Chapter 23: Arterial Disease

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 versus 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 patients with claudication will need intervention because of disabling extremity pain. The 5-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.

Since 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 claudication, postprandial abdominal pain from mesenteric ischemia, and arm pain with axillo-subclavian 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. The pain syndrome of arterial disease is usually 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.

The Vascular History

Appropriate history should be focused based 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.

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 lower extremity pain on ambulation has intermittent claudication that occurs in certain muscle groups; for example, calf pain upon exercise usually reflects superficial femoral artery 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 gazer’s 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.

The Vascular Physical Examination

Specific vascular examination should include abdominal aortic palpation, carotid artery examination, and pulse examination of the lower extremity (femoral, popliteal, posterior tibial, and dorsalis pedis arteries). The abdomen should be palpated for an abdominal aortic aneurysm, detected as an expansile pulse above the level of the umbilicus. It should also 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 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 (TOS) can result in occlusion or aneurysm formation of the subclavian artery. Distal embolization is a manifestation of TOS; 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 is usually 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 lower extremity vascular examination, the femoral pulse is usually 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 should also 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 later in this chapter.

After reconstructive vascular surgery, the graft may be available for examination, depending on its type and course. The in situ lower extremity 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 can usually 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 less than 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 is measured in both upper extremities using the highest systolic blood pressure as the denominator for the ABI. The ankle pressure is determined by placing a blood pressure 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 less than 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 ABI ≥1.40 and require additional noninvasive diagnostic testing to evaluate for peripheral artery disease. Alternative tests include toe-brachial pressures, pulse volume recordings, transcutaneous oxygen measurements, or vascular imaging (duplex ultrasound).

Segmental Limb Pressures

By placing serial blood pressure cuffs down the lower extremity 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. This 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 greater than 1.0, and a value of less than 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 ≥250 mmHg and ABIs >1.40. In this situation, absolute toe and ankle pressures can be measured to gauge critical limb ischemia. Ankle pressures less than 50 mmHg or toe pressures less than 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 (TBI) <0.70 is abnormal. False-positive results with the TBI 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 blood 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, so as 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.

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 peripheral artery disease.

Radiologic 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 computed tomography angiography.⁴ Few surgeons rely solely on duplex ultrasonography for preoperative planning in lower extremity revascularizations; but with experience, lower extremity arteries can be insonated to determine anatomy, and the functional significance of lesions can be determined by calculation of degree of stenosis from velocity ratios. 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 intravenous 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 in-stent 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

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 because 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 drop-out; 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.

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 also been 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.

Preoperative Cardiac Evaluation

The most important and most controversial aspect of preoperative evaluation in patients with atherosclerotic disease requiring surgical intervention is the detection and subsequent management of associated coronary artery disease.⁷ Several studies have documented the existence of significant coronary artery disease 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 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 prior to vascular surgical procedures impact 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 (CARP) trial showed that coronary revascularization in patients with peripheral vascular disease and significant coronary artery disease, 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 prior to 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 β-blockade, as well as use of antiplatelet medication, statins, and angiotensin-converting enzyme inhibitors, is encouraged in vascular patients.^10,11

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, reduced morbidity and mortality in endovascular interventions, and 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-inch guidewire. A 21-gauge micropuncture needle will accept a 0.018-inch 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 prior to 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 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 superficial femoral artery (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 because 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.

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 inches. For most aortoiliac procedures, a 0.035-inch wire is most commonly used, whereas the smaller diameter 0.018-inch 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 facilitate 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, which 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 5- to 9-French inner diameter, but with open surgical exposure of the CFA, sheaths as large as 26 French 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.

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 and 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 and 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, placing a stent or stent graft if warranted.

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 and 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 on 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 internal carotid artery. These stents are always oversized by 1 to 2 mm relative to the largest diameter of normal vessel adjacent to the lesion in order to prevent immediate migration.

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 stents. This makes them ideal for short-segment lesions, especially those that involve the ostia such as proximal common iliac or renal artery stenosis.

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 peripheral arterial disease.^13,14

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.

Endovascular aneurysm repair using the concept of stent grafts was initiated by Parodi in 1991.¹⁵ Since that time, a large number of endografts have been inserted under the auspice of clinical trials initially and now as Food and Drug Administration (FDA)–approved devices. Current available FDA-approved devices include the following: (a) AneuRx device (Medtronic/AVE, Santa Rosa, CA); (b) Gore Excluder device (WL Gore & Associates, Flagstaff, AZ); (c) Endologix Powerlink device (Endologix Inc., Irvine, CA); (d) Zenith device (Cook Inc., Bloomington, IN); (e) Talent device (Medtronic/AVE, Santa Rosa, CA); and (f) Endurant device (Medtronic/AVE, Santa Rosa, CA) for the treatment of abdominal aortic aneurysms. 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 greater than 60° of angulation. For those patients with associated common iliac artery aneurysmal disease, endovascular treatment can be achieved by initial coil embolization of the ipsilateral hypogastric artery with extension of the endovascular device into the external iliac artery. Newer generation endografts, including devices such as AFX Endovascular AAA System (Endologix Inc., Irvine, CA), Aorfix Flexible Stent (Lombard Medical Inc., Framingham, MA), and Ovation Prime Stent (TriVascular Inc., Santa Rosa, CA), are designed to overcome previous challenges of difficult anatomy by incorporating more flexible stents and lower profile delivery systems. Clinical trials are under way with devices that will expand indications to aneurysms involving the visceral segment of the abdominal aorta. The FDA has similarly approved several thoracic endograft devices 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.^16,17,18 More experience with these devices exists in both Europe and Asia, and trials are under way in the United States with several devices.

Atherosclerotic occlusive plaque is by far the most common pathology seen in the carotid artery bifurcation. Thirty percent to 60% of all ischemic strokes are related to atherosclerotic carotid bifurcation occlusive disease. In the following section, we first focus our discussion on the 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, we provide a review on other less common nonatherosclerotic diseases involving the extracranial carotid artery, including kink and coil, fibromuscular dysplasia, 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.¹⁹ 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, to decreased flow resulting from proximal arterial stenosis and poor collateral network. Common causes of ischemic strokes are cardiogenic emboli in 35%, carotid artery disease in 30%, lacunar in 10%, miscellaneous in 10%, and idiopathic in 15%.¹⁹ The term cerebrovascular accident is often 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 is usually 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 internal carotid artery 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 internal carotid artery, 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 (<50%), moderate (50%–69%), and severe (70%–99%). Severe carotid stenosis is a strong predictor for stroke.²⁰ 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.

Clinical Manifestations of Cerebral Ischemia

TIA is a focal loss of neurologic function, lasting for less than 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 for those with either 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.

Patients who suffer cerebrovascular accidents 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 grey 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 Hollenhorst plaque. These plaques are frequently derived from cholesterol embolization from the carotid bifurcation and warrant further investigation. Additionally, several ocular symptoms may be caused by microembolization from extracranial carotid diseases including monocular visual 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 cerebrovascular accidents are lateralized or focal neurologic deficits. 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 paresthesia. 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 internal carotid artery 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 resembles that in the internal carotid artery, as 80% of the flow is directed to the internal carotid artery, with waveforms that have broad systolic peaks and 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 internal carotid artery. Characteristically, the peak systolic velocity is increased at the site of the vessel stenosis. The end-diastolic velocity is increased with greater degree of stenosis. In addition, stenosis of the internal carotid artery can lead to color shifts with color mosaics indicating a poststenotic turbulence. Dampening of the Doppler velocity waveforms is typically seen in areas distal to severe carotid stenosis where blood flow is reduced. It is well known that occlusion of the ipsilateral internal carotid artery 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 internal carotid artery, the ipsilateral common carotid artery displays high flow resistance waveforms, similar to those seen in the external carotid artery. If there is a significant stenosis in the proximal common carotid artery, 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 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 greater than 125 cm/s with extensive spectral broadening. For stenosis in the range of 80% to 99%, the peak systolic velocity is greater than 125 cm/s, and peak diastolic velocity is greater than 140 cm/s. The ratio of internal carotid to common carotid artery peak systolic velocity has also been part of various ultrasound diagnostic classifications. A ratio greater than 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).²¹

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.²² 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 tomography (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.²³ 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.

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 last few 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, and 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 detail later in this chapter. We generally use CTA or MRA 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.

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%.¹⁹ According to the Cardiovascular Health Study, a longitudinal population-based study of coronary artery disease and stroke in men and women, the prevalence of TIA in men was 2.7% for ages of 65 and 69 and 3.6% for ages 75 to 79; the prevalence in women was 1.4% and 4.1%, respectively.²⁴ 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.²⁵

Symptomatic Carotid Stenosis

Currently, most stroke neurologists prescribe both aspirin and clopidogrel for secondary stroke prevention in patients who have experienced a TIA or stroke.¹⁹ 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 (ECST) and the North American Symptomatic Carotid Endarterectomy Trial (NASCET), have both shown a significant risk reduction in stroke for patients with symptomatic high-grade stenosis (70%–99%) undergoing carotid endarterectomy when compared to medical therapy alone.^26,27 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, yet they both studies had similar results.²⁸ 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 NASCET 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%–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 versus 22% in the medically treated group.²⁹ 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 ECST 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 versus medical therapy.²⁷

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.²⁹ 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).³⁰

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 occurrence rate of neurologic symptoms was 4% in a cohort of 167 patients with asymptomatic cervical bruits followed prospectively by serial carotid duplex scan.³¹ 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 internal carotid artery 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 (ACAS), which evaluated the benefits of medical management with antiplatelet therapy versus carotid endarterectomy.³² 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 (ACST), recently confirmed similar beneficial stroke risk reduction for patients with asymptomatic, greater than 70% carotid stenosis undergoing endarterectomy versus medical therapy.³³ 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%–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%–79%) remains controversial.

Carotid Endarterectomy versus Angioplasty and Stenting

Currently, the argument is no longer whether 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 produce the same benefits demonstrated by carotid endarterectomy. Since carotid artery stenting was approved by the FDA for clinical application in 2004, 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 more challenging procedure, because it requires complex catheter-based skills using the 0.014-inch guidewire system and distal protection device. Moreover, current carotid stent devices predominantly use the monorail guidewire system, which requires more technical agility compared with 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 in part due 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.³⁴ 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% confidence interval, 0.86 to 2.04). Additionally, a 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 several prospective randomized trials comparing the efficacy of carotid stenting versus endarterectomy are available for review.³⁵ Two recently published randomized controlled trial, the Carotid Revascularization Endarterectomy Versus Stent Trial (CREST) and the International Carotid Stenting Study (ICSS) have reported somewhat differing results.³⁶ CREST compared the efficacy of carotid endarterectomy and carotid stenting in both symptomatic and asymptomatic patients.³⁷ Primary end points included 30-day periprocedural composite death, stroke, myocardial infarction, or any ipsilateral stroke up to 4 years. CREST investigators reported no difference between stenting (5.2%) and endarterectomy (4.5%) in terms of primary end point. When each variable was independently analyzed, there was a higher rate of stroke in the stenting group at 30 days (4.1% vs. 2.3%) and a higher rate of myocardial infarction in the endarterectomy group (2.3% vs. 1.1%). The ICSS was a multicenter, international, randomized controlled trial comparing carotid stenting versus endarterectomy in patients with symptomatic carotid stenosis.³⁸ The risk of stroke, death, and myocardial infarction in the stenting group (8.5%) was significantly higher than in the surgical arm (5.2%). The finding that carotid endarterectomy is safer than carotid stenting is also supported by the results of an MRI substudy, which showed significantly more new lesions by diffusion-weighted imaging in the carotid stenting than the carotid endarterectomy patients.

All available randomized studies have provided some answers and raised some questions. Some ongoing clinical trials will undoubtedly provide more insights on the efficacy of carotid stenting in the near future. Currently, the Society for Vascular Surgeons recommends carotid endarterectomy as first-line treatment for most symptomatic patients with stenosis of 50% to 99% and asymptomatic patients with stenosis of 60% to 99%.³⁹ The perioperative risk of stroke and death in asymptomatic patients must be below 3% to ensure benefit for the patient. Carotid artery stenting should be reserved for symptomatic patients with stenosis of 50% to 99% at high risk for carotid endarterectomy for anatomic or medical reasons. Carotid artery stenting is not recommended for asymptomatic patients at this time. Asymptomatic patients at high risk for intervention or with a life expectancy of less than 3 years should be considered for medical management as the first-line therapy.

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 versus eversion endarterectomy, and patch versus primary closure. Various anesthetic options are available for 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 (EEG) 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 EEG 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 common carotid artery. This muscle can be divided. The carotid fascia is incised, and the common carotid artery is exposed. The common carotid artery 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 intravenous 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 12th 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 internal carotid artery. For high bifurcation, division of the posterior belly of the digastric muscle is helpful in establishing distal exposure of the internal carotid artery.

Intravenous heparin sulfate (1 mg/kg) is routinely administered just prior to carotid clamping. The internal carotid artery 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 common carotid artery and extended into the bulb and past the occlusive plaque into the normal part of the internal carotid artery. Endarterectomy is carried out to remove the occlusive plaque (Fig. 23-18). If necessary, a temporary shunt can be inserted from the common carotid artery to the internal carotid artery 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 internal carotid artery 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 has also been advocated for removing the plaque from the internal carotid artery. In the eversion technique, the internal carotid artery 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.⁴⁰ Surgeons will likely continue to use the technique of their choice. Just prior to completion of the anastomosis to close the arteriotomy, we thoroughly flush the vessels of any potential debris. When the arteriotomy is closed, flow is restored to the external carotid artery first and to the internal carotid artery second. Intravenous 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 asserted in the operating room prior to transfer to the recovery area.

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 internal carotid artery. 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 hematoma. The reported incidence of postoperative cranial nerve palsies after carotid endarterectomy varies from 1% to 30%.⁴¹ 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 anatomic conditions based on angiographic evaluation in which carotid artery stenting should be avoided due to increased procedure-related risks (Table 23-5). In preparation for carotid stenting, the patient should be given oral clopidogrel 3 days prior to the intervention if the patient was not already taking the drug. The procedure is done in either the operating room with angiographic capabilities or in a dedicated angiography room. The patient is placed in the supine position. The patient’s blood pressure and cardiac rhythm are closely monitored.

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, we insert a diagnostic 5- or 6-French sheath in the CFA. A diagnostic arch aortogram is obtained. The carotid artery to be treated is then selected using a 5-French 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 common carotid artery, a 0.035-inch, 260-cm long stiff guidewire is placed in the ipsilateral external carotid artery. Anticoagulation with intravenous bivalirudin bolus (0.75 mg/kg) followed by an infusion rate of 2.5 mg/kg/h for the remainder of the procedure is routinely administered. Next the diagnostic catheter is withdrawn and a 90-cm, 6-French guiding sheath is advanced into the common carotid artery 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-inch platform. The size selection is typically based on the size of common carotid artery. 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 balloon. It is 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 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.

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 with carotid endarterectomy. However, the clinical significance of the distal embolization detected by TCD is not clear because most are asymptomatic. Acute carotid stent thrombosis is rare. The incidence of in-stent 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 not infrequently. However, velocity criteria are being formulated to determine the severity of in-stent restenosis after carotid stenting by ultrasound duplex.⁴² It appears that systolic velocities exceeding 300 to 400 cm/s would represent >70% to 80% restenosis. Bradycardia and hypotension occur in up to 20% of patients undergoing carotid stenting.⁴³ 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.

Nonatherosclerotic Disease of the Carotid Artery

Carotid Coil and Kink

A carotid coil consists of an excessive elongation of the internal carotid artery 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 are 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 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.

Fibromuscular Dysplasia

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 is also involved.⁴⁴ 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 histologic 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 can also involve the renal and external iliac arteries. It is estimated that approximately 40% of patients with FMD present with a TIA due to embolization of platelet aggregates.⁴⁴ 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.

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 remain 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’s syndrome, α₁-antitrypsin deficiency, or FMD, may predispose to carotid artery dissection. Iatrogenic dissections can also 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 internal carotid artery distal to the bulb. Uncommonly, the dissection can start in the common carotid artery or is an extension of a more proximal aortic dissection. Medical therapy has been the accepted primary treatment of symptomatic of 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.

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 is generally 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 are rare. Pseudoaneurysms of the carotid artery can result from injury or infection. Mycotic aneurysms often involved 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.⁴⁵

Carotid Body Tumor

The carotid body originates from the third branchial arch and from neuro-ectodermal derived neural crest lineage. The normal carotid body is located in the adventitia or periadventitial tissue at the bifurcation of the common carotid artery (Fig. 23-27). The gland is innervated by the glossopharyngeal nerve. Its blood supply is derived predominantly from the external carotid artery but can also 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.

Symptoms related to the endocrine products of the carotid body tumor are rare. Patients usually present between the fifth and seventh decades 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 MRI is usually 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 less than 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.⁴⁶ With good-resolution CT and MRI, arteriography is usually 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 is usually 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 internal carotid artery. Medical management with antiplatelet or anticoagulation therapy is usually 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.

Despite 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 10th leading cause of death in men in this country.⁴⁷ The incidence appears to be increasing, and this is due in part to improvements in diagnostic imaging and, more importantly, 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 1964.⁴⁸ Nearly two decades later, Parodi and colleagues reported the first successful endovascular repair of AAA using a stent graft device.¹⁵ Since then, a variety of stent graft technologies have been developed to treat 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 of AAA in order to provide adequate evaluation and education to patients and their families. The purpose of this section is to outline the treatment options for AAAs, including conventional repair and endovascular approach. Advantages and potential complications of these treatments will also be addressed.

Causes and Risk Factors

The pathogenesis of aneurysmal disease of the aorta is complex and multifactorial. A degenerative process in the aortic wall is the most common cause of AAA development.⁴⁹ Matrix metalloproteinases (MMP), proteolytic enzymes, are found abundantly in the wall of AAA. Atherosclerotic disease, age, male sex, smoking history, family history, hypertension, coronary artery disease, and chronic obstructive pulmonary disease are associated with the development of AAA.^50,51 Diabetes and black race have negative association with AAA.⁵⁰ Other less common causes include inflammation, infection, and connective tissue disease. Inflammatory AAA accounts for 5% to 10% of all AAAs.⁵² In contrast to atherosclerotic AAA, the inflammatory variant is characterized pathologically by marked thickening of the aneurysm wall, fibrosis of the adjacent retroperitoneum, and rigid adherence of the adjacent structures to the anterior aneurysm wall.⁵³ Male sex and smoking are even stronger risk factors in inflammatory AAA.⁵⁴ Smoking cessation is the first step of medical therapy, followed by surgical repair. Infectious or mycotic AAA is rare but is associated with high mortality.⁵⁵ Patients with connective tissue disorders such as Marfan’s syndrome and Ehlers-Danlos syndrome tend to have more extensive and larger aneurysms at a younger age.⁵⁶

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/year. 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 are 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.^57,58 Based on best available evidence, the annualized risk of rupture is given in Table 23-8. The rupture risk is quite low below 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 Aneurysm Detection and Management (ADAM) study, 80% of all AAAs that were followed in this manner eventually came to repair within 5 years.⁵⁸

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 are usually found incidentally during workup 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 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 blood pressure control with intravenous antihypertensive agents and undergoes repair 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 operating room with a presumed diagnosis of a ruptured AAA.

Overall mortality of AAA rupture is 71% to 77%, which includes all out-of-hospital and in-hospital deaths, as compared with 2% to 6% for elective open surgical repair.⁵⁹ Nearly 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 greater than 30 mm or 1.5 times the adjacent diameter of the normal aorta (Fig. 23-28). Male aortas tend to be larger than female aortas, and there is generalized growth of the aortic diameter with each decade of life. Ninety percent of AAAs are infrarenal in location and have a fusiform morphology. There is a higher predilection for juxtarenal and suprarenal AAAs in women compared with 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.

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; common iliac artery, which can range from 8 to 16 mm; and external iliac arteries, which can range from 6 to 10 mm. Morphologically, the aortic neck can manifest complex angulation above and below the renal arteries due to 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 significant from hemodynamic standpoint, severe iliac calcifications combined with extreme tortuosity can pose a formidable challenge during endovascular repair.

Diagnostic Evaluation

Preoperative evaluation should include routine history and physical exam with particular attention to (a) any symptoms referable to the aneurysm, which may impact the timing of repair; (b) 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) lower extremity 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 thus the screening modality of choice, 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 intravenous contrast-enhanced, 2.5- to 3.0-mm slice spiral CT of the chest, abdomen, and pelvis can be performed in less than 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) are 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.

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 one’s 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 <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. While a retroperitoneal incision is a well-accepted surgical approach, a midline transabdominal incision remains the more common approach for open aortic aneurysm operation. Since the abdominal incision can lead to significant pain and discomfort, an epidural catheter can be placed prior to 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. Intravenous heparin (100 IU/kg) is given followed by clamping of the proximal and distal segments of the aneurysm. The aneurysm sac is open next, and a prosthetic graft is used to reconstruct the aorta. If the aneurysm only involves 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 aorto-bi-iliac or aorto-bi-femoral 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.

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 gastrointestinal 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%.⁶⁰ 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.⁶⁰

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.⁶¹ However, if the partial-thickness ischemia progresses to full-thickness gangrene and peritonitis, mortality can be as high as 90%.⁶¹

The incidence of prosthetic graft infection ranges between 1% and 4% after open repair.⁶¹ 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

Over 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 compared with 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 nonaneurysmal aortoiliac segment and thereby endoluminally excluding the aneurysm from the aortic circulation (Fig. 23-32). Unlike open surgical repair, the aneurysm sac is not resected, which is subjected for potential aneurysm expansion or even rupture. Importantly, aortic branches, such as lumbar arteries or the inferior mesenteric artery (IMA), are occluded, which can lead to persistent aneurysm pressurization and aneurysm expansion. Currently, the following nine devices are available for elective repair of intact infrarenal AAA: AneuRx device (Medtronic/AVE, Santa Rosa, CA), Gore Excluder device (WL Gore & Associates, Flagstaff, AZ), Endologix Powerlink device (Endologix Inc., Irvine, CA), Zenith device (Cook Inc., Bloomington, IN), Talent device (Medtronic/AVE, Santa Rosa, CA), Endurant device (Medtronic/AVE, Santa Rosa, CA), AFX Endovascular AAA System (Endologix Inc., Irvine, CA), Aorfix Flexible Stent (Lombard Medical Inc., Framingham, MA), and Ovation Prime Stent (TriVascular Inc., Santa Rosa, CA). Despite some differences in physical appearance, mechanical properties, and materials, they will be discussed collectively for this chapter. Most of these devices are 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.

A severe limitation of the endovascular repair devices is the need for adequate proximal neck to achieve a durable sealing zone. Several techniques have been proposed to overcome this limitation. These include fenestrated or branched endografts and the “chimney,” “snorkel,” and “periscope” techniques. The fenestrated stent grafts rely on precise alignment between the fenestration and the corresponding visceral artery.⁶² Multiple clinical trials using customized fenestrated stent graft for the treatment of short-necked and juxtarenal aortic aneurysm repair have shown promising short- and mid-term results.^63,64 However, restricted access to these investigational devices and the delays due to device customization limit the current use of these devices to a few centers. Alternatively, some centers have reported good results with intraoperative surgeon-modified endograft to create fenestrations for the treatment of complex aortic aneurysms in high-risk patients.⁶⁵ Further development of the fenestrated techniques also opens the way for endovascular treatment of suprarenal and thoracoabdominal aneurysm.⁶⁶ Recently, an “off-the-shelf” Zenith Fenestrated AAA endovascular graft has been approved by the FDA. This device has fenestrations or scallops in the graft material to allow the proximal edge of the stent graft to be placed above the renal arteries while still permitting blood flow to vessels accommodated by the fenestrations or scallops. The “chimney” technique involves placing renal or mesenteric stents parallel to the aortic stent graft to preserve blood flow in the visceral aortic branches.⁶⁷ This technique has been suggested as a rescue procedure for visceral arteries that have been covered by the stent graft during endovascular repair.⁶⁸ The review of literature showed that open surgery remains a safe and effective treatment option for good-risk patients with juxtarenal aortic aneurysm.⁶⁹ Fenestrated endovascular repair is associated with low mortality and compares favorably with open surgery in terms of morbidity, especially renal function impairment and cardiac complications.⁶⁹ The “chimney” technique demonstrated feasibility, but because of the limited number of reports and the lack of long-term data, it should be considered only in acute poor surgical risk patients and in case of unintentional visceral artery coverage or elective poor surgical cases for fenestrated endovascular repair.⁶⁹

Patient Selection for Endovascular Aortic Aneurysm Repair

Anatomic eligibility for endovascular repair is mainly based on three areas: the proximal aortic neck, common iliac arteries, and 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 mid-wall to mid-wall 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 common iliac artery. The external iliac artery may serve as an alternate site when the ipsilateral common iliac artery is aneurysmal or ectatic. The treatable diameters of common iliac arteries range from 8 to 20 mm, and there should be at least 20 mm of patent artery of uniform diameter to allow adequate fixation. Finally, at least one of two common femoral and external iliac arteries must be at least 7 mm in diameter in order 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 time and intraoperative complications. Using these criteria, approximately 60% of all AAAs are anatomic candidates for endovascular repair.

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, whereas center-line measurements usually overestimate the length. Angiographic measurements using a marker catheter are invasive, require contrast and radiation exposure, and are also inaccurate because they fail to account for 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 our institution, 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.

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, avoiding respiratory complications or prolonged mechanical ventilation. Because the abdominal cavity has not been entered, the risk of gastrointestinal complications, such as ileus, ventral hernia, or bowel obstruction due to intestinal adhesion, is also 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. Since 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%.⁷⁰ 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 less than 0.8%.⁷¹

Stent graft iliac limb dysfunction resulting in thrombosis has been reported following endovascular repair.^18,70 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.^18,60,70 Graft limb separation or dislocation has also been reported.^18,60,70

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.⁷² 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.^18,71 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 (Mucomyst) 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.⁷³

Bilateral transverse oblique incisions are made just below the inguinal ligament to expose approximately 2 to 3 cm of CFA 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, CA). Review of reported series on this technique suggest a technical success rate of 95% for medium-size sheaths ranging from 12 to 16 French, and 75% success for 18- to 24-French 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. Intravenous heparin at 80 IU/kg are 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 immediate 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, and bare stents are performed as needed. The procedure is concluded with routine repairs of the femoral arteries and closure of the groin incisions. The patients recover 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 intensive care unit, this is rarely needed. Most patients can be started on a regular diet that evening and discharged the next morning.

Surveillance Following Endovascular Aortic Aneurysm Repair

Life-long 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, and 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 “birds-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 can sometimes only be detected on a plain film and not on a CT scan.

Results from Clinical Studies Comparing Endovascular versus Open Repair

The primary success rate after endovascular repair of AAA has been reported to be as high as 95%.^18,59 The less invasive nature of this procedure is appealing to many physicians and patients. In addition, virtually all reports indicate a decreased blood loss, transfusion requirements, and length of intensive care unit and hospital stay for endovascular repair of AAAs compared with the standard surgical approach.^18,59,74 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 versus open repair and 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 who are eligible for both types of repair. Two such European trials have recently published short-term outcome data that are unbiased in design.

The DREAM trial is a multicenter randomized trial that compared open versus endovascular repair among a group of 345 patients at 28 European centers using multiple different devices including Gore, AneuRx, and Zenith.⁷⁵ 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 versus 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 group versus 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 Endovascular Repair-1 (EVAR-1) trial is also a multicenter randomized trial that compared open to endoluminal repair.⁷⁴ 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 group and 1.7% in the endoluminal group. The in-hospital mortality rate was also increased in the open when compared to the endoluminal group (6.2% vs. 2.1%). As expected, the secondary intervention rate was higher in the endoluminal group (9.8% vs. 5.8%). Complication rates were not reported in the EVAR-1 trial. Criticisms can be applied to both of these trials. Patients had to be eligible for either type of repair in order to be included in the study. Consequently, these findings cannot be generalized to patients who are too sick to undergo open surgery or to patients whose anatomy precludes them from undergoing endovascular repair.

The Open Versus Endovascular Repair (OVER) Veterans Affairs Cooperative Study Group randomly assigned 881 patients with asymptomatic AAAs who were candidates for both procedures to either endovascular repair (n = 444) or open repair (n = 437) and followed them for up to 9 years.⁷⁶ Reduction in perioperative mortality with endovascular repair was sustained at 3 years but not thereafter. There was no difference in primary outcome of all-cause mortality. Endovascular repair and open repair resulted in similar long-term survival. Six aneurysm ruptures were confirmed in the endovascular repair group versus none in the open repair group. Rupture after endovascular repair remains a concern. A significant interaction was observed between age and type of treatment. Endovascular repair led to increased long-term survival among younger patients but not among older patients, for whom a greater benefit from the endovascular approach had been expected.

Device-Specific Outcome

Matsumura and associates compared endoluminal versus open repair using the Excluder device.⁷⁷ In their review, they demonstrated a 30-day mortality rate of 1% along with endoleak rates of 17% and 20% at 1- and 2-year intervals, respectively.⁷⁷ 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 with endoluminal repair in low-risk patients and endoluminal repair in high-risk patients.⁷⁸ They reported a 30-day mortality rate of 3.5%, which was equal to the open group. The endoleak rates were 7.4% and 5.4% at 1- and 2-year intervals, respectively. There was a 5.3% migration of 5 mm at 1 year. Freedom from rupture was 100% in the low-risk group and 98.9% in the high-risk endoluminal group at 2 years. Experience with the AneuRx device has been reported by Zarins.⁷⁹ In this 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.⁸⁰ 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 neck. 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 healthcare services mandates a critical analysis of the economic impact of any new medical technology on the market. The in-hospital costs for both endovascular and open repair include graft cost, operating room fees, radiology, pharmacy, ancillary care, intensive care unit 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.^81,82 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 associated further corroborates previous studies.⁸³ In their review, despite decreased hospital and intensive care unit stays and utilization 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 in-hospital costs and do not even begin to address secondary costs such as postoperative surveillance that is required with endovascular repair. In the OVER trial, endovascular repair was found to be a cost-effective alternative to open repair in the U.S. Veterans Affairs healthcare system for at least the first 2 years.⁸⁴ The primary outcomes were mean total healthcare cost per life-year and per quality-adjusted life-year. There were no differences found in survival, quality of life, and costs after 2 years between the endovascular and the open group. Although graft costs were higher in the endovascular group, length of stay was shorter, resulting in lower cost of AAA repair hospitalization in the endovascular group. Costs remained lower after 2 years in the endovascular group, but the difference was no longer significant.

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.⁸⁵ In general, over 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, 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, whereas 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.

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.^85,86 Although seen as 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 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 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, whereas in the late period, the endoleak 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. Finally, 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 are initially considered type IV but persist become type III endoleaks by definition, because this indicates a more significant material defect than simple porosity or a suture hole.

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.⁸⁷ This phenomenon has been described as endotension. Although it was initially thought that an endoleak was really present but simply not detected, case 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.⁸⁸ 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 10% to 15% per year risk of secondary interventions following endovascular AAA repair.^18,78,89 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 that an annual rupture rate of approximately 1% to 1.5% per year after endovascular repair.^18,78,89 The EUROSTAR registry reports a rupture rate of 2.3% over 15.4 months in patients with an endoleak, compared with 0.3% in those without.⁹⁰ 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 aneurysms can lead to the development of attachment-site leaks and device failure, caused in part by aneurysm remodeling resulting in stent migration or kinking.⁹¹ Mehta and colleagues reported that 63% of delayed AAA ruptures after endovascular repair were caused by type I endoleaks with endograft migration, 11% by type I without migration, 19% by type II, and the rest of unknown type.⁹²

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.⁹³ Emergent endovascular repair should be considered in these patients since it is potentially much faster and less likely to cause physiologic stress than open conversion. Several reports have shown that endovascular repair can be performed successfully in patients previously treated with endoluminal prostheses.^94,95

Vascular occlusive disease of the mesenteric vessels is a relatively uncommon but potentially devastating condition that generally presents in patients over 60 years of age, is three times more frequent in women, and has been recognized as an entity since 1936.⁹⁶ 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.⁹⁷ Other etiologies exist and include FMD, panarteritis nodosa, arteritis, and celiac artery compression from a median arcuate ligament, but they are unusual and have an incidence of one in nine compared with 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 superior mesenteric artery, 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 (SMA in 5% and celiac trunk in 4% of cases).⁹⁸ 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 of pathophysiology, mesenteric ischemia is considered one of the most catastrophic vascular disorders with mortality rates ranging from 50% to 75%. Delays in diagnosis and treatment are the main contributing factors in its high mortality. It is estimated that mesenteric ischemia accounts for 1 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 gastrointestinal system: the celiac artery (CA), the superior mesenteric artery (SMA), and the 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 mid-colon); and the IMA supplies the hindgut (mid-colon to rectum). The CA and SMA arise from the ventral surface of the infradiaphragmatic suprarenal abdominal aorta, whereas 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. In order 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 since 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 networks 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.

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 gastrointestinal 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 gastrointestinal collateral circulation. The postprandial pain frequently occurs in the mid-abdomen, 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: (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 superior mesenteric artery (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.

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 celiac artery by the diaphragm, which is termed 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, which involves the mesenteric arteries, or after coarctation repair. Finally, other unusual causes of ischemia include mesenteric arteritis, radiation arteritis, and cholesterol emboli.

Clinical Manifestations

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 due to the extensive collateral development. However, when intestinal blood flow is unable to meet the physiologic gastrointestinal demands, mesenteric insufficiency ensues. The classical 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 gastrointestinal tract workup for the above symptoms prior to referral to a vascular service.

The typical patient who develops nonocclusive mesenteric ischemia is an elderly patient who has multiple comorbidities, such as 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 celiac artery 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 symptoms are nonspecific, but the pain is localized in the upper abdomen, which may be precipitated by meals.

Diagnostic Evaluation

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 prior to the evaluation by a vascular service, the patients have undergone an extensive workup 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 workup that should include CT scan of the abdomen and evaluation by 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.^99,100 A peak systolic velocity in the SMA >275 cm/s demonstrated a sensitivity of 92%, specificity of 96%, and overall accuracy of 96% for detecting >70% stenosis. The same authors found sensitivity and specificity of 87% and 82%, respectively, with an accuracy of 82% in predicting >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 CT with three-dimensional reconstruction (Fig. 23-40) and MRA (Fig. 23-41) have been promising in providing clear radiographic assessment of the mesenteric vessels.

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).

Mesenteric arteriography can also 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 Foley catheter should be placed for hemodynamic status monitoring. Appropriate antibiotics are given prior to 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 prior to 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 mid-jejunum 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 intravenous 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 smoother 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.¹⁰¹

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.¹⁰¹

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 celiac artery 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. Some surgeons advocate careful celiac plexus sympathectomy in addition to arcuate ligament decompression to ensure good treatment outcome.¹⁰² 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.^103,104 A recent review of laparoscopic and open median arcuate ligament release cases in the literature by Jimenez and colleagues showed both approaches to be effective in symptom relief (85%), with no difference in late symptom recurrence rate (6.8% in the open group and 5.7% in the laparoscopic group).¹⁰⁵

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 at a high operative risk category. Endovascular therapy is also suited in 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.¹⁰⁶ 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, since 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%.¹⁰⁶ 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 >30% or the presence of dissection after angioplasty. Restenosis after PTA is also an indication for stent placement.¹⁰⁷

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, IL) or recombinant tissue plasminogen activator (Activase; Genentech, South San Francisco, CA), 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 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 in order to achieve successful catheter-directed thrombolysis, 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 intravenous 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 operating room 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, MA), or SOS Omni catheter (Angiodynamics, Queensbury, NY). Once the mesenteric artery is cannulated, systemic heparin (5000 IU) is administered intravenously. A selective mesenteric angiogram is then performed to identify the diseased segment, which is followed by the placement of a 0.035-inch or less traumatic 0.014- to 0.018-inch 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 6-French 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 warrants mesenteric stent placement. Moreover, atherosclerotic involvement of the proximal mesenteric artery or vessel orifice should be treated with balloon-expandable stent placement. These stents can be placed over a low-profile 0.014- or 0.018-inch 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 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.¹⁰⁸

Clinical Results of Interventions for Mesenteric Ischemia

The first successful percutaneous angioplasty of the SMA was reported in 1980.¹⁰⁹ Since 1995, multiple series and scattered case reports have reported results from endovascular management of mesenteric occlusive disease.^101,108 A literature review by AbuRahma and colleagues in 2003 showed that endovascular intervention had an overall technical success rate of 91%, early and late pain relief rates 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.¹⁰⁸

In our review of the literature from published series since 1995, restenosis developed in 22% of patients during 24.5 months of average follow-up.¹⁰¹ The long-term clinical relief without reintervention was 82%. Among the patients who experienced 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, while it slightly increases the technical success rate, is not correlated with any substantial overall clinical benefit or improved long-term patency rates.

In contrast to endovascular treatment, open surgical techniques have achieved an immediate clinical success rate that approaches 100%, a surgical mortality rate of 0% to 17%, and an operative morbidity rate that ranges from 19% to 54% in a number of different series.^101,104,106 AbuRahma and colleagues reported their experience of endovascular interventions of 22 patients with symptomatic mesenteric ischemia due to either SMA or CA stenosis.¹⁰⁸ They noted an excellent initial technical and clinical success rates, which were 96% (23 of 24 patients) and 95% (21 of 22 patients), respectively, with no perioperative mortality or major morbidity. During a mean follow-up of 26 months (range, 1–54 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 relative high incidence of late restenosis.¹⁰⁸

Several studies have attempted to compare the endovascular with the standard open surgical approach.^110,111 The results of the open surgery appear to be more durable, but it tends 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.¹¹¹ With both patient cohorts having similar baseline comorbidities and symptom duration, there was no difference in early in-hospital 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.¹¹¹

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 from progressing to occlusion, and placement of drug-eluting stents. One such example is a recent nonrandomized study to compare the outcomes of mesenteric angioplasty using covered stents or bare metal stents in patients undergoing primary or reintervention for chronic mesenteric ischemia. The study showed that covered stents are associated with less restenosis (18% vs. 47%), symptom recurrence (18% vs. 50%), and reintervention (9% vs. 44%) at 24 months and better primary patency at 3 years (92% vs. 52%) than bare metal stents in the primary intervention group.¹¹² Similar results were found in the reintervention group as well.

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.¹¹³ 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 blood pressure. 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 consider 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).¹¹⁴ 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 arteries.¹¹⁵

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.¹¹⁶ 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.¹¹⁶ 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.

Clinical Manifestations

Renovascular hypertension is the most common sequela of renal artery occlusive disease. Its prevalence varies from 2% in patients with diastolic blood pressure greater than 100 mmHg to almost 30% in those with diastolic blood pressure over 125 mmHg.¹¹⁴ Clinical features that may indicate the presence of renovascular hypertension include the following: (a) systolic and diastolic upper abdominal bruits; (b) diastolic hypertension of greater than 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 angiotensin-converting enzyme inhibitors; and (g) development of hypertension during childhood.

All patients with significant hypertension, especially elevated diastolic blood pressure, 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.

Diagnostic 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 prior to 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. The following 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 prior to intervention.

Captopril renal scanning is a functional study that assesses renal perfusion before and after administration of the angiotensin-converting enzyme 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. A 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 greater than 180 cm/s and the ratio of these velocities to those in the aorta of greater than 3.5 (Table 23-11). Renal artery duplex is a technically demanding exam, 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 exam and is typically the initial screening test for patients with suspected renal artery occlusive disease.

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 (RVRR), of greater than 1.5 is indicative of functionally important renovascular hypertension, and it also predicts a favorable response from renovascular revascularization. Since 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 greater than 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 less than 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 to be considerably greater than 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 intravenous 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 prior to making plans for operative or endovascular treatment.

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 is also associated with activation of the renin-angiotensin cascade.

Treatment Indications

The therapeutic goals in patients with renovascular disease include: (a) improved blood pressure control, in order 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).

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:

• Inability to adequately control hypertension despite appropriate antihypertensive regimen.

• 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.

Prior to 1990, the most common treatment modality in patients with renal artery occlusive disease is 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. In the event that the surgeon plans to perform a side-to-side anastomosis between the conduit and the renal artery, this 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 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 revascularization 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. 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 nonatherosclerotic vascular disease had improvement in hypertension, but only 43% were completely cured and taken off antihypertensives.¹¹⁷ Patients younger than age 45 fair better, with a cure rate of 68% and 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 rates were 3.1% and 0% in the atherosclerotic and nonatherosclerotic groups, respectively.

Renal function improvement occurs within the first week of the operation in approximately two thirds of patients. A progressive decrease in the GFR is seen after this initial improvement, but the rate of decrease is less compared with patients who did not respond at all to operative intervention. Up to three quarters of patients were permanently removed from dialysis in a large series.¹¹⁸ Favorable response of renal function to revascularization improves overall survival.

Endovascular Treatment

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 is usually performed to assess the immediate results. The technical aspect of an endovascular renal artery revascularization is discussed 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. A selective renal angiogram is then performed to confirm position, and the lesion is crossed with either 0.035-inch or a 0.018- to 0.014-inch guidewires. It is important to maintain the distal wire position without movement in the tertiary renal branches during 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 and provides 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 diameter 4 mm 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 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 μg 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.¹¹⁹ In contrast, significantly greater minor complications were associated with the endovascular cohort, with a minor complication rate of 48% compared with 7% in the surgical group.¹¹⁹ In a prospective randomized study that compared the clinical outcome of renal artery balloon angioplasty versus stenting for renal ostial atherosclerotic lesion, comparable complications rates were found in the two groups (39% vs. 43%, respectively). However, the incidence of restenosis at 6 months was significantly higher in the balloon angioplasty cohort than the stenting group (48% vs. 14%, respectively). This study underscores the clinical superiority of renal stenting compared to renal balloon angioplasty alone in patients with ostial stenosis.¹²⁰

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 FMD such as hypertension or renal insufficiency usually respond well to renal artery balloon angioplasty alone.¹²¹ 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.¹²¹ 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.¹²¹

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.¹²² 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 blood pressure was controlled between the two groups. However, the degree and dose of antihypertensive medications were 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.

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.¹²³ The technical success of the procedure was 99%. The mean blood pressure values were 173 ± 25/88 ± 17 mmHg prior to stent implantation and 146 ± 20/77 ± 12 mmHg 6 months after renal artery stenting (P <0.01). Angiographic follow-up with 67 patients (mean 8.7 ± 5 months) demonstrated that 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.¹²⁴ Patients were followed for a mean of 27 months with measurements of blood pressure and serum creatinine, duplex sonography, and intra-arterial angiography. Five-year patency was 84.5% (mean follow-up, 27 months). Restenosis occurred in 8 of 74 arteries (11%), but after reintervention, the secondary 5-year patency rate was 92.4%. Hypertension 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 serum creatinine levels to determine the response of renal function following endovascular intervention.¹²⁵ In a study reported by Harden and colleagues who performed 33 renal artery stenting procedures in 32 patients with renal insufficiency, they noted that renal function improved or stabilized in 22 patients (69%).¹²⁶ 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 serum creatinine versus time.¹²⁵ A total of 61 renal stenting procedures were performed in 33 patients, and 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 7 patients. The study concluded 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.^{123,124,126,127,128,129,130,131,132} 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.¹³³ 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% of patients 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.

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 lower extremity circulation. If the aortoiliac plaques reach sufficient mass and 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 of this disease entity will enable physicians to prescribe the appropriate treatment strategy, which may alleviate symptoms and improve quality of life.

Diagnostic Evaluation

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, which reveals either a peak systolic velocity ratio ≥2.5 at the site of stenosis and or a monophasic waveform. Noninvasive tests such as pulse volume recordings (PVRs) of the lower extremity 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 PFA. Presence of pelvic and groin collaterals is important to provide 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 disk 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 is often 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 superior mesenteric artery 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 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 lower extremity tissue wound, and lower extremity microembolization that arises from aortoiliac lesions.

Disease Classification

Based on the atherosclerotic disease pattern, aortoiliac occlusive disease can be classified into three 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 (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 becomes 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,” which represents microembolization into the distal vascular bed (Fig. 23-53). Type II aortoiliac disease represents a more diffuse atherosclerotic progression that involves predominately the abdominal aorta with disease extension into the common iliac artery. This disease pattern affects approximately 25% 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.

The most commonly used classification system of iliac lesions has been set forth by the TransAtlantic Inter-Society Consensus (TASC) 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 document, the commission has not only made allowances for treatment of more extensive lesions, but also takes 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.^2,134

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 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, aortobifemoral bypass 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. Aortobifemoral bypass reliably relieves symptoms, has excellent long-term patency (approximately 70%–80% at 10 years), and can be completed with a tolerable perioperative mortality (2%–3%).¹³⁵

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, since visualization from the left flank is very poor. Tunneling of a graft to the right femoral artery is also 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 gastrointestinal 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 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.

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.

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 because it is associated with greater blood loss and 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 common iliac arteries; however, at present, aortoiliac PTA, stents, and other catheter-based therapies have become first-line treatment 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 external iliac artery 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 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 blood pressure 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 ipsilaterally at the CFA bifurcation into the SFA and PFA. 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%.¹³⁶ 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.¹³⁶

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.¹³⁶

Femorofemoral Bypass

A femorofemoral bypass is another option for patients with unilateral stenosis or occlusion of the common or external iliac artery 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.¹³⁷ 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.¹³⁷ Depending on the skills of the interventionalist or surgeon, many iliac lesions classified as TASC 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 common iliac artery, external iliac artery, or uninvolved limb of an aortobifemoral bypass. A conduit of Dacron, PTFE, or autologous vein is tunneled through the anteromedial portion of the obturator membrane to the distal SFA or popliteal artery. The obturator membrane must be divided sharply so as 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.¹³⁸ 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.^138,139

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%. It is usually the result of technical oversight or coagulation abnormality.¹⁴⁰ Acute limb ischemia 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 prior to restoring blood flow. Acute thrombosis of an aortofemoral graft limb in the early perioperative period occurs in 1% to 3% of patients.¹⁴⁰ 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).

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 a 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% over a 22-year period.¹⁴¹ 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 after the index operation.^140,141 Anastomotic pseudoaneurysms occur in 1% and 5% of femoral anastomoses in patients with aortofemoral grafts.¹⁴² Predisposing factors to pseudoaneurysm formation include progression of degenerative changes within the host artery, excessive tension at the anastomosis, and infection.¹⁴² 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.^141,142 Use of prophylactic antibiotics and meticulous surgical technique are vital in preventing contamination of the graft at the time of implantation. If infection appears localized to a single groin, graft preservation and local measures such as antibiotic irrigation, aggressive debridement, and soft tissue coverage with rotational muscle flaps may prove successful. 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 gastrointestinal 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 gastrointestinal tract with this configuration.^141,142 Treatment of aortoenteric fistula requires resection of all prosthetic material, closure of the infrarenal abdominal aorta, repair of the gastrointestinal 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 10-French 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 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 is generally sufficient in most cases. Large Palmaz-type stents mounted on XXL balloons (Meditech, Westwood, MA) have been successfully used and may be inflated up to 25 mm in diameter if needed. Newer self-expanding stents have also 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 recommend 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. Since calcified aortic stenoses are prone to rupture during dilation, it is recommended to be cognizant of the extent of the calcification 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 common iliac arteries, using a retrograde approach, and inflated. Simultaneous balloon dilatation at the origins of both common iliac arteries is advocated, even in the presence of unilateral lesion, to protect the contralateral common iliac artery from dissection or plaque embolization. Calcified lesions that 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.¹⁴³ 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%.¹⁴⁴ In more recent years, stents have been used to reconstruct the aortic bifurcation.¹⁴⁵ 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%.¹⁴⁵ In the largest series reported, the primary patency at 3 years was 79%.¹⁴⁶

Endovascular Treatment for Iliac Artery Disease

Percutaneous Transluminal Angioplasty

PTA is most useful in the treatment of isolated iliac stenoses of less than 4 cm in length. When used for stenoses rather than occlusion, a 2-year patency of 86% can be achieved.¹⁴⁷ 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 common iliac artery 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-inch guidewire (i.e., Bentson-type wire) or hydrophilic wire and a 5-French 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-French Berenstein catheter (Cordis Corp., Miami Lakes, FL) is used to probe the occlusion. The lesion can be crossed in most instances (5%–20% failure rate) with a hydrophilic guidewire or occasionally with its stiffer back end. As soon as the guidewire has crossed the obstruction and lies within the ipsilateral external iliac artery 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 “roadmap” imaging software, which 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 common iliac arteries will accommodate 8- to 10-mm diameter balloons, whereas most external iliac arteries 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 catheter-directed thrombolysis. If guidewire traversal is challenging, it is unlikely that catheter-directed thrombolysis will be beneficial. Investigators have found that routine thrombolysis and balloon dilation of occluded arteries prior to stent placement are associated with an increased incidence of distal embolic events.¹⁴⁸ 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 across the treated segment.¹⁴⁹ 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.¹⁵⁰

Primary Stenting versus Selective Stenting in Iliac Arteries

Primary stenting rather than selective stenting should be considered for longer iliac lesions and for all TASC C and D lesions. The primary patency rates at 1, 2, and 3 years were 96%, 90%, and 72%, respectively, for longer lesions (>5 cm) that were primarily stented versus 46%, 46%, and 28%, respectively, with selective stenting.¹⁵⁰ Primary stenting is generally advocated for chronic iliac artery occlusions, recurrent stenosis after previous iliac PTA, and complex stenoses with eccentric, calcified, ulcerated plaques or plaques with spontaneous dissection. All of 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.¹⁵⁰ It is believed that direct stent placement without predilation significantly reduces the risk of distal embolization by trapping potentially embologenic material between the arterial wall and the stent mesh. While 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 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.¹⁵¹ 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 C and D lesions.¹⁵² Bosiers and colleagues published a series of 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.¹⁵³ 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.¹⁴⁰ 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 catheter-directed thrombolysis. 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 of aortobifemoral bypass 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 receiving aortoiliac reconstruction remains 10 to 15 years less than anticipated for a normal age- and sex-matched population. Twenty-five percent 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.¹⁴²

Compared with conventional aortobifemoral bypass, 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 a 70% to 75% graft patency rate at 10 years after aortobifemoral reconstruction.¹⁵⁴ Due in part to factors including continued refinements in anesthetic management, intraoperative monitoring, and postoperative intensive care, low perioperative mortality rates for aortobifemoral bypass can be achieved commonly in today’s clinical practice. The most recent systematic review and meta-analysis of 5358 patients who underwent direct open bypass or endovascular treatment for aortoiliac occlusive disease demonstrated superior durability for open bypass, although with longer length of stay and increased risk for complications and mortality, when compared to the endovascular approach.¹⁵⁵ In this study, poor preoperative runoff was greater in the open bypass group (50.0% vs. 24.6%). Mean length of hospital stay was 13 days for open bypass versus 4 days for endovascular treatment procedures. The open bypass group experienced more complications (18.0% vs. 13.4%) and greater 30-day mortality (2.6% vs. 0.7%). At 1, 3, and 5 years, pooled primary patency rates were greater in the open bypass group (94.8% vs. 86.0%, 86.0% vs. 80.0%, and 82.7% vs. 71.4%, respectively); the same was true for secondary patency (95.7% vs. 90.0%, 91.5 vs. 86.5%, and 91.0% vs. 82.5%, respectively).

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 colleagues 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.¹⁵⁶ 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 from 54% to 92%.¹⁵⁷ The reported technical and initial clinical success of balloon angioplasty in iliac artery occlusions ranges from 78% to 98%, and the 3-year patency rates range from 48% to 85%.¹⁵⁷

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 external iliac artery adversely affects both primary and assisted-primary patency. Following angioplasty of the common iliac artery, patency rates were 81% and 52% at 1 and 6 years, respectively; whereas, after external iliac artery angioplasty, they were 74% and 48% at 1 and 4 years, respectively.¹⁵⁸ Although some literature supports location of the lesion in the external iliac artery as a factor that adversely affects both primary and assisted-primary patency, this has not been a universal finding.¹⁵⁸ Female patients are also reported to have lower patency rates than males following iliac PTA, with or without stent placement in the external iliac artery.¹⁵⁹

Stenting of the iliac arteries provides a durable and curative treatment, with a 3-year patency rate of 41% to 92% for stenosis and a 3-year patency rate of 64% to 85% and 4-year patency rate of 54% to 78% for occlusions.¹⁵⁷ A meta-analysis of 2116 patients by Bosch and Hunink showed that aortoiliac stenting 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.¹⁶⁰ Park and colleagues presented long-term follow-up results in a cohort of patients with all four TASC 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.¹⁶¹ Leville and colleagues achieved primary and secondary patency rates of 76% and 90%, respectively, after 3 years, in a cohort of patients who received stents for iliac occlusions.¹⁶² 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 classifications in terms of primary and secondary patency rates.¹⁶² They concluded that presence of TASC 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 embologenic potential or recanalized chronic iliac occlusions may be an exception. In the Dutch Iliac Stent 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.¹⁵¹ 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.¹⁵¹

The symptoms of lower extremity occlusive disease are classified into two large categories: acute limb ischemia (ALI) and chronic limb ischemia (CLI). Ninety percent of acute ischemia cases 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 lower extremity that manifest from asymptomatic to limb-threatening gangrene. As the population ages, the prevalence of chronic occlusive disease of the lower extremity 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 lower extremity occlusive disease. However, despite rapidly evolving endovascular technology, lower extremity 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.¹⁶³ Leng and his colleagues scanned 784 subjects using ultrasound in a random sample of men and women age 56 to 77 years. Of the subjects who were scanned, 64% demonstrated atherosclerotic plaque.¹⁶⁴ However, a large number of patients had occlusive disease without significant symptoms. In a study by Schroll and Munck, only 19% of patients with peripheral vascular disease were symptomatic.¹⁶⁵ Using ABIs, Stoffers and colleagues scanned 3171 individuals between the ages of 45 and 75 and identified that 6.9% of patients had ABIs <0.95, only 22% of whom had symptoms.¹⁶⁶ In addition, they demonstrated that 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 confirmed 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.

Diagnostic Evaluation

The diagnosis of lower extremity occlusive disease is often made based on 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 blood pressure 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).

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 greater than 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.¹⁶⁷ 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 a accumulative sensitivity of 80% and specificity of over 95%.¹⁶⁸ Adding an ultrasound contrast agent further increases the sensitivity and specificity of ultrasound technology.¹⁶⁹ Other noninvasive imaging technologies, such as MRA and CTA, are rapidly evolving and gaining popularity in the diagnosis of lower extremity occlusive disease (Figs. 23-59 and 23-60).

Contrast angiography remains the gold standard 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 lower extremity muscles, particularly during exercise. Intermittent claudication is pain affecting the calf and, less commonly, the thigh and buttock that 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. Regarding the 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 nonatherosclerotic conditions can also cause symptoms consistent with intermittent lower extremity 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 are also common, occur above the medial malleolus, usually in an area with the skin changes of lipodermatosclerosis, and cause mild discomfort. Neuropathic ulcers are usually 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.

Lower Extremity Occlusive Disease Classification

Lower extremity occlusive disease may range from exhibiting no symptoms to limb-threatening gangrene. There are two major classifications developed 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).¹⁷⁰

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; and 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 (Table 23-19).

The most clinically useful classification of lower extremity atherosclerotic disease should be based on the morphologic character of the lesions. The TASC taskforce published a guideline separating lower extremity 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 less than 3 cm in length and do not involve the origins of the 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 less than 3 cm in length. Type C lesions are multiple stenoses or occlusions greater than 15 cm in length or recurrent stenoses or occlusions that need treatment after two endovascular interventions. Type D lesions are those with complete occlusion of CFA, SFA, or popliteal artery.²

In a similar fashion, infrapopliteal arterial diseases are classified into four types based on TASC guideline (Fig. 23-61). Type A lesions are single lesions less than 1 cm in length not involving the trifurcation. Type B lesions are multiple lesions less than 1 cm in length or single lesions shorter than 1 cm involving the trifurcation. Type C lesions are lesions that extensively involve trifurcation or 1- to 4-cm stenotic or 1- to 2-cm occlusive lesions. Type D lesions are occlusions longer than 2 cm or diffuse lesions.²

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. While 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 lower extremity ALI 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, and 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 ≥2 weeks in duration compared with acute thrombosis.¹⁷¹

Arterial Embolism

The heart is the most common source of distal emboli, which accounts 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 can also 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 endocarditis and acute bacterial endocarditis are the more common causes. Infected emboli can seed the recipient vessel wall, creating mycotic aneurysms.

An electrocardiogram (ECG) will diagnose atrial fibrillation. A transthoracic or transesophageal echocardiogram should be performed looking 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 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 crosses through 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 lower extremity 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 lower extremity 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 lower extremity ischemia is 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 are 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 operating room 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 considers 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 lower extremity should be immediately anticoagulated. This will prevent propagation of the clot into unaffected vascular beds. Intravenous fluid should be started and a Foley catheter inserted to monitor urine output. Baseline labs should be obtained and creatinine levels noted. A hypercoagulable workup should be performed prior to 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 five-fold more frequently than thrombolysis. Three randomized studies have investigated the role of catheter-directed thrombolytic therapy in the treatment of ALI.¹⁷²

Endovascular Treatment

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 are 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 wash-out 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).

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 lower extremity arterial thrombosis. The utility of these thrombectomy devices is that they can be used as standalone 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.^173,174

Surgical Treatment

Embolectomy

When a decision is made to proceed with open surgical intervention, the abdomen, contralateral groin, and entire lower extremity 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 the techniques previously described. 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, because 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 because 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 catheter-directed thrombolysis 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.¹⁷⁵ Hematoma at the vascular puncture site has been reported in 12% to 17% of cases. Gastrointestinal 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.^167,172 Lytic agents are absolutely contraindicated in patients with intracranial surgery, intracranial hemorrhage within the last 3 months, or 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: reperfusion and compartment syndromes. Other procedure-related complications 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 lower extremity and causes of recurrent thrombosis are listed in Table 23-22.

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 greater than 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% of cases. 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.

Clinical Manifestations of Chronic Limb Ischemia

The term CLI 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 less than 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 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 less than 70 mmHg or a toe systolic pressure less than 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.

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 PFA can bypass the occlusion and reconstitute the popliteal artery. Symptom development is a function of the extent of occlusion, adequacy of collaterals, and the activity level of the patients.

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 greater than 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 artery disease, resulting in a high risk for ischemic events. Hertzer and associates reviewed coronary angiographies on 1000 patients undergoing elective vascular procedure and identified 25% of concomitant correctable coronary artery disease including 21% in patients undergoing elective peripheral vascular intervention.⁸ Conte and associates analyzed their 20-year experience in 1642 open lower extremity reconstructive surgeries and concluded that patients requiring lower extremity reconstruction presented an increasingly complex medical and surgical challenge compared with the previous decade in a tertiary practice setting.¹⁷⁶ With aging of the population, a growing number of vascular patients have prohibitive medical cormobidities and 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 lower extremity peripheral arterial diseases 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 may not be amendable to endovascular treatment or may be associated with poor outcomes, such as long segment occlusion, heavily calcified lesion, orifice lesion, or lesions that cannot be traversed by a guidewire. Proper selection of patients and techniques is critical in achieving good long-term outcome.

Endovascular intervention for lower extremity occlusive disease is continuously evolving. Success and patency rates of endovascular intervention are closely related to the anatomic and morphologic characteristics of the treated lesions. The TASC work group made recommendations on the intervention strategies of lower extremity arterial diseases based on the morphologic characteristics. Based on TASC 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 for infrapopliteal endovascular intervention due to higher complication and lower success rates. The treatment is restricted for patients with limb-threatening ischemia who lack surgical alternatives. However, with further advancement of endovascular technology and the development of new devices, endovascular intervention is becoming 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 lower extremity occlusive disease. As described by TASC 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 prior to endovascular therapy.

Endovascular Treatment

Technical Considerations

A sterile field is required in either an operating room or an angiography suite with image capability. The most common and safest access site is CFA via either a retrograde or an 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 to help access a pulseless CFA including ultrasound-guided puncture, using a micropuncture kit, and targeting calcification in a calcified vessel. The 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-inch guidewires are used for femoropopliteal lesions, and 0.014- or 0.018-inch guidewires are used for infrapopliteal access. Hydrophilic-coated wires, such as Glidewires, 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 manipulating 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 us traversed, one needs to pay particular attention on 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 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, and cutting balloon; the most commonly used atherectomy techniques include percutaneous atherectomy catheter and laser atherectomy device.

Systemic anticoagulation should be maintained routinely during lower extremity arterial interventions to minimize the risk of pericatheter thrombosis. Unfractionated heparin is the most commonly used agent, administered using a weight-based formula. We typically use 80 to 100 mg/kg initial bolus for therapeutic procedure to achieve an activated clotting time above 250 seconds upon catheter insertion and administer a subsequent 1000 units for each additional hour of the procedure. Newer agents, such as low molecular weight heparin, platelet IIb/IIIa inhibitors, direct thrombin inhibitors, 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 the procedure, 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 lower extremity interventions unless otherwise contraindicated.

Percutaneous Transluminal Balloon Angioplasty

After the lesion is crossed with a wire, an appropriated 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 is disappeared and the balloon is at the full profile. Frequently, several inflations are required to achieve a 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.

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 complications at the entry site and for crossing the tight lesions. Upon inflation, most balloons do not rewrap to their preinflation diameter and assume larger profiles. Furthermore, trackability, pushability, and crossability of the balloon should be considered when choosing a particular type of balloon. 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 lower extremity occlusive diseases. Studies have shown that PTA of femoropopliteal segment achieved over 90% technical success rate and 38% to 58% 5-year primary patency rates.^177,178,179 However, efficacy of PTA is highly dependent on anatomic selection and patient condition.¹³⁴ PTA of lesions longer than 7 to 10 cm offers limited patency, whereas PTA of shorter lesions, such as those less than 3 cm, has fairly good results. Lofberg and associates performed 127 femoropopliteal PTA procedures and reported a primary 5-year success rate of 12% in limbs with occlusion longer than 5 cm versus 32% in limbs with occlusion less than 5 cm in length.¹⁸⁰ 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%, with the best results being for patients with claudication and stenotic lesions.¹⁷⁹ Distal runoff is another powerful predictor of long-term success. Johnston analyzed 254 consecutive patients who underwent femoral and popliteal PTA and reported a 5-year patency rate of 53% for stenotic lesions and 36% for occlusive lesions in patients with good runoff versus a 5-year patency rate of 31% for stenotic lesions and 16% for occlusive lesions in patients with poor runoff.¹⁷⁸ Literature reviews showed that 5-year patency rates varied from 27% to 67% based on runoff status.¹⁷⁹

Due to limited success with infrapopliteal PTA, the indication for infrapopliteal PTA is stringent and 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, 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.¹⁸¹ In patients with favorable anatomies, the 2-year limb salvage rate after infrapopliteal PTA is expected to exceed 80%.

Subintimal Angioplasty

The technique of subintimal angioplasty 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. Subintimal angioplasty is recommended for chronic occlusion, long segment of lesion, and heavily calcified lesions. In addition, this technique is applicable for vessels with diffuse disease and for vessels that had previously failed an intraluminal approach, when 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 break back into the true lumen distal to the lesion. The occluded lumen is recanalized through the subintimal plan. Subintimal angioplasty can be performed through either an ipsilateral antegrade or contralateral retrograde approach 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 guide wire, usually an angled hydrophilic wire, such as a 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 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 prior to 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 30% luminal reduction is confirmed on completion angiogram.

Multiple studies have demonstrated the efficacy of subintimal angioplasty. Bolia and colleagues reported their extensive experiences on subintimal angioplasty for treating long-segment occlusions of infrainguinal vessels.^182,183 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.^184,185 Treiman and colleagues treated 25 patients with 6- to 18-cm femoropopliteal occlusion and achieved a technical success rate of 92% and a 13-month primary patency rate of 92%,¹⁸⁵ whereas Lipsitz and associates reported a technical success rate of 87% in 39 treated patients and a 12-month cumulative patency rate of 74%.¹⁸⁴ In addition, Ingle and associates reported a technical success rate of 87% in 67 patients with femoropopliteal lesions and a 36-month limb salvage rate of 94%.¹⁸⁶ 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 for reocclusion and distal embolization after PTA. In addition, an endoluminal stent is potentially beneficial for early restenosis after PTA. Drug-eluting stents are currently under investigation in the United States and may be promising in decreasing restenosis rates.

Although technical success rates are high, 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.^134,187 Gray and associates stented 58 limbs after suboptimal PTA for long SFA lesions and demonstrated a 1-year primary patency rate of 22%.¹⁸⁸ However, Mewissen treated 137 limbs using self-expanding SMART nitinol stents in patients with TASC A, B, and C femoropopliteal lesions and reported a 1-year primary patency of 76% and a 24-month primary patency rate of 60%.¹⁸⁹ 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 trial.¹⁹⁰ The German Multicenter Experience was a retrospective review of 111 SFA stenting procedures and predicted that the 6-month patency rate for SMART stents was 82% versus 37% for the Wallstent. The BLASTER (Bilateral Lower Arterial Stenting Employing Reopro) Trial evaluated the feasibility of using nitinol stents with and without intravenous abciximab for the treatment of femoral artery disease, and the preliminary results showed a 1-year clinical patency rate of 83%.¹⁹¹

Furthermore, the drug-eluting stent, which proved effective in decreasing restenosis in coronary intervention, may offer another promising alternative in lower extremity 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 drug-eluting stent clinical trial used Cordis Cypher SMART stents coated with sirolimus (SIROCCO trial).¹⁹² The SIROCCO results showed binary in-lesion restenosis rates of 0% in the sirolimus-eluting group versus 23.5% in the noneluting group at 6-month follow-up angiography. The PaRADISE (Preventing Amputations Using Drug-Eluting Stents) Trial investigated the efficacy and safety of using balloon-expandable drug-eluting stents to prevent amputations in patients with below-the-knee critical limb ischemia.¹³ One hundred six patients (118 limbs) were treated with drug-eluting stents in this prospective, nonrandomized trial. There were 228 drug-eluting stents implanted (83% Cypher [Cordis, Johnson & Johnson, Warren, NJ], 17% Taxus [Boston Scientific, Maple Grove, MN]). The average length treated was 60 mm. The 3-year cumulative incidence of amputation was 6%, the survival rate was 71%, and the amputation-free survival rate was 68%. Only 12% of patients who died had a preceding major amputation. Rutherford category, age, creatinine level, and dialysis were predictors of death but not amputation. Target limb revascularization occurred in 15% of patients.

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 anatomic 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 & Associates, Flagstaff, AZ) is the most commonly used device in the United States and is composed of an ultra-thin PTFE graft externally supported by self-expanding nitinol meshwork. The Viabahn device has a specific delivery mechanism by pulling back the attached string, which results in 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 at an average 7-month follow-up.¹⁹³ 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 comparable to surgical bypass, with a significantly shorter hospital stay (0.9 vs. 3.1 days).¹⁹⁴ A recent randomized prospective study comparing the treatment of SFA occlusive disease percutaneously with an expanded PTFE (ePTFE)/nitinol self-expanding stent graft (stent graft) versus surgical femoral to above-knee popliteal artery bypass with synthetic graft material showed no difference between the two groups with respect to primary or secondary patency rates at 48 months.¹⁹⁵ Mean total lesion length of the treated arterial segment in the stent graft group was 25.6 cm. The stent graft group demonstrated a primary patency of 72%, 63%, 63%, and 59% with a secondary patency of 83%, 74%, 74%, and 74% at 12, 24, 36, and 48 months, respectively. The surgical femoral-popliteal group demonstrated a primary patency of 76%, 63%, 63%, and 58% with a secondary patency of 86%, 76%, 76%, and 71% at 12, 24, 36, and 48 months, respectively. The authors concluded that ePTFE/nitinol self-expanding stent graft placement can be offered as an alternative to treatment of the SFA segment for revascularization when prosthetic bypass is being considered or when autologous conduit is unavailable.

Atherectomy

The basic principle of atherectomy is to remove the atheroma from obstructed arterial vessels. The currently available atherectomy devices can be generally categorized into directional, nondirectional, orbital, and rotational types based on their mecahnism. A few examples of FDA-approved atherectomy devices are Simpson AtheroCath (DVI, Redwood City, CA), Transluminal Extraction Catheter (Interventional Technologies, San Diego, CA), Thoratec recanalization arterial catheter (Thoratec, Pleasanton, CA), Auth Rotablator (Heart Technologies, Redmond, WA), SilverHawk system (FoxHollow Technologies, Redwood City, CA), Jetstream atherectomy system (Bayer, Indianola, PA), Diamondback 360° orbital atherectomy device (Cardiovascular Systems, Inc., St. Paul, MN), and Rotablator system (Boston Scientific Corporation, Natick, MA). 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 Thoratec 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. SilverHawk device is a monorail catheter designed to overcome the drawbacks of a directional atherectomy catheter. 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. Jetstream atherectomy system is a rotating, aspirating catheter with tip sizes of 1.6 and 1.8 mm for tibial arteries, and an expandable catheter with a tip size ranging from 2.1 to 3.4 mm for active removal of atherosclerotic debris and thrombus. The Diamondback 360° orbital atherectomy device uses a drive shaft with an eccentrically mounted, diamond-coated crown to create an orbital spin. As the speed of the crown increases from centrifugal force, it sands wider spaces, thereby providing variability in its working range. It can create a lumen that is >1.75 times the crossing profile depending on the size of the grit and the eccentricity of the offset. The greater the speed of the crown, the larger is the arc of debulking and, ultimately, the resultant lumen size. A constant flow of saline solution is delivered by a roller pump that lubricates the device and helps to flush the debris. The Rotablator system high-speed rotational device uses calcium ablation to achieve larger lumens. It has been used for more than 20 years to treat challenging, calcified coronary artery disease. The diamond-coated burr is designed to preferentially engage calcium and modify lesion compliance.