, in contrast to the 5- to 10-day stay required after conventional
open surgical repair. In most clinical practices, patients who have had an endovascular repair are routinely transferred
to a general vascular ward from the postanesthesia recovery unit, avoiding admission to a more costly intensive care
unit (ICU).
Because an abdominal incision is not necessary in endovascular repair, the procedure is particularly beneficial in patients
with severe pulmonary disease such as chronic obstructive pulmonary disease or emphysema. Patients can sustain
adequate breathing in the postoperative period, thereby avoiding respiratory complications or prolonged mechanical
ventilation. Because the abdominal cavity has not been entered, the risk of GI complications such as ileus, ventral
hernia, or bowel obstruction due to intestinal adhesion also is greatly reduced. Moreover, regional or epidural anesthesia
can be used, avoiding the risks associated with general anesthesia in patients with severe cardiopulmonary dysfunction.
Despite its many advantages, endovascular repair does have potential complications. Because the stent graft device is
attached endoluminally within the abdominal aorta, an endoleak due to incomplete stent graft exclusion of the aneurysm
can occur. With this type of leak, blood flow persists outside the lumen of the endoluminal graft but within an aneurysm
sac. A meta-analysis of 1118 patients who underwent successful endovascular repair found an endoleak incidence of
24%.48 Although a small endoleak usually poses little clinical significance because it will typically become thrombosed
spontaneously, a large or persistent endoleak may lead to continuous aneurysm perfusion and ultimately to aneurysm
rupture. The rupture rate following an endovascular AAA repair has been reported to be <0.8%.49
Stent graft iliac limb dysfunction resulting in thrombosis has been reported following endovascular repair.16,48 One
possible cause is aneurysm remodeling, resulting in a shortening in the aortic length, which can cause the stent graft to
kink. Alternatively, progression of an underlying iliac atherosclerotic lesion may cause compression of the iliac limb and
ultimately result in graft-limb occlusion. Treatment options include thrombolysis or graft thrombectomy to determine the
underlying cause and possibly additional stent graft placement. Renal artery occlusion may occur due to improper stent
graft positioning or migration.16,46,48 Graft limb separation or dislocation also has been reported.16,46,48
In patients with AAA and concurrent iliac artery aneurysms who undergo preoperative coil embolization of the internal
iliac artery, 20 to 45% experience symptoms of pelvic ischemia.50 These symptoms may include buttock claudication,
impotence, gluteal skin sloughing, and colonic ischemia. Other complications pertaining to endovascular repair relate to
the access site and include groin hematoma and wound infection. Occasionally, the stent graft device can malfunction by
either failing to deploy or dislodging during the deployment procedure.16,49 If the device cannot be salvaged or rescued
endoluminally, open surgical repair of the aneurysm may be necessary.
TECHNICAL CONSIDERATIONS OF ENDOVASCULAR AORTIC ANEURYSM REPAIR

Although endovascular AAA repair may be performed in any venue with appropriate digital fluoroscopic imaging
capability, due to the need for absolute sterility and aseptic technique, it is most safely performed in a surgical suite.
The patient is prepped and draped just as in open AAA repair. Patients with renal insufficiency should be started on
perioperative oral N-acetylcysteine and sodium bicarbonate infusion to reduce the risk of contrast nephropathy. A
variety of anesthetic options may be used. Regional anesthesia may be appropriate for patients with pulmonary disease.
There are reports of success with local anesthetics alone, as the incisions are typically smaller than a typical open
inguinal hernia repair.51
Bilateral transverse oblique incisions are made just below the inguinal ligament to expose approximately 2 to 3 cm of
common femoral arteries and obtain proximal control. Special attention is paid to avoid the groin crease to decrease the
risk of wound complications. Some have advocated a completely percutaneous access using the "pre-close" technique
with the Perclose suture-mediated vascular closure device (Abbott Perclose, Redwood City, Calif). Review of reported
series on this technique suggest a technical success rate of 95% for medium size sheaths ranging from 12F to 16F, and
75% success for 18F to 24F sizes.
Transfemoral access is obtained using standard Seldinger technique. Initial soft-tipped starter guidewires are exchanged
for stiff guidewires that are advanced to the thoracic arch. IV heparin at 80 IU/kg is administered and the activated
clotting time is maintained at 200 to 250 seconds. These guidewires provide the necessary support for the subsequent
introduction of the large-diameter delivery catheters and devices. In the absence of special anatomic considerations, the
primary device is inserted through the right side and the contralateral iliac limb is inserted through the left side. After
administration of heparin, the delivery catheter or the introducer sheath is advanced to the L1–L2 vertebral space, which
typically marks the location of the renal arteries. An angiographic catheter is advanced from the contralateral femoral
artery to the same level.
A road-mapping aortogram is obtained to localize the renal arteries. The primary device is rotated to the desired
orientation and deployed immediately below the lowest renal artery (Fig. 23-33). The angiographic catheter is replaced
with a directional catheter and an angled guidewire, and the opening for the contralateral limb on the main device is
cannulated. Intrastent passage of the guidewire is confirmed, and the angled guidewire is replaced with a stiff
guidewire. The contralateral iliac limb is inserted into the docking opening of the primary device and deployed. A
completion angiogram is performed looking for patency of the renal and hypogastric arteries, the device limbs, proximal
and distal fixation, and endoleak. Adjunctive interventions, including additional devices, balloons, bare stents, etc., are
performed as needed. The procedure is concluded with routine repairs of the femoral arteries and closure of the groin
incisions. The patients are recovered in the recovery room for 2 to 4 hours and admitted to the general care floor.
Although in the past, patients were admitted to the ICU, this is rarely needed. Most patients can be started on a regular
diet that evening and discharged the next morning.
Fig. 23-33.
A. During an endovascular aortic aneurysm repair, the main endograft device is inserted through a femoral artery approach. B.
The device is deployed in the aorta just below the renal arteries. C. A contralateral iliac endograft device is inserted through a
contralateral gate opening that is next deployed. D. Completion deployment of the endograft device should fully exclude an aortic
aneurysm while arterial flow to the renal and hypogastric arteries should remain patent.
SURVEILLANCE FOLLOWING ENDOVASCULAR AORTIC ANEURYSM REPAIR

Lifelong follow-up is essential to the long-term success after endovascular AAA repair. Indeed, one may go so far as to
say that absence of appropriate follow-up is tantamount to not having had a repair at all. A triple-phase (noncontrast,
contrast, delayed) spiral CT scan and a four-view (anteroposterior, lateral, and two obliques) abdominal x-ray should be
obtained within the first month. Subsequent imaging can be obtained at 6-month intervals in the first 1 to 2 years and
yearly thereafter. After the first 6 months, patients who cannot travel easily may obtain their studies locally and submit
them for review. The CT scan is for detection of endoleaks, subtle proximal migrations, and changes in aneurysm size.
The abdominal x-ray gives a "bird's-eye" view of the overall morphology of the stent graft. Subtle changes in
conformation of the iliac limbs relative to each other and/or the spine can provide early signs of impending component
separation or loss of fixation. Further, stent fractures and/or suture breaks that can compromise long-term device
integrity sometimes only can be detected on a plain film and not on a CT scan.
Results from Clinical Studies Comparing Endovascular vs. Open Repair

The primary success rate after endovascular repair of AAA has been reported to be as high as 95%.16,45 The less
invasive nature of this procedure is appealing to many physicians and patients. In addition, virtually all reports indicate
decreased blood loss, transfusion requirements, and length of ICU and hospital stay for endovascular repair of AAAs
when compared to the standard surgical approach.16,45,52 With the advent of bifurcated grafts and improved delivery
systems in the future, the only real limitation will be cost. When evaluating the literature for results from clinical series,
it is important to look at a comparison of endoluminal vs. open repair, device specific outcome, and cost analysis
studies.
Early reports on results with endovascular repair were often flawed due to selection biases. This is because from its
inception, endovascular repair has been used mostly in patients who are at higher risk for open repair. At the same
time, only patients with favorable anatomy including less tortuosity and the presence of a suitable infrarenal neck were
considered for endovascular repair. Randomization is also difficult because most patients who anatomically qualify for
endovascular repair would withdraw from the study if randomized to open repair. Consequently, there are very few
randomized, controlled trials that have compared outcomes in patients with similar risk factors and anatomy that are
eligible for both types of repair. Two such European trials have published short-term outcome data that are unbiased in
design.
The DREAM trial is a multicenter randomized trial that compared open vs. endovascular repair among a group of 345
patients at 28 European centers using multiple different devices including: Gore, AneuRx, and Zenith.53 Patients were
included only if they were considered to be candidates for both types of repairs. The operative mortality rate was 4.6%
in the operative group vs. 1.2% in the endoluminal group at 30 days. When looking at the combined rate of operative
mortality and severe complications, there was an incidence of 9.8% in the open-repair vs. 4.7% in the endoluminal
group. The difference here was largely due to the higher frequency of pulmonary complications seen in the open group.
There was a higher incidence of graft-related complications in the endoluminal group. There was no difference in the
nonvascular-local complication rate among the two groups.
The EVAR-1 trial is also a multicenter randomized trial that compared open to endoluminal repair.52 This study was
conducted on 1082 patients at 34 centers in the United Kingdom using all available devices. Short-term mortality at 30
days was 4.7% in the open and 1.7% in the endoluminal group. The inhospital mortality rate was also increased in the
open when compared to the endoluminal group (6.2 to 2.1%). As expected, the secondary-intervention rate was higher
in the endoluminal group (9.8 to 5.8%). Complication rates were not reported with the EVAR-1 trial. There are criticisms
that can be applied to both of these trials. Patients had to be eligible for either type of repair to be included in the study.
Consequently, these findings cannot be generalized for patients who are too sick to undergo open surgery or in those
patients whose anatomy precludes them from undergoing endovascular repair.
DEVICE-SPECIFIC OUTCOME
Matsmura and associates compared endoluminal to open repair using the Excluder device.54 In their review, they
demonstrated a 30-day mortality rate of 1% along with an endoleak rate of 17 and 20% at 1 and 2-year intervals.54
The limb narrowing, limb migration, and trunk migration were all 1% at 2 years. There were no deployment failures or
early conversions. There was an annual 7% reintervention rate. Aneurysm growth was demonstrated in 14% of patients
at 2 years. The Zenith device by Cook has been studied by Greenberg and associates, who compared standard surgical
repair to endoluminal repair in low-risk patients as well as endoluminal repair in high-risk patients.55 They reported a
30-day mortality rate of 3.5% that was equal to the open group. The rate of endoleak was 7.4 and 5.4% at 1 and 2-
year intervals. There was a 5.3% migration of 5 mm after 1 year. Freedom from rupture was 100% in the low-risk and
98.9% in the high-risk endoluminal group at 2 years. Experience with the AneuRx device has been reported by Zarins
and associates.56 In their 4-year review, they found a 30-day mortality rate of 2.8%. Endoleak rate at 4 years was
13.9%, aneurysm enlargement was 11.5%, and stent graft migration was 9.5%. Freedom from rupture was noted to be
98.4% at 4 years. Criado and associates have reported on their 1-year experience with the Talent LPS device by
Medtronic.57 They report a 30-day mortality rate of 0.8%. Endoleak rate was 10%. Three deployment failures were
noted, and freedom from rupture was 100%. Aneurysm growth and migration rates were divided into three different
neck-size groups. Patients with a wide neck (>26 mm) had a 3% growth and migration rate. Narrow-neck patients (<26
mm) had a 1% growth rate and a 2% migration rate. Interestingly, short-neck patients (<15 mm) had no aneurysm
growths and a 2% migration rate.
COST ANALYSIS
The current climate of cost containment and limited reimbursement for heath care services mandates a critical analysis
of the economic impact of any new medical technology on the market. The inhospital costs for both endovascular and
open repair include graft cost, OR fees, radiology, pharmacy, ancillary care, ICU charges, and floor charges. Despite the
improved morbidity and mortality rates, several early studies have reported no cost benefit with the application of
endovascular repair.58,59 The limiting factor appears to be the cost of the device. Despite commercialization of
endovascular repair, the device costs are still in the range of $5000 to $6000 with no signs of abating. A recent report
by Angle and associates further corroborates previous studies.60 In their review, despite decreased hospital and ICU
stays and use of pharmacy and respiratory services, cost of endovascular repair was 1.74 times greater than the
standard surgical approach. In addition, these cost analysis studies are centered on inhospital costs and do not even
begin to address secondary costs such as postoperative surveillance that is required with endovascular repair.
Classification and Management of Endoleak

An endoleak is an extravasation of contrast outside the stent graft and within the aneurysm sac (Fig. 23-34). It can be
present in up to 20 to 30% of all endovascular AAA repairs in the early postoperative period.61 In general, over one half
of these endoleaks will resolve spontaneously during the first 6 months, resulting in a 10% incidence of chronic
endoleaks in all cases beyond the first year of follow-up. Endoleaks can be detected using conventional angiography,
contrast CT (Fig. 23-35), MRA (magnetic resonance angiography), and color flow duplex ultrasound. Although there is
no recognized gold standard, in practice, angiography is considered the least sensitive but most specific for
characterizing the source of the endoleak, while the CT scan is the most sensitive but least specific. Widespread
availability and reliability that is relatively independent of technique have made the CT scan the de facto standard
imaging modality for postoperative surveillance. Conversely, routine use of duplex ultrasound and MRA has been limited
by the lack of proper equipment and local expertise. On the other hand, investigational techniques such as time-
resolved MRA may provide greater sensitivity and specificity than either angiography or CT in the future.
Fig. 23-34.
Four types of endoleak that include: type I endoleak = attachment site leak; type II endoleak = side branch leak caused by
lumbar or side branches; type III endoleak = endograft junctional leak due to overlapping device components; type IV endoleak
= endograft fabric or porosity leak.
Fig. 23-35.
A computed tomographic scan demonstrating an endoleak (small arrow) as evidenced by contrast flow outside the aortic
endograft (long arrow).
Four types of endoleaks have been described (Table 23-10). Type I endoleak refers to fixation-related leaks that occur
at the proximal or distal attachment sites. These represent less than 5% of all endoleaks and are seen as an early blush
of contrast into the aneurysm sac from the proximal or distal ends of the device during completion angiography.61,62
Although seen as a marker of poor patient selection or inadequate repair, over 80% of these leaks spontaneously seal in
the first 6 months. Persistent type I endoleaks, on the other hand, require prompt treatment. Type II endoleak refers to
retrograde flow originating from a lumbar, inferior mesenteric, accessory renal, or hypogastric artery. They are the most
common type of endoleak, accounting for 20 to 30% of all cases, and about one half resolve spontaneously. On
angiography, they are seen as a late filling of the aneurysm sac from a branch vessel(s). Type II endoleaks carry a
relatively benign natural history and do not merit intervention unless associated with aneurysm growth. Type III
endoleaks refer to a failure of device integrity or component separation from modular systems. If detected
intraoperatively or in the early perioperative period, it is usually from inadequate overlap between two stent grafts,
while in the late period, it may be from a fabric tear or junctional separation from conformational changes of the
aneurysm. Regardless of the etiology or timing, these should be promptly repaired. And lastly, type IV endoleak refers
to the diffuse, early blush seen during completion angiography due to graft porosity and/or suture holes of some
Dacron-based devices. It does not have any clinical significance and usually cannot be seen after 48 hours and heparin
reversal. Endoleaks that have initially been considered type IV that persist become type III endoleaks by definition, as it
indicates a more significant material defect than simple porosity or a suture hole.
Table 23-10 Endoleak Classification
Classification Description
Type I endoleak Attachment site leak
Type II endoleak Side branch leak caused by lumbar or inferior mesenteric artery
Type III endoleak Junctional leak (of overlapping endograft components)
Type IV endoleak Endograft fabric or porosity leak
ENDOTENSION FOLLOWING ENDOVASCULAR AORTIC ANEURYSM REPAIR

In approximately 5% of cases after an apparently successful endovascular repair, the aneurysm continues to grow
without any demonstrable endoleak.63 This phenomenon has been described as endotension. Although it was initially
thought that an endoleak was really present but simply not detected, cases have been reported where the aneurysm has
been surgically opened and the contents were completely devoid of any blood and no extravasation could be found. The
mechanism of continued pressurization of the aneurysm sac following successful exclusion from the arterial circulation
remains unsolved at this time. One putative mechanism has been linked to a transudative process related to certain
expanded PTFE graft materials.64 More importantly, however, the natural history of these enlarging aneurysms without
endoleaks is unknown, but to date there has been no evidence to suggest that they carry an increased risk of rupture.
Conservatively speaking, until further, long-term data become available, if the patient is a suitable surgical risk, elective
open conversion should be considered.
SECONDARY INTERVENTIONS FOLLOWING ENDOVASCULAR AORTIC ANEURYSM

REPAIR
There is approximately a 10 to 15% per year risk of secondary interventions following endovascular AAA repair.16,55,65
These procedures are critical in the long-term success of the primary procedure in prevention of aneurysm rupture and
aneurysm-related death. These secondary procedures, in order of frequency, include proximal or distal extender
placement for migrations, highly-selective or translumbar embolization for type II endoleaks, direct surgical or
laparoscopic branch vessel ligations, bridging cuffs for component separations, and late open surgical conversions.
Multiple large series have reported an annual rupture rate of approximately 1 to 1.5% per year after endovascular
repair.16,55,65 The EUROSTAR registry reports a rupture rate of 2.3% over a 15-month period in patients with an
endoleak, compared with 0.3% in those without.66 Various causes of late ruptures have been reported in the literature,
although presence of a persistent endoleak with aneurysm enlargement remains a common culprit for this complication.
It has been shown that even successfully excluded aneurysm can lead to the development of attachment-site leaks and
device failure, caused in part by aneurysm remodeling resulting in stent migration or kinking.67
Treatment of rupture may be open conversion or endovascular stent graft placement. May and associates reported a
mortality rate of 43% in those patients who underwent open conversion.68 Emergent endovascular repair should be
considered in these patients because it is potentially much faster and incurs less physiologic stress than open
conversion. Several reports have shown that endovascular repair can be performed successfully in patients previously
treated with endoluminal prostheses.69,70
MESENTERIC ARTERY DISEASE

Vascular occlusive disease of the mesenteric vessels is a relatively uncommon but potentially devastating condition that
generally presents in patients more than 60 years of age, is three times more frequent in women, and has been
recognized as an entity since 1936.71 The incidence of such a disease is low and represents 2% of the revascularization
operations for atheromatous lesions. The most common cause of mesenteric ischemia is atherosclerotic vascular
disease. Autopsy studies have demonstrated splanchnic atherosclerosis in 35 to 70% of cases.72 Other etiologies exist
and include FMD, panarteritis nodosa, arteritis, and celiac artery (CA) compression from a median arcuate ligament, but
they are unusual and have an incidence of one in nine compared to that of atherosclerosis.
Chronic mesenteric ischemia is related to a lack of blood supply in the splanchnic region and is caused by disease in one
or more visceral arteries: the celiac trunk, the SMA, and the IMA. Mesenteric ischemia is thought to occur when two of
the three visceral vessels are affected with severe stenosis or occlusion; however, in as many as 9% of cases, only a
single vessel is involved [superior mesenteric artery (SMA) in 5% and celiac trunk in 4% of cases].73 This disease
process may evolve in a chronic fashion, as in the case of progressive luminal obliteration due to atherosclerosis. On the
other hand, mesenteric ischemia can occur suddenly, as in the case of thromboembolism. Despite recent progress in
perioperative management and better understanding in pathophysiology, mesenteric ischemia is considered one of the
most catastrophic vascular disorders, with mortality rates ranging from 50 to 75%. Delay in diagnosis and treatment are
the main contributing factors in its high mortality. It is estimated that mesenteric ischemia accounts for one in every
1000 hospital admissions in this country. The prevalence is rising due in part to the increased awareness of this disease,
the advanced age of the population, and the significant comorbidity of these elderly patients. Early recognition and
prompt treatment before the onset of irreversible intestinal ischemia are essential to improve the outcome.
Anatomy and Pathophysiology

Mesenteric arterial circulation is remarkable for its rich collateral network. Three main mesenteric arteries provide the
arterial perfusion to the GI system: the CA, SMA, and IMA. In general, the CA provides arterial circulation to the foregut
(distal esophagus to duodenum), hepatobiliary system, and spleen; the SMA supplies the midgut (jejunum to midcolon);
and the IMA supplies the hindgut (midcolon to rectum). The CA and SMA arise from the ventral surface of the
infradiaphragmatic suprarenal abdominal aorta, while the IMA originates from the left lateral portion of the infrarenal
aorta. These anatomic origins in relation to the aorta are important when a mesenteric angiogram is performed to
determine the luminal patency. To fully visualize the origins of the CA and SMA, it is necessary to perform both an
anteroposterior and a lateral projection of the aorta because most arterial occlusive lesions occur in the proximal
segments of these mesenteric trunks.
Because of the abundant collateral flow between these mesenteric arteries, progressive diminution of flow in one or
even two of the main mesenteric trunks is usually tolerated, provided that uninvolved mesenteric branches can enlarge
over time to provide sufficient compensatory collateral flow. In contrast, acute occlusion of a main mesenteric trunk may
result in profound ischemia due to lack of sufficient collateral flow. Collateral network between the CA and the SMA exist
primarily through the superior and inferior pancreaticoduodenal arteries. The IMA may provide collateral arterial flow to
the SMA through the marginal artery of Drummond, the arc of Riolan, and other unnamed retroperitoneal collateral
vessels termed meandering mesenteric arteries (Fig. 23-36). Lastly, collateral visceral vessels may provide important
arterial flow to the IMA and the hindgut through the hypogastric arteries and the hemorrhoidal arterial network.
Fig. 23-36.
An aortogram showing a prominent collateral vessel that is the arc of Riolan (arrow) in a patient with an inferior mesenteric artery
occlusion. This vessel network provides collateral flow between the superior mesenteric artery and inferior mesenteric artery.
Regulation of mesenteric blood flow is largely modulated by both hormonal and neural stimuli, which characteristically
regulate systemic blood flow. In addition, the mesenteric circulation responds to the GI contents. Hormonal regulation is
mediated by splanchnic vasodilators such as nitric oxide, glucagon, and vasoactive intestinal peptide. Certain intrinsic
vasoconstrictors such as vasopressin can diminish the mesenteric blood flow. On the other hand, neural regulation is
provided by the extensive visceral autonomic innervation.
Clinical manifestation of mesenteric ischemia is predominantly postprandial abdominal pain, which signifies that the
increased oxygen demand of digestion is not met by the GI collateral circulation. The postprandial pain frequently occurs
in the midabdomen, suggesting that the diversion of blood flow from the SMA to supply the stomach impairs perfusion
to the small bowel. This leads to transient anaerobic metabolism and acidosis. Persistent or profound mesenteric
ischemia will lead to mucosal compromise with release of intracellular contents and by-products of anaerobic
metabolism to the splanchnic and systemic circulation. Injured bowel mucosa allows unimpeded influx of toxic
substances from the bowel lumen with systemic consequences. If full-thickness necrosis occurs in the bowel wall,
intestinal perforation ensues, which will lead to peritonitis. Concomitant atherosclerotic disease in cardiac or systemic
circulation frequently compounds the diagnostic and therapeutic complexity of mesenteric ischemia.
Types of Mesenteric Artery Occlusive Disease

There are three major mechanisms of visceral ischemia involving the mesenteric arteries, which include: (a) acute
mesenteric ischemia, which can be either embolic or thrombotic in origin; (b) chronic mesenteric ischemia; and (c)
nonocclusive mesenteric ischemia. Despite the variability of these syndromes, a common anatomic pathology is involved
in these processes. The SMA is the most commonly involved vessel in acute mesenteric ischemia. Acute thrombosis
occurs in patients with underlying mesenteric atherosclerosis, which typically involves the origin of the mesenteric
arteries while sparing the collateral branches. In acute embolic mesenteric ischemia, the emboli typically originate from
a cardiac source and frequently occur in patients with atrial fibrillation or following myocardial infarction (Figs. 23-37
and 23-38). Nonocclusive mesenteric ischemia is characterized by a low flow state in otherwise normal mesenteric
arteries, and most frequently occurs in critically ill patients on vasopressors. Finally, chronic mesenteric ischemia is a
functional consequence of a long-standing atherosclerotic process that typically involves at least two of the three main
mesenteric vessels. The gradual development of the occlusive process allows the development of collateral vessels that
prevent the manifestations of acute ischemia, but are not sufficient to meet the high postprandial intestinal oxygen
requirements, giving rise to the classical symptoms of postprandial abdominal pain and the resultant food fear.
Fig. 23-37.
An anteroposterior view of a selective superior mesenteric artery angiogram showed an abrupt cutoff of the middle colic artery,
which was caused by emboli (arrow) due to atrial fibrillation.
Fig. 23-38.
A lateral mesenteric angiogram showing an abrupt cutoff of the proximal superior mesenteric artery, which is consistent with
superior mesenteric artery embolism (arrow).
Several less common syndromes of visceral ischemia involving the mesenteric arteries can also cause serious
debilitation. Chronic mesenteric ischemic symptoms can occur due to extrinsic compression of the CA by the diaphragm,
which is termed the median arcuate ligament syndrome, or celiac artery compression syndrome. Acute visceral ischemia
may occur following an aortic operation, due to ligation of the IMA in the absence of adequate collateral vessels.
Furthermore, acute visceral ischemia may develop in aortic dissection that involves the mesenteric arteries, or after
coarctation repair. Finally, other unusual causes of ischemia include mesenteric arteritis, radiation arteritis, and
cholesterol emboli.
Abdominal pain out of proportion to physical findings is the classic presentation in patients with acute mesenteric
ischemia and occurs following an embolic or thrombotic ischemic event of the SMA. Other manifestations include sudden
onset of abdominal cramps in patients with underlying cardiac or atherosclerotic disease, often associated with bloody
diarrhea, as a result of mucosal sloughing secondary to ischemia. Fever, nausea, vomiting, and abdominal distention are
some common but nonspecific manifestations. Diffuse abdominal tenderness, rebound, and rigidity are late signs and
usually indicate bowel infarction and necrosis.
Clinical manifestations of chronic mesenteric ischemia are more subtle owing to the extensive collateral development.
However, when intestinal blood flow is unable to meet the physiologic GI demands, mesenteric insufficiency ensues. The
classic symptoms include postprandial abdominal pain, "food fear," and weight loss. Persistent nausea, and occasionally
diarrhea, may coexist. Diagnosis remains challenging, and most of the patients will undergo an extensive and expensive
GI tract work-up for the above symptoms before referral to a vascular service.
The typical patients who develop nonocclusive mesenteric ischemia are elderly patients. Comorbidities include
congestive heart failure, acute myocardial infarction with cardiogenic shock, hypovolemic or hemorrhagic shock, sepsis,
pancreatitis, and administration of digitalis or vasoconstrictor agents such as epinephrine. Abdominal pain is only
present in approximately 70% of these patients. When present, the pain is usually severe but may vary in location,
character, and intensity. In the absence of abdominal pain, progressive abdominal distention with acidosis may be an
early sign of ischemia and impending bowel infarction.
Abdominal pain due to narrowing of the origin of the CA may occur as a result of extrinsic compression or impingement
by the median arcuate ligament (Fig. 23-39). This condition is known as celiac artery compression syndrome or median
arcuate ligament syndrome. Angiographically, there is CA compression that augments with deep expiration, and

poststenotic dilatation. The CA compression syndrome has been implicated in some variants of chronic mesenteric
ischemia. Most patients are young females between 20 and 40 years of age. Abdominal symptom is nonspecific, but the
pain is localized in the upper abdomen, which may be precipitated by meals.
Fig. 23-39.
A lateral projection of the magnetic resonance angiography of the aorta showing a chronic compression of the celiac artery
(arrow) by the median arcuate ligament.
The differential diagnosis of acute mesenteric ischemia includes other causes of severe abdominal pain of acute onset,
such as perforated viscus, intestinal obstruction, pancreatitis, cholecystitis, and nephrolithiasis. Laboratory evaluation is
neither sensitive nor specific in distinguishing these various diagnoses. In the setting of mesenteric ischemia, complete
blood count may reveal hemoconcentration and leukocytosis. Metabolic acidosis develops as a result of anaerobic
metabolism. Elevated serum amylase may indicate a diagnosis of pancreatitis, but is also common in the setting of
intestinal infarction. Finally, increased lactate levels, hyperkalemia, and azotemia may occur in the late stages of
mesenteric ischemia.
Plain abdominal radiographs may provide helpful information to exclude other causes of abdominal pain such as
intestinal obstruction, perforation, or volvulus, which may exhibit symptoms mimicking intestinal ischemia.
Pneumoperitoneum, pneumatosis intestinalis, and gas in the portal vein may indicate infarcted bowel. In contrast,
radiographic appearance of an adynamic ileus with a gasless abdomen is the most common finding in patients with
acute mesenteric ischemia.
Upper endoscopy, colonoscopy, or barium radiography does not provide any useful information when evaluating acute
mesenteric ischemia. Moreover, barium enema is contraindicated if the diagnosis of mesenteric ischemia is being
considered. The intraluminal barium can obscure accurate visualization of mesenteric circulation during angiography. In
addition, intraperitoneal leakage of barium can occur in the setting of intestinal perforation, which can lead to added
therapeutic challenges during mesenteric revascularization.
Diagnosis of chronic mesenteric ischemia can be more challenging. Usually, before the evaluation by a vascular service,
the patients have undergone an extensive work-up for the symptoms of chronic abdominal pain, weight loss, and
anorexia. Rarely, the vascular surgeon is the first to encounter a patient with the above symptoms. In this situation, it is
advisable to keep in mind that mesenteric ischemia is a rare entity, and that a full diagnostic work-up that should
include CT scan of the abdomen and evaluation by a gastroenterologist should be performed. Mesenteric occlusive
disease may coexist with malignancy, and symptoms of mesenteric vessel stenosis may be the result of extrinsic
compression by a tumor.
Duplex ultrasonography is a valuable noninvasive means of assessing the patency of the mesenteric vessels. Moneta
and associates evaluated the use of duplex ultrasound in the diagnosis of mesenteric occlusive disease in a blinded
prospective study.74,75 A peak systolic velocity in the SMA >275 cm/s demonstrated a sensitivity of 92%, specificity of
96%, and an overall accuracy of 96% for detecting more than 70% stenosis. The same authors found sensitivity and
specificity of 87% and 82%, respectively, with an accuracy of 82% in predicting more than 70% celiac trunk stenosis.
Duplex has been successfully used for follow-up after open surgical reconstruction or endovascular treatment of the
mesenteric vessels to assess recurrence of the disease. Finally, spiral computed tomography with three-dimensional
reconstruction (Fig. 23-40) as well as MRA (Fig. 23-41) have been promising in providing clear radiographic assessment
of the mesenteric vessels.
Fig. 23-40.
Computed tomographic angiogram of the abdomen with three-dimensional reconstruction provides a clear view of the celiac
artery, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA).
Fig. 23-41.
A cross-sectional view of a magnetic resonance angiography provides a clear view of the luminal patency of the superior
mesenteric artery.
The definitive diagnosis of mesenteric vascular disease is made by biplanar mesenteric arteriography, which should be
performed promptly in any patient with suspected mesenteric occlusion. It typically shows occlusion or near-occlusion of
the CA and SMA at or near their origins from the aorta. In most cases, the IMA has been previously occluded secondary
to diffuse infrarenal aortic atherosclerosis. The differentiation of the different types of mesenteric arterial occlusion may
be suggested with biplanar mesenteric arteriogram. Mesenteric emboli typically lodge at the orifice of the middle colic
artery, which creates a "meniscus sign" with an abrupt cutoff of a normal proximal SMA several centimeters from its
origin on the aorta. Mesenteric thrombosis, in contrast, occurs at the most proximal SMA, which tapers off at 1 to 2 cm
from its origin. In the case of chronic mesenteric occlusion, the appearance of collateral circulation is typically present.
Nonocclusive mesenteric ischemia produces an arteriographic image of segmental mesenteric vasospasm with a
relatively normal appearing main SMA trunk (Fig. 23-42).
Fig. 23-42.
Mesenteric arteriogram showing nonocclusive mesenteric ischemia as evidenced by diffuse spasm of intestinal arcades with poor
filling of intramural vessels.
Mesenteric arteriography also can play a therapeutic role. Once the diagnosis of nonocclusive mesenteric ischemia is
made on the arteriogram, an infusion catheter can be placed at the SMA orifice and vasodilating agents such as
papaverine can be administered intra-arterially. The papaverine infusion may be continued postoperatively to treat
persistent vasospasm, a common occurrence following mesenteric reperfusion. Transcatheter thrombolytic therapy has
little role in the management of thrombotic mesenteric occlusion. Although thrombolytic agents may transiently
recannulate the occluded vessels, the underlying occlusive lesions require definitive treatment. Furthermore,
thrombolytic therapy typically requires a prolonged period of time to restore perfusion, during which the intestinal
viability will be difficult to assess.
A word of caution would be appropriate here regarding patients with typical history of chronic intestinal angina who
present with an acute abdomen and classical findings of peritoneal irritation. Arteriography is the gold standard for the
diagnosis of mesenteric occlusive disease; however, it can be a time-consuming diagnostic modality. In this group of
patients, immediate exploration for assessment of intestinal viability and vascular reconstruction is the best choice.
Surgical Repair
ACUTE EMBOLIC MESENTERIC ISCHEMIA
Initial management of patients with acute mesenteric ischemia includes fluid resuscitation and systemic anticoagulation
with heparin to prevent further thrombus propagation. Significant metabolic acidosis not responding to fluid
resuscitation should be corrected with sodium bicarbonate. A central venous catheter, peripheral arterial catheter, and a
Foley catheter should be placed for hemodynamic status monitoring. Appropriate antibiotics are given before surgical
exploration. The operative management of acute mesenteric ischemia is dictated by the cause of the occlusion. It is
helpful to obtain a preoperative mesenteric arteriogram to confirm the diagnosis and to plan appropriate treatment
options. However, the diagnosis of mesenteric ischemia frequently cannot be established before surgical exploration;
and therefore, patients in a moribund condition with acute abdominal symptoms should undergo immediate surgical
exploration, avoiding the delay required to perform an arteriogram.
The primary goal of surgical treatment in embolic mesenteric ischemia is to restore arterial perfusion with removal of
the embolus from the vessel. The abdomen is explored through a midline incision, which often reveals variable degrees
of intestinal ischemia from the midjejunum to the ascending or transverse colon. The transverse colon is lifted
superiorly, and the small intestine is reflected toward the right upper quadrant. The SMA is approached at the root of
the small bowel mesentery, usually as it emerges from beneath the pancreas to cross over the junction of the third and
fourth portions of the duodenum. Alternatively, the SMA can be approached by incising the retroperitoneum lateral to
the fourth portion of the duodenum, which is rotated medially to expose the SMA. Once the proximal SMA is identified
and controlled with vascular clamps, a transverse arteriotomy is made to extract the embolus, using standard balloon
embolectomy catheters. In the event the embolus has lodged more distally, exposure of the distal SMA may be obtained
in the root of the small bowel mesentery by isolating individual jejunal and ileal branches to allow a more
comprehensive thromboembolectomy. Following the restoration of SMA flow, an assessment of intestinal viability must
be made, and nonviable bowel must be resected. Several methods have been described to evaluate the viability of the
intestine, which include intraoperative IV fluorescein injection and inspection with a Wood's lamp, and Doppler
assessment of antimesenteric intestinal arterial pulsations. A second-look procedure should be considered in many
patients, and is performed 24 to 48 hours following embolectomy. The goal of the procedure is reassessment of the
extent of bowel viability, which may not be obvious immediately following the initial embolectomy. If nonviable intestine
is evident in the second-look procedure, additional bowel resections should be performed at that time.
ACUTE THROMBOTIC MESENTERIC ISCHEMIA

Thrombotic mesenteric ischemia usually involves a severely atherosclerotic vessel, typically the proximal CA and SMA.
Therefore, these patients require a reconstructive procedure to the SMA to bypass the proximal occlusive lesion and
restore adequate mesenteric flow. The saphenous vein is the graft material of choice, and prosthetic materials should be
avoided in patients with nonviable bowel, due to the risk of bacterial contamination if resection of necrotic intestine is
performed. The bypass graft may originate from either the aorta or iliac artery. Advantages from using the supraceliac
infradiaphragmatic aorta as opposed to the infrarenal aorta as the inflow vessel include a more smooth graft
configuration with less chance of kinking, and the absence of atherosclerotic disease in the supraceliac aortic segment.
Exposure of the supraceliac aorta is technically more challenging and time consuming than that of the iliac artery,
which, unless calcified, is an appropriate inflow. Patency rates are similar regardless of inflow vessel choice.76
CHRONIC MESENTERIC ISCHEMIA

The therapeutic goal in patients with chronic mesenteric ischemia is to revascularize mesenteric circulation and prevent
the development of bowel infarction. Mesenteric occlusive disease can be treated successfully by either transaortic
endarterectomy or mesenteric artery bypass. Transaortic endarterectomy is indicated for ostial lesions of patent CA and
SMA. A left medial rotation is performed, and the aorta and the mesenteric branches are exposed. A lateral aortotomy is
performed, encompassing both the CA and SMA orifices. The visceral arteries must be adequately mobilized so that the
termination site of endarterectomy can be visualized. Otherwise, an intimal flap may develop, which can lead to early
thrombosis or distal embolization.
For occlusive lesions located 1 to 2 cm distal to the mesenteric origin, mesenteric artery bypass should be performed.
Multiple mesenteric arteries are typically involved in chronic mesenteric ischemia, and both the CA and SMA should be
revascularized whenever possible. In general, bypass grafting may be performed either antegrade from the supraceliac
aorta or retrograde from either the infrarenal aorta or iliac artery. Both autogenous saphenous vein grafts and prosthetic
grafts have been used with satisfactory and equivalent success. An antegrade bypass also can be performed using a
small-caliber bifurcated graft from the supraceliac aorta to both the CA and SMA, which yields an excellent long-term
result.76
CELIAC ARTERY COMPRESSION SYNDROME

The decision to intervene in patients with CA compression syndrome should be based on both an appropriate symptom
complex and the finding of CA compression in the absence of other findings to explain the symptoms. The treatment
goal is to release the ligamentous structure that compresses the proximal CA and to correct any persistent stricture by
bypass grafting. The patient should be cautioned that relief of the celiac compression cannot be guaranteed to relieve
the symptoms. In a number of reports on endovascular management of chronic mesenteric ischemia, the presence of CA
compression syndrome has been identified as a major factor of technical failure and recurrence. Therefore, angioplasty
and stenting should not be undertaken if extrinsic compression of the CA by the median arcuate ligament is suspected
based on preoperative imaging studies. Open surgical treatment should be performed instead.77,78
Endovascular Treatment
CHRONIC MESENTERIC ISCHEMIA
Endovascular treatment of mesenteric artery stenosis or short segment occlusion by balloon dilatation or stent
placement represents a less invasive therapeutic alternative to open surgical intervention, particularly in patients whose
medical comorbidities place them in a high operative risk category. Endovascular therapy is also suited to patients with
recurrent disease or anastomotic stenosis following previous open mesenteric revascularization. Prophylactic mesenteric
revascularization is rarely performed in the asymptomatic patient undergoing an aortic procedure for other indications.79
However, the natural history of untreated chronic mesenteric ischemia may justify revascularization in some minimally
symptomatic or asymptomatic patients if the operative risks are acceptable, because the first clinical presentation may
be acute intestinal ischemia in as many as 50% of the patients, with a mortality rate that ranges from 15 to 70%.79 This
is particularly true when the SMA is involved. Mesenteric angioplasty and stenting is particularly suitable for this patient
subgroup given its low morbidity and mortality. Because of the limited experience with stent use in mesenteric vessels,
appropriate indications for primary stent placement have not been clearly defined. Guidelines generally include calcified
ostial stenoses, high-grade eccentric stenoses, chronic occlusions, and significant residual stenosis greater than 30% or
the presence of dissection after angioplasty. Restenosis after PTA is also an indication for stent placement.80
ACUTE MESENTERIC ISCHEMIA

Catheter-directed thrombolytic therapy is a potentially useful treatment modality for acute mesenteric ischemia, which
can be initiated with intra-arterial delivery of thrombolytic agent into the mesenteric thrombus at the time of diagnostic
angiography. Various thrombolytic medications, including urokinase (Abbokinase, Abbott Laboratory, North Chicago, Ill)
or recombinant tissue plasminogen activator (Activase, Genentech, South San Francisco, Calif), have been reported to
be successful in a small series of case reports. Catheter-directed thrombolytic therapy has a higher probability of
restoring mesenteric blood flow success when performed within 12 hours of symptom onset. Successful resolution of a
mesenteric thrombus will facilitate the identification of the underlying mesenteric occlusive disease process. As a result,
subsequent operative mesenteric revascularization or mesenteric balloon angioplasty and stenting may be performed
electively to correct the mesenteric stenosis. There are two main drawbacks with regard to thrombolytic therapy in
mesenteric ischemia. Percutaneous, catheter-directed thrombolysis (CDT) does not allow the possibility to inspect the
potentially ischemic intestine following restoration of the mesenteric flow. Additionally, a prolonged period of time may
be necessary to achieve successful CDT, due in part to serial angiographic surveillance to document thrombus
resolution. An incomplete or unsuccessful thrombolysis may lead to delayed operative revascularization, which may
further necessitate bowel resection for irreversible intestinal necrosis. Therefore, catheter-directed thrombolytic therapy
for acute mesenteric ischemia should only be considered in selected patients under a closely scrutinized clinical protocol.
NONOCCLUSIVE MESENTERIC ISCHEMIA

The treatment of nonocclusive mesenteric ischemia is primarily pharmacologic with selective mesenteric arterial
catheterization followed by infusion of vasodilatory agents such as tolazoline or papaverine. Once the diagnosis is made
on the mesenteric arteriography (see Fig. 23-42), intra-arterial papaverine is given at a dose of 30 to 60 mg/h. This
must be coupled with the cessation of other vasoconstricting agents. Concomitant IV heparin should be administered to
prevent thrombosis in the cannulated vessels. Treatment strategy thereafter is dependent on the patient's clinical
response to the vasodilator therapy. If abdominal symptoms improve, mesenteric arteriography should be repeated to
document the resolution of vasospasm. The patient's hemodynamic status must be carefully monitored during
papaverine infusion, as significant hypotension can develop in the event that the infusion catheter migrates into the
aorta, which can lead to systemic circulation of papaverine. Surgical exploration is indicated if the patient develops signs
of continued bowel ischemia or infarction as evidenced by rebound tenderness or involuntary guarding. In these
circumstances, papaverine infusion should be continued intraoperatively and postoperatively. The OR should be kept as
warm as possible, and warm irrigation fluid and laparotomy pads should be used to prevent further intestinal
vasoconstriction during exploration.
TECHNIQUES OF ENDOVASCULAR INTERVENTIONS

To perform endovascular mesenteric revascularization, intraluminal access is performed via a femoral or brachial artery
approach. Once an introducer sheath is placed in the femoral artery, an anteroposterior and lateral aortogram just below
the level of the diaphragm is obtained with a pigtail catheter to identify the origin of the CA and SMA. Initial
catheterization of the mesenteric artery can be performed using a variety of selective angled catheters, which include
the RDC, Cobra-2, Simmons I (Boston Scientific/Meditech, Natick, Mass), or SOS Omni catheter (AngioDynamics,
Queensbury, NY). Once the mesenteric artery is cannulated, systemic heparin (5000 IU) is administered IV. A selective
mesenteric angiogram is then performed to identify the diseased segment, which is followed by the placement of a
0.035-in or less traumatic 0.014- to 0.018-in guidewire to cross the stenotic lesion. Once the guidewire is placed across
the stenosis, the catheter is carefully advanced over the guidewire across the lesion. In the event that the mesenteric
artery is severely angulated as it arises from the aorta, a second stiffer guidewire (Amplatz or Rosen Guidewire, Boston
Scientific) may be exchanged through the catheter to facilitate the placement of a 6F guiding sheath (Pinnacle, Boston
Scientific).
With the image intensifier angled in a lateral position to fully visualize the proximal mesenteric segment, a balloon
angioplasty is advanced over the guidewire through the guiding sheath and positioned across the stenosis. The balloon
diameter should be chosen based on the vessel size of the adjacent normal mesenteric vessel. Once balloon angioplasty
is completed, a postangioplasty angiogram is necessary to document the procedural result. Radiographic evidence of
either residual stenosis or mesenteric artery dissection constitutes suboptimal angioplasty results that warrant
mesenteric stent placement. Moreover, atherosclerotic involvement of the proximal mesenteric artery or vessel orifice
should be treated with a balloon-expandable stent placement. These stents can be placed over a low profile 0.014- or
0.018-in guidewire system. It is preferable to deliver the balloon-mounted stent through a guiding sheath, which is
positioned just proximal to the mesenteric orifice while the balloon-mounted stent is advanced across the stenosis. The
stent is next deployed by expanding the angioplasty balloon to its designated inflation pressure. The balloon is then
deflated and carefully withdrawn through the guiding sheath.
Completion angiogram is performed by hand injecting a small volume of contrast though the guiding sheath. It is critical
to maintain the guidewire access until a satisfactory completion angiogram is obtained. If the completion angiogram
reveals suboptimal radiographic results, such as residual stenosis or dissection, additional catheter-based intervention
can be performed through the same guidewire. These interventions may include repeat balloon angioplasty for residual
stenosis or additional stent placement for mesenteric artery dissection. During the procedure, intra-arterial infusion of
papaverine or nitroglycerine can be used to decrease vasospasm. Administration of antiplatelet agents is also
recommended, for at least 6 months or even indefinitely if other risk factors of cardiovascular disease are present.
COMPLICATIONS OF ENDOVASCULAR TREATMENT

Complications are not common and rarely become life threatening. These include access site thrombosis, hematomas,
and infection. Dissection can occur during PTA and is managed with placement of a stent. Balloon-mounted stents are
preferred over the self-expanding ones because of the higher radial force and the more precise placement. Distal
embolization has also been reported but it never resulted in acute intestinal ischemia, likely due to the rich network of
collaterals already developed.81
Clinical Results of Interventions for Mesenteric Ischemia

The first successful percutaneous angioplasty of the SMA was reported in 1980.82 Since 1995, 11 series and multiple
scattered case reports have reported results from endovascular management of mesenteric occlusive disease.76,81 In a
literature review, Aburhama and associates showed that endovascular intervention had an overall technical success rate
of 91%, early and late pain relief of 84 and 71%, respectively, and 30-day morbidity and mortality rates of 16.4 and
4.3, respectively. The average patency was 63% during an average 26-month follow-up.81
In a recent review of the literature from published series since 1995, restenosis was developed in 22% of patients
during 24.5 months of average follow-up.76 The long-term clinical relief without reintervention was 82%. Among the
patients that had a technical failure, 15 were ultimately diagnosed with median arcuate ligament syndrome and
underwent successful surgical treatment, an observation that emphasizes the need for careful patient selection.
Interestingly, the addition of selective stenting after PTA that was started in 1998 slightly increases the technical
success rate, but is not correlated with any substantial overall clinical benefit or improved, long-term patency rates.
In contrast to the endovascular treatment, open surgical techniques have achieved an immediate clinical success that
approaches 100%, a surgical mortality rate from 0 to 17%, and an operative morbidity rate that ranges from 19 to 54%
in a number of different series.76,78,79 AbuRahma and colleagues reported their experience of endovascular
interventions of 22 patients with symptomatic mesenteric ischemia due to either SMA or CA stenosis.81 They noted
excellent initial technical and clinical success rates, which were 96% (23/24) and 95% (21/22), respectively, with no
perioperative mortality or major morbidity. During a mean follow-up of 26 months (range 1 to 54 months), the primary
late clinical success rate was 61% and freedom from recurrent stenosis was 30%.The freedom from recurrent stenosis
rates at 1, 2, 3, and 4 years were 65%, 47%, 39%, and 13%, respectively. The authors concluded that mesenteric
stenting, which provides excellent early results, is associated with a relatively high incidence of late restenosis.81
Several studies have attempted to compare the endovascular to standard open surgical approach.83,84 The results of
the open surgery appear to be more durable, but tend to be associated with higher morbidity and mortality rates and an
overall longer hospital stay. In one study that compared the clinical outcome of open revascularization with
percutaneous stenting for patients with chronic mesenteric ischemia, 28 patients underwent endovascular treatment and
85 patients underwent open mesenteric bypass grafting.84 Both patient cohorts had similar baseline comorbidities and
symptom duration, so there was no difference in early inhospital complication or mortality rates. Moreover, both groups
had similar 3-year cumulative recurrent stenosis and mortality rates. However, patients treated with mesenteric stenting
had a significantly higher incidence of recurrent symptoms. The authors concluded that operative mesenteric
revascularization should be offered to patients with low surgical risk.84
Based on the above results one could argue that mesenteric angioplasty and stenting demonstrate an inferior technical
and clinical success rate. Long-term patency rates appear to also be superior with the open technique. There is a
general consensus, however, that the endovascular approach is associated with lower morbidity and mortality rates and
is therefore more suitable for high-risk patients. One should also keep in mind that practices representing standard of
care for stent placement today were absent in the early era of endovascular experience. These include perioperative
heparinization and short-term antiplatelet therapy, use of stents with higher radial force, routine use of postoperative
surveillance with arterial duplex and early reintervention to prevent a high-grade stenosis to progress to occlusion, and
placement of drug-eluting stents (DES).
RENAL ARTERY DISEASE

Obstructive lesions of the renal artery can produce hypertension, resulting in a condition known as renovascular
hypertension, which is the most common form of hypertension amenable to therapeutic intervention, and affects 5 to
10% of all hypertensive patients in the United States.85 Patients with renovascular hypertension are at an increased risk
for irreversible end-organ dysfunction, including permanent kidney damage, if inadequate pharmacologic therapies are
used to control the BP. The majority of patients with renal artery obstructive disease have vascular lesions of either
atherosclerotic disease or fibrodysplasia involving the renal arteries. The proximal portion of the renal artery represents
the most common location for the development of atherosclerotic disease. It is well established that renal artery
intervention, either by surgical or endovascular revascularization, provides an effective treatment for controlling
renovascular hypertension as well as preserving renal function. The decision for intervention is complex, and needs to
take into consideration a variety of anatomic, physiologic, and clinical features, unique for the individual patient.
Etiology
Approximately 80% of all renal artery occlusive lesions are caused by atherosclerosis, which typically involves a short
segment of the renal artery ostia, and represents spillover disease from a severely atheromatous aorta (Fig. 23-43).86
Atherosclerotic lesions are bilateral in two thirds of patients. Individuals with this disease commonly present during the
sixth decade of life. Men are affected twice as frequently as women. Atherosclerotic lesions in other territories such as
the coronary, mesenteric, cerebrovascular, and peripheral arterial circulation are common. When a unilateral lesion is
present, the disease process equally affects the right and left renal artery.87
Fig. 23-43.
Occlusive disease of the renal artery typically involves the renal ostium (arrow) as a spillover plaque extension from aortic
atherosclerosis.
The second most common cause of renal artery stenosis is FMD, which accounts for 20% of cases, and is most
frequently encountered in young, often multiparous women.88 FMD of the renal artery represents a heterogeneous
group of lesions that can produce histopathologic changes in the intima, media, or adventitia. The most common variety
consists of medial fibroplasia, in which thickened fibromuscular ridges alternate with attenuated media producing the
classic angiographic "string of beads" appearance (Figs. 23-44 and 23-45). The cause of medial fibroplasia remains
unclear. Most common theories involve a modification of arterial smooth muscle cells in response to estrogenic stimuli
during the reproductive years, unusual traction forces on affected vessels, and mural ischemia from impairment of vasa
vasorum blood flow.88 Fibromuscular hyperplasia usually affects the distal two thirds of the main renal artery, and the
right renal artery is affected more frequently than the left. Other less common causes of renal artery stenosis include
renal artery aneurysm (compressing the adjacent normal renal artery), arteriovenous malformations, neurofibromatosis,
renal artery dissections, renal artery trauma, Takayasu's arteritis, and renal arteriovenous fistula.
Fig. 23-44.
Abdominal aortogram revealed a left renal artery fibromuscular dysplasia (arrows) with a characteristic "string of beads"
appearance.
Fig. 23-45.
Magnetic resonance angiography of the abdominal aorta revealed the presence of a left renal artery fibromuscular dysplasia
(arrows).
Renovascular hypertension is the most common sequelae of renal artery occlusive disease. Its prevalence varies from
2% in patients with diastolic BP >100 mmHg, to almost 30% in those with diastolic BP over 125 mmHg.86 Clinical
features that may indicate the presence of renovascular hypertension include the following: (a) systolic and diastolic
upper abdominal bruits, (b) diastolic hypertension of >115 mmHg, (c) rapid onset of hypertension after the age of 50
years, (d) a sudden worsening of mild to moderate essential hypertension, (e) hypertension that is difficult to control
with three or more antihypertensives, (f) development of renal insufficiency after ACE inhibitors, and (g) development of
hypertension during childhood.
All patients with significant hypertension, especially elevated diastolic BP, must be considered as suspect for
renovascular disease. Young adults with hypertension have a great deal to gain by avoiding lifelong treatment if
renovascular hypertension is diagnosed and corrected. Appropriate diagnostic studies and intervention must be timely
instituted to detect the possibility of renovascular hypertension in patients with primary hypertension who present for
clinical evaluation.
The diagnostic requisites for renovascular hypertension include both hypertension and renal artery stenosis. Impairment
of the renal function may coexist, although the occurrence of renal insufficiency before the development of hypertension
is uncommon. Nearly all diagnostic studies for renovascular hypertension evaluate either the anatomic stenosis or renal
parenchymal dysfunction attributed to the stenosis. This section provides an overview of the strengths and limitations of
the most common tests used in the diagnostic evaluation of the patient with suspected renovascular hypertension before
intervention.
Captopril renal scanning is a functional study that assesses renal perfusion before and after administration of the ACE
inhibitor captopril. Captopril inhibits the secretion of angiotensin II. Through this mechanism it reduces the efferent
arteriole vasoconstriction and, as a result, the glomerular filtration rate (GFR). The test consists of a baseline renal scan,
and a second renal scan after captopril administration. Positive result indicates that captopril administration (a)
increases the time to peak activity to more than 11 minutes or (b) the GFR ratio between sides increases to greater than
1.5:1 compared to a normal baseline scan. Significant parenchymal disease limits the reliability of this study.
Renal artery duplex ultrasonography is a noninvasive test of assessing renal artery stenosis both by visualization of the
vessel and measurement of the effect of stenosis on blood flow velocity and waveforms. The presence of a severe renal
artery stenosis correlates with peak systolic velocities of >180 cm/s and the ratio of these velocities to those in the
aorta of >3.5 (Table 23-11). Renal artery duplex is a technically demanding examination, requiring a substantial amount
of operator expertise. In addition, the presence of bowel gas and obesity make the exam difficult to perform and
interpret. However, in experienced hands and with appropriate patient selection, it can be a high-yield examination and
is typically the initial screening test for patients with suspected renal artery occlusive disease.
Table 23-11 Renal Duplex Diagnostic Criteria
Renal Artery Diameter Reduction Renal Artery PSV RAR

Normal <180 cm/s <3.5
<60% ≥180 cm/s <3.5
≥60% ≥180 cm/s ≥3.5
Occlusion No signal No signal
PSV = peak systolic velocity; RAR = renal-to-aortic ratio.
Selective catheterization of the renal vein via a femoral vein approach for assessing renin activity is a more invasive test
of detecting the physiologic sequelae of renal artery stenosis. If unilateral disease is present the affected kidney should
secrete high levels of renin while the contralateral kidney should have low renin production. A ratio between the two
kidneys, or the renal vein renin ratio, of >1.5 is indicative of functionally important renovascular hypertension, and it
also predicts a favorable response from renovascular revascularization. Because this study assesses the ratio between
the two kidneys, it is not useful in patients with bilateral disease because both kidneys may secrete abnormally elevated
renin levels.
The renal:systemic renin index (RSRI) is calculated by subtracting systemic renin activity from individual renal vein
renin activity and dividing the remainder by systemic renin activity. This value represents the contribution of each
kidney to renin production. In the absence of renal artery stenosis, the renal vein renin activity from each kidney is
typically 24% or 0.24 higher than the systemic level. As the result, the total of both kidneys' renin activity is usually
48% greater than the systemic activity, a value that represents a steady state of renal renin activity. The RSRI of the
affected kidney in patients with renovascular hypertension is >0.24. In the case of unilateral renal artery stenosis with
normal contralateral kidney, the increase in ipsilateral renin release is normally balanced by suppression of the
contralateral kidney renin production, which results in a drop in its RSRI to <0.24. Bilateral renal artery disease may
negate the contralateral compensatory response, and the autonomous release of renin from both diseased kidneys may
result in the sum of the individual RSRIs being considerably >0.48. The prognostic value of RSRI remains limited in that
approximately 10% of patients with favorable clinical response following renovascular revascularization do not exhibit
contralateral renin suppression. As a result, the use of RSRI must be applied with caution in the management of patients
with renovascular hypertension.
MRA with IV gadolinium contrast enhancement has been increasingly used for renal artery imaging because of its ability
to provide high-resolution images (Figs. 23-46 and 23-47) while using a minimally nephrotoxic agent. Flow void may be
inaccurately interpreted as occlusion or stenosis in MRA. Therefore, unless the quality of the image analysis software is
superior, MRA should be interpreted with caution and used in conjunction with other modalities before making plans for
operative or endovascular treatment.
Fig. 23-46.
Magnetic resonance angiography of the abdominal aorta revealed bilateral normal renal arteries.
Fig. 23-47.
Magnetic resonance angiography of the abdominal aorta revealed bilateral ostial renal artery stenosis (arrows).
DSA remains the gold standard to assess renal artery occlusive disease. A flush aortogram is performed first so that any
accessory renal arteries can be detected and the origins of all the renal arteries are adequately displayed. The presence
of collateral vessels circumventing a renal artery stenosis strongly supports the hemodynamic importance of the
stenosis. A pressure gradient of 10 mmHg or greater is necessary for collateral vessel development, which also is
associated with activation of the renin-angiotensin cascade.
Treatment Indications
The therapeutic goals in patients with renovascular disease include: (a) improved BP control to prevent end-organ
damage on systems such as the cerebral, coronary, pulmonary, and peripheral circulations; and (b) preservation and
possibly improvement of the renal function (Table 23-12).
Table 23-12 Indications for Renal Artery Revascularization
Angiography criteria
Fibromuscular dysplasia lesion
Pressure gradient >20 mmHg
Affected/unaffected kidney renin ratio >1.5:1
Clinical criteria
Refractory or rapidly progressive hypertension
Hypertension associated with flash pulmonary edema without coronary artery disease
Rapidly progressive deterioration in renal function
Intolerance to antihypertensive medications
Chronic renal insufficiency related to bilateral renal artery occlusive disease or stenosis to a solitary functioning
kidney
Dialysis-dependent renal failure in a patient with renal artery stenosis but without another definite cause of end-stage
renal disease
Recurrent congestive heart failure or flash pulmonary edema not attributable to active coronary ischemia
The indications for endovascular treatment for renal artery occlusive disease include 70% or greater stenosis of one or
both renal arteries and at least one of the following clinical criteria:
n Inability to adequately control hypertension despite appropriate antihypertensive regimen.
n Chronic renal insufficiency related to bilateral renal artery occlusive disease or stenosis to a solitary
functioning kidney.
n Dialysis-dependent renal failure in a patient with renal artery stenosis but without another definite cause of
end-stage renal disease.
n Recurrent congestive heart failure or flash pulmonary edema not attributable to active coronary ischemia.
Before 1990, the most common treatment modality in patients with renal artery occlusive disease was surgical
revascularization, with either renal artery bypass grafting or renal artery endarterectomy. The advancement of
endovascular therapy in the past decade has led to various minimally invasive treatment strategies such as renal artery
balloon angioplasty or stenting to control hypertension or to preserve renal function.
Surgical Reconstruction
The typical approach for surgical renal artery revascularization involves a midline xiphoid-to-pubis incision. The posterior
peritoneum is incised, and the duodenum is mobilized to the right, starting at the ligament of Treitz. The left renal hilum
can be exposed by extending the retroperitoneal dissection to the left along the avascular plane along the inferior border
of the pancreas. Mobilization of the left renal vein is essential in these cases and can be achieved by dividing the
gonadal, iliolumbar, and adrenal veins. The proximal portion of the right renal artery can be exposed through the base
of the mesentery by retraction of the left renal vein cephalad and the vena cava to the right. Accessing the most distal
portion of the right renal artery requires a Kocher maneuver and duodenal mobilization. Another approach useful for
treating bilateral renal artery lesions involves mobilization of the entire small bowel and the right colon, with a dissection
that starts at the ligament of Treitz, and proceeds toward the cecum and then along the line of Todd in the right
paracolic gutter. Simultaneous dissection along the inferior border of the pancreas provides additional visualization of
the left renal artery. Finally, division of the diaphragmatic crura that encircle the suprarenal aorta may sometimes be
necessary to achieve suprarenal clamping.
TYPES OF SURGICAL RECONSTRUCTION

Aortorenal bypass is the most frequently performed reconstruction of ostial occlusive renal artery disease. After proximal
and distal control is obtained, an elliptical segment of the aorta is excised, and the proximal anastomosis is performed in
end-to-side fashion. Autologous vein is the preferred conduit. If the vein is not suitable, then prosthetic material can be
used. An end-to-end anastomosis is then performed between the conduit of choice and the renal artery using either a 6-
0 or 7-0 polypropylene suture. The length of the arteriotomy needs to be at least three times the diameter of the renal
artery to prevent anastomotic restenosis. If the surgeon plans to perform a side-to-side anastomosis between the
conduit and the renal artery, then it is performed first, and the aortic anastomosis follows.
Endarterectomy, either transrenal or transaortic, is an alternative to bypass for short ostial lesions, or in patients with
multiple renal arteries. The transrenal endarterectomy is performed with a transverse longitudinal incision on the aorta
that extends into the diseased renal artery. After the plaque removal, the arteriotomy is closed with a prosthetic patch.
Transaortic endarterectomy is well suited for patients with multiple renal arteries and short ostial lesions. The aorta is
opened longitudinally and aortic sleeve endarterectomy is performed, followed by eversion endarterectomy of the renal
arteries. Adequate mobilization of the renal arteries is essential for a safe and complete endarterectomy.
Hepatorenal and splenorenal bypass are alternative options of revascularizations for patients who might not tolerate
aortic clamping, or for those with calcified aorta that precludes adequate control. For hepatorenal bypass, a right
subcostal incision is used, and the hepatic artery is exposed with an incision in the lesser omentum. A Kocher maneuver
is performed, the right renal vein is identified and mobilized, and the right renal artery is identified and controlled
posteriorly to the vein. The greater saphenous vein is the conduit of choice. The anastomosis is performed end to side
with the common hepatic artery, and end to end with the renal artery anterior to the inferior vena cava. The splenorenal
bypass is performed via a left subcostal incision. The splenic artery is mobilized from the lesser sac, brought through a
retropancreatic plane, and anastomosed end to end to the renal artery.
Reimplantation of the renal artery is an attractive option of reconstruction in children, or in adults with ostial lesions. A
redundant renal artery is a prerequisite for the procedure. After mobilization, the artery is transected and spatulated,
eversion endarterectomy is performed, if necessary, and an end-to-side anastomosis with the aorta is created.
Clinical Results of Surgical Repair

Results reflect the need for performance of renal artery bypass in high-volume and experienced centers. In a review
from a large tertiary center, 92% of the patients with non-atherosclerotic vascular disease had good response to
hypertension, but only 43% were completely cured and were taken off antihypertensives.89 Patients younger than 45
years old fare better with a cure rate of 68% and an improvement rate of 32%. In patients with atherosclerotic renal
artery disease, the cure rate was even smaller (12%), and the overall response to hypertension rate was 85%. The
operative mortality was 3.1% and 0% in the atherosclerotic and non-atherosclerotic groups, respectively.
Renal function improvement occurs within the first week of the operation in approximately two thirds of the patients. A
progressive decrease in the GFR is seen after this initial improvement, but the rate of decrease is less compared to the
group of patients who did not respond at all to operative intervention. Up to three fourths of patients were permanently
removed from dialysis in a large series.90 Favorable response of renal function to revascularization improves overall
survival.
Endovascular treatment of renal artery occlusive disease was first introduced by Grüntzig who successfully dilated a
renal artery stenosis using a balloon catheter technique. This technique requires passage of a guidewire under
fluoroscopic control typically from a femoral artery approach to across the stenosis in the renal artery. A balloon-dilating
catheter is passed over the guidewire and positioned within the area of stenosis and inflated to produce a controlled
disruption of the arterial wall. Alternatively, a balloon-mounted, expandable stent can be used to primarily dilate the
renal artery stenosis. Completion angiography usually is performed to assess the immediate results. The technical
aspect of an endovascular renal artery revascularization is discussed in Techniques of Renal Artery Angioplasty and
Stenting below.
TECHNIQUES OF RENAL ARTERY ANGIOPLASTY AND STENTING

Access to the renal artery for endovascular intervention is typically performed via a femoral artery approach, although a
brachial artery approach can be considered in the event of severe aortoiliac occlusive disease, aortoiliac aneurysm, or
severe caudal renal artery angulation. Once an introducer sheath is placed in the femoral artery, an aortogram is
performed with a pigtail catheter placed in the suprarenal aorta. Additional oblique views are frequently necessary to
more precisely visualize the orifice of the stenosed renal artery and thoroughly assess the presence of accessory renal
arteries. Noniodinated contrast agents such as carbon dioxide and gadolinium can be used in endovascular renal
intervention in patients with renal dysfunction or history of allergic reaction.
After systemic heparinization, catheterization of the renal artery can be performed using a variety of selective angled
catheters including the RDC, Cobra-2, Simmons I, or SOS Omni catheter (Boston Scientific/Meditech, Natick, Mass;
Cook, Bloomington, Ind; Medtronic, Santa Rosa, Calif, Cordis, Warren, NJ; or AngioDynamics, Queensbury, NY). A
selective renal angiogram is then performed to confirm position, and the lesion is crossed with either a 0.035-in or a
0.018- to 0.014-in guidewire. It is important to maintain the distal wire position without movement in the tertiary renal
branches while guiding sheath placement to reduce the possibility of parenchymal perforation and spasm. A guiding
sheath or a guiding catheter is then advanced at the orifice of the renal artery to provide a secure access for balloon and
stent deployment.
Balloon angioplasty is performed with a balloon sized to the diameter of the normal renal artery adjacent to the
stenosis. Choosing a balloon with a 4-mm diameter is a reasonable first choice. The luminal diameter of the renal artery
can be further assessed by comparing it to the fully inflated balloon. Such a comparison may provide a reference guide
to determine whether renal artery dilatation with a larger diameter angioplasty balloon is necessary.
Once balloon angioplasty of the renal artery is completed, an angiogram is performed to document the procedural
result. Radiographic evidence of either residual stenosis or renal artery dissection constitutes suboptimal angioplasty
results, which warrants an immediate renal artery stent placement. Moreover, atherosclerotic involvement of the very
proximal renal artery that involves the vessel orifice typically requires stent placement. A balloon-expandable stent is
typically used, and is positioned in such a way so that it protrudes into the aorta by 1 to 2 mm. The size of the stent is
determined by the size of the renal artery, taking into account a desirable 10 to 20% oversizing. After the stent
deployment, the angiogram is repeated and, upon a satisfactory result, the devices are withdrawn. It is critical to
maintain the guidewire access across the renal lesion until satisfactory completion angiogram is obtained. Spasm of the
branches of the renal artery will usually respond to nitroglycerin 100 to 200 mcg administered through the guiding
sheath directly into the renal artery.
While endovascular therapy of renal artery occlusive disease is considerably less invasive than conventional renal artery
bypass operation, complications relating to this treatment modality can occur. In a study in which Guzman and
colleagues compared the complications following renal artery angioplasty and surgical revascularization, the authors
noted that major complication rates following endovascular and surgical treatment were 17% and 31%, respectively. In
contrast, significantly greater minor complications were associated with the endovascular cohort, which was 48%, in
contrast to 7% in the surgical group.91 In a prospective randomized study that compared the clinical outcome of renal
artery balloon angioplasty vs. stenting for renal ostial atherosclerotic lesion, comparable complications rates were found
in the two groups, which were 39% and 43%, respectively. However, the incidence of restenosis rate at 6 months was
significantly higher in the balloon angioplasty cohort than the stenting group, which was 48% in contrast to 14% at 6
months. This study underscores the clinical superiority of renal stenting compared to renal balloon angioplasty alone in
patients with ostial stenosis.92
Deterioration in renal function, albeit transient, is a common complication following endovascular renal artery
intervention. This is most likely the combined result of the use of iodinated contrast, and the occurrence of renal
parenchymal embolism due to wire and catheter manipulation. In most cases, this is a temporary problem, as
supportive care with adequate fluid hydration is sufficient to reverse the renal dysfunction. However, transient
hemodialysis may become necessary in approximately 1% of patients. Other complications include vascular access
complications (bleeding, hematoma, femoral nerve injury, arteriovenous fistula, and pseudoaneurysm), target vessel
dissection, perinephric hematoma, early postoperative renal artery thrombosis, and extremity atheroembolism from
thrombus in the aorta or the iliac arteries.
Clinical Results of Endovascular Interventions

PERCUTANEOUS TRANSLUMINAL BALLOON ANGIOPLASTY
FMD of the renal artery is the most common treatment indication for percutaneous, transluminal balloon angioplasty.
Patients with symptomatic FM, such as hypertension or renal insufficiency, usually respond well to renal artery balloon
angioplasty alone.93 In contrast, balloon angioplasty generally is not an effective treatment for patients with renal artery
stenosis or proximal occlusive disease of the renal artery, due to the high incidence of restenosis with balloon
angioplasty alone. In the latter group of patients, primary stent placement is the preferred endovascular treatment. The
long-term benefit of renal artery balloon angioplasty in patients with FMD was reported by Surowiec and colleagues.93
They followed 14 patients who underwent 19 interventions on 18 renal artery segments. The technical success rate of
balloon angioplasty for FMD was 95%. Primary patency rates were 81%, 69%, 69%, and 69% at 2, 4, 6, and 8 years,
respectively. Assisted primary patency rates were 87%, 87%, 87%, and 87% at 2, 4, 6, and 8 years, respectively. The
restenosis rate was 25% at 8 years. Clinical benefit, as defined by either improved or cured hypertension, was found in
79% of patients overall, with two thirds of patients having maintained this benefit at 8 years. The authors concluded
that balloon angioplasty is highly effective in symptomatic FMD with excellent durable functional benefits.93
The utility of balloon angioplasty alone in the treatment of renovascular hypertension appears to be limited. Van
Jaarsveld and associates performed a prospective study in which patients with renal artery stenosis were randomized to
either drug therapy or balloon angioplasty treatment.94 A total of 106 patients with 50% diameter stenosis or greater
plus hypertension or renal insufficiency were randomized in the study. At 3 months, there was no difference in the
degree to which BP was controlled between the two groups. However, the degree and dose of antihypertensive
medications was slightly lowered in the balloon angioplasty group. The above advantage of the angioplasty group
completely disappeared at 12 months, making the authors conclude that, in the treatment of patients with hypertension
and renal artery stenosis, percutaneous transluminal balloon angioplasty alone offers minimal advantage over
antihypertensive drug therapy.
RENAL ARTERY STENTING

Endovascular stent placement is the treatment of choice for patients with symptomatic or high-grade renal artery
occlusive disease (Fig. 23-48). This is due in part to the high incidence of restenosis with balloon angioplasty alone,
particularly in the setting of ostial stenosis. Renal artery stenting is also indicated for renal artery dissection caused by
balloon angioplasty or other catheter-based interventions. Numerous studies have clearly demonstrated the clinical
efficacy of renal artery stenting when compared to balloon angioplasty alone in patients with high-grade renal artery
stenosis.
Fig. 23-48.
Renal artery stenting. A. Focal lesion in the renal artery (arrow). B. Poststenting angiogram reveals a satisfactory result following
a renal artery stenting placement (arrow).
White and colleagues conducted a study to evaluate the role of renal artery stenting in patients with poorly controlled
hypertension and renal artery lesions that did not respond well to balloon angioplasty alone.95 The technical success of
the procedure was 99%. The mean BP values were 173 ± 25/88 ± 17 mmHg before stent implantation and 146 ± 20/77
± 12 mmHg 6 months after renal artery stenting (P <.01). Angiographic follow-up with 67 patients (mean 8.7 ± 5
months) demonstrated restenosis, as defined by 50% or greater luminal narrowing, occurred in 15 patients (19%). The
study concluded that renal artery stenting is a highly effective treatment for renovascular hypertension, with a low
angiographic restenosis rate. In another similar study, Blum and colleagues prospectively performed renal artery
stenting in 68 patients (74 lesions) with ostial renal artery stenosis and suboptimal balloon angioplasty.96 Patients were
followed for a mean of 27 months with measurements of BP and serum creatinine (Scr), duplex sonography, and intra-
arterial angiography. Five-year patency was 84.5% (mean follow-up was 27 months). Restenosis occurred in eight of 74
arteries (11%), but, after reintervention, the secondary, 5-year patency rate was 92.4%. BP was cured or improved in
78% of patients. The authors concluded that primary stent placement is an effective treatment for renal artery stenosis
involving the ostium.
The clinical utility of renal artery stenting in renal function preservation was analyzed by several studies, which
measured serial Scr levels to determine the response of renal function following endovascular intervention.97 In a study
reported by Harden and colleagues, who performed 33 renal artery stentings in 32 patients with renal insufficiency, they
noted that renal function improved or stabilized in 22 patients (69%).98 In a similar study, Watson and associates
evaluated the effect of renal artery stenting on renal function by comparing the slopes of the regression lines derived
from the reciprocal of Scr vs. time.97 With a total of 61 renal stentings performed in 33 patients, the authors found that
after stent placement, the slopes of the reciprocal of the serum creatinine (1/Scr) were positive in 18 patients and less
negative in seven patients. The study concludes that in patients with chronic renal insufficiency due to obstructive renal
artery stenosis, renal artery stenting is effective in improving or stabilizing renal function.
The clinical outcome of several large clinical studies of renal artery stenting in the treatment of renovascular
hypertension or chronic renal insufficiency is shown in Table 23-13.95,96,98–104 These studies uniformly demonstrated
an excellent technical success rate with low incidence of restenosis or procedural-related complications. A similar
analysis was reported by Leertouwer and colleagues who performed a meta-analysis of 14 studies comparing patients
with renal arterial stent placement to those who underwent balloon angioplasty alone for renal arterial stenosis.105 The
study found that stent placement proved highly successful, with an initial technical success of 98%. The overall cure rate
for hypertension was 20%, whereas hypertension was improved in 49%. Renal function improved in 30% and stabilized
in 38% of patients. The restenosis rate at follow-up of 6 to 29 months was 17%. Renal stenting resulted in a higher
technical success rate and a lower restenosis rate when compared to balloon angioplasty alone.
Table 23-13 Clinical Outcome of Renal Artery Stent Placement in the Treatment of
Renovascular Hypertension and Renal Insufficiency
Author Year Patient Technical Follow- Renal Renovascular Complications Restenosis

No. Success Up Insufficiency Hypertension (%) (%)
(%) (mo) (%) (%)
(%)
Stable Improved Cured Improved
Iannone102 1996 63 99 10 45 36 4 35 13 14
Harden98 1997 32 100 6 34 34 N/A N/A 3 13
Blum96 1997 68 100 27 N/A N/A 16 62 0 11
White95 1997 100 99 6 N/A 20 N/A N/A 2 19
Shannon104 1998 21 100 9 29 43 N/A N/A 9 0
Rundback103 1998 45 94 17 N/A N/A N/A N/A 9 25
Dorros100 1998 163 100 48 N/A N/A 3 51 11 N/A
Henry101 1999 210 99 25 N/A 29 19 61 3 9
Bush99 2001 73 89 20 21 38 13 61 12 16
N/A = not available.
AORTOILIAC OCCLUSIVE DISEASE

The distal abdominal aorta and the iliac arteries are common sites affected by atherosclerosis. The symptoms and
natural history of the atherosclerotic process affecting the aortoiliac arterial segment are influenced by the disease
distribution and extent. Atherosclerotic plaques may cause clinical symptoms by restricting blood flow due to luminal
obstruction or by embolizing atherosclerotic debris to the LE circulation. If the aortoiliac plaques reach sufficient mass
that impinge on the arterial lumen, obstruction of blood flow to lower extremities occurs. Various risk factors exist that
can lead to the development of aortoiliac occlusive disease. Recognition of these factors and understanding this disease
entity will enable physicians to prescribe the appropriate treatment strategy that may alleviate symptoms and improve
quality of life.
On clinical examination, patients often have weakened femoral pulses and a reduced ABI. Verification of iliac occlusive
disease is usually made by color duplex scanning that reveals either a peak systolic velocity ratio of 2.5 or greater at the
site of stenosis and/or a monophasic waveform. Noninvasive tests such as pulse volume recording (PVR) of the LE with
estimation of the thigh-brachial pressure index may be suggestive of aortoiliac disease. MRA and multidetector CTA are
increasingly being used to determine the extent and type of obstruction. DSA offers the interventionalist the benefit of
making a diagnosis and the option of performing an endovascular treatment in a single session. Angiography provides
important information regarding distal arterial runoff vessels as well as the patency of the profunda femoris artery
(PFA). Presence of pelvic and groin collaterals is important in providing crucial collateral flow in maintaining lower limb
viability. It must be emphasized, however, that patients should be subjected to angiography only if their symptoms
warrant surgical intervention.
Differential Diagnosis
Degenerative hip or spine disease, lumbar disc herniation, spinal stenosis, diabetic neuropathy, and other
neuromuscular problems can produce symptoms that may be mistaken for vascular claudication. Such cases can be
distinguished from true claudication by the fact that the discomfort from neuromuscular problems often is relieved by
sitting or lying down, as opposed to cessation of ambulation. In addition, complaints that are experienced upon standing
suggest nonvascular causes. When confusion persists, the use of noninvasive vascular laboratory testing modalities,
including treadmill exercise, can help establish the diagnosis.
Collateral Arterial Network

The principal collateral pathways in severe aortoiliac artery occlusive disease or chronic aortic occlusion that may
provide blood flow distal to the aortoiliac lesion include: (a) the SMA to the distal IMA via its superior hemorrhoidal
branch to the middle and inferior hemorrhoidals to the internal iliac artery (39%); (b) the lumbar arteries to the
superior gluteal artery to the internal iliac system (37%); (c) the lumbar arteries to the lateral and deep circumflex
arteries to the common femoral artery (CFA) (12%); and (d) Winslow's pathway from the subclavian to the superior
epigastric artery to the inferior epigastric artery to the external iliac arteries at the groin (Fig. 23-49). In general,
treatment indications for aortoiliac artery occlusive disease include disabling claudication, ischemic rest pain, nonhealing
LE tissue wound, and LE microembolization that arise from aortoiliac lesions.
Fig. 23-49.
Pertinent collateral pathways are developed in the event of chronic severe aortoiliac occlusive disease. As illustrated in this
multidetector computed tomography angiography, these collaterals include epigastric arteries (large white arrows), an enlarged
inferior mesenteric artery (white arrowhead), and enlarged lumbar arteries (black arrows).
Disease Classification
Based on the atherosclerotic disease pattern, aortoiliac occlusive disease can be classified into three various types (Fig.
23-50). Type I aortoiliac disease, which occurs in 5 to 10% of patients, is confined to the distal abdominal aorta and
common iliac vessels (Fig. 23-51). Due to the localized nature of this type of aortic obstruction and formation of
collateral blood flow around the occluded segment, limb-threatening symptoms are rare in the absence of more distal
disease (Fig. 23-52). This type of aortoiliac occlusive disease occurs in a relatively younger group of patients (aged in
their mid-50s), compared with patients who have more femoropopliteal disease. Patients with a type I disease pattern
have a lower incidence of hypertension and diabetes, but a significant frequency of abnormal blood lipid levels,
particularly type IV hyperlipoproteinemia. Symptoms typically consist of bilateral thigh or buttock claudication and
fatigue. Men report diminished penile tumescence and may have complete loss of erectile function. These symptoms in
the absence of femoral pulses constitute Leriche's syndrome. Rest pain is unusual with isolated aortoiliac disease unless
distal disease coexists. Occasionally patients report a prolonged history of thigh and buttock claudication that recently
has become more severe. It is likely that this group has underlying aortoiliac disease that has progressed to acute
occlusion of the terminal aorta. Others may present with "trash foot" that represents microembolization into the distal
vascular bed (Fig. 23-53).
Fig. 23-50.
Aortoiliac disease can be classified into three types. Type I represents focal disease affecting the distal aorta and proximal
common iliac artery. Type II represents diffuse aortoiliac disease above the inguinal ligament. Type III represents multisegment
occlusive disease involving aortoiliac and infrainguinal arterial vessels.
Fig. 23-51.
Type I aortoiliac disease is confined to the distal abdominal aorta (long arrow) or proximal common iliac arteries. Due to the
localized nature of this type of aortic obstruction and formation of collateral blood flow around the occluded segment (short
arrows), limb-threatening symptoms are rare in the absence of more distal disease.
Fig. 23-52.
Multidetector computed tomography angiography of the aortoiliac artery circulation in a 63-year-old man with buttock
claudication. Three-dimensional image reconstruction showing intra-arterial calcification of the aorta (large arrows) and right
common iliac artery (small arrows). This is consistent with a type I aortoiliac occlusive disease.
Fig. 23-53.
Atherosclerotic disease involving the aortoiliac segment can result in microembolization of the lower leg circulation, resulting in
trash foot or digital gangrene of toes.
Type II aortoiliac disease represents a more diffuse atherosclerotic progression that involves predominately the
abdominal aorta with disease extension into the CIA. This disease pattern affects approximately 25% of patients with
aortoiliac occlusive disease. Type III aortoiliac occlusive disease, which affects approximately 65% of patients with
aortoiliac occlusive disease, is widespread disease that is seen above and below the inguinal ligament (Fig. 23-54).
Patients with "multilevel" disease are older, more commonly male (with a male-to-female ratio of 6:1), and much more
likely to have diabetes, hypertension, and associated atherosclerotic disease involving cerebral, coronary, and visceral
arteries. Progression of the occlusive process is more likely in these patients than in those with localized aortoiliac
disease. For these reasons, most patients with a type III pattern tend to present with symptoms of advanced ischemia
and require revascularization for limb salvage rather than for claudication. These patients have a decreased 10-year life
expectancy when compared to patients with localized aortoiliac disease.
Fig. 23-54.
Type III aortoiliac occlusive disease is a multilevel disease pattern that affects the aortoiliac segment as well as infrainguinal
femoropopliteal vessels. Most patients with this disease pattern tend to present with symptoms of advanced ischemia and require
revascularization for limb salvage rather than for claudication.
The most commonly used classification system of iliac lesions has been set forth by the TASC II group with
recommended treatment options. This lesion classification categorizes the extent of atherosclerosis and has suggested a
therapeutic approach based on this classification (Table 23-14 and Fig. 23-55).2 According to this consensus document,
endovascular therapy is the treatment of choice for type A lesions, and surgery is the treatment of choice for type D
lesions. Endovascular treatment is the preferred treatment for type B lesions, and surgery is the preferred treatment for
good-risk patients with type C lesions. In comparison to the 2000 TASC II document, the commission has not only made
allowances for treatment of more extensive lesions, but also took into account the continuing evolution of endovascular
technology and the skills of individual interventionalists when stating that the patient's comorbidities, fully informed
patient preference, and the local operator's long-term success rates must be considered when making treatment
decisions for type B and type C lesions.2,106
Table 23-14 TASC II Classification of Aortoiliac Occlusive Lesions
Type A lesions
Unilateral or bilateral stenoses of CIA
Unilateral or bilateral single short (≤3 cm) stenosis of EIA
Type B lesions
Short (≤3 cm) stenosis of infrarenal aorta
Unilateral CIA occlusion
Single or multiple stenosis totaling 3–10 cm involving the EIA not extending into the CFA
Unilateral EIA occlusion not involving the origins of internal iliac or CFA
Type C lesions
Bilateral CIA occlusions
Bilateral EIA stenoses 3–10 cm long not extending into the CFA
Unilateral EIA stenosis extending into the CFA
Unilateral EIA occlusion that involves the origins of internal iliac and/or CFA
Heavily calcified unilateral EIA occlusion with or without involvement of origins of internal iliac and/or CFA
Type D lesions
Infrarenal aortoiliac occlusion
Diffuse disease involving the aorta and both iliac arteries requiring treatment
Diffuse multiple stenoses involving the unilateral CIA, EIA, and CFA
Unilateral occlusions of both CIA and EIA
Bilateral occlusions of EIA
Iliac stenoses in patients with AAA requiring treatment and not amenable to endograft placement or other lesions
requiring open aortic or iliac surgery
AAA = abdominal aortic aneurysm; CFA = common femoral artery; CIA = common iliac artery; EIA = external iliac
artery; TASC II = Trans-Atlantic Inter-Society Consensus.
Fig. 23-55.
Schematic depiction of Trans-Atlantic Inter-Society Consensus classification of aortoiliac occlusive lesions.
General Treatment Considerations

There is no effective medical therapy for the management of aortoiliac disease, but control of risk factors may help slow
progression of atherosclerosis. Patients should have hypertension, hyperlipidemia, and diabetes mellitus controlled. They
should be advised to stop smoking. Most patients are empirically placed on antiplatelet therapy. A graduated exercise
program may improve walking efficiency, endothelial function, and metabolic adaptations in skeletal muscle, but, there
is usually minimal improvement in patients with aortoiliac disease who are treated with these measures. Failure to
respond to exercise and/or drug therapy should prompt consideration for limb revascularization. Patients with buttock
claudication and reduced or absent femoral pulses who fail to respond to exercise and drug therapy should be
considered for revascularization because they are less likely than patients with more distal lesions to improve without
concomitant surgical or endovascular intervention.
Surgical Reconstruction of Aortoiliac Occlusive Disease

AORTOBIFEMORAL BYPASS
Surgical options for treatment of aortoiliac occlusive diseases consist of various configurations of aortobifemoral bypass
(ABF) grafting, various types of extra-anatomic bypass grafts, and aortoiliac endarterectomy. The procedure performed
is determined by several factors, including anatomic distribution of the disease, clinical condition of the patient, and
personal preference of the surgeon.
In most cases, ABF is performed because patients usually have disease in both iliac systems. Although one side may be
more severely affected than the other, progression does occur, and bilateral bypass does not complicate the procedure
or add to the physiologic stress of the operation. ABF reliably relieves symptoms, has excellent long-term patency
(approximately 70 to 75% at 10 years), and can be completed with a tolerable perioperative mortality (2 to 3%).107
TECHNICAL CONSIDERATIONS FOR AORTOBIFEMORAL BYPASS

Both femoral arteries are initially exposed to ensure that they are adequate for the distal anastomoses. The abdomen is
then opened in the midline, the small intestine is retracted to the right, and the posterior peritoneum overlying the aorta
is incised. A retroperitoneal approach may be selected as an alternative in certain situations. This approach involves
making a left flank incision and displacing the peritoneum and its contents to the right. Such an approach is
contraindicated if the right renal artery is acutely occluded, because visualization from the left flank is very poor.
Tunneling of a graft to the right femoral artery also is more difficult from a retroperitoneal approach, but can be
achieved. The retroperitoneal approach has been reputed to be better tolerated than midline laparotomy for patients
with multiple previous abdominal operations and with severe pulmonary disease. Further proposed advantages of the
retroperitoneal approach include less GI disturbance, decreased third-space fluid losses, and ease with which the
pararenal aorta can be accessed. There are randomized reports, however, that support and refute the superiority of this
approach. A collagen-impregnated, knitted Dacron graft is used to perform the proximal aortic anastomosis, which can
then be made in either an end-to-end or end-to-side fashion using 3-0 polypropylene suture. The proximal anastomosis
should be made as close as possible to the renal arteries to decrease the incidence of restenosis from progression of the
atherosclerotic occlusive process in the future.
An end-to-end proximal aortic anastomosis is necessary in those patients with an aortic aneurysm or complete aortic
occlusion extending up to the renal arteries (Fig. 23-56). Although in theory, the end-to-end configuration allows for less
turbulence and less chance of competitive flow with still patent host iliac vessels, there have not been consistent results
to substantiate differences in patency between end-to-end and end-to-side grafts. Relative indications for an end-to-side
proximal aortic anastomosis include the presence of large aberrant renal arteries, an unusually large IMA with poor
back-bleeding, suggesting inadequate collateralization, and/or occlusive disease involving bilateral external iliac arteries.
Under such circumstances, end-to-end bypass from the proximal aorta to the femoral level devascularizes the pelvic
region because there is no antegrade or retrograde flow in the occluded external iliac arteries to supply the hypogastric
arteries. As a result of the pelvic devascularization, there is an increased incidence of impotence, postoperative colon
ischemia, buttock ischemia, and paraplegia secondary to spinal cord ischemia, despite the presence of excellent femoral
and distal pulses.
Fig. 23-56.
In an end-to-end proximal aortic anastomosis, the aorta is divided in half. The proximal end of the aorta is anastomosed to the
end of a prosthetic graft while the distal divided aortic stump is oversewn.
An end-to-side proximal aortic anastomosis can be associated with certain disadvantages, which include the potential for
distal embolization when applying a partially occlusive aortic clamp (Fig. 23-57). Furthermore, the distal aorta often
proceeds to total occlusion after an end-to-side anastomosis. There may also be a higher incidence of aortoenteric
fistula following construction of end-to-side proximal anastomoses because the anterior projection makes subsequent
tissue coverage and reperitonealization of the graft more difficult. The limbs of the graft are tunneled through the
retroperitoneum to the groin, where an end-to-side anastomosis is fashioned between the graft and the bifurcation of
the CFA using 5-0 polypropylene suture. Endarterectomy or patch angioplasty of the profunda femoris may be required
concurrently. Once the anastomoses have been fashioned and the graft thoroughly flushed, the clamps are removed and
the surgeon carefully controls the degree of aortic occlusion until full flow is re-established. During this period the
patient must be carefully monitored for hypotension. Declamping hypotension is a complication of sudden restoration of
aortic flow, particularly following prolonged occlusion. Once flow has been re-established, the peritoneum is carefully
reapproximated over the prosthesis to prevent fistulization into the intestine.
Fig. 23-57.
In an end-to-side aortic anastomosis, the end of a prosthetic graft is connected to the side of an aortic incision.
Despite the presence of multilevel disease in most patients, a properly performed aortobifemoral operation can provide
arterial inflow and alleviate claudication symptoms in 70 to 80% of patients; however, 10 to 15% of patients will require
simultaneous outflow reconstruction to address distal ischemia and facilitate limb salvage. The advantage of
concomitant distal revascularization is avoidance of reoperation in a scarred groin. As a rule, if the profunda femoris can
accept a 4-mm probe and if a No. 3 Fogarty embolectomy catheter can be passed distally for 20 cm or more, the PFA
will be sufficient for outflow and concomitant distal revascularization is not necessary.
AORTIC ENDARTERECTOMY
Aortoiliac endarterectomy is rarely performed, as it is associated with greater blood loss, greater sexual dysfunction, and
is more difficult to perform. Long-term patency is comparable with aortobifemoral grafting, and thus it remains a
reasonable option in cases in which the risk of infection of a graft is excessive, because it involves no prosthetic tissue.
Aortoiliac endarterectomy was useful when disease was localized to either the aorta or CIAs; however, at present,
aortoiliac PTA, stents, and other catheter-based therapies have become first-line treatments in this scenario.
Endarterectomy should not be performed if the aorta is aneurysmal because of continued aneurysmal degeneration of
the endarterectomized segment. If there is total occlusion of the aorta to the level of the renal arteries, aortic
transection several centimeters below the renal arteries with thrombectomy of the aortic cuff followed by graft insertion
is easier and more expeditious when compared to endarterectomy. Involvement of the EIA makes aortic endarterectomy
more difficult to complete because of decreased vessel diameter, increased length, and exposure issues. The ability to
establish an appropriate endarterectomy plane is compromised due to the muscular and inherently adherent nature of
the media in this location. There is a higher incidence of early thrombosis and late failure with extended aortoiliofemoral
endarterectomy when compared to bypass grafting as a result of recurrent stenosis.
AXILLOFEMORAL BYPASS
An axillofemoral bypass is an extra-anatomic reconstruction that derives arterial inflow from the axillary artery to the
femoral artery. This is a treatment option for those patients with medical comorbidities that prohibit an abdominal
vascular reconstruction. It may be performed under local anesthesia and is used for limb salvage. Extra-anatomic
bypasses have lower patency when compared to aortobifemoral, and therefore, are seldom recommended for
claudication. Before performing this operation, the surgeon should check pulses and BP in both arms to ensure that
there is no obvious disease affecting flow through the axillary system. Angiography of the axillosubclavian vasculature is
not necessary, but can be helpful if performed at the time of aortography. The axillary artery is exposed below the
clavicle, and a 6- to 8-mm externally reinforced PTFE graft is tunneled subcutaneously down the lateral chest wall and
lateral abdomen to the groin. It is anastomosed to the ipsilateral distal at the CFA bifurcation into the superficial femoral
and profunda femoris arteries. A femorofemoral crossover graft using a 6- to 8-mm externally reinforced PTFE graft is
then used to revascularize the opposite extremity if necessary. Reported patency rates over 5 years vary from 30 to
80%.108 Paradoxically, although it is a less complex procedure than aortofemoral grafting, the mortality rate is higher
(10%), reflecting the compromised medical status of these patients.108
ILIOFEMORAL BYPASS
One option for patients with unilateral occlusion of the distal common iliac or external iliac arteries is iliofemoral grafting
(Fig. 23-58). Long-term patency is comparable to aortounifemoral bypass and because the procedure can be performed
using a retroperitoneal approach without clamping the aorta, the perioperative mortality is less.108
Fig. 23-58.
A. Skin markings showing the incisions of an iliofemoral bypass. B. A prosthetic bypass graft is used for an iliofemoral artery
bypass in which the proximal anastomosis is connected to the common iliac artery (long arrow) while the distal anastomosis is
connected to the common femoral artery (short arrow).
FEMOROFEMORAL BYPASS
A femorofemoral bypass is another option for patients with unilateral stenosis or occlusion of the common or EIA who
have rest pain, tissue loss, or intractable claudication. The primary (assisted) patency at 5 years is reported to be 60 to
70%, and, although this is inferior when compared to aortofemoral bypass, there are physiologic benefits, especially for
patients with multiple comorbidities, because it is not necessary to cross-clamp the aorta.109 There are no studies
supporting the superiority of unsupported or externally supported PTFE over Dacron for choice of conduit. The fear of
the recipient extremity stealing blood from the extremity ipsilateral to the donor limb is not realized unless the donor
iliac artery and donor outflow arteries are diseased.109 Depending on the skills of the interventionalist/surgeon, many
iliac lesions classified as TASC II B, C, or D can now be addressed using an endovascular approach, thus obviating the
need to perform a femorofemoral bypass. Additionally, femorofemoral bypass can be used as an adjuvant procedure
after iliac inflow has been optimized with endovascular methods.
OBTURATOR BYPASS
An obturator bypass is used to reconstruct arterial anatomy in patients with groin sepsis resulting from prior prosthetic
grafting, intra-arterial drug abuse, groin neoplasm, or damage from prior groin irradiation. This bypass can originate
from the CIA, EIA, or uninvolved limb of an ABF. A conduit of Dacron, PTFE, or autologous vein is tunneled through the
anteromedial portion of the obturator membrane to the distal superficial femoral or popliteal artery. The obturator
membrane must be divided sharply so as to avoid injury to adjacent structures, and care must be taken to identify the
obturator artery and nerve that pass posterolaterally. After the bypass is completed and the wounds isolated, the
infected area is entered, the involved arteries are débrided to healthy tissue, and vascularized muscle flaps are
mobilized to cover the ligated ends.110 There have been varied results in terms of patency and limb salvage for
obturator bypass. Some authors have reported 57% 5-year patency and 77% 5-year limb salvage rates, whereas others
have shown a high rate of reinfection and low patency requiring reintervention.110,111
THORACOFEMORAL BYPASS
The indications for thoracofemoral bypass are (a) multiple prior surgeries with a failed infrarenal aortic reconstruction
and (b) infected aortic prosthesis. This procedure is more physiologically demanding than other extra-anatomic
reconstructions because the patient must not only tolerate clamping the descending thoracic aorta but also performance
of a left thoracotomy. The graft is tunneled to the left CFA from the left thorax posterior to the left kidney in the anterior
axillary line using a small incision in the periphery of the diaphragm and an incision in the left inguinal ligament to gain
access to the extraperitoneal space from below. The right limb is tunneled in the space of Retzius in an attempt to
decrease kinking that is more likely to occur with subcutaneous, suprapubic tunneling. Thoracofemoral bypass has long-
term patency comparable to aortofemoral bypass.
Complications of Surgical Aortoiliac Reconstruction

With current surgical techniques and conduits, early postoperative hemorrhage is unusual and occurs in 1 to 2% of
cases. It is usually the result of technical oversight or coagulation abnormality.112 Acute limb ischemia (ALI) occurring
after aortoiliac surgery may be the result of acute thrombosis or distal thromboembolism. The surgeon can prevent
thromboembolic events by (a) avoiding excessive manipulation of the aorta, (b) ensuring adequate systemic
heparinization, (c) judicious placement of vascular clamps, and (d) thorough flushing before restoring blood flow. Acute
thrombosis of an aortofemoral graft limb in the early perioperative period occurs in 1 to 3% of patients.112
Thrombectomy of the graft limb is performed through a transverse opening in the hood of the graft at the femoral
anastomosis. With this approach, it is possible to inspect the interior of the anastomosis and pass embolectomy
catheters distally to clear the superficial femoral and profunda arteries. Various complications may be encountered
following aortoiliac or aortobifemoral reconstruction (Table 23-15).
Table 23-15 Perioperative Complications of Aortobifemoral Bypass Grafting
Medical complications
Perioperative myocardial infarction
Respiratory failure
Ischemia-induced renal failure
Bleeding from IV heparinization
Stroke
Procedure-related complications
Early
Declamping shock
Graft thrombosis
Retroperitoneal bleeding
Groin hematoma
Bowel ischemia/infarction
Peripheral embolization
Erectile dysfunction
Lymphatic leak
Chylous ascites
Paraplegia
Late
Graft infection
Anastomotic pseudoaneurysm
Aortoenteric fistula
Aortourinary fistula
Graft thrombosis
Intestinal ischemia following aortic reconstruction occurs in approximately 2% of cases; however, with colonoscopy,
mucosal ischemia, which is a milder form, is seen more frequently. The surgeon can identify patients who require
concomitant revascularization of the IMA, hypogastric arteries, or mesenteric arteries by examining the preoperative
arteriogram for the presence of associated occlusive lesions in the celiac axis, the superior mesenteric arteries, or both.
Likewise patients with patent and enlarged IMA or a history of prior colonic resections will benefit from IMA
reimplantation.
In a comprehensive review of 747 patients who had aortoiliac operations for occlusive disease, secondary operations for
late complications such as reocclusion, pseudoaneurysms, and infection were necessary in 21% of cases over a 22-year
period.113 The most frequent late complication is graft thrombosis. Limb occlusion occurs in 5 to 10% of patients within
5 years of the index operation and in 15 to 30% of patients 10 years or more after the index operation.112,113
Anastomotic pseudoaneurysms occur in 1 to 5% of femoral anastomoses in patients with aortofemoral grafts.114
Predisposing factors to pseudoaneurysm formation include progression of degenerative changes within the host artery,
excessive tension at the anastomosis, and infection.114 Due to the associated risks of thrombosis, distal embolization,
infection, and rupture, anastomotic aneurysms should be repaired expeditiously.
Infection following aortoiliac reconstruction is a devastating complication that occurs in 1% of cases. Femoral
anastomoses of aortofemoral reconstructions and axillofemoral bypasses are prone to infection.113,114 Use of
prophylactic antibiotics and meticulous surgical technique are vital in preventing contamination of the graft at the time
of implantation. If infection appears to be localized to a single groin, one may consider the treatment strategies of graft
preservation, aggressive local wound débridement, antibiotic solution irrigation, and soft tissue coverage with rotational
muscle flaps. This nonexcisional treatment approach may be useful in selective cases of localized femoral graft infection.
Most patients with infected aortoiliofemoral reconstructions usually require graft excision and revascularization via
remote uncontaminated routes or the use of in situ replacement to clear the infective process and maintain limb
viability. Aortoenteric fistula and associated GI hemorrhage are devastating complications, with a 50% incidence of
death or limb loss. The incidence of aortoenteric fistula formation appears to be higher after an end-to-side proximal
anastomosis, because it is more difficult to cover the prosthesis with viable tissue and avoid contact with the GI tract
with this configuration.113,114 Treatment of aortoenteric fistula requires resection of all prosthetic material, closure of
the infrarenal abdominal aorta, repair of the GI tract, and revascularization by means of an extra-anatomic graft.
Endovascular Treatment for Aortic Disease

Although aortofemoral bypass surgery has excellent long-term patency and can be performed with low mortality rates,
there are patients who are unable to withstand the physiologic stress of longer open procedures performed under
general anesthesia, which require aortic cross-clamping, and which are associated with greater blood loss. These
patients are more suited to endovascular interventions despite the decreased durability and requirement for more
frequent reinterventions.
FOCAL AORTIC STENOSIS

The endovascular technique used to treat infrarenal aortic stenoses is similar to that used for iliac artery disease.
Bilateral CFA access is established followed by insertion of a 10F sheath. The lesion is crossed using a hydrophilic wire
and a supporting selective catheter and then changed for a stiffer guidewire. A self-expanding nitinol stent or a balloon-
expandable stent mounted on a larger caliber angioplasty balloon is implanted followed by adequate postdilation. At the
physician's discretion, "kissing" stents, simultaneous bilateral proximal iliac stents, are deployed if the lesion is in the
distal aorta in the proximity of the aortic bifurcation. The role of covered stents such as cuffs made for endoluminal
abdominal aortic aneurysm (AAA) repair has not been rigorously studied. The aortic diameter should be sized with a
calibrated catheter during the angiography or by preintervention CT scanning to avoid undersizing. Balloon size will
range from 12 to 18 mm in most cases. A single stent generally is sufficient in most cases. Large Palmaz-type stents
mounted on XXL balloons (Meditech, Westwood, Mass) have been successfully used and may be inflated up to 25 mm in
diameter if needed. Newer self-expanding stents also have been used. Concentric aortic stenosis may encroach upon the
IMA and coverage of this vessel may be unavoidable. Care should be taken to use low inflation pressures (5 mmHg) to
minimize the risk of aortic rupture. Patient complaints of back or abdominal pain during balloon inflation should be taken
seriously, as they may suggest impending rupture. In case of a calcified small caliber, hypoplastic aorta (≤12 mm,
typically in female patients), it is recommended to use smaller diameter stents. To achieve clinical improvement, these
patients can be recanalized to an aortic diameter of 8 or 9 mm. Distal embolization is one of the potential complications
of endovascular treatment for aortic stenoses. Full heparinization, meticulous technique during wire and catheter
manipulations, and primary stenting reduce the risk of this complication. Because calcified aortic stenoses are prone to
rupture during dilation, it is recommended that the extent of the calcification should be determined beforehand with
preoperative CT scans. In case of aortic rupture, as long as wire access has been maintained, an occlusion balloon can
be inflated proximal to the disrupted segment to achieve hemostasis and the rupture can be covered with a stent graft
or repaired with open surgery.
OCCLUSIVE LESIONS OF THE AORTIC BIFURCATION

Occlusive lesions are treated with the kissing balloon technique to avoid dislodging aortic plaque. Two angioplasty
balloons of equal size are positioned across the ostia of the CIAs, using a retrograde approach, and inflated.
Simultaneous balloon dilatation at the origins of both CIAs is advocated, even in the presence of a unilateral lesion, to
protect the contralateral CIA from dissection or plaque embolization. Calcified lesions, which typically occur at the aortic
bifurcation, are not amenable to balloon dilatation, and frequently require that a distal aortic reconstruction be
performed using "kissing stents." Fears that the proximal ends of the stents that extend into the distal aorta will become
a nidus for thrombus formation, or cause hemolysis have not been realized. The results are difficult to interpret because
these bifurcation lesions are usually included in studies with iliac artery lesions. Patency rates for aortic bifurcation PTA
range from 76 to 92% at 3 years.115 The largest series reported to date includes 79 patients with aortic bifurcation
lesions. The cumulative clinical success rate at a mean of 4 years was 93%.116 In more recent years, stents have been
used to reconstruct the aortic bifurcation.117 The kissing stent technique is well suited for orificial lesions. Technical
success with kissing stents at the aortic bifurcation has been reported to be 95 to 100%.117 In the largest series
reported, the primary patency at 3 years was 79%.118
Endovascular Treatment for Iliac Artery Disease

PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY
PTA is most useful in the treatment of isolated iliac stenoses of <4 cm in length. When used for stenoses rather than
occlusion, a 2-year patency of 86% can be achieved.119 The complication rate is approximately 2%, consisting of distal
embolization, medial dissection, and acute thrombosis.
Technical Considerations for Iliac Interventions

Crossing a high-grade stenosis or occlusion can be challenging in the iliac arteries. It is vital to image the lesion well
because multiple views and use of the image intensifier will frequently uncover the anatomic reason for the difficulty.
Frequently, the difficulty is the result of vessel tortuosity that cannot be appreciated on the original view. Use of an
angled hydrophilic guidewire and an angled catheter can provide steering and add extra support for the wire trying to
cross the lesion. Patience, persistence, and periodic reimaging will facilitate the crossing of a lesion in the great majority
of cases. Guidewire traversal must be achieved for performance of endovascular iliac intervention. Over 90% of iliac
occlusions can be passed with simple guidewire techniques.
The preferred approach for recanalizing a CIA occlusion is retrograde passage of devices from an ipsilateral CFA
puncture because, in this manner, distance to the lesion is short and access is straighter. A stenosis is normally crossed
using a combination of a soft-tip 0.035-in guidewire (i.e., Bentson type wire) or hydrophilic wire and a 5 F straight or
selective catheter. One of the hazards of retrograde recanalization is that the guidewire stays in a subintimal location,
and cannot be redirected into the true lumen at the aortic bifurcation. There are several approaches that can be used to
achieve re-entry of total chronic occlusions. Specialized catheters allow passage of a needle and guidewire across the
intima distal to the occlusion. Intravascular ultrasound can be used for true lumen re-entry under fluoroscopic guidance.
Another method of achieving true lumen re-entry involves performing the recanalization from an antegrade contralateral
CFA approach. A 4 F Berenstein catheter (Cordis Corp., Miami Lakes, FL) is used to probe the occlusion. The lesion can
be crossed in most instances (5 to 20% failure rate) with a hydrophilic guidewire or, occasionally, with its stiffer back
end. As soon as the guidewire crosses the obstruction and lies within the ipsilateral EIA lumen, it is snared and partially
pulled out of the ipsilateral CFA. A short catheter is then inserted in a retrograde fashion over the wire end into the
abdominal aorta proximal to the lesion. The hydrophilic guidewire is then exchanged for a stiffer Amplatz (Boston
Scientific, Natick, MA) guidewire to facilitate iliac stenting.
Obtaining arterial access when there are absent femoral pulsations is aided by the use of ultrasound guidance and
"road-map" imaging software that is available on modern angiographic equipment. When the lesion is successfully
crossed, balloons of an appropriate size and length are selected for the angioplasty. Most CIAs will accommodate 8- to
10-mm diameter balloons, while most EIAs will accommodate 6- to 8-mm diameter balloons. Inflation is performed with
caution, especially if there is heavy calcification, and should be guided by patient discomfort, pressure gauge readings,
and changes in balloon outline.
If guidewire traversal is straightforward, consideration should be given to the presence of an acute thrombosis that may
benefit from CDT. If guidewire traversal is challenging, it is unlikely that CDT will be beneficial. Investigators have found
that routine thrombolysis and balloon dilation of occluded arteries before stent placement is associated with an
increased incidence of distal embolic events.120 Stents should be placed after inadequate angioplasty. Stents are
warranted when there is a greater than 30% residual stenosis, when there is a flow-limiting dissection, or when there is
a pressure gradient of 5 mmHg or greater across the treated segment.121 Placement of stents can precipitate distal
embolization in up to 10%, especially if lesions are friable and vulnerable to manipulation. Routine primary stent
placement is not recommended because it has not been found to be superior to selective stenting in terms of outcomes
or cost.122
PRIMARY STENTING VS. SELECTIVE STENTING IN ILIAC ARTERIES

Primary stenting rather than selective stenting should be considered for longer iliac lesions and for all TASC II C and D
lesions. The primary patency rates at 1, 2, and 3 years were 96%, 90%, and 72% for longer lesions (>5 cm) that were
primarily stented vs. 46%, 46%, and 28% with selective stenting.122 Primary stenting generally is advocated for chronic
iliac artery occlusions, recurrent stenosis after previous iliac PTA, and for complex stenoses with eccentric, calcified,
ulcerated plaques, or plaques with spontaneous dissection. All these lesions are prone to distal embolization during
manipulation of wires and angioplasty balloons. Distal embolization with isolated PTA is not common for uncomplicated
lesions, but can occur in up to 24% of cases, when treating ulcerated plaques, aortoiliac bifurcation lesions, or iliac
occlusions.122 It is believed that direct stent placement without predilation significantly reduces the risk of distal
embolization by trapping potentially emboligenic material between the arterial wall and the stent mesh. Although PTA
has demonstrated excellent results in focal stenoses of the abdominal aorta and iliacs, primary stenting in these
locations is safe, improves patency rates, reduces the degree of restenosis when compared with PTA alone, and also
decreases the risk of distal embolization. Additional potential advantages of direct stenting include shorter procedural
time and less radiation exposure. The Dutch Iliac Stent Trial has provided evidence that refutes the superiority of
primary stenting over angioplasty alone.123 Most interventionalists continue to perform angioplasty first and stent
selectively for inadequate results. The approach to aortoiliac stenting is intuitive. Individual judgment and experience
are important in the decision-making process, and there are lesions with unstable morphology such as long occlusions,
ulceration, and dissection that warrant primary stenting.
STENT GRAFT PLACEMENT FOR AORTOILIAC INTERVENTIONS

Stent grafts have been used to treat complex iliac lesions in an attempt to exclude these sources of embolization. A
recent report suggested that the use of stent grafts was beneficial for TASC II C and D lesions.124 Bosiers and
colleagues published a series involving 91 limbs with diseased iliacs that they treated with 107 stent grafts. They
reported successful deployment in all patients without distal embolization or vessel rupture and a primary patency rate
of 91.1% at 1-year follow-up.125 The authors commented about their concerns of causing embolization during
placement of the stent grafts and recommended that, once an occlusion was traversed with the guidewire, to gently
predilate with a 5-mm balloon, followed by smooth stent graft insertion into the newly created channel. The role of stent
grafts in aortoiliac occlusive disease has not been fully elucidated yet.
Complications of Endovascular Aortoiliac Interventions

Iliac artery angioplasty is associated with a 2 to 4% major complication rate and 4 to 15% minor complication rate.
Many of these minor complications are related to the arterial puncture site. The most frequent complications relate to
access site cannulation. Hemorrhage can range from the more common access site hematoma to the rarer
retroperitoneal and intraperitoneal hemorrhage. Distal embolization occurs in 2 to 10% of iliac PTA and stenting
procedures.112 Percutaneous catheter aspiration should be the initial treatment for calf vessel embolization, but, for
larger emboli such as those that lodge in the profunda femoris or common femoral arteries, surgical embolectomy may
be required because the embolic material contains atherosclerotic plaque, which is not amenable to transcatheter
aspiration or CDT. The incidence of pseudoaneurysm formation at the puncture site is 0.5%. The treatment of choice for
pseudoaneurysms >2 cm in diameter is percutaneous thrombin injection under ultrasound guidance. Arterial rupture
may complicate the procedure in 0.3% of cases. Tamponade of the ruptured artery with an occlusion balloon should be
performed, and a covered stent should be placed. In case of failure, surgical treatment is required.
Clinical Results Comparing Surgical and Endovascular Treatment of

Aortoiliac Disease
The mortality risk for ABF in patients with isolated, localized aortoiliac disease is relatively low, whereas, for patients
with concomitant atherosclerosis in coronary, carotid, and visceral vessels, mortality and morbidity are higher. For this
reason, the cumulative long-term survival rate for patients having aortoiliac reconstruction remains 10 to 15 years less
than anticipated for a normal age- and sex-matched population. Twenty-five to 30% of patients with concomitant
atherosclerosis in other vascular distributions are dead within 5 years, and 50 to 60% will have died by 10 years.114
Compared with conventional ABF, common iliac angioplasty was shown to have a 10 to 20% lower overall patency rate.
It should be noted that these results were reported in early trials that used older generations of endovascular
equipment. With continued progress and newer angioplasty balloons and stenting practices, more comparable outcomes
are being reported. Review of the literature confirms that there is an 85 to 90% graft patency rate at 5 years and 70 to
75% at 10 years after aortobifemoral reconstruction.126 Due in part to factors including continued refinements in
anesthetic management, intraoperative monitoring, and postoperative intensive care, low perioperative mortality rates
for ABF can be achieved commonly in today's clinical practice.
Despite its lower long-term success, common iliac angioplasty is a useful procedure in patients with focal disease and
mild symptoms in whom a major surgical revascularization is not justified. Angioplasty of the iliac vessels can be a
useful adjunct to distal surgical bypass as well, increasing the success of distal revascularization and eliminating the
risks associated with aortoiliac bypass. Thus, with long-term patency less than, but comparable to, open surgical
bypass, and with more favorable morbidity rates, iliac angioplasty has become a well-accepted modality of treatment for
iliac occlusive disease. Ideal iliac angioplasty lesions are nonocclusive and short. Patency after intervention is better
when lesions occur in larger diameter vessels, when stenoses rather than occlusions are treated, when runoff vessels
are patent, and when the indication for intervention is lifestyle-limiting claudication rather than critical limb ischemia.
Becker and associates estimated a 5-year patency rate of 72% in an analysis of 2697 cases of iliac angioplasty and
noted a better patency (79%) in claudicants.127 Less favorable results are obtained with long stenoses, external iliac
stenoses, and tandem lesions. The reported technical and initial clinical success of balloon angioplasty in iliac artery
stenoses exceeds 90% in most series and the 5-year patency rates range between 54 and 92%.128 The reported
technical and initial clinical success of balloon angioplasty in iliac artery occlusions ranges between 78 and 98% and the
3-year patency rates range between 48 and 85%.128
Factors reported to affect the patency of aortoiliac endovascular interventions adversely include quality of runoff vessels,
severity of ischemia, and length of diseased segments treated. Likewise, as vessel diameter and flow rates change, so
do success rates after angioplasty. It was reported in the literature that location of the lesion at the EIA adversely
affects both primary and assisted-primary patency. Following angioplasty of the CIA, patency rates were 81 and 52% at
1 and 6 years, whereas, after EIA angioplasty, they were 74 and 48% at 1 and 4 years.129 Although there is literature
that supports location of the lesion in the EIA as a factor that adversely affects both primary and assisted-primary
patency, this has not been a universal finding.129 Female patients are also reported to have lower patency rates than
males following iliac PTA, with or without stent placement in the EIA.130
Stenting of the iliac arteries provides a durable and curative treatment, with a 3-year patency rate of 41 to 92% for
stenoses and a 3-year patency rate of 64 to 85% and 4-year patency rate of 54 to 78% for occlusions.128 A meta-
analysis of 2116 patients by Bosch and Hunink showed that aortoiliac PTA resulted in a 39% improvement in long-term
patency compared to balloon angioplasty, despite the fact that complication rates and 30-day mortality rates did not
differ significantly.131 Park and colleagues presented long-term follow-up results in a cohort of patients with all four
TASC II types of iliac lesions. The authors presented primary patency rates of 87%, 83%, 61%, and 49% at 3, 5, 7, and
10 years, respectively, after the index intervention.132 Leville and associates achieved primary and secondary patency
rates of 76 and 90%, respectively, after 3 years, in a cohort of patients that they stented for iliac occlusions. The
authors postulated that endovascular treatment for iliac occlusive disease should be extended to type C and D lesions,
because they observed no detectable differences between the four TASC II classifications in terms of primary and
secondary patency rates.133 They concluded that presence of TASC II C and D lesions should not preclude endovascular
treatment and believe that endovascular attempts should be exhausted before open surgical repair of iliac occlusions is
attempted because of the decreased perioperative morbidity and good midterm durability.
Not all results have been in favor of stenting, and, at present, universal primary stenting cannot be recommended.
Although stents are often used to improve the outcome of PTA, there is no general consensus that stenting should be
mandatory in all iliac lesions. Complex, ulcerated iliac lesions with high emboligenic potential or recanalized chronic iliac
occlusions may be an exception. In the Dutch Iliac Trial, primary stenting did not prove to be superior to iliac
angioplasty and selective stenting. The researchers in this prospective, randomized, multicenter study concluded that
balloon angioplasty with selective stenting had comparable 2-year patency rates with primary stenting; 77 and 78%,
respectively. It must be noted, however, that it was necessary to stent 43% of the patients in the PTA treatment group
due to unsatisfactory angioplasty results.123 The 5-year outcomes between the two groups were also similar, with 82
and 80% of the treated iliac segments remaining free of the need for new revascularization procedures after a mean
follow-up of 5.6 ± 1.3 years.123
LOWER EXTREMITY ARTERIAL OCCLUSIVE DISEASE

The symptoms of LE occlusive disease are classified into two large categories: ALI and chronic limb ischemia (CLI).
Ninety percent (90%) of acute ischemias are either thrombotic or embolic. Frequently, sudden onset of limb-threatening
ischemia may be the result of acute exacerbation of the pre-existing atherosclerotic disease. Chronic ischemia is largely
due to atherosclerotic changes of the LE that manifest from asymptomatic to limb-threatening gangrene. As the
population ages, the prevalence of chronic occlusive disease of the LE is increasing and it significantly influences
lifestyle, morbidity, and mortality. In addition, multiple comorbid conditions increase risks of surgical procedures.
Endovascular interventions become an important alternative in treating LE occlusive disease. However, despite rapid
evolving endovascular technology, LE endovascular intervention continues to be one of the most controversial areas of
endovascular therapy.
Epidemiology
In a detailed review of the literature, McDaniel and Cronenwett concluded that claudication occurred in 1.8% of patients
under 60 years of age, 3.7% of patients between 60 and 70 years of age, and 5.2% of patients over 70 years of age.134
Leng and his colleagues scanned 784 subjects using ultrasound in a random sample of men and women ages 56 to 77
years. Of the subjects that were scanned, 64% demonstrated atherosclerotic plaque.135 However, a large number of
patients had occlusive disease without significant symptoms. In a study by Schroll and Munck, only 19% of the patients
with peripheral vascular disease were symptomatic.136 Using ankle-brachial indices (ABIs), Stoffers and colleagues
scanned 3171 individuals between the ages of 45 and 75 and identified 6.9% of patients who had ABIs <0.95, only 22%
of whom had symptoms.137 In addition, they demonstrate that the concomitant cardiovascular and cerebrovascular
diseases were three to four times higher among the group with asymptomatic peripheral vascular diseases than those
without peripheral vascular disease. Furthermore, they confirm that 68% of all peripheral arterial obstructive diseases
were unknown to the primary care physician and this group mainly represented less advanced cases of atherosclerosis.
However, among patients with an ABI ratio <0.75, 42% were unknown to the primary physicians.
The diagnosis of LE occlusive disease often is made based upon a focused history and physical examination, and
confirmed by the imaging studies. A well-performed physical examination often reveals the site of lesions by detecting
changes in pulses, temperature, and appearances. The bedside ABIs using BP cuff also aid in diagnosis. Various clinical
signs and symptoms are useful to differentiate conditions of viable, threatened, and irreversible limb ischemia caused by
arterial insufficiency (Table 23-16).
Table 23-16 Signs and Symptoms of Acute Limb Ischemia
Category
Description Viable Threatened Irreversible
Clinical description Not immediately Salvageable if promptly Major tissue loss, amputation
threatened treated unavoidable
Capillary return Intact Intact, slow Absent (marbling)
Muscle weakness None Mild, partial Profound, paralysis (rigor)
Sensory loss None Mild, incomplete Profound anesthetic
Arteriovenous Doppler Audible Inaudible or audible Inaudible
finding
Noninvasive studies are important in documenting the severity of occlusive disease objectively. Ultrasound Dopplers
measuring ABIs and segmental pressures are widely used in North America and Europe. Normal ABI is >1.0. In patients
with claudication, ABIs decrease to 0.5 to 0.9 and to even lower levels in patients with rest pain or tissue loss.138
Segmental pressures are helpful in identifying the level of involvement. Decrease in segmental pressure between two
segments indicates significant disease. Ultrasound duplex scans are used to identify the site of lesion by revealing flow
disturbance and velocity changes. A meta-analysis of 71 studies by Koelemay and associates confirmed that duplex
scanning is accurate for assessing arterial occlusive disease in patients suffering from claudication or critical ischemia,
with an accumulative sensitivity of 80% and specificity of over 95%.139 Adding an ultrasound contrast agent further
increases sensitivity and specificity to ultrasound technology.140 Other noninvasive imaging technologies such as MRA
and CTA are rapidly evolving and gaining popularity in the diagnosis of LE occlusive disease (Figs. 23-59 and 23-60).
Fig. 23-59.
A high-resolution computed tomography angiography of a patient with normal right lower extremity arterial circulation. Distal
occlusive disease is noted in the left tibial arteries (arrow).
Fig. 23-60.
A. A multidetector computed tomographic angiography of a patient with an infrapopliteal arterial circulation. B. Pedal arterial
circulation. The high spatial resolution and image quality of these images show three patent infrapopliteal runoff vessels and
patent pedal vessels at the foot level.
Contrast angiography remains the gold standard in imaging study. Using contrast angiography, interventionists can
locate and size the anatomic significant lesions and measure the pressure gradient across the lesion, as well as plan for
potential intervention. Angiography is, however, semi-invasive and should be confined to patients for whom surgical or
percutaneous intervention is contemplated. Patients with borderline renal function may need to have alternate contrast
agents such as gadolinium or carbon dioxide to avoid contrast-induced nephrotoxicity.
Differential Diagnosis
Arterial insufficiency frequently leads to muscle ischemic pain involving the LE muscularly, particularly during exercise.
Intermittent claudication is pain affecting the calf, and, less commonly, the thigh and buttock, which is induced by
exercise and relieved by rest. Symptom severity varies from mild to severe. Intermittent claudication occurs as a result
of muscle ischemia during exercise caused by obstruction to arterial flow. For differential diagnosis of intermittent
claudication, there are a variety of neurologic, musculoskeletal, and venous conditions that may produce symptoms of
calf pain (Table 23-17). Additionally, various non-atherosclerotic conditions also can cause symptoms consistent with
intermittent LE claudication (Table 23-18). Nocturnal calf muscle spasms or night cramps are not indicative of arterial
disease. They are common but are difficult to diagnose with certainty. Foot ulceration is not always the result of arterial
insufficiency. Ischemic ulcers occur on the toes or lateral side of the foot and are painful. By comparison, venous ulcers,
which also are common, occur above the medial malleolus. These venous stasis ulcers are typically surrounded by a
peripheral area of darkened skin discoloration that is also known as lipodermatosclerosis. Neuropathic ulcers usually are
found on weight-bearing surfaces, have thick calluses, and are pain free. Ulcers may be the result of more than one
etiology. Rest pain must be distinguished from peripheral neuropathy, which is prevalent in diabetic patients. Patients
with diabetic neuropathy tend to have decreased vibration and position sense and decreased reflexes. Spinal stenosis
causes pain that is exacerbated with standing and back extension.
Table 23-17 Differential Diagnosis of Intermittent Claudication
Condition Location of Characteristic Onset Effect of Effect of Body Other

Pain or Discomfort Relative to Rest Position Characteristics
Discomfort Exercise
Intermittent Calf muscles Cramping pain After same Quickly None Reproducible
claudication degree of relieved
(calf) exercise
Chronic Calf muscles Tight, bursting After much Subsides Relief speeded Typically heavy-
compartment pain exercise (e.g., very slowly by elevation muscled athletes
syndrome jogging)
Venous Entire leg, but Tight, bursting After walking Subsides Relief speeded History of iliofemoral
claudication usually worse pain slowly by elevation deep venous
in thigh and thrombosis, signs of
groin venous congestion,
edema
Nerve root Radiates down Sharp Soon, if not Not quickly Relief may be History of back
compression leg, usually lancinating pain immediately relieved aided by problems
(e.g., herniated posteriorly after onset (also often adjusting back
disk) present at position
rest)
Symptomatic Behind knee, Swelling, With exercise Present at None Not intermittent
Baker's cyst down calf soreness, rest
tenderness
Intermittent Hip, thigh, Aching After same Quickly None Reproducible
claudication buttocks discomfort, degree of relieved
(hip, thigh, weakness exercise
buttock)
Hip arthritis Hip, thigh, Aching After variable Not quickly More Variable, may relate
buttocks discomfort degree of relieved comfortable to activity level,

exercise (and may sitting, weight weather changes
be present taken off legs
at rest)
Spinal cord Hip, thigh, Weakness more After walking Relieved by Relief by Frequent history of
compression buttocks than pain or standing for stopping lumbar spine back problems,
(follows same length of only if flexion (sitting provoked by
dermatome) time position or stooping increased intra-
changed forward) abdominal pressure
pressure
Intermittent Foot, arch Severe deep After same Quickly None Reproducible
claudication pain and degree of relieved
(foot) numbness exercise
Arthritic, Foot, arch Aching pain After variable Not quickly May be relieved Variable, may relate
inflammatory degree of relieved by not bearing to activity level
process exercise (and may weight
be present
at rest)
Table 23-18 Non-Atherosclerotic Causes of Intermittent Claudication
Aortic coarctation
Arterial fibrodysplasia
Iliac syndrome of the cyclist
Peripheral emboli
Persistent sciatic artery
Popliteal aneurysm
Popliteal cyst
Popliteal entrapment
Primary vascular tumors
Pseudoxanthoma elasticum
Remote trauma or radiation injury
Takayasu's disease
Thromboangiitis obliterans
Lower Extremity Occlusive Disease Classification

LE occlusive disease may range from exhibiting no symptoms to limb-threatening gangrene. There are two major
classifications based on the clinical presentations.
The Fontaine classification uses four stages: Fontaine I is the stage when patients are asymptomatic; Fontaine II is
when they have mild (IIa) or severe (IIb) claudication; Fontaine III is when they have ischemic rest pain; and Fontaine
IV is when patients suffer tissue loss such as ulceration or gangrene (Table 23-19).141
Table 23-19 Classification of Peripheral Arterial Disease Based on the Fontaine and
Rutherford Classifications
Fontaine Classification Rutherford Classification

Stage Clinical Grade Category Clinical
I Asymptomatic 0 0 Asymptomatic
IIa Mild claudication I 1 Mild claudication
IIb Moderate to severe claudication I 2 Moderate claudication
I 3 Severe claudication
III Ischemic rest pain II 4 Ischemic rest pain
IV Ulceration or gangrene III 5 Minor tissue loss

III 6 Major tissue loss
The Rutherford classification has four grades (0–III) and seven categories (0–6). Asymptomatic patients are classified
into category 0; claudicants are stratified into grade I and divided into three categories based on the severity of the
symptoms; patients with rest pain belong to grade II and category 4; patients with tissue loss are classified into grade
III and categories 5 and 6, based on the significance of the tissue loss.2 These clinical classifications help to establish
uniform standards in evaluating and reporting the results of diagnostic measurements and therapeutic interventions
(see Table 23-19).
The most clinically useful classification of LE atherosclerotic disease should be based on morphologic characters of the
lesions. The TASC II task force published a guideline separating LE arterial diseases into femoropopliteal and
infrapopliteal lesions (Table 23-20). This guideline is particularly useful in determining intervention strategies based on
the disease classifications. Based on the guideline, femoropopliteal lesions are divided into four types: A, B, C, and D.
Type A lesions are single focal lesions <3 cm in length that did not involve the origins of the superficial femoral artery
(SFA) or the distal popliteal artery; Type B lesions are single lesions 3 to 5 cm in length not involving the distal popliteal
artery or multiple or heavily calcified lesions <3 cm in length; Type C lesions are multiple stenoses or occlusions >15 cm
in length, or recurrent stenoses or occlusions that need treatment after two endovascular interventions. Type D lesions
were those with complete occlusion of CFA, SFA, or popliteal artery.2
Table 23-20 TASC II Classification of Femoral Popliteal Occlusive Lesions
Type A lesions
Single stenosis ≤10 cm in length
Single occlusion ≤5 cm in length
Type B lesions
Multiple lesions (stenoses or occlusions), each ≤5 cm
Single stenosis or occlusion ≤15 cm not involving the infra geniculate popliteal artery
Single or multiple lesions in the absence of continuous tibial vessels to improve inflow for a distal bypass
Heavily calcified occlusion ≤5 cm in length
Single popliteal stenosis
Type C lesions
Multiple stenoses or occlusions totaling >15 cm with or without heavy calcification
Recurrent stenoses or occlusions that need treatment after two endovascular interventions
Type D lesions
Chronic total occlusions of CFA or SFA (>20 cm, involving the popliteal artery)
Chronic total occlusion of popliteal artery and proximal trifurcation vessels
CFA = common femoral artery; SFA = superficial femoral artery; TASC II = Trans-Atlantic Inter-Society Consensus.
In a similar fashion, infrapopliteal arterial diseases are classified into four types based on TASC II guideline (Fig. 23-61).
Type A lesions are single lesions <1 cm in length not involving the trifurcation; Type B lesions are multiple lesions <1
cm in length or single lesions shorter than 1 cm involving the trifurcation; Type C lesions are those lesions extensively
involving trifurcation or those that are 1- to 4-cm stenotic or 1- to 2-cm occlusive lesions; Type D lesions are occlusions
longer than 2 cm or diffuse diseases.2
Fig. 23-61.
Schematic depiction of Trans-Atlantic Inter-Society Consensus classification of femoral popliteal occlusive lesions.
Etiology of Acute Limb Ischemia

ALI is defined as sudden loss of limb perfusion and the term is applicable up to 2 weeks after an initiating event.
Although the instances of acute leg ischemia caused by emboli have decreased due to more effective treatment of
rheumatic fever and atrial fibrillation, the incidence of thrombotic acute leg ischemia has increased. Even with the
extensive use of newer endovascular techniques including thrombolysis, most published series report a 10 to 30% 30-
day amputation rate.2 The short-term mortality of patients presenting with acute ischemia is 15 to 20%. The most
common etiologies of ALI include embolism, native vessel thrombosis, reconstruction thrombosis, trauma, and
complications of peripheral aneurysm. Most cases of acute LE ischemia are the result of thrombosis of a prosthetic
conduit. This stems from increased use of prosthetic conduits to address CLI.
Presenting symptoms in ALI are pain and loss of sensory or motor function. The abruptness and time of onset of the
pain, its location and intensity, as well as change in severity over time, should all be taken into consideration. The
duration and intensity of the pain and presence of motor or sensory changes are very important in clinical decision
making and urgency of revascularization. Thrombolysis may be less effective for thrombosis of a 2-week or longer
duration compared with acute thrombosis.142
ARTERIAL EMBOLISM
The heart is the most common source of distal emboli, which account for more than 90% of peripheral arterial embolic
events. Atrial fibrillation is the most common source. Sudden cardioversion results in the dilated noncontractile atrial
appendage regaining contractile activity, which can dislodge the contained thrombus. Other cardiac sources include
mural thrombus overlying a myocardial infarction, or thrombus forming within a dilated left ventricular aneurysm. Mural
thrombi also can develop within a ventricle dilated by cardiomyopathy. Emboli that arise from a ventricular aneurysm or
from a dilated cardiomyopathy can be very large and can lodge at the aortic bifurcation (saddle embolus), thus
rendering both legs ischemic. Diseased valves are another source of distal embolization. Historically, this occurred as a
result of rheumatic heart disease. Currently, subacute and acute bacterial endocarditis are the more common causes.
Infected emboli can seed the recipient vessel wall, creating mycotic aneurysms.
An electrocardiogram will diagnose atrial fibrillation. A transthoracic or transesophageal echocardiogram should be
performed to look for a cardiac source. It is important to seek other sources of the embolus using CT scanning of the
descending thoracic and abdominal aorta. More unusual sources include mural thrombus from an aortic aneurysm and,
occasionally, idiopathic arterial-to-arterial thrombus occurs, usually from a thrombus that has formed in an
atherosclerotic aortic arch or descending thoracic aorta. The presence of mobile plaque on transesophageal
echocardiography is suggestive of this source.
Paradoxical embolus occurs when a patient has a patent foramen ovale and an embolus from a deep venous thrombosis
which embolizes across the atrial defect into the left side of the heart and passes into the peripheral circulation. This is
diagnosed using a bubble echocardiography, in which air bubbles introduced into the venous circulation can be seen
traversing the septal defect.
ARTERIAL THROMBOSIS
Thrombosis can occur in native arteries and in arterial reconstructions. Patients with thrombosed arterial segments often
have an underlying atherosclerotic lesion at the site of thrombosis, or aneurysmal degeneration with mural thrombosis.
It is important to obtain a history, determine risk factors for atherosclerosis and hypercoagulable status, and examine
the contralateral extremity for circulatory problems. Patients with thrombosis of prior arterial reconstructions have limb
incisions from previous surgery, and graft occlusion can be confirmed with duplex imaging.
Clinical Manifestations of Acute Limb Ischemia

Acute LE ischemia manifests with the "five Ps": pain, pallor, paresthesias, paralysis, and pulselessness, to which some
add a sixth "P"—poikilothermia or "perishing cold." Pain is the usual symptom that causes a patient to present to the
emergency room. The most common location for an embolus to lodge in the leg is at the common femoral bifurcation.
Typically a patient will complain of foot and calf pain. Pulses are absent and there may be diminution of sensation.
Inability to move the affected muscle group is a sign of very severe ischemia and necessitates urgent revascularization.
During evaluation of the affected extremity, it is important to compare findings with the contralateral limb. Clinical
evaluation is extremely important in determining the etiology and location of the obstruction. One of the most important
pieces of information to obtain is whether the patient has had prior vascular procedures or if there is a history of LE
claudication. Either of these features suggests pre-existing vascular disease, renders revascularization more
complicated, and usually mandates angiography to permit surgical planning. On the contrary, in a patient with no
history suggestive of prior vascular disease, the etiology is most likely embolic and simple thrombectomy is more likely
to be successful.
Absent bilateral femoral pulses in a patient with bilateral LE ischemia are most likely due to saddle embolus to the aortic
bifurcation. A palpable femoral pulse and absent popliteal and distal pulses may either be due to distal common femoral
embolus (the pulse being palpable above the level of occlusion) or embolus to the superficial femoral or popliteal
arteries. Typically, emboli lodge at arterial bifurcations where they are trapped due to sudden reductions in arterial
diameter. A popliteal trifurcation embolus will present with calf ischemia and absent pedal pulses, possibly with a
popliteal pulse present. The finding of palpable contralateral pulses and the absence of ipsilateral pulses in the acutely
ischemic leg is suggestive of an embolus, irrespective of presence of Doppler signals. Arteriography is not mandatory in
patients without antecedent history suggestive of vascular disease; nevertheless, all patients should be positioned on
the OR table in such a way that fluoroscopic access to the entire inflow and outflow tract is possible, if necessary.
The main question to be answered by the history and physical examination is the severity of the ALI, which is the major
consideration in early management decisions. Patients with ALI should be evaluated in a fashion that takes into
consideration the severity and duration of ischemia at the time of presentation. Ideally, all patients with acute ischemia
should be investigated with imaging, especially if there is an antecedent vascular reconstruction; however, the clinical
condition and access to resources must guide further investigations.2 Unnecessary delays can result in amputation.
Arteriography, if it can be performed in a timely fashion, is an excellent modality for localizing obstructions and deciding
which type of intervention (endovascular, embolectomy, or bypass) patients will benefit more from. One of the goals of
treatment for ALI is to prevent thrombus propagation; therefore, expedient anticoagulation with heparin is indicated as
soon as the diagnosis is suspected.
Treatment Considerations for Acute Limb Ischemia

In the absence of any significant contraindication, the patient with an ischemic LE should be immediately anticoagulated.
This will prevent propagation of the clot into unaffected vascular beds. IV fluid should be started and a Foley catheter
inserted to monitor urine output. Baseline labs should be obtained and creatinine levels noted. A hypercoagulable work-
up should be performed before initiation of heparin if there is sufficient suspicion. According to results from randomized
trials, there is no clear superiority for thrombolysis over surgery in terms of 30-day limb salvage or mortality. Access to
each treatment option is a major issue in the decision-making process, as time is often critical. National registry data
from the United States reveal that surgery is used three- to fivefold more frequently than thrombolysis. Three
randomized studies have investigated the role of catheter-directed thrombolytic therapy in the treatment of ALI.143
The potential to reduce mortality and morbidity while achieving limb salvage is the impetus that makes thrombolysis
preferable to open surgery as first-line treatment in patients with ALI (class I and IIa). Advantages of thrombolytic
therapy over balloon embolectomy include the reduced endothelial trauma and potential for more gradual and complete
clot lysis in branch vessels usually too small to access by embolectomy balloons. It is hoped that the more gradual clot
dissolution with thrombolysis may decrease the incidence of reperfusion injury that is encountered after open surgical
procedures where rapid return of blood flow may precipitate compartment syndrome. Skeletal muscle tissue appears to
be most vulnerable to ischemia. Pathophysiologic studies reveal that irreversible damage to muscle tissue starts after 3
hours of ischemia and is nearly complete at 6 hours. Progressive microvascular damage appears to follow rather than
precede skeletal muscle tissue damage. The more severe the cellular damage, the greater the microvascular changes.
When the musculature and microvasculature are severely damaged, amputation rather than attempts at
revascularization may be the most prudent course to prevent washout of toxic by-product from the ischemic limb into
the systemic circulation. The mortality rate associated with reperfusion syndrome is high, because of the development of
concomitant adult respiratory distress syndrome, shock, disseminated intravascular coagulation, and renal failure.
Patients with small-vessel occlusion are poor candidates for surgery because they lack distal target vessels to use for
bypass. These patients should be offered a trial of thrombolysis unless they have contraindications to thrombolysis or
their ischemia is so severe that the time needed to achieve adequate lysis is considered too long. The major
contraindications of thrombolysis are recent stroke, intracranial primary malignancy, brain metastases, or intracranial
surgical intervention. Relative contraindications for performance of thrombolysis include renal insufficiency, allergy to
contrast material, cardiac thrombus, diabetic retinopathy, coagulopathy, and recent arterial puncture or surgery (Table
23-21).
Table 23-21 Contraindications to Thrombolytic Therapy
Absolute contraindications
Established cerebrovascular events (including transient ischemic attack) within last 2 mo
Active bleeding diathesis
Recent (<10 d) GI bleeding
Neurosurgery (intracranial or spinal) within last 3 mo
Intracranial trauma within last 3 mo
Intracranial malignancy or metastasis
Relative major contraindications
Cardiopulmonary resuscitation within last 10 d
Major nonvascular surgery or trauma within last 10 d
Uncontrolled hypertension (>180 mmHg systolic or >110 mmHg diastolic)
Puncture of noncompressible vessel
Intracranial tumor
Recent eye surgery
Minor contraindications
Hepatic failure, particularly with coagulopathy
Bacterial endocarditis
Pregnancy
Diabetic hemorrhagic retinopathy
Advances in clot removal techniques with percutaneous mechanical thrombectomy and thromboaspiration may extend
the applicability of this intervention to patients with more advanced degrees of ALI (class IIb) and contraindications to
thrombolysis. Several thrombectomy devices have received FDA approval for acute LE arterial thrombosis. The utility of
these thrombectomy devices is that they can be used as stand-alone therapy when there are contraindications for
thrombolytic therapy. Additionally, these thrombectomy devices can be used in conjunction with thrombolytic agents, for
pharmacomechanical thrombectomy, to enhance clot lysis, and to limit the doses and time required for
thrombolysis.144,145
Surgical Treatment
EMBOLECTOMY
When a decision is made to proceed with open surgical intervention, the abdomen, contralateral groin, and entire LE are
prepped in the field. The groin is opened through a vertical incision, exposing the CFA and its bifurcation. Frequently,
the location of the embolus at the femoral bifurcation is readily apparent by the presence of a palpable proximal femoral
pulse, which disappears distally. The artery is clamped and opened transversely over the bifurcation. Thrombus is
extracted by passing a Fogarty balloon embolectomy catheter. Good back-bleeding and antegrade bleeding suggest that
the entire clot has been removed. Embolic material often forms a cast of the vessel and is sent for culture and histologic
examination. Completion angiography is advisable to ascertain the adequacy of clot removal. The artery is then closed
and the patient fully anticoagulated.
When an embolus lodges in the popliteal artery, in most cases it can be extracted via a femoral incision using a balloon
embolectomy catheter approach. A femoral approach is preferred because the larger diameter of the femoral artery
results in decreased likelihood of arterial compromise when the arteriotomy is closed. The disadvantage with using the
femoral approach for embolectomy is the greater difficulty involved in directing the embolectomy catheter into each of
the infrapopliteal arteries. Use of fluoroscopic imaging and an over-the-wire thrombectomy catheter can overcome this
problem. Alternatively, use of a separate incision to expose the popliteal bifurcation may be necessary to achieve a
complete thrombectomy.
A more complex situation arises when a patient has antecedent peripheral vascular disease and in situ thrombosis
develops on top of pre-existing atheroma because, frequently, embolectomy catheters will not pass through these
occlusions. Similarly, when a bypass graft fails, it is usually due to progression of atheroma proximal or distal to the
graft anastomoses, or to intrinsic stenoses that develop within a vein graft. In these scenarios, expeditious angiography
is useful, to determine the extent of the occlusion, to search for inflow and distal outflow vessels, and to decide whether
thrombolysis or surgery will be the better intervention. Although the surgeon's preference tends to dictate the approach
selected, the decision is based on the presence or absence of good target vessels and availability of a suitable bypass
conduit. If there are good distal vessels and the saphenous vein is suitable, surgical bypass is recommended, as it is
fast, durable, and reliable. In the absence of a good distal target and saphenous vein, or in a patient at high risk for
surgery, lysis is recommended.
BYPASS GRAFT THROMBECTOMY

Bypass thrombectomy is more likely to succeed with prosthetic bypasses. Bypass graft revision or replacement is more
appropriate for acute vein graft failures as they are less likely to respond to thrombolysis and require some type of
revision such as valve lysis, interposition, or extension. Thrombectomy of autogenous grafts is prone to failure unless an
anatomic cause for failure such as a retained valve or unligated side branch is found and corrected. The performance of
a fasciotomy to circumvent reperfusion injury/compartment syndrome is an important consideration.
Complications Related to Treatment for Acute Limb Ischemia

Adverse events related to CDT are primarily related to bleeding complications. The overall risk of hemorrhagic stroke
from a thrombolysis procedure has been reported to be 1 to 2.3%, with 50% of hemorrhagic complications occurring
during the thrombolytic procedure.146 Hematoma at the vascular puncture site has been reported in 12 to 17% of
cases. GI bleeding is reported in 5 to 10% of cases. Hematuria following thrombolysis is uncommon and should prompt
a search for urinary tumors. Hemorrhage requiring transfusion can occur in approximately 25% of patients undergoing
thrombolysis.138,143 Lytic agents are absolutely contraindicated in patients with intracranial surgery, intracranial
hemorrhage within the last 3 months, or in the presence of any active bleeding. Most bleeding complications occur at
the arterial puncture sites, but concealed retroperitoneal bleeding is possible. The most feared complication that patients
can sustain is intracerebral hemorrhage. Older patients may be more susceptible to this complication and thus many
interventionalists are extremely reticent to use thrombolysis in patients older than 80 years of age.
Patients who are treated for acute ischemia are susceptible to two major complications following revascularization,
which include reperfusion and compartment syndromes. Other procedure-related complications can include arterial
rethrombosis, recurrent embolization, and arterial injuries secondary to the balloon catheter manipulations.
Reperfusion of the ischemic limb is variable in its physiologic effects and directly relates to the severity and extent of the
ischemia. Patients with a saddle embolus of the aortic bifurcation and severely ischemic limbs may develop the full-
blown "reperfusion syndrome," whereas patients with minimal muscle ischemia who are reperfused in a timely fashion
essentially develop no effects. Many patients with ALI have severe underlying cardiac disease and are unable to tolerate
even short ischemic periods. Complications occurring after revascularization of the LE and causes of recurrent
thrombosis are listed in Table 23-22.
Table 23-22 Complications of Arterial Revascularization
Compartment syndrome
Ischemic neuropathy
Muscle necrosis
Recurrent thrombosis
Lower leg swelling
Reperfusion syndrome
Hypotension
Hyperkalemia
Myoglobinuria
Renal failure
Compartment syndrome occurs after prolonged ischemia is followed by reperfusion. The capillaries leak fluid into the
interstitial space in the muscles, which are enclosed within a nondistensible fascial envelope. When the pressure inside
the compartment exceeds the capillary perfusion pressure, nutrient flow ceases and progressive ischemia occurs, even
in the presence of peripheral pulses. Consequently, every patient who has sustained an ischemic event and is reperfused
is monitored for compartment syndrome, which is characterized by excessive pain in the compartment, pain on passive
stretching of the compartment, and sensory loss due to nerve compression of the nerves coursing though the
compartment (Table 23-23 and Fig. 23-62). The most commonly affected compartment is the anterior compartment in
the leg. Numbness in the web space between the first and second toes is diagnostic due to compression of the deep
peroneal nerve. Compartment pressure is measured by inserting an arterial line into the compartment and recording the
pressure. Although controversial, pressures >20 mmHg are an indication for fasciotomy. Compartment pressures are
relieved in the leg by medial and lateral incisions. Through the medial incision, long openings are then made in the
fascia of the superficial and deep posterior compartments. Through the lateral incision, the anterior and peroneal
compartments are opened. Both skin and fascial incisions should be of adequate length to ensure full compartment
decompression. Laboratory evidence of rhabdomyolysis is seen in 20%. The myoglobin from damaged muscle
precipitates in kidney tubules and causes acute tubular necrosis. Alkalinization of urine increases the solubility of
myoglobin, thus preventing it from crystallizing in the tubules. In addition to alkalinization, therapy consists of forced
saline diuresis and removal of the source of dead muscle that is releasing the myoglobin.
Table 23-23 Fascial Compartments of the Lower Leg
Anterior Lateral Compartment Superficial Posterior Deep Posterior

Compartment Compartment Compartment
Muscles Tibialis anterior Peroneus longus Gastrocnemius Tibialis posterior
Extensor digitorum Peroneus brevis Plantaris Flexor digitorum longus
longus
Peroneus tertius Soleus Flexor hallucis longus
Extensor hallucis
longus
Extensor digitorum
brevis
Extensor hallucis
brevis
Artery Anterior tibial artery Anterior and posterior tibial — Posterior tibial artery
branches of the popliteal artery
Peroneal artery
Nerve Deep peroneal Superficial peroneal nerve — Tibial nerve
nerve
Fig. 23-62.
Schematic illustration of fascial compartments of the lower extremity.
Clinical Manifestations of Chronic Limb Ischemia

The term chronic limb ischemia is reserved for patients with objectively proven arterial occlusive disease and symptoms
lasting for more than 2 weeks. Symptoms include rest pain and tissue loss such as ulceration or gangrene (Table 23-
24). The diagnosis should be corroborated with noninvasive diagnostic tests such as the ABI, toe pressures, and
transcutaneous oxygen measurements. Ischemic rest pain most commonly occurs below an ankle pressure of 50 mmHg
or a toe pressure <30 mmHg.2 Ulcers are not always of an ischemic etiology (Table 23-25). In many instances, there
are other etiologic factors (traumatic, venous, or neuropathic) that are contributory, but it is underlying peripheral
arterial disease (PAD) that may be responsible for delayed or absent healing (Fig. 23-63). Healing of ulcers requires an
inflammatory response and greater perfusion than is required to support intact skin and underlying tissues. As a result,
the ankle and toe pressure levels needed for healing are higher than the pressures seen with ischemic rest pain. For
patients with ulcers or gangrene, the presence of CLI is suggested by an ankle pressure <70 mmHg or a toe systolic
pressure <50 mmHg.2 It is important to understand that there is no definite consensus regarding the vascular
hemodynamic parameters required to make the diagnosis of CLI.
Table 23-24 Clinical Categories of Chronic Limb Ischemia
Grade Category Clinical Description Objective Criteria

0 0 Asymptomatic—no hemodynamically Normal treadmill or reactive hyperemia test
significant occlusive disease
1 Mild claudication Able to complete treadmill exercisea; AP after exercise
>50 mmHg but at least 20 mmHg lower than resting
value
I 2 Moderate claudication Between categories 1 and 3
3 Severe claudication Cannot complete standard treadmill exercisea and AP
after exercise <50 mmHg
IIb 4 Ischemic rest pain Resting AP <40 mmHg, flat or barely pulsatile ankle or

metatarsal PVR; TP <30 mmHg
IIIb 5 Minor tissue loss—nonhealing ulcer, focal Resting AP <60 mmHg, ankle or metatarsal PVR flat

gangrene with diffuse pedal ischemia or barely pulsatile; TP <40 mmHg
6 Major tissue loss—extending above TM level, Same as category 5
functional foot no longer salvageable
a
5 minutes at 2 miles per hour on a 12% incline of treadmill exercise.
b
Grades II and III, categories 4, 5, and 6, are encompassed by the term chronic critical ischemia.
AP = ankle pressure; PVR = pulse volume recording; TM = transmetatarsal; TP = toe pressure.
Table 23-25 Symptoms and Signs of Neuropathic Ulcer versus Ischemic Ulcer
Neuropathic Ulcer Ischemic Ulcer

Painless Painful
Normal pulses Absent pulses
Regular margins, typically punched-out appearance Irregular margin
Often located on plantar surface of foot Commonly located on toes, glabrous margins
Presence of calluses Calluses absent or infrequent
Loss of sensation, reflexes, and vibration Variable sensory findings
Increased in blood flow (atrioventricular shunting) Decreased in blood flow
Collapsed veins
Dilated veins Cold foot
Dry, warm foot No bony deformities
Bony deformities Pale and cyanotic in appearance
Red or hyperemic in appearance
Fig. 23-63.
A. A neuropathic ulcer is characterized by a punched-out appearance with loss of sensation in the surrounding skin. The foot may
be warm to touch, and pulses may be present in the distal pedal arteries. B. An ischemic ulcer is characterized by a gangrenous
skin change in the foot or toes. The foot is usually cold to touch with absent pedal pulses. The foot is painful to touch with
decreased distal capillary refills.
One of the most common sites for occlusive disease is in the distal SFA as it passes deep through the adductor canal. It
may be that the entrapment by the adductor hiatus prevents the compensatory dilation that occurs in atherosclerotic
vessels. Stenoses, which develop here, progress to occlusion of the distal third of the SFA (Fig. 23-64). When distal SFA
occlusion develops slowly, it may be totally asymptomatic because of development of collaterals from the proximal SFA
or the profunda femoris artery (PFA) can bypass the occlusion and reconstitute the popliteal artery. Symptom
development is a function of the extent of occlusion, adequacy of collaterals, and also the activity level of the patients.
Fig. 23-64.
Computed tomography angiogram of a patient with an occluded left superficial femoral artery (single long arrow) with

reconstituted superficial femoral artery at the level of midthigh. Diffuse arterial calcifications (double small arrows) are noted in
the mid and distal left superficial femoral arteries.
Presenting symptoms of femoropopliteal occlusive disease are broadly classified into two types: limb-threatening and
non–limb-threatening ischemia. Claudication is non–limb-threatening, while rest pain, ulceration, and gangrene are
limb-threatening and warrant urgent intervention. Occlusive disease of the femoral artery may be isolated or occur in
conjunction with multilevel disease that involves both the aortoiliac segment and the tibial vessels. Symptoms in
patients with multilevel disease are more severe than in those with single-level disease. Pain from isolated SFA and
popliteal occlusion typically manifests as calf claudication. Cramping pain develops in the calf on ambulation, occurs at a
reproducible distance, and is relieved by rest. Activities such as climbing stairs or going uphill also exacerbate the pain.
Many patients report worsening symptoms during cold weather. It is important to evaluate whether the symptoms are
progressive or static. In >70% of patients, the disease is stable, particularly with risk factor modification.
Progression of the underlying atherosclerotic process is more likely to occur in patients with diabetes, those who
continue to smoke, and those who fail to modify their atherosclerotic risk factors. In comparison, rest pain is constant,
and usually occurs in the forefoot across the metatarsophalangeal joint. It is worse at night and requires placing the foot
in a dependent position to improve symptoms. Patients may report that they either sleep in a chair or hang the foot off
the side of the bed. The pain is severe and relentless, even with narcotics. Ischemic ulceration most commonly involves
the toes. Any toe can be affected. Occasionally, ulcers develop on the dorsum of the foot. Ulceration can occur in
atypical positions in an ischemic foot from trauma such as friction from poorly fitting shoes. Injury to a foot with
borderline ischemia can convert an otherwise stable situation into one that is limb-threatening. The initial development
of gangrene commonly involves the digits. As with all vascular patients, it is important to evaluate their risk factors,
intercurrent cardiac diseases, and any prior vascular interventions.
Treatment Considerations for Chronic Limb Ischemia

Patients with vascular diseases frequently have complicated medical comorbidities. Careful patient evaluation and
selection should be performed for any peripheral arterial vascular procedure. The fundamental principle is to assess not
only the surgical risk from the peripheral arterial system but also the global nature of the atherosclerotic process. Full
cardiac evaluations are often necessary due to the high incidence of concomitant atherosclerotic coronary arteries
disease, resulting in a high risk for ischemic events. Hertzer and associates reviewed coronary angiographies on 1000
patients undergoing elective vascular procedures and identified 25% of concomitant correctable CAD, including 21% in
patients undergoing elective peripheral vascular intervention.8 Conte and associates analyzed their 20-year experience
in a tertiary practice setting in 1642 open LE reconstructive surgeries and concluded that patients requiring LE
reconstruction presented an increasingly complex medical and surgical challenge compared with the previous decade.147
With aging of the population, there are a growing number of vascular patients who have prohibitive medical
comorbidities that are deemed high-risk for open surgical repair. Endovascular intervention provides an attractive
alternative.
As for open surgical repair, the clinical indications for endovascular intervention of LE PADs include lifestyle-limiting
claudication, ischemic rest pain, and tissue loss or gangrene. Importantly, endovascular procedures should be performed
by a competent vascular interventionist who understands the vascular disease process and is familiar with a variety of
endovascular techniques. In addition, certain lesions such as long segment occlusion, heavily calcified lesion, orifice
lesion, or lesions that can be not be traversed by a guidewire may not be amendable to endovascular treatment or may
be associated with poor outcomes. A proper selection of patients and techniques is critical in achieving a good long-term
outcome.
Endovascular intervention for LE occlusive disease is continuously evolving. Success and patency rates of endovascular
intervention are closely related to the anatomic and morphologic characters of the treated lesions. The TASC II work
group made recommendations on the intervention strategies of LE arterial diseases based on the morphologic
characters. Based on the TASC II guidelines, endovascular treatment is recommended for type A lesions, open surgery
is recommended for Type D lesions, and no recommendations were made for Types B and C lesions. However, with rapid
advancement in endovascular technologies, there are increased numbers of lesions amendable to endovascular
interventions.
There is less literature support on infrapopliteal endovascular intervention due to higher complication and lower success
rates. The treatment is restricted to patients with limb-threatening ischemia who lack surgical alternatives. However,
with further advancement of endovascular technology and the development of new devices, endovascular intervention
will become an integral part of treatment (Table 23-26). By itself or combined with open technique, percutaneous
intervention plays an important role in therapeutic options for LE occlusive disease. As described by the TASC II
guidelines, four criteria should be measured to evaluate the clinical success of the treatment: improvement in walking
distance, symptomatic improvement, quality of life, and overall graft patency. These criteria should all be carefully
weighed and evaluated for each individual before endovascular therapy.
Table 23-26 Summary of Endovascular Treatment Strategies Using Device-Based

Infrapopliteal Intervention
Intervention Advantages Disadvantages

Angioplasty Easy to use Failure in long lesions, calcified lesions,
and disease at multiple levels
Broad range of applications
Balloon- Overcomes arterial recoil from angioplasty Crushability can lead to restenosis

expandable stent Useful in treatment of flow-limiting dissection Poor distal runoff can result in stent
thrombosis; limited data
Self-expanding Vessel conformability and wall apposition prevents Limited sizes; limited data; multicenter
stent kinking and crushing of stent trials under way
Bioabsorbable Overcomes arterial recoil from angioplasty Limited data; multicenter trials under

stent way
Absorbed long-term to prevent risk of stent thrombosis
Cryoplasty Reduces the risk of flow-limiting dissection, therefore Short-term results of a multicenter trial

reducing the need for stent implantation are promising; however, long-term data
are limited
Cutting balloon Useful in anastomotic segments of bypass grafts and Limited data
instent restenosis where "watermelon seeding" can
prevent adequate expansion of plaque
Mechanical Allows for debulking of plaque without the need for Limited use in areas of heavy
atherectomy stent implantation in most cases calcification
Allows for removal of plaque for histologic analysis No large, randomized, prospective trial
comparing this technique to angioplasty
and stenting
Laser Useful in acute thrombotic and chronic total occlusions Minimal data in infrapopliteal arteries

Need adjunctive treatment with
angioplasty, stenting, or atherectomy
TECHNICAL CONSIDERATIONS
A sterile field is required in either an OR or an angiography suite with image capability. The most common and safest
access site is the CFA via either a retrograde or antegrade approach. For diagnostic angiography, arterial access should
be contralateral to the symptomatic sides. For therapeutic procedures, location of the lesion and the anatomic structures
of the arterial tree determine the puncture site. To avoid puncturing the iliac artery or SFA, the femoral head is located
under the fluoroscopy and used as the guide for the level of needle entry. In addition, there are several useful
techniques in helping access a pulseless CFA, including puncturing guided by ultrasound, using a micropuncture kit, and
targeting calcification in a calcified vessel. An antegrade approach may be challenging, particularly in obese patients.
Meticulous technique is crucial in preventing complications, and a bony landmark can be used as guidance to ensure CFA
puncture.
Traversing the lesion with a wire is the most critical part of the procedure. Typically, 0.035-in guidewires are used for
femoropopliteal lesions and 0.014- or 0.018-in guidewires are used for infrapopliteal access. Hydrophilic-coated wires,
such as Glide wires, are useful in navigating through tight stenosis or occlusion. An angled-tip wire with a torque device
may be helpful in crossing an eccentric lesion, and a shaped selective catheter is frequently used in helping manipulate
the wire across the lesion. The soft and floppy end of the wire is carefully advanced, crossing the lesion under
fluoroscopy, and gentle force is applied while manipulating the wire. Once the lesion has been traversed, one needs to
pay particular attention to the tip of the wire to ensure a secure wire access and avoid vessel wall perforation or
dissection.
Once the access to the diseased vessel is secured and the wire has successfully traversed the lesion, several treatment
modalities can be used either used alone or in conjunction with others, including angioplasty, stent or stent graft
placement, and atherectomy. The available angioplasty techniques are balloon angioplasty, cryoplasty, subintimal
angioplasty (SA), and cutting balloon. The most commonly used atherectomy techniques include percutaneous
atherectomy catheter and laser atherectomy device.
Systemic anticoagulation should be maintained routinely during LE arterial interventions to minimize the risk of
pericatheter thrombosis. Unfractionated heparin is the most commonly used agent, given on a weight-based formula. It
is a common clinical practice to use a 80 to 100 mg/kg initial bolus for a therapeutic procedure to achieve the activated
clotting time above 250 seconds on the catheter insertion and subsequently 1000 units for each additional hour of the
procedure. Newer agents such as low molecular weight heparin, platelet IIb/IIIa inhibitor, direct thrombin inhibitor, or
recombinant hirudin have been available and can be used either alone or in conjunction with heparin, particularly in
patients sensitive to unfractionated heparin. After procedures, all patients are placed on antiplatelet therapy such as
aspirin. Additional antiplatelet agents such as clopidogrel (Plavix) are given to selected patients with stent placement for
at least 6 weeks after LE interventions, unless otherwise contraindicated.
Percutaneous Transluminal Balloon Angioplasty

After the lesion is crossed with a wire, an appropriate balloon angioplasty catheter is selected and tracked along the wire
to traverse the lesion. The length of the selected catheter should be slightly longer than the lesion and the diameter
should be equal to the adjacent normal vessel. The balloon tends to be approximately 10 to 20% oversized. The
radiopaque markers of the balloon catheter are placed so that they will straddle the lesion. Then, the balloon is inflated
with saline and contrast mixture to allow visualization of the insufflation process under the fluoroscopy (Fig. 23-65). The
patient may experience mild pain, which is not uncommon. However, severe pain can be indicative of vessel rupture,
dissection, or other complications. An angiography is crucial in confirming the intraluminal location of the catheter and
absence of contrast extravasation. The inflation is continued until the waist of the atherosclerotic lesion disappears and
the balloon is at full profile. Frequently, several inflations are required to achieve full profile of the balloon (Fig. 23-66).
Occasionally, a lower profile balloon is needed to predilate the tight stenosis so that the selected balloon catheter can
cross the lesion.
Fig. 23-65.
angioplasty catheter that inflated a dilating balloon and expanded the flow lumen. C. Completion angiogram demonstrating
satisfactory radiographic result.
Fig. 23-66.
treated with cryoplasty, which lowered the balloon catheter temperature to a temporary freezing state during the balloon
angioplasty procedure (double arrows). C. Completion angiogram demonstrated satisfactory result with no evidence of vessel
dissection.
Besides length and diameter, the operators need to be familiar with several balloon characters. Noncompliant and low-
compliant balloons tend to be inflated to their preset diameter and offer greater dilating force at the site of stenosis.
Low-compliant balloons are the mainstay for peripheral intervention. A balloon with a low profile is used to minimize
complication at the entry site and for crossing the tight lesions. Upon inflation, most balloons do not rewrap to their
preinflation diameter and assume a larger profile. Furthermore, trackability, pushability, and crossability of the balloon
should be considered when choosing a particular type. Lastly, shoulder length is an important characteristic when
performing PTA to avoid injury to the adjacent arterial segments. After PTA, a completion angiogram is performed while
the wire is still in place. Leaving the wire in place provides access for repeating the procedure if the result is
unsatisfactory.
PTA is an established and effective therapy for select patients with LE occlusive diseases. Studies have shown that PTA
of the femoropopliteal segment achieved over a 90% technical success rate and a 38 to 58% 5-year primary patency
rate.148–150 However, efficacy of PTA is highly dependent upon anatomic selection and patient condition.106 PTA of
lesions longer than 7 to 10 cm offer limited patency, while PTA of shorter lesions, such as those that are <3 cm, have
fairly good results. Lofberg and associates performed 127 femoropopliteal PTA procedures and reported a primary 5-
year success rate of 12% in limbs with an occlusion longer than 5 cm vs. 32% in limbs with an occlusion <5 cm in
length.151 Occlusive lesions have much worse initial technical success rates than stenotic lesions. Concentric lesions
respond better to PTA than eccentric lesions, and heavy calcifications have a negative impact on success rates. A meta-
analysis by Hunink and associates showed that adjusted 5-year primary patencies after angioplasty of femoropopliteal
lesions varied from 12 to 68%, the best results being for patients with claudication and stenotic lesions.150 Distal runoff
is another powerful predictor of long-term success. Johnston analyzed 254 consecutive patients who underwent femoral
and popliteal PTA and reported that 5-year patency rates of 53% for stenotic lesions and 36% for occlusive lesions in
patients with good runoffs vs. a 5-year patency of 31% for stenotic lesions and 16% for occlusive lesions in patients
with poor runoff.149 Literature reviews showed that 5-year patency rates varied from 27 to 67% based on the runoff
statuses.150
Due to limited success with infrapopliteal PTA, the indication for infrapopliteal artery PTA is stringent, reserved for limb
salvage. Current patency rates from infrapopliteal PTA can be improved further by proper patient selection, ensuring
straight-line flow to the foot in at least one tibial vessel, and close patient surveillance for early reintervention. Possible
future advances including the use of drug-eluting stents (DES), cutting balloons, and atherectomy devices are being
investigated to improve clinical outcomes following endovascular interventions on the tibial arteries. Varty and
associates reported a 1-year limb salvage rate of 77% in patients with critical ischemia who underwent infrapopliteal
PTA.152 In patients with favorable anatomies, a 2-year limb salvage rate after infrapopliteal artery PTA is expected to
exceed 80%.
SUBINTIMAL ANGIOPLASTY
The technique of SA was first described in 1987 when successful establishment of flow was made by accidental creation
of a subintimal channel during treatment of a long popliteal artery occlusion. SA is recommended for chronic occlusion,
long segments of lesion, and heavily calcified lesions. In addition, this technique is applicable for vessels with diffuse
diseases and for vessels that had previously failed an intraluminal approach because it is difficult to negotiate the wire
across the entire diseased segment without dissection.
The principle of this technique is to bypass the occlusion by deliberately creating a subintimal dissection plan
commencing proximal to the lesion and continuing in the subintimal space before breaking back into the true lumen
distal to the lesion. The occluded lumen is recanalized through the subintimal plan. SA can be performed through either
ipsilateral antegrade or contralateral retrograde using the CFA approach. If selecting contralateral CFA puncture, a long
guiding sheath is placed across the aortic bifurcation to provide access for the femoropopliteal and infrapopliteal vessels.
The subintimal dissection is initiated at the origin of an occlusion by directing the tip of an angled guidewire, usually an
angled hydrophilic wire such as Glidewire. A supporting catheter is used to guide the tip of the guidewire away from the
important collaterals. When the wire is advanced, a loop is naturally formed at the tip of the guidewire. Once the
subintimal plan is entered, the wire tends to move freely in the dissection space. Subintimal location of the wire and the
catheter can be confirmed by injecting a small amount of diluted contrast. At this point, the wire and the catheter are
then advanced along the subintimal plan until the occlusion segment is passed. A loss of resistance is often encountered
as the guidewire re-enters the true lumen distal to the occlusion. Recanalization is confirmed by advancing the catheter
over the guidewire beyond the point of re-entry and obtaining an angiogram. This is followed by a balloon angioplasty.
To confirm the patency following balloon dilatation, a completion angiogram is performed before withdrawing the
catheter and wire. If flow is impaired, repeat balloon dilatation may be necessary. Frequently, a stent is required to
maintain a patent lumen and treat residual stenosis if more than a 30% luminal reduction is confirmed on completion
angiogram.
Multiple studies have demonstrated the efficacy of SA. Bolia and his colleagues and London and his colleagues reported
their extensive experiences on SA for treating long segment occlusions of infrainguinal vessels.153,154 They achieved a
technical success rate of over 80% for both femoropopliteal and tibial arteries. One-year patency rates varied from 53%
for infrapopliteal vessels to 71% for femoropopliteal segments. Limb salvage rates reached over 80% at 12 months.
They also reported that the factors influencing patency are smoking, number of runoff vessels, and occlusion length.
Studies by other groups showed similar results.155,156 Treiman and colleagues treated 25 patients with 6- to 18-cm
femoropopliteal occlusion and achieved a technical success rate of 92% and a 12-month primary patency rate of
92%,156 while Lipsitz and associates reported a technical success rate of 87% in treating 39 patients and achieved a 12-
month cumulative patency rate of 74%.155 Additionally, Ingle and associates reported a technical success rate of 87%
on 67 patients with femoropopliteal lesions and a 36-month limb salvage rate of 94%.157 As demonstrated herein,
although technical success rates are similar in most series, the patency rates vary widely in different studies. Patient
selection, anatomic character, and lesion locations may account for the wide range of outcomes.
STENT PLACEMENT
Although suggested by Dotter during the late 1960s, the use of an endoluminal stent was not pursued until the
limitations of PTA were widely recognized. There are several situations where stent placement is appealing. The primary
indication is the potential salvage of an unacceptable angioplasty result. Stent placement is typically used when residual
stenosis after PTA is 30% or greater. An endoluminal stent is also used for dissection, perforation, and other PTA
complications. Primary stent placement has become a viable alternative for treating ulcerative lesions that may
potentially be the source for embolization. Primary stent is also used to treat occlusive lesions that have a tendency of
reocclusion and distal embolization after PTA. In addition, an endoluminal stent is potentially beneficial for early
restenosis post-PTA. DESs are currently under investigation in the United States and may be promising in decreasing
restenotic rates.
Even though technical success rates are high, a published series on femoropopliteal artery stents show that patency
rates are comparable to PTA alone with primary patency rates varying from 18 to 72% at 3 years.106,158 Gray and
associates stented 58 limbs after suboptimal PTA for long SFA lesions and demonstrated a 1-year primary patency rate
of 22%.159 However, Mewissen treated 137 limbs using self-expanding SMART nitinol stents in patients with TASC II A,
B, and C femoropopliteal lesions and reported a 1-year primary patency rate of 76% and a 24-month primary patency
rate of 60%.160 Appropriate patient selection and the anatomic characteristics of the lesions are crucial in the success of
treatment outcomes. Additionally, stent characteristics may contribute to the patency rate.
Several clinical studies have demonstrated the significant improvements of the new generation of nitinol stents for the
SFA lesions: the German Multicenter Experience, the Mewissen trial, the BLASTER Trial, and the SIROCCO trials.161 The
German Multicenter Experience was a retrospective review of 111 SFA stenting procedures and found the 6-month
patency rates for Smart stents and Wall stents were 82% and 37%, respectively. The BLASTER (Bilateral Lower Arterial
Stenting Employing Reopro) Trial evaluated the feasibility of using nitinol stents with and without IV abciximab for the
treatment of femoral artery disease. Preliminary results showed a 1-year clinical patency rate of 83%.162
Furthermore, DESs, which proved effective at decreasing restenosis in coronary intervention, may offer another
promising alternative in LE diseases. The drug, released over a period of time, interferes with smooth muscle cell
proliferation, the main cellular element and source of extracellular-matrix–producing restenosis. The first DES clinical
trial used Cordis Cypher SMART stents coated with sirolimus (SIROCCO trial).163 The SIROCCO results showed binary
inlesion restenosis rates of 0% in the sirolimus-eluting group vs. 23.5% in the noneluting group at 6-month follow-up
angiography.
STENT GRAFT
The concept of endobypass using stent graft in treating atherosclerotic SFA disease has been entertained. A stent graft
is placed percutaneously across a long segment or multiple segments of lesions and is used to create a femoropopliteal
bypass. Theoretically, endobypass has the potential of being as successful as surgical bypass graft by relining the vessel
wall in its anatomical position without the negative impact of anastomosis. Stent grafts can be divided into two
categories: unsupported and fully supported. The unsupported grafts consist of segments of bypass graft, such as PTFE,
with an expandable stent at one or both ends. The unsupported grafts are flexible with a low profile, but prone to
external compression. The supported stent grafts consist of a metallic skeleton covered with graft fabric. The presence
of a dense metal skeleton promotes an extensive inflammatory response and increases the risk of thrombosis. There is
no FDA-approved stent graft for peripheral intervention. However, Viabahn (WL Gore, Calif) is the most commonly used
device in the United States, composed of an ultrathin PTFE graft externally supported by a self-expanding nitinol
meshwork. The Viabahn device has a specific delivery mechanism—pulling back the attached string—which results in a
proximal-to-distal delivery of the endoprosthesis.
Although it is an intriguing concept, data on endobypass results are limited and the graft thrombosis rate is high.
Additionally, covering major collateral vessels can potentially jeopardize the viability of the limb if stent graft occlusion
occurs. Bauermeister treated 35 patients with Hemobahn and reported a 28.6% occlusion rate on an average 7-month
follow-up.164 Kedora and colleagues recently conducted a prospective, randomized study comparing covered
PTFE/nitinol self-expanding stent grafts with prosthetic above-the-knee femoropopliteal bypass. Fifty limbs were
randomized into each group. Primary patency at 1-year was approximately 74% for both cohorts, with a mean follow-up
of 18 months. The covered nitinol PTFE stent graft in the SFA had a 1-year patency rate comparable to surgical bypass,
with a significantly shorter hospital stay (0.9 vs. 3.1 days).165
ATHERECTOMY
The basic principle of atherectomy is to remove the atheroma from obstructed arterial vessels. There are currently five
atherectomy devices approved by the FDA: Simpson AtheroCath (DVI, Redwood City, Calif), Transluminal Extraction
Catheter (Interventional Technologies, San Diego, Calif), Theratec recanalization arterial catheter (Trac-Wright), Auth
Rotablator (Heart Technologies, Redmond, Wash), and SilverHawk system (FoxHollow Technologies, Redwood City,
Calif). These devices either cut and remove or pulverize the atheroma plaques.
The Simpson AtheroCath has a directional cutting element that is exposed to one third of the circumference of the
arterial wall. The atheroma protruding into the window is excised and pushed into the collection chamber. The
Transluminal Extraction Catheter has an over-the-wire, nondirectional cutter mounted on the distal end of a torque tube.
The excised atheroma is simultaneously removed by aspiration through the torque tube. The Theratec recanalization
arterial catheter is a nondirectional, noncoaxial, atheroablative device. The rotating cam tip pulverizes the atheromatous
lesion into minute particles. The Auth Rotablator is a nondirectional, coaxial, atheroablative device with a metal burr
embedded with fine diamond chips. Lastly, the SilverHawk device, approved by the FDA for peripheral use in 2003, is a
monorail catheter designed to overcome the drawback of direction atherectomy catheter, such as the Simpson
AtheroCath. The working end consists of a hinged housing unit containing a carbide cutting blade. The blade is activated
from the motor drive unit and the catheter is then advanced through the length of the lesion. Once each pass is
completed, the cutter then packs the tissue into the distal end of the nosecone to maximize collection capacity. The
SilverHawk can then either be removed or torqued to treat a different quadrant in the same lesion or other lesions.
Despite the promising early technical and clinical success, the mid- and long-term results have been disappointing due
to a high incidence of restenosis. However, a multicenter clinical registry of plaque atherectomy in patients with
femoropopliteal occlusive disease showed potential clinical efficacy of this technology as the 6- and 12-month rates of
survival free of target lesion revascularization were 90 and 80%, respectively.166 Importantly, nearly three fourths
(73%) of patients treated with plaque excision modality did not require adjunctive endovascular therapy as infrainguinal
stenting was necessary in only 6.3% of lesions. Results from the TALON registry support the role of plaque excision in
selective patients with LE arterial disease.166
Laser Atherectomy
Since laser atherectomy was reported in the 1960s, a variety of innovative approaches have been developed in an effort
to overcome the limitation of laser angioplasty. Recent developments in excimer laser technology have led to increased
optimism regarding the ability to safely deliver laser energy. Excimer laser atherectomy approved by the FDA for
peripheral artery intervention uses precision laser energy control (shallow tissue penetration) and safer wavelengths
(ultraviolet as opposed to the infrared spectra in older laser technology), which decreases perforation and thermal injury
to the treated vessels.
A laser atherectomy catheter, with diameters varying from 0.9 mm to 2.5 mm, is tracked over the guidewire to the
desired target. Once activated, the excimer laser uses ultraviolet energy to ablate the lesion and create a
nonthrombogenic arterial lumen. This lumen is further dilated by an angioplasty balloon. Because the excimer laser can
potentially reduce the rate of distal embolization by evaporating the lesion, it may be used as an adjunct tool for ostial
lesions and lesions that can be traversed by a wire but not an angioplasty balloon catheter.
Several studies regarding the use of excimer laser atherectomy combined with balloon angioplasty on LE occlusive
disease have shown promising clinical outcomes.167,168 Peripheral excimer laser angioplasty trials involved 318 patients
with chronic SFA occlusion. They achieved a technical success rate of 83.2%, a 1-year primary patency rate of 33.6%,
and an assisted primary patency rate of 65%.168 Steinkamp and his colleagues treated 127 patients with long-segment
of popliteal artery occlusion using laser atherectomy followed by balloon angioplasty and reported a 3-year primary
patency rate of 22%.169 The multicenter clinical trial evaluating the use of laser angioplasty for critical limb ischemia
supports the efficacy of this treatment modality in selective patients as the 6-month primary patency rate and clinical
improvement were 33 and 89%, respectively.167
Complications of Endovascular Interventions

ANGIOPLASTY-RELATED COMPLICATIONS
Complications related to PTA vary widely, including dissection, rupture, embolization, pseudoaneurysms, restenosis,
hematoma, and acute occlusion secondary to thrombosis, vasospasm, or intimal injury. Clark and associates analyzed
the data from 205 patients in the SCVIR Transluminal Angioplasty and Revascularization registry and reported a
complication rate of 7.3% for patients undergoing femoropopliteal angioplasty.170 Minor complications accounted for
75% of the cases, including distal emboli (41.7%), puncture site hematomas (41.7%), contained vessel rupture (8.3%),
and vagal reactions (8.3%). In another study, Axisa and colleagues reported an overall rate of significant complications
for patients undergoing PTA of the lower extremities as 4.2%, including retroperitoneal bleeding (0.2%), false aneurysm
(0.2%), ALI (1.5%), and vessel perforation (1.7%).171
Complications limiting the application of SA are parallel to those of PTA. A study investigating the use of SA in 65
patients with SFA occlusion found that complications developed in 15% of patients.172 These complications included
significant stenosis (44%), SFA rupture (6%), distal embolization (3%), retroperitoneal hemorrhage (1.5%), and
pseudoaneurysm (1.5%). Additional complications reported consist of perforation, thrombosis, dissection, and
extensions beyond the planned re-entry site.173 Importantly, damage to significant collateral vessels may occur in 1 to
1.5% of patient who undergo SA. If a successful channel is not achieved in this situation, the patient may have a
compromised distal circulation that necessitates distal bypass. Cryoplasty is a modified form of angioplasty, and long-
term results on LE intervention are not yet available. Fava and associates treated 15 patients with femoropopliteal
disease and had a 13% complication rate involving guidewire dissection and PTA-induced dissection of a tandem lesion
remote to the cryoplasty zone.174
ENDOLUMINAL STENT AND STENT GRAFT–RELATED COMPLICATIONS

In addition to the aforementioned complications with angioplasty, endoluminal stents are associated with the risk of
stent fraction and deformity. The adductor canal has nonlaminar flow dynamics, especially with walking. The forces
exerted on the SFA include torsion, compression, extension, and flexion. These forces exert significant stress on the SFA
and stents. In addition, the LE is subject to external trauma, which further increases the risk of stent deformity and
fracture (Fig. 23-67). The SIROCCO study showed that stent fracture, although not associated with clinical symptoms,
occurs in 18.2% of the procedures involving both the DES and control stent.163
Fig. 23-67.
Due to various geometric forces, including torsion, compression, extension, and flexion, which exert on the superficial femoral
artery, stent fracture (arrows) is a known complication following superficial femoral artery stent placement.
Stent grafts may present an additional complication of covering important collaterals, which results in compromised
distal circulation. A prospective study evaluating Hemobahn stent grafts in the treatment of femoropopliteal arterial
occlusions demonstrated a 23% immediate complication rate, including distal embolization (7.7%), groin hematoma
(13.5%), and arteriovenous fistula (1.9%).175
ATHERECTOMY-RELATED COMPLICATIONS
Overall complication rates associated with atherectomy range from 15.4 to 42.8% and include spasm, thrombosis,
dissection, perforation, distal emboli, no reflow, and hematoma.176,177 Jahnke and associates conducted a prospective
study evaluating high-speed, rotational atherectomy in 15 patients with infrapopliteal occlusive disease. They yielded a
94% technical success rate, which was complicated by vessel rupture (5%), distal embolization (5%), and arterial
spasm (5%).175 Although the excimer laser atherectomy reduces embolic events by evaporating the lesion,
embolization still remains a problematic complication. Studies show that distal embolic events occur in 3 to 4% of
procedures, and perforation in 2.2 to 4.3% of cases.168,169 Other complications compromising laser atherectomy
therapy include acute reocclusion, vasospasm, direct vessel injury, and dissection.
Surgical Treatment for Chronic Limb Ischemia Due to Femoropopliteal

Disease
ENDARTERECTOMY
Endarterectomy has a limited, albeit important, role in LE occlusive disease. It is most frequently used when there is
disease in the CFA or involving the PFA. In this procedure, the surgeon opens the diseased segment longitudinally and
develops a cleavage plane within the media that is developed proximally and distally. This permits the inner layer
containing the atheroma to be excised. Great care must be taken at the distal end of the endarterectomy to ensure
either a smooth transition or to tack down the distal endpoint to prevent the flow from elevating a potentially occlusive
atheromatous flap. Currently, there is essentially no role for long open endarterectomy in the treatment of SFA stenoses
or occlusions. The high incidence of restenosis is what limits use of endarterectomy in this location. Short-segment
stenoses are more appropriately treated with balloon angioplasty. Endarterectomy using a catheter-based approach
(e.g., Moll endarterectomy device) supplemented with stent grafting or stenting across the endpoint of the
endarterectomy is currently being re-evaluated; however, no long-term data are available.
BYPASS GRAFTING
Bypass grafting remains the primary intervention for LE occlusive disease. The type of bypass and conduit are important
variables to consider. Patients with occlusive disease limited to the SFA, who have at least 4 cm (ideally 10 cm) of
normal popliteal artery reconstituted above the knee joint and at least one continuous vessel to the foot, can be treated
with an above-knee (AK) femoropopliteal bypass graft. Despite the fact that in this above-knee location, the differential
patencies between prosthetic (PTFE) and vein graft are comparable; undoubtedly, it remains ideal to use a saphenous
vein as the bypass conduit, if possible. Saving the vein for future coronary artery bypass or distal leg bypass grafting
has been shown to be a flawed argument. One must also take into consideration that the consequences to the vascular
outflow after a thrombosed prosthetic are worse than after a thrombosed vein graft.
When the disease extends to involve the popliteal artery or the tibial vessels, the surgeon must select an appropriate
outflow vessel to perform a bypass. Suitable outflow vessels are defined as uninterrupted flow channels beyond the
anastomosis into the foot. In order of descending preference, they are: AK popliteal artery, below-knee (BK) popliteal
artery, posterior tibial artery, anterior tibial artery, and peroneal artery. In patients with diabetes, it is frequently the
peroneal artery that is spared. Although the peroneal artery has no direct flow into the foot, collateralization to the
posterior tibial and anterior tibial arteries makes it an appropriate outflow vessel. There is no objective evidence to
preferentially select tibial over peroneal arteries if they are vessels of equal caliber and quality. The dorsalis pedis, which
is the continuation of the anterior tibial in the foot, is frequently spared from atherosclerotic disease and can be used as
a target for distal bypasses. Patency is affected by the length of the bypass (longer bypasses have reduced patency),
quality of the recipient artery, extent of runoff to the foot, and quality of the conduit (saphenous vein/graft). Five-year
assisted patency rates for infrapopliteal venous bypasses are 60%. Venous conduits also have been shown to be suitable
for bypasses to plantar arteries. In this location, venous conduits have a 3-year limb salvage of 84% and a 3-year
secondary patency of 74%.2 A meta-analysis suggests unsatisfactory results when PTFE-coated grafts are used to
bypass to infrapopliteal arteries. In this location, prosthetic grafts have a 5-year primary patency rate of 30.5%.178
Additionally, due to distal embolization and compromise of outflow vessels, prosthetic graft occlusion may have more
severe consequences than vein graft occlusion.178
Two techniques are used for distal bypass grafting: reversed saphenous vein grafting and in situ saphenous vein
grafting. There is no difference in outcomes (patency or limb salvage) between these techniques.2 In the former, the
vein is excised in its entirety from the leg using open or endoscopic vein harvest, reversed to render the valves
nonfunctional, and tunneled from the CFA inflow to the distal target vessels. End-to-side anastomoses are then created.
Several adjunctive techniques have been tried to improve the patency of bypass grafts to tibial arteries. Creation of an
arteriovenous fistula at the distal anastomosis is one option, but it has not been shown to improve patency.179 Another
method involves creating various configurations of vein cuffs or patches at the distal anastomosis in an attempt to
streamline the flow and to reduce the likelihood of neointimal hyperplasia. Results with this approach are more
promising, especially when done to improve patency of a below-the-knee prosthetic; however, there are no definitive
comparative trials that support the superiority of one configuration over another.
AMPUTATION
Primary amputation is defined as an amputation that is performed without a prior attempt at surgical or endovascular
revascularization. It is rarely necessary in patients who, as a result of neglect, present with class III ALI. Primary
amputation may play a role in patients with critical limb ischemia who are deemed nonambulatory because of knee
contractures, debilitating strokes, or dementia.
Complications of Surgical Reconstruction

VEIN GRAFT STENOSES
Fifteen percent of vein grafts will develop intrinsic stenoses within the first 18 months following implantation.
Consequently, patients with a vein graft were entered into duplex surveillance protocols (scans every 3 months) to
detect elevated (>300 cm/s) or abnormally low (<45 cm/s) graft velocities early. Stenoses greater than 50%, especially
if associated with changes in ABI, should be repaired to prevent graft thrombosis. Repair usually entails patch
angioplasty or short-segment venous interposition, but PTA/stenting is an option for short, focal lesions. Grafts with
stenoses that are identified and repaired before thrombosis have assisted primary patency identical to primary patency,
whereas a thrombosed autogenous bypass has limited longevity, resulting from ischemic injury to the vein wall.
Secondary patency is markedly inferior to primary assisted patency. The recommendation for routine duplex ultrasound
surveillance of autogenous infrainguinal bypasses was recently brought into question by a randomized, controlled trial
that demonstrated no cost benefit or quality-of-life improvement after 18 months in patients with femoropopliteal
venous bypasses.180 Many surgeons continue with programs of vein graft surveillance, as has been suggested in older
trials, awaiting further confirmation of the findings from the more recent study. When intervening on a failing
infrainguinal bypass, the original indication for surgery is an important consideration. Limb salvage rates for occluded
grafts are better if the indication for the original bypass was claudication rather than rest pain or tissue loss. An acutely
occluded infrainguinal graft (≤30 postoperative days) has a 25% limb salvage rate.181
LIMB SWELLING
Limb swelling is common following revascularization and usually returns to baseline within 2 to 3 months. The etiology is
multifactorial, with lymphatic interruption, interstitial edema, and disruption of venous drainage all contributing. Limb
swelling tends to worsen with repeat revascularization (see Table 23-22).
WOUND INFECTION
Because the most common inflow vessel for distal bypass is the CFA, groin infection is common and occurs in 7% of
cases.182 When an autogenous conduit such as a saphenous vein is used, most infection can be managed with local
wound care because it involves the subcutaneous tissue or skin rather than infection of the actual vein. When a
prosthetic graft has been used, management of graft infection is a major undertaking. Infection of a LE prosthetic
bypass graft is associated with a significant amputation rate because of the tendency for graft thrombosis and
anastomotic disruption. Prosthetic graft infections cannot be eradicated with antibiotics, and they mandate graft excision
and complex revascularization using a vein, if available.
Choice of Conduit for Infrainguinal Bypass Grafting

AUTOGENOUS VEIN
Autogenous vein is superior to prosthetic conduits for all infrainguinal bypasses, even in the AK position. This preference
is applicable not only for the initial bypass but also for reoperative cases. For long bypasses, ipsilateral great saphenous
vein (GSV), contralateral GSV, small saphenous vein, arm vein, and spliced vein are used, in decreasing order of
preference. If only a short segment of vein is missing, the SFA can be endarterectomized and the proximal anastomosis
performed distally to decrease the length of the conduit and to avoid harvesting and splicing additional vein. When GSV
is not available and a relatively short bypass is necessary, arm vein or small saphenous vein is effective. Small
saphenous vein is of particular use when a posterior approach is used. If a longer bypass with vein is necessary, arm
vein is preferable because it is less awkward to harvest. Another conduit alternative is to harvest the upper arm basilic,
median cubital, and cephalic veins in continuity, while incising valves in the basilic segment and using the cephalic
segment in reversed configuration to provide a relatively long, unspliced autogenous conduit.183
CRYOPRESERVED GRAFTS
Cryopreserved grafts are usually cadaveric arteries or veins that have been subjected to rate-controlled freezing with
dimethyl sulfoxide and other cryopreservants. Cryopreserved vein grafts are more expensive than prosthetic grafts and
are more prone to failure. The endothelial lining is lost as part of the freezing process, making these grafts prone to
early thrombosis. Cryopreserved grafts also are prone to aneurysmal degeneration. Despite the fact that these grafts
have not performed as well as prosthetic bypasses and autogenous vein in clinical practice, they can still play a role
when revascularization is required following removal of infected prosthetic bypass grafts, especially when autogenous
vein is unavailable to create a new bypass through clean tissue planes.184
HUMAN UMBILICAL VEIN

Human umbilical vein (HUV) is less commonly used than PTFE, because it is thicker and more cumbersome to handle
and because of concerns about aneurysmal degeneration. HUV allografts are stabilized with glutaraldehyde and do not
have viable cells or antigenic reactivity. These grafts have poor handling characteristics and require extra care when
suturing because of an outer Dacron mesh wrapping, which is used to decrease aneurysmal degeneration. Dardik and
colleagues have reported favorable results after using HUV and an adjunctive distal arteriovenous fistula.185 One trial
comparing HUV with PTFE and saphenous vein showed that HUV was better than PTFE but worse than saphenous vein in
terms of 5-year patency in the AK location.186 In a systematic review, HUV appears to perform better than
cryopreserved veins.187
PROSTHETIC CONDUITS AND ADJUNCTIVE MODIFICATIONS

If vein is truly unavailable, PTFE or Dacron is the best option for AK bypass. The addition of rings to PTFE did not confer
benefit in a single prospective, randomized clinical trial.188 For infrageniculate prosthetic bypasses, use of a vein patch,
cuff, or other venous anastomotic modification can improve patency (52% patency at 2 years for PTFE with vein cuff vs.
29% for PTFE with no cuff) and also improve limb salvage (84% vs. 62%).189
Although prosthetic grafts are readily available, easy to handle, and do not require extensive dissection to harvest, their
propensity to undergo thrombosis and develop neointimal hyperplasia makes them a less favorable alternative when
compared to vein. In a recent review of vein and prosthetic AK femoropopliteal bypasses, the 5-year primary patency
rates were reported to be 74 and 39%, respectively.190 Outcomes were even worse for BK prosthetic bypasses.
Unfortunately, the use of autologous venous conduits is not possible in as many as 30% of patients. The GSV may be
unsuitable because of small size and poor quality or unavailable due to prior harvest.
Methods to improve prosthetic graft performance have consisted of altering the geometry at the distal anastomosis to
get the benefit obtained with vein cuffs (Distaflo, Bard Peripheral Vascular, Tempe, Ariz) and covalently bonding agents
onto the luminal surface with anticoagulant, anti-inflammatory and antiproliferative characteristics (Propaten, Gore,
Flagstaff, Ariz). One randomized trial that compared precuffed PTFE and PTFE with a vein cuff enrolled 104 patients at
10 centers. Eighty-nine patients were randomized to 47 precuffed PTFE bypasses and 44 bypasses with a vein cuff. At 1
and 2 years, primary patency rates were 52 and 49% for the precuffed group and 62 and 44% for the vein cuffed group,
respectively. At 1 year and 2 years, the limb salvage rate was 72 and 65% for the precuffed group and 75 and 62% in
the vein cuffed group, respectively. Although numbers are small and follow-up short, the midterm analysis revealed that
Distaflo precuffed grafts and PTFE grafts with vein cuff had similar results. The authors concluded that a precuffed graft
was a reasonable alternative for infragenicular reconstruction in the absence of saphenous vein.191 Other authors have
been less optimistic and question if there is any benefit derived from geometrically altering prosthetic conduits.192
Another approach for improving outcomes when using prosthetic for bypass grafts involves bonding anticoagulants to
the conduit. The Gore Propaten graft has heparin bonded onto the luminal surface of the PTFE graft using Carmeda
BioActive Surface technology, which immobilizes the heparin molecule with a single covalent bond that does not alter its
anticoagulant properties.193 The heparin binding does not alter the microstructure and handling characteristics of the
PTFE. A prospective, randomized trial by Devine and associates suggested that heparin-bonded Dacron or PTFE was
superior to plain PTFE for AK popliteal bypasses. The 3-year primary patency for the heparin-bonded grafts was 55%
compared with 42% for PTFE (P <.044). Both of these patency rates are inferior to GSV; however, if the improved
results with heparin bonding continue to be substantiated, then heparin-bonded prosthetic grafts will become the
preferred conduit for AK bypass in the absence of suitable vein.194 A recent review of available studies with this graft
showed an 80% 1-year patency for BK bypasses.195 Randomized, controlled clinical trials with more patients and longer
follow-up are necessary to validate whether the PROPATEN vascular graft is superior to other prosthetics, and if, indeed,
it is comparable to autogenous vein for BK interventions.
Clinical Results of Surgical and Endovascular Interventions for

Femoropopliteal Occlusive Disease
Balloon angioplasty of the femoropopliteal vessels has not enjoyed the degree of success seen with iliac angioplasty.
Patency in this region is dependent upon whether the patient presents with claudication vs. limb-threatening ischemia,
the status of the distal runoff vessels, and lesion morphology.2 Initial technical success for femoropopliteal angioplasty is
seen in 80 to 90% of cases, with failures to cross a lesion occurring in 7% of stenoses and 18% of occlusive lesions.
Studies have shown that PTA of the femoropopliteal segment achieved greater than a 90% technical success rate and
had a 59% primary patency rate at 5-years.148,149 PTA of lesions longer than 7 to 10 cm results in compromised
patency, while PTA of shorter lesions (<3 cm) gives fairly good results. Lofberg and associates performed 127
femoropopliteal PTA procedures and reported a primary patency rate at 5-year follow-up of 12% in limbs with occlusion
longer than 5 cm vs. 32% in limbs with occlusion <5 cm in length.151 Occlusive lesions have much worse initial
technical success rates than stenotic lesions. Concentric lesions respond better to PTA than eccentric lesions, and heavy
calcifications have a negative impact on success rates. Distal runoff is another powerful predictor of long-term success.
Johnston and associates analyzed 254 consecutive patients who underwent femoropopliteal PTA and reported a 5-year
patency rate of 53% for stenotic lesions and 36% for occlusive lesions in patients with good runoff vs. 5-year patency of
31% for stenotic lesions and 16% for occlusive lesions in patients with poor runoff.149 A meta-analysis by Hunink and
colleagues showed that adjusted 5-year primary patencies after angioplasty of femoropopliteal lesions varied from 12 to
68%, the best results occurring in patients with claudication and stenotic lesions.150 Although the initial technical
success is better for stenoses than occlusions, long-term patency rates for stenoses and short occlusions have been
variable and there have been conflicting results regarding the efficacy of stent use. Early published series that examined
efficacy of femoropopliteal artery stents showed patency rates that were comparable to stand-alone PTA with primary
patency rates varying from 18 to 72% at 3 years.158 Patient selection and the anatomic character of the lesions may
play important roles in the outcomes. Additionally, stent characteristics may contribute to the patency rate. Several
clinical studies have demonstrated significant improvements in patency when the newer generations of nitinol stents are
used to treat SFA lesions.160,196
Mewissen treated 137 lower limbs in 122 patients with CLI, secondary to TASC II A (n = 12) or TASC II B or C (n = 125)
lesions in the SFA. Patients were treated with Cordis SMART self-expanding nitinol stents. Binary restenosis (>50%) was
measured by standard duplex velocity criteria at various postintervention intervals. Primary stent patency, defined as
absence of binary restenosis in this study, was calculated by life table methods from the time of intervention. The mean
lesion length was 12.2 cm (range, 4 to 28 cm). The technical success was 98%. Mean follow-up was 302 days. The
primary stent patency rates were 92%, 76%, 66%, and 60% at 6, 12, 18, and 24-months, respectively.160 Fereira and
associates treated 59 patients who had 74 femoropopliteal lesions (60% TASC II D) with Zilver nitinol self-expanding
stents (COOK, Bloomington, Ind). Mean recanalization length was 19 cm (range 3 to 53 cm). Mean follow-up time was
2.4 years (range 3 days to 4.8 years). Kaplan-Meier estimates for primary patency rates were 90%, 78%, 74%, 69%,
and 69% at 1, 2, 3, 4, and 4.8 years, respectively.197
There is general agreement that for suboptimal PTA of an SFA lesion, stent placement is indicated, but a recent
randomized trial by Schillinger and associates suggests that primary stenting results in lower restenosis rates than PTA
and selective stenting. Restenosis rates at 2 years were 45.7% vs. 69.2% in favor of primary stenting compared with
PTA and optional secondary stenting using an intention-to-treat analysis (P = .031). Consistently, stenting, both primary
and selective, was superior to stand-alone PTA with respect to the occurrence of restenosis (49.2% vs. 74.3%; P
= .028) by a treatment-received analysis.198
Nitinol bare metal stents that are designed specifically for BK interventions are showing very encouraging results.
Bosiers and colleagues reported their 12-month results using the commercially available non–drug-eluting Xpert (Abbott
Vascular, Santa Clara, Calif) nitinol stent system in BK arterial interventions.199 They had a 12-month primary patency
rate of 76.3%, and a limb salvage rate of 95.9%. They followed patients to 12 months and performed angiography with
quantitative vessel analysis on the 73% of patients available. Angiography revealed a binary restenosis rate (>50%) of
only 20.5%, which is comparable to well-accepted coronary DES study outcomes. The authors attributed this optimal
performance to the maintenance of flow dynamics because the stent was specifically designed for use in small
vessels.199 Kickuth and colleagues also have obtained good results using the Xpert stent. After stent placement, the
primary cumulative patency rate at 6 months for the study group of 35 patients was 82%. The sustained clinical
improvement rate as evidenced by improved ABI was 80%, and freedom from major amputation was 100% at the 6-
month follow-up. The rate of major complications was 17%.200
Wolf and associates published a multicenter, prospective randomized trial comparing PTA with bypass in 263 men who
had iliac, femoral, or popliteal artery obstruction.201 In 56 patients, cumulative 1-year primary patency after PTA was
43% and, after bypass surgery, was 82%, demonstrating that for long SFA stenoses or occlusions, surgery is better
than PTA. Another recent randomized study (BASIL trial) of 452 patients with CLI demonstrated no difference in
amputation-free survival at 6 months between surgery and PTA/stenting. The authors commented that surgery was
somewhat more expensive and recommended that endovascular intervention should be used as first-line therapy,
especially in medically unfit patients. They did conclude that at 2-year follow-up, healthy patients without medical
comorbidities derived greater benefit from surgery because it was associated with decreased need for reintervention and
had a decreased hazard ratio in terms of all-cause mortality.202 Using the 2000 TASC II definitions and a Markov state
transition model decision analysis, Nolan and colleagues showed that PTA/stenting surpasses bypass efficacy for TASC II
C lesions if PTA/stenting primary patency is greater than 32% at 5 years, patient age is >80 years, and/or GSV bypass
operative mortality is greater than 6%.106,203
NON-ATHEROSCLEROTIC DISORDERS OF BLOOD VESSELS

The majority of cases of peripheral vascular disease that are seen by vascular surgeons are attributable to underlying
atherosclerosis. Non-atherosclerotic disease states that result in arterial pathology are less commonly encountered, but
are nonetheless important, as they are potentially treatable lesions that may mimic atherosclerotic lesions and result in
vascular insufficiency (see Table 23-18). A thorough knowledge of these rare disease states is important for the
practicing vascular surgeon to make medical recommendations and provide appropriate surgical treatment.
Giant Cell Arteritis (Temporal Arteritis)

Giant cell arteritis is also known as temporal arteritis, which is a systemic chronic inflammatory vascular disease with
many characteristics similar to those of Takayasu's disease. The histologic and pathologic changes as well as laboratory
findings are similar. Patients tend to be white women over the age of 50 years old, with a high incidence in Scandinavia
and among women of Northern European descent. Genetic factors may play a role in disease pathogenesis, with a
human leukocyte antigen (HLA) variant having been identified. Differences exist between Takayasu's and giant cell
arteritis in terms of presentation, disease location, and therapeutic efficacy. The inflammatory process typically involves
the aorta and its extracranial branches, of which the superficial temporal artery is specifically affected.
The clinical syndrome begins with a prodromal phase of constitutional symptoms, including headache, fever, malaise,
and myalgia. The patients may be initially diagnosed with coexisting polymyalgia rheumatica; an HLA-related association
may exist between the two diseases. As a result of vascular narrowing and end-organ ischemia, complications may
occur such as visual alterations, including blindness and mural weakness, resulting in acute aortic dissection that may be
devastating. Ischemic optic neuritis resulting in partial or complete blindness occurs in up to 40% of patients and is
considered a medical emergency. Cerebral symptoms occur when the disease process extends to the carotid arteries.
Jaw claudication and temporal artery tenderness may be experienced. Aortic lesions usually are asymptomatic until later
stages and consist of thoracic aneurysms and aortic dissections.
The diagnostic gold standard is a temporal artery biopsy, which will show the classic histologic findings of multinucleated
giant cells with a dense perivascular inflammatory infiltrate. Treatment regimens are centered on corticosteroids, and
giant cell arteritis tends to rapidly respond. Remission rates are high, and treatment tends to have a beneficial and
preventative effect on the development of subsequent vascular complications.
Takayasu's Arteritis
Takayasu's arteritis is a rare but well-recognized chronic inflammatory arteritis affecting large vessels, predominantly
the aorta and its main branches (Table 23-27).204 Chronic vessel inflammation leads to wall thickening, fibrosis,
stenosis, and thrombus formation. Symptoms are related to end-organ ischemia. The acute inflammation can destroy
the arterial media and lead to aneurysm formation. This rare autoimmune disease occurs predominantly in women
between the ages of 10 and 40 years old who are of Asian descent. Genetic studies have demonstrated a high frequency
of HLA haplotypes in patients from Japan and Mexico, suggesting increased susceptibility to developing the disease in
patients with certain alleles. However, these associations have not been seen in North America. Vascular inflammation
leads to arterial wall thickening, stenosis, and eventually, fibrosis and thrombus formation. The pathologic changes
produce stenosis, dilation, aneurysm formation, and/or occlusion.
Table 23-27 Angiographic Classification of Takayasu's Arteritis
Type Vessel Involvement

I Branches from the aortic arch
IIa Ascending aorta, aortic arch and its branches
IIb Ascending aorta, aortic arch and its branches, thoracic descending aorta
III Thoracic descending aorta, abdominal aorta, and/or renal arteries
IV Abdominal aorta and/or renal arteries
V Combined features of types IIb and IV
Involvement of the coronary or pulmonary arteries are designated as C (+) or P (+), respectively.
The clinical course of Takayasu's arteritis begins with a "prepulseless" phase in which the patient demonstrates
constitutional symptoms. These include fever, anorexia, weight loss, general malaise, arthralgias, and malnutrition. As
the inflammation progresses and stenoses develop, more characteristic features of the disease become evident. During
the chronic phase, the disease is inactive or "burned out." It is during this latter stage that patients most frequently
present with bruits and vascular insufficiency according to the arterial bed involved. Laboratory data may show
elevations in erythrocyte sedimentation rate, C-reactive protein, white blood cell count, or conversely, anemia may
predominate. Characteristic clinical features during the second phase vary according to the involved vascular bed and
include hypertension reflecting renal artery stenosis, retinopathy, aortic regurgitation, cerebrovascular symptoms,
angina and congestive heart failure, abdominal pain or GI bleeding, pulmonary hypertension, or extremity claudication.
The gold standard for diagnosis remains angiography showing narrowing or occlusion of the entire aorta or its primary
branches, or focal or segmental changes in large arteries in the upper or lower extremities. Six types of Takayasu's
arteritis exist and are graded in terms of severity: type I, affecting the aorta and arch vessels; type IIa, affecting the
ascending aorta, aortic arch, and branches; type IIb, affecting the ascending aorta, aortic arch and branches, and
thoracic descending aorta; type III, affecting the thoracic descending aorta, abdominal aorta, and/or renal arteries; type
IV, affecting the abdominal aorta and/or renal arteries; and type V, with combined features of types IIb and IV.204
Treatment consists of steroid therapy initially, with cytotoxic agents used in patients who do not achieve remission.
Surgical treatment is performed only in advanced stages, and bypass needs to be delayed during active phases of
inflammation. There is no role for endarterectomy, and synthetic or autogenous bypass grafts need to be placed onto
disease-free segments of vessels. For focal lesions, there have been reports of success with angioplasty.205–207
Ehlers-Danlos Syndrome
Ehlers-Danlos syndrome is one of the more significant inheritable disorders affecting the connective tissue, along with
Marfan syndrome. This syndrome represents a heterogeneous group of connective tissue disorders (types I through IV)
that were first described in 1682 by van Meekeren.208 It is an autosomal dominant disorder affecting approximately one
in 5000 persons that is characterized by skin elasticity, joint hypermobility, tissue fragility, multiple ecchymoses, and
subcutaneous pseudotumors. Ehlers-Danlos syndrome is a disorder of fibrillar collagen metabolism with identifiable,
specific defects that have been found in the collagen biosynthetic pathway that produce clinically distinct forms of this
disease. Ten different phenotypes have been described, each with variable modes of inheritance and biochemical
defects. Of the four basic types of collagen found in the body, the predominant type in blood vessels is type III. Within
the vessel wall, type III collagen contributes to structural integrity and tensile strength, as well as playing a role in
platelet aggregation and thrombus formation.
Of the three types of Ehlers-Danlos syndrome that have arterial complications, type IV represents 5% of cases and is
the one most likely to be seen by a vascular surgeon. These patients synthesize abnormal type III collagen (mutation
COL3A1), and represent 5% of all cases.208 Affected individuals do not show the typical skin and joint manifestations,
and thus typically present for diagnosis when a major vascular catastrophe occurs. In a review of 36 patients with this
disorder, Cikrit and colleagues reported a 44% mortality rate from major hemorrhage before any surgical
intervention.209 In the 20 patients who underwent 29 vascular procedures, there was a 29% mortality rate. Arterial
rupture, aneurysm formation, and acute aortic dissection may occur in any major artery, with the most frequent site of
rupture being the abdominal cavity. Repair is problematic, as the vessel wall is soft and sutures pull through the fragile
tissue. Ligation may be the only option in many circumstances.
Marfan Syndrome
Another heterogeneous heritable disorder of connective tissue, Marfan syndrome is characterized by abnormal
musculoskeletal, ocular, and cardiovascular features first described by Antoine Marfan in 1896.210 The inborn error of
metabolism in this syndrome has been localized to the long arm of chromosome 15 (15q21.3). Defects occur in fibrillin,
a basic protein in the microfibrillar apparatus that serves as a backbone for elastin, which is one of the main
extracellular structural proteins in blood vessels. This is an autosomal dominant gene with high penetrance; however,
approximately 15 to 20% of cases are secondary to new spontaneous mutations.210
Classic recognizable features of Marfan syndrome include tall stature, long limbs (dolichostenomelia), long fingers
(arachnodactyly), joint hyperextensibility, chest wall deformities, and scoliosis. Ocular manifestations are flattened
corneas, lens subluxation, and myopia. Ninety-five percent of patients have cardiovascular involvement, which may
include ascending aortic dilatation, mitral valve prolapse, valvular regurgitation, and aortic dissection. Skin, central
nervous system, and pulmonary features may be present as well. Aortic root dilatation will generally occur in all
patients. This may not be evident on standard chest radiograph until dilatation has resulted in an ascending aortic
aneurysm, aortic valve regurgitation, or dissection. Left untreated, the cardiovascular complications are devastating and
reduce the life expectancy to about 40 years for men and slightly higher for women. Death is usually attributable to life-
threatening complications of aortic regurgitation, dissection, and rupture after the ascending aorta has dilated to 6 cm
or more.
Aggressive medical management with beta-adrenergic blocking agents and other BP lowering regimens is crucial to
treatment. Surgical intervention entails replacement of the aortic root with a composite valve graft (e.g., Bentall
procedure).205 Prophylactic operative repair is indicated for an aneurysm >5.5 cm, with an acceptable perioperative
mortality of less than 5%.
Pseudoxanthoma Elasticum
Pseudoxanthoma elasticum is a rare inherited disorder of connective tissue that is characterized by an unbalanced
elastic fiber metabolism and synthesis, resulting in fragmentation and calcification of the fibers. Clinical manifestations
occur in the skin, ocular, GI, and cardiovascular systems.206 Characteristic skin lesions are seen in the axilla, antecubital
and popliteal fossae, and groin. The yellow, xanthoma-like papules occur in redundant folds of skin and are said to
resemble plucked chicken skin. The inheritance pattern includes both autosomal dominant and recessive types and has a
prevalence of one in 160,000 individuals.183 The ATP-binding cassette subfamily C member 6 (ABCC6) gene has been
demonstrated to be responsible, and 43 mutations have been identified, all of which lead to calcification of the internal
elastic laminae of medium-sized vessel walls.206
Cardiovascular features are common and include premature CAD, cerebrovascular disease, renovascular hypertension,
diminished peripheral pulses, and restrictive cardiomyopathy. Symptom onset typically occurs in the second decade of
life, with onset at an average age of 13 years. Patients should be counseled to reduce potential contributing factors for
atherosclerosis such as tobacco use and high cholesterol levels. Calcium intake should be restricted in adolescents, as a
positive correlation has been found between disease severity and calcium intake.206 Surgical management involves
standard vascular techniques, with the exception that arterial conduits should not be used in cardiac bypass.
Kawasaki Disease
Kawasaki disease was first described in 1967, as a mucocutaneous lymph node syndrome occurring in young children. In
most studies, more than one half of the patients are younger than 2 years of age, with a higher prevalence in boys.207
Although originally described in Japan, the disease is found worldwide. An infectious agent may be causative; however,
no specific agent has been identified. Immune activation with the contribution of cytokines, elastases, growth factors,
and metalloproteinases is believed to be a mechanism for inflammation and aneurysm formation. Coronary artery
aneurysms, the hallmark of the disease, histologically demonstrate a panarteritis with fibrinoid necrosis. Coronary
arteriography may show occlusions, recanalization, and localized stenosis, in addition to multiple aneurysms. A variety
of constitutional symptoms and signs resulting from systemic vasculitis are present in the acute phase of the illness.207
Medical therapy for Kawasaki disease clearly decreases the manifestations of coronary artery involvement. IV gamma
globulin and aspirin therapy are most successful if begun within the first 10 days of illness. Up to 20% of untreated
patients will develop coronary arterial lesions.207 A long-term, low-dose aspirin therapy regimen usually is
recommended.
Inflammatory Arteritis and Vasculitis

Chronic inflammatory arteritis and vasculitis (i.e., inflammatory changes within veins as well as arteries) include a
spectrum of disease processes caused by immunologic mechanisms. These terms signify a necrotizing transmural
inflammation of the vessel wall associated with antigen-antibody immune complex deposition within the endothelium.
These conditions show pronounced cellular infiltration in the adventitia, thickened intimal fibrosis, and organized
thrombus.204 These disease processes may clinically mimic atherosclerosis, and most are treated by corticosteroid
therapy or chemotherapeutic agents. Even so, it is important to recognize distinguishing characteristics of each disease
to establish the course of treatment and long-term prognosis. A classification system of systemic vasculitis by vessel
size is shown in Table 23-28.
Table 23-28 Classification of Vasculitis Based on Vessel Involvement
Large vessel vasculitis

Takayasu's arteritis
Giant cell arteritis
Behçet's disease
Medium-sized vessel vasculitis
Polyarteritis nodosa
Kawasaki disease
Buerger's disease
Small vessel vasculitis
Hypersensitivity angiitis
Behçet's Disease
Behçet's disease is a rare syndrome characterized by oral and genital ulcerations and ocular inflammation, affecting
males in Japan and the Mediterranean. An HLA linkage has been found, indicating a genetic component to the etiology.
Vascular involvement is seen in 7 to 38% of patients, and is localized to the abdominal aorta, femoral artery, and
pulmonary artery.211 Vascular lesions also may include venous complications such as deep venous thrombosis or
superficial thrombophlebitis. Arterial aneurysmal degeneration can occur; however, this is an uncommon, albeit
potentially devastating, complication. Multiple true aneurysms and pseudoaneurysms may develop, and rupture of an
aortic aneurysm is the major cause of death in patients with Behçet's disease.212
Histologically, degeneration of the vasa vasorum with surrounding perivascular lymphocyte infiltration is seen, along
with thickening of the elastic laminae around the tunica media.213 Aneurysm formation is believed to be associated with
a loss of the nutrient flow and elastic component of the vessels, leading to progressive dilatation. Multiple aneurysms
are relatively common, with a reported occurrence of 36% in affected Japanese patients.212Furthermore,
pseudoaneurysm formation after surgical bypass is common at anastomotic suture lines due to the vascular wall fragility
and medial destruction. Systemic therapy with corticosteroids and immunosuppressive agents may diminish symptoms
related to the inflammatory process; however, they have no effect on the rate of disease progression and arterial
degeneration.212
Polyarteritis Nodosa
Polyarteritis nodosa (PAN) is another systemic inflammatory disease process, which is characterized by a necrotizing
inflammation of medium-sized or small arteries that spares the smallest blood vessels (i.e., arterioles and capillaries).
This disease predominantly affects men more than women by a 2:1 ratio. PAN develops subacutely, with constitutional
symptoms that last for weeks to months. Intermittent, low-grade fever, malaise, weight loss, and myalgia are common
presenting symptoms. As medium-sized vessels lie within the deep dermis, cutaneous manifestations occur in the form
of livedo reticularis, nodules, ulcerations, and digital ischemia.214 Skin biopsies of these lesions may be sufficient for
diagnosis. Inflammation may be seen histologically, with pleomorphic cellular infiltrates and segmental transmural
necrosis leading to aneurysm formation.
Neuritis from nerve infarction occurs in 60% of patients, and GI complications in up to 50%.215 Additionally, renal
involvement is found in 40%, and manifests as microaneurysms within the kidney or segmental infarctions. Cardiac
disease is a rare finding except at autopsy, where thickened, diseased coronary arteries may be seen, as well as patchy
myocardial necrosis. Patients may succumb to renal failure, intestinal hemorrhage, or perforation. End-organ ischemia
from vascular occlusion or aneurysm rupture can be disastrous complications with high mortality rates. The mainstay of
treatment is steroid and cytotoxic agent therapy. Up to 50% of patients with active PAN will experience remission with
high dosing.215
Radiation-Induced Arteritis
Radiation-induced arteritis results from progressive stenosis due to endothelial damage that leads to cellular
proliferation and fibrosis. These are well-described complications of combined irradiation and chemotherapy for the
treatment of head and neck malignancy. Arterial lesions are known complications of radiation and are similar to those
found in atherosclerotic occlusive disease. A history of therapeutic irradiation to the neck can complicate the
management of carotid artery occlusive disease. Radiation-induced damage to blood vessels has been well studied. The
small capillaries and sinusoids are most susceptible to radiation effects, as endothelial cells are the most radiosensitive
cells. The radiation effects on the medium and large-sized arteries include myointimal proliferation, with or without lipid
deposits, and thrombosis. Characteristically, irregular, spindle-shaped cells are seen replacing the normal endothelial
cells in the healing phase. Occlusive lesions develop in the irradiated carotid arteries, and are either the result of vessel
wall fibrosis, or, more commonly, due to accelerated atherosclerosis. Neurologic complications related to radiation-
induced carotid artery disease are similar to those due to nonirradiated atherosclerotic occlusive disease.
Rupture of the carotid artery has been reported following neck irradiation, and is likely related to local wound
complication and superimposed infection. The diagnosis of radiation arteritis is based on the clinical history and
confirmation of the occlusive lesion by duplex ultrasound, MRA, CTA, or subtraction angiography. Irradiated lesions can
be confined to the irradiated segment of the ICA with the remaining part of the vessel spared of disease.
Characteristically, the radiation-induced atherosclerotic lesion does not involve the carotid bulb, unlike the nonradiated
atherosclerotic lesions. The indications for intervention in radiation-induced carotid lesions are the same for
atherosclerotic carotid occlusive lesions as previously discussed in the "Treatment of Carotid Occlusive Disease" section.
However, asymptomatic irradiated carotid artery lesions should be considered for intervention because they can be more
prone to progression and development of neurologic complications. Endovascular treatment with carotid
angioplasty/stenting has become the treatment of choice for radiation-induced lesions, although surgical endarterectomy
and bypass have been shown to be safe. The rate of recurrent stenosis is higher in radiation-induced carotid lesions,
whether stented or surgically treated.
Raynaud's Syndrome
First described in 1862 by Maurice Raynaud, the term Raynaud's syndrome applies to a heterogeneous symptom array
associated with peripheral vasospasm, more commonly occurring in the upper extremities. The characteristically
intermittent vasospasm classically follows exposure to various stimuli, including cold temperatures, tobacco, or
emotional stress. Formerly, a distinction was made between Raynaud's "disease" and Raynaud's "phenomenon" for
describing a benign disease occurring in isolation or a more severe disease secondary to another underlying disorder,
respectively. However, many patients develop collagen vascular disorders at some point after the onset of vasospastic
symptoms; progression to a connective tissue disorder ranges from 11 to 65% in reported series.211,216 Therefore, the
term Raynaud's syndrome is now used to encompass both the primary and secondary conditions.
Characteristic color changes occur in response to the arteriolar vasospasm, ranging from intense pallor to cyanosis to
redness as the vasospasm occurs. The digital vessels then relax, eventually leading to reactive hyperemia. The majority
of patients are young women <40 years of age. Up to 70 to 90% of reported patients are women, although many
patients with only mild symptoms may never present for treatment. Geographic regions located in cooler, damp climates
such as the Pacific Northwest and Scandinavian countries have a higher reported prevalence of the syndrome. Certain
occupational groups, such as those that use vibrating tools, may be more predisposed to Raynaud's syndrome or digital
ischemia. The exact pathophysiologic mechanism behind the development of such severe vasospasm remains elusive,
and much attention has focused on increased levels of alpha2-adrenergic receptors and their hypersensitivity in patients
with Raynaud's syndrome, as well as abnormalities in the thermoregulatory response, which is governed by the
sympathetic nervous system.211
The diagnosis of severe vasospasm may be made using noninvasive measurements in the vascular laboratory.
Angiography is usually reserved for those who have digital ulceration and an embolic or obstructive cause is believed to
be present and potentially surgically correctable. Different changes in digital BP will occur in patients with Raynaud's
syndrome. Normal individuals will show only a slight decrease in digital BP in response to external cold stimuli, whereas
those with Raynaud's syndrome will show a similar curve until a critical temperature is reached.211 It is at this point that
arterial closure acutely occurs.
There is no cure for Raynaud's syndrome, thus all treatments mainly palliate symptoms and decrease the severity and,
perhaps, frequency of attacks. Conservative measures predominate, including the wearing of gloves, use of electric or
chemically activated hand warmers, avoiding occupational exposure to vibratory tools, abstinence from tobacco, or
relocating to a warmer, dryer climate. The majority (90%) of patients will respond to avoidance of cold and other
stimuli. The remaining 10% of patients with more persistent or severe syndromes can be treated with a variety of
vasodilatory drugs, albeit with only a 30 to 60% response rate. Calcium-channel blocking agents such as diltiazem and
nifedipine are the drugs of choice. The selective serotonin reuptake inhibitor fluoxetine has been shown to reduce the
frequency and duration of vasospastic episodes.211 IV infusions of prostaglandins have been reserved for nonresponders
with severe symptoms.
Surgical therapy is limited to débridement of digital ulcerations and amputation of gangrenous digits, which are rare
complications. Upper extremity sympathectomy may provide relief in 60 to 70% of patients; however, the results are
short lived with a gradual recurrence of symptoms in 60% within 10 years.211,216
Fibromuscular Dysplasia
Fibromuscular dysplasia (FMD) is a vasculopathy of uncertain etiology that is characterized by segmental arterial
involvement. Histologically, fibrous tissue proliferation, smooth muscle cell hyperplasia, and elastic fiber destruction
alternate with mural thinning.213 The characteristic beaded appearance of FMD is due to areas of medial thinning
alternating with areas of stenosis. Most commonly affected are medium-sized arteries, including the internal carotid,
renal, vertebral, subclavian, mesenteric, and iliac arteries. The ICA is the second most common site of involvement after
the renal arteries. FMD occurs most frequently in women (90%) and is recognized at approximately 55 years of age.
Only 10% of patients with FMD will have complications attributable to the disease.213 Pathologically, FMD is a
heterogeneous group of four distinct types of lesions that are subgrouped, based on the predominant site of involvement
within the vessel wall. Of the four types (medial fibroplasia, intimal fibroplasia, medial hyperplasia, and perimedial
dysplasia), medial fibroplasia is the most common pathologic type, affecting the ICA and the renal artery, and occurring
in 85% of reported cases.213
The two main clinical syndromes associated with FMD are transient ischemic attacks from disease in the ICA, and
hypertension from renal artery involvement. Symptoms produced by FMD are generally secondary to associated arterial
stenosis, and are clinically indistinguishable from those caused by atherosclerotic disease. Often, asymptomatic disease
is found incidentally on conventional angiographic studies being performed for other reasons. Within the ICA, FMD
lesions tend to be located higher in the extracranial segment than with atherosclerotic lesions, and may not be readily
demonstrated by duplex scan.
Clinically, symptoms are due to encroachment on the vessel lumen and a reduction in flow. Additionally, thrombi may
form in areas of mural dilatation from a stagnation of flow, leading to distal embolization. Surgical treatment has been
favored for symptomatic patients with angiographically proven disease. Owing to the distal location of FMD lesions in the
extracranial carotid artery, resection and repair is not usually feasible. Instead, graduated luminal dilatation under direct
vision has been used successfully in patients, with antiplatelet therapy continued postoperatively. Percutaneous
transluminal angioplasty (PTA) has been used effectively in patients with FMD-induced hypertension. Several series have
documented a high technical success rate, with recurrence rates of 8 to 23% at more than 1 year.217 However, the
therapeutic effect of BP control may continue to be observed despite restenosis. Surgical reconstruction of the renal
arteries for FMD has good long-term results and is recommended for recurrent lesions after angioplasty.217 Open
balloon angioplasty of the ICA has been described, which allows for precise fluoroscopic guidance, rather than blind
dilatation with calibrated metal probes, and back-bleeding after dilatation to eliminate cerebral embolization.218 Distal
neuroprotective devices may allow this procedure to be performed completely percutaneously, by lessening the threat of
cerebral emboli.
Non-Atherosclerotic Disease Affecting the Popliteal Artery Disease

There are three distinct non-atherosclerotic disease entities that may result in LE claudication that predominantly occur
in 40- to 50-year-old men. Adventitial cystic disease, popliteal artery entrapment syndrome, and Buerger's disease
should be considered in any young patients presenting with intermittent claudication.
ADVENTITIAL CYSTIC DISEASE OF THE POPLITEAL ARTERY

The first successful operative repair of popliteal artery occlusion caused by a cyst arising from the adventitia was
reported in 1954 by Ejrup and Hierton.218 Adventitial cystic disease is a rare arterial condition occurring at an incidence
of 0.1%, usually in the popliteal artery. This disease affects men in a ratio of approximately 5:1 and appears
predominantly in the fourth and fifth decades. The incidence is approximately one in 1200 cases of claudication or one in
1000 peripheral arteriograms.218 The predominance of reported cases is found in Japan and Europe. However, this
disease may affect other vascular sites such as the femoral, external iliac, radial, ulnar, and brachial arteries. Besides
claudication as a symptom, this diagnosis should be considered in young patients who have a mass in a nonaxial vessel
in proximity to a related joint. These synovial-like, mucin-filled cysts reside in the subadventitial layer of the vessel wall
and have a similar macroscopic appearance to ganglion cysts. Despite this similarity and suggestion of a joint origin for
these lesions, histochemical markers have failed to link the cystic lining to synovium.
Patients presenting at a young age with bilateral LE claudication and minimal risk factors for atheroma formation should
be evaluated for adventitial cystic disease, as well as the other two non-atherosclerotic vascular lesions described
herein. Because of luminal encroachment and compression, peripheral pulses may be present in the limb when
extended, but then can disappear during knee joint flexion. Noninvasive studies may suggest arterial stenosis with
elevated velocities. Color flow duplex scanning followed by T2-weighted MRI now appears to be the best diagnostic
choice. Angiography will demonstrate a smooth, well-defined, crescent-shaped filling defect, the classic "scimitar"
sign.218 There may be associated calcification in the cyst wall and no other evidence of atherosclerotic occlusive disease.
Various therapeutic methods have been described for the treatment of adventitial cystic disease. The recommended
treatments are excision of the cyst with the cystic wall, enucleation, or simple aspiration when the artery is stenotic.
Retention of the cystic lining leads to continued secretion of the cystic fluid and recurrent lesions. In 30% of patients
who have an occluded artery, resection of the affected artery, followed by an interposition graft using autogenous
saphenous vein, is recommended.
POPLITEAL ARTERY ENTRAPMENT SYNDROME

Love and colleagues first coined the term popliteal artery entrapment in 1965 to describe a syndrome combining
muscular involvement with arterial ischemia occurring behind the knee, with the successful surgical repair having taken
place 6 years earlier.214 This is a rare disorder with an estimated prevalence of 0.16% that occurs with a male-to-
female ratio of 15:1. Five types of anatomic entrapment have been defined, according to the position of the medial head
of the gastrocnemius muscle, abnormal muscle slips or tendinous bands, or the course of the popliteal artery itself
(Table 23-29). Concomitant popliteal vein impingement occurs in up to 30%. Twenty-five percent of cases are bilateral.
Table 23-29 Classification of Popliteal Entrapment Syndrome
Type Description
I Popliteal artery is displaced medially around a normal medial head of the gastrocnemius
II Medial head of gastrocnemius, which arises lateral to popliteal artery
III Popliteal artery is compressed by an accessory slip of muscle form medial head of gastrocnemius
IV Entrapment by a deeper popliteus muscle
V Any of the above plus popliteal vein
VI Functional entrapment
The typical patient presents with swelling and claudication of isolated calf muscle groups following vigorous physical
activity. Various differential diagnoses must be considered when encountering patients with symptoms and signs
suggestive of popliteal artery entrapment syndrome (Table 23-30). In a large series of 240 patients reported by
Turnipseed, the median age for surgical treatment was 28.5 years.214 Noninvasive studies with ankle-brachial indices
should be performed with the knee extended and the foot in a neutral, forced plantar, and dorsiflexed position. A drop in
pressure of 50% or greater or dampening of the plethysmographic waveforms in plantar or dorsiflexion is a classic
finding. Contraction of the gastrocnemius should compress the entrapped popliteal artery. The sudden onset of signs
and symptoms of acute ischemia with absent distal pulses is consistent with popliteal artery occlusion secondary to
entrapment. Other conditions resulting from entrapment are thrombus formation with distal emboli or popliteal
aneurysmal degeneration. Although CT and MRI have been used, angiography remains the most widely used test.
Angiography performed with the foot in a neutral position may demonstrate classical medial deviation of the popliteal
artery or normal anatomic positioning. Coexisting abnormalities may include stenosis, luminal irregularity, delayed flow,
aneurysm, or complete occlusion. Diagnostic accuracy is increased with the use of ankle stress view–active plantar
flexion and passive dorsiflexion.
Table 23-30 Differential Diagnosis for Popliteal Entrapment Syndrome
Vascular etiologies
Atherosclerosis
Buerger's disease
Trauma
Popliteal aneurysm
Adventitial cystic disease
Extrinsic compression
Cardiac embolism
Deep vein thrombosis
Venous entrapment
Musculoskeletal etiologies
Gastrocnemius or soleus strain
Periostitis
Compartment syndrome
Stress fractures
Tibialis posterior tendonitis
Muscular anomalies
General neurologic etiologies
Spinal stenosis
The treatment of popliteal artery entrapment consists of surgical decompression of the impinged artery with possible
arterial reconstruction. Division of the anomalous musculotendinous insertion site with or without saphenous vein
interposition grafting to bypass the damaged arterial segment has been described to be the procedure of choice. The
natural history of entrapment is progressive arterial degeneration, leading to complete arterial thrombosis. In such
instances, thrombolytic therapy is needed with subsequent release of the functional arterial impairment. Lysis will
improve distal runoff and may improve limb-salvage and bypass patency rates.
Buerger's Disease (Thromboangiitis Obliterans)

Buerger's disease, also known as thromboangiitis obliterans, is a progressive non-atherosclerotic segmental
inflammatory disease that most often affects small and medium-sized arteries, veins, and nerves of the upper and lower
extremities.219 The clinical and pathologic findings of this disease entity were published in 1908 by Leo Buerger in a
description of 11 amputated limbs.219 The typical age range for occurrence is 20 to 50 years old, and the disorder is
more frequently found in males who smoke. The upper extremities may be involved, and a migratory superficial
phlebitis may be present in up to 16% of patients, thus indicating a systemic inflammatory response. In young adults
presenting to the Mayo Clinic (1953–1981) with lower limb ischemia, Buerger's disease was diagnosed in 24%.219
Conversely, the diagnosis was made in 9% of patients with ischemic finger ulcerations. The cause of thromboangiitis
obliterans is unknown; however, use of or exposure to tobacco is essential to both the diagnosis and progression of the
disease.
Pathologically, thrombosis occurs in small to medium-sized arteries and veins with associated dense polymorphonuclear
leukocyte aggregation, microabscesses, and multinucleated giant cells. The chronic phase of the disease shows a
decrease in the hypercellularity and frequent recanalization of the vessel lumen. End-stage lesions demonstrate
organized thrombus and blood vessel fibrosis. Although the disease is common in Asia, North American males do not
appear to have any particular predisposition, as the diagnosis is made in less than 1% of patients with severe limb
ischemia.
Buerger's disease typically presents in young male smokers, with symptoms beginning before age 40 years old. Patients
initially present with foot, leg, arm, or hand claudication, which may be mistaken for joint or neuromuscular problems.
Progression of the disease leads to calf claudication and eventually ischemic rest pain and ulcerations on the toes, feet,
or fingers. A complete history should exclude diabetes, hyperlipidemia, or autoimmune disease as possible etiologies for
the occlusive lesions. Because it is likely that multiple limbs are involved, angiography should be performed of all four
limbs. Even if symptoms are not yet present in a limb, angiographic findings may be demonstrated. Characteristic
angiographic findings show disease confinement to the distal circulation, usually infrapopliteal and distal to the brachial
artery. The occlusions are segmental and show "skip" lesions with extensive collateralization, the so-called "corkscrew
collaterals."
The treatment of thromboangiitis obliterans revolves around strict smoking cessation. In patients who are able to
abstain, disease remission is impressive and amputation avoidance is increased. In the experience reported from the
Oregon Health Sciences Center, no disease progression with associated tissue loss occurred after discontinuation of
tobacco. The role of surgical intervention is minimal in Buerger's disease, as there is often no acceptable target vessel
for bypass. Furthermore, autogenous vein conduits are limited secondary to coexisting migratory thrombophlebitis. Mills
and associates reported their results of 31% limb loss in 26 patients over 15 years, thus authenticating the virulence of
Buerger's disease involving the lower extremities.219 In addition, others have described a significant discrepancy in limb
loss in patients that continued to smoke vs. those who discontinued tobacco use (35 vs. 67%).
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Schwartz's Principles of Surgery > Chapter 23. Arterial Disease >

GENERAL APPROACH TO THE VASCULAR PATIENT

Table 23-1 Pertinent Elements in Vascular History

Vascular Physical Examination

Table 23-2 Grading Scales for Peripheral Pulses

Traditional Scale Basic Scale

Noninvasive Diagnostic Evaluation of the Vascular Patient

SEGMENTAL LIMB PRESSURES

PULSE VOLUME RECORDING

Radiological Evaluation of the Vascular Patient

COMPUTED TOMOGRAPHY ANGIOGRAPHY

MAGNETIC RESONANCE ANGIOGRAPHY

PREOPERATIVE CARDIAC EVALUATION

BASIC PRINCIPLES OF ENDOVASCULAR THERAPY

Needles and Access

CAROTID ARTERY DISEASE

Epidemiology and Etiology of Carotid Occlusive Disease

Clinical Manifestations of Cerebral Ischemia

Normal <125 <2.0 <40 None

50–69 125–230 2.0–4.0 40–100 ≥50

Treatment of Carotid Occlusive Disease

Symptomatic Carotid Stenosis

ASYMPTOMATIC CAROTID STENOSIS

Carotid Endarterectomy vs. Angioplasty and Stenting

Anatomical Factors Physiological Factors

Surgical Techniques of Carotid Endarterectomy

A temporary carotid shunt is inserted from the common carotid artery (long arrow) to the internal carotid artery (short arrow)

COMPLICATIONS OF CAROTID ENDARTERECTOMY

Techniques of Carotid Angioplasty and Stenting

Table 23-6 Commonly Used Embolic Protection Devices (EPDs)

Mechanism Name of EPD Pore Size (micrometers)

Flow reversala Parodi Neuro Protection (Gore) N/A

COMPLICATIONS OF CAROTID STENTING

Non-Atherosclerotic Disease of the Carotid Artery

CAROTID ARTERY DISSECTION

CAROTID ARTERY ANEURYSMS

CAROTID BODY TUMOR

ABDOMINAL AORTIC ANEURYSM

Natural History of Aortic Aneurysm

Normal aorta 2–3 0 0 (unless AAA develops)

Surgical Repair of Abdominal Aortic Aneurysm

ADVANTAGES AND RISKS OF OPEN ABDOMINAL AORTIC ANEURYSM REPAIR

Endovascular Repair of Abdominal Aortic Aneurysm

PATIENT SELECTION FOR ENDOVASCULAR AORTIC ANEURYSM REPAIR

Table 23-9 Ideal Characteristics of an Aneurysm for Endovascular Abdominal Aortic

ADVANTAGES AND RISKS OF ENDOVASCULAR REPAIR

TECHNICAL CONSIDERATIONS OF ENDOVASCULAR AORTIC ANEURYSM REPAIR

SURVEILLANCE FOLLOWING ENDOVASCULAR AORTIC ANEURYSM REPAIR

Results from Clinical Studies Comparing Endovascular vs. Open Repair

Classification and Management of Endoleak

Table 23-10 Endoleak Classification

ENDOTENSION FOLLOWING ENDOVASCULAR AORTIC ANEURYSM REPAIR

SECONDARY INTERVENTIONS FOLLOWING ENDOVASCULAR AORTIC ANEURYSM

MESENTERIC ARTERY DISEASE

Anatomy and Pathophysiology

Types of Mesenteric Artery Occlusive Disease

arcuate ligament syndrome. Angiographically, there is CA compression that augments with deep expiration, and

ACUTE THROMBOTIC MESENTERIC ISCHEMIA

CHRONIC MESENTERIC ISCHEMIA

CELIAC ARTERY COMPRESSION SYNDROME