Aortoiliac Occlusive Disease 

Updated: Aug 21, 2017
Author: Khanjan H Nagarsheth, MD, MBA; Chief Editor: Vincent Lopez Rowe, MD 

Overview

Background

In patients with peripheral arterial disease (PAD), obstructing plaques caused by atherosclerotic occlusive disease commonly occur in the infrarenal aorta and iliac arteries. Atherosclerotic plaques may induce symptoms either by obstructing blood flow or by breaking apart and embolizing atherosclerotic and/or thrombotic debris to more distal blood vessels. If the plaques are large enough to impinge on the arterial lumen, reduction of blood flow to the extremities occurs.

Several risk factors exist for development of the arterial lesions, and recognition of these factors enables physicians to prescribe nonoperative treatment that may alleviate symptoms as well as prolong life.

Aortoiliac occlusive disease (AIOD) occurs commonly in patients with PAD. Significant lesions in the aortoiliac arterial segment are exposed easily by palpation of the femoral pulses. Any diminution of the palpable femoral pulse indicates that a more proximal obstruction exists.

Obstructive lesions may be present in the infrarenal aorta, common iliac artery, internal iliac (hypogastric) artery, external iliac artery, or combinations of any or all of these vessels. Occasionally, degenerated nonstenotic atheromatous disease exists in these vessels and may manifest by atheroembolism to the foot, the "blue toe" or "trash foot" syndrome. Generally, patients with aortoiliac PAD have a poorer general prognosis than those with more distal PAD.[1]

Before prosthetic grafts for aortic bypasses became available, the first direct surgical reconstructions on the aorta were performed using the technique of thromboendarterectomy (TEA), first described by Dos Santos of Lisbon in 1947.[2] The initial procedure was performed on a patient with superficial femoral artery (SFA) obstruction, and Dos Santos termed the procedure disobliteration. Wylie adapted this technique to the aortoiliac region and, in 1951, performed the first aortoiliac endarterectomy in the United States.[3]

With the discovery of suitable prosthetic graft materials for aortic replacement in the 1960s, surgical treatment of AIOD became available to even more patients.

In 1964, Dotter first performed percutaneous iliac angioplasty using a coaxial system of metal dilators.[4] This procedure proved to have limited application, because of the cumbersome nature of the device. However, Dotter's early work paved the way for Grüntzig, who, in 1974, developed a catheter with an inflatable polyvinyl chloride balloon that could be passed over a guide wire.[5] This device became the cornerstone for the percutaneous treatment of arterial occlusive lesions today.

In 1985, Palmaz introduced the first stent that helped to improve the results of angioplasty for arterial occlusive disease.[6] Since the advent of angioplasty and stenting, the technology has evolved at an astronomic rate. The design and quality of endovascular devices, as well as the ease and accuracy of performing the procedures, have improved. These improvements have led to improved patient outcomes following endovascular interventions for AIOD.

Surgical treatment of AIOD has been well standardized for many years, and the outcomes are quite good. However, the additional techniques of percutaneous transluminal angioplasty (PTA) and stenting have provided more alternatives to open surgery and make successful approaches available to patients who may have been considered at an unacceptably high risk for conventional open surgical repairs.

Catheter-based endovascular treatments for AIOD offer the advantages of less morbidity, faster recovery, and shorter hospital stays. In fact, most endovascular interventions today are simply performed as outpatient procedures.

This article reviews the risk factors for development of atherosclerotic occlusive disease of the aorta and iliac arteries and describes the natural history, diagnosis, and treatment of the disease.

For patient education resources, see the Cholesterol Center, as well as High Cholesterol and Cholesterol FAQs.

Pathophysiology

Atherosclerosis is an extraordinarily complex degenerative disease with no known single cause. However, many variables are known to contribute to the development of atherosclerotic lesions. One popular theory emphasizes that atherosclerosis occurs as a response to arterial injury. Factors that are known to be injurious to the arterial wall include the following:

  • Mechanical factors, such as hypertension and low wall shear stress
  • Chemical factors, such as nicotine, hyperlipidemia, hyperglycemia, and homocysteine

Lipid accumulation begins in the smooth-muscle cells and macrophages that occur as an inflammatory response to endothelial injury, and the "fatty streak" begins to form in the arterial wall. The atheroma consists of differing compositions of cholesterol, cholesterol esters, and triglycerides. Some plaques are unstable, and fissures occur on the surface of the plaque that expose the circulating platelets to the inner elements of the atheroma.

Platelet aggregation then is stimulated. Platelets bind to fibrin through activation of the glycoprotein (GP) IIb/IIIa receptor on the platelets, and a fresh blood clot forms in the area of plaque breakdown. These unstable plaques are prone to atheromatous embolization and/or propagation of clot that eventually can occlude the arterial lumen.

If the atheroma enlarges enough to occupy at least 50% of the arterial lumen, the flow velocity of blood through that stenosis can significantly increase. The oxygen requirements of the lower extremity at rest are low enough that even with a moderate proximal stenosis, no increase in blood flow velocity occurs. During exercise, however, the oxygen debt that occurs in ischemic muscle cannot be relieved, because of the proximal obstruction of blood flow; this results in claudication symptoms.

In more advanced cases, critical tissue ischemia occurs, and neuropathic rest pain or tissue loss ensues. However, critical limb ischemia (CLI) is seldom, if ever, caused by AIOD alone. Commonly, in patients with CLI, multiple arterial segments are involved in the occlusive atherosclerotic process.

Three distinct arterial segments distal to the visceral bearing portion of the abdominal aorta may become diseased by atherosclerosis, as follows:

  • Type I atherosclerosis involves the infrarenal aorta and the common iliac arteries only; the vessels distal to the common iliac arteries usually are normal or only minimally diseased; this pattern of atherosclerosis is present in about 5-10% of patients with PAD and occurs more commonly in women
  • Type II atherosclerosis involves the infrarenal aorta and the common and external iliac arteries and may extend into the common femoral arteries; this pattern is observed in 35% of patients with PAD
  • Type III atherosclerosis is the most severe form and, unfortunately, also the most common; this pattern of atherosclerosis involves the infrarenal aorta and the iliac, femoral, popliteal, and tibial arteries

Diabetes mellitus is a risk factor that results in a characteristic pattern of atherosclerotic lesions in patients with PAD. The proximal inflow vessels (aorta, iliac arteries) tend be normal. However, the femoropopliteal segment (including the deep femoral artery), and especially the proximal tibial arteries, are usually severely diseased. Fortunately, the distal tibial and plantar vessels may be normal, enabling successful arterial reconstruction for limb-threatening ischemia.

Etiology

Atherosclerosis is the most common cause of occlusive plaques in the aorta and iliac arteries. Several risk factors exist for the development of atherosclerotic plaques in the aortoiliac arterial segment. Cigarette smoking and hypercholesterolemia are observed more commonly in patients with AIOD than in those with infrainguinal occlusive disease. In addition, patients with AIOD tend to be younger and less likely to have diabetes.

An uncommon cause of aortic obstruction is Takayasu disease, a nonspecific arteritis that may cause obstruction of the abdominal aorta and its branches. The etiology of Takayasu disease is not known. For the purposes of this article, only occlusive lesions caused by atherosclerosis are considered.

Epidemiology

At least 50% of patients with PAD have no symptoms, and therefore, the exact incidence and prevalence of the condition is unknown. However, the incidence of PAD is known to increase with advancing age, so that by age 70 years, as much as 25% of the US population is affected. Occlusive disease involving the aortoiliac arterial segment occurs commonly in patients with PAD and is second only to occlusive disease of the SFA in frequency.

Prognosis

Outcomes after aortic operations for AIOD are measured in terms of operative mortality and patency of the arterial reconstruction over time. These outcomes are similar for aortoiliac TEA and aortofemoral bypass (AFB). The 30-day operative mortality is 2-3%. Long-term patency is excellent too: 85-90% at 5 years after AFB or TEA. If patients continue to smoke, however, these excellent patency rates are reduced by half.

Outcomes for extra-anatomic (axillofemoral or femorofemoral) bypasses are clearly not as good as those for either AFB or aortoiliac TEA. Operative mortality might be expected to be better for extra-anatomic bypass than for AFB because of the extracavitary nature of these procedures and the absence of the requirement for aortic occlusion during the operation. However, the operative mortality (0-4% for femorofemoral bypass; 2-11% for axillobifemoral bypass) reflects the selected patients in whom these procedures are performed. The 5-year primary patency rate with extra-anatomic bypass for AIOD is 19-50% for axillobifemoral bypass and 44-85% for femorofemoral bypass.

In a study of 92 patients with AIOD who underwent AFB (n=72), aortioiliac bypass (n=15), or both (n=5), Lee et al reported overall primary patency rates of 86.2% at 5 years and 77.6% at 10 years,[7] as well as a 10-year limb salvage rate of 97.7% and an overall survival rate of 91.7%.

Endovascular techniques (ie, PTA and stent placement) offer alternatives to conventional surgical repair. Therefore, understanding the outcomes offered with such interventions is important.

Although isolated stenosis of the infrarenal aorta or common iliac artery is uncommon, this lesion is suited ideally to PTA, stent placement, or both. For localized segmental occlusive disease in the aorta, PTA can achieve initial technical success rates of 95%, with 5-year patency rates of 80-87%. For iliac lesions, PTA yields initial success rates of 93-97%, with 5-year patency rates of 54-85%. These results seem to be improved when arterial stents are used either primarily or as an adjunct to PTA for the treatment of iliac artery stenosis.

One study investigating the effects of heavy calcification in stent-implanted iliac arteries showed that iliac stents in heavily calcified lesions presented significant residual stenosis; however, even in cases with incomplete expansion of the stent, further blockage was not found, and all stents remained anatomically patent.[8]

In a systematic review and meta-analysis designed to examine the clinical outcomes of endovascular and open bypass treatment for AIOD, Indes et al found that endovascular treatment was associated with shorter hospital stays, lower complication rates, and reduced 30-day mortality, whereas open bypass was associated with higher primary and secondary patency rates at 1, 3, and 5 years.[9]

 

Presentation

History and Physical Examination

The most common symptom of patients with hemodynamically significant aortoiliac disease (AIOD) is claudication (from Latin claudicatio ["limping, lameness"]). The symptom complex of claudication is defined as muscle cramps in the leg(s) that occur after exercise and are relieved by resting. In any individual patient, the exercise distance at which claudication occurs is quite constant.

Claudication usually occurs first in the calf muscles, though thigh, hip, and buttocks muscles also can be affected when more extensive proximal lesions are present. The location of the muscle pain (ie, calf vs thigh) does not necessarily correlate with the level of arterial obstruction. However, more proximal symptoms (ie, buttocks or thigh claudication) are generally associated with severe AIOD.

Symptoms of buttock claudication can occur in association with erectile dysfunction in patients with absent femoral pulses. This constellation of symptoms, termed Leriche syndrome (after the surgeon who described it in 1923), occurs when either preocclusive stenosis or complete occlusion of the infrarenal aorta is present as a result of to severe aortic atherosclerosis. Because of the chronic nature of the occlusive process leading to the development of rich collateral blood supply to the lower extremity, limb-threatening ischemia seldom occurs.

 

Workup

Laboratory Studies

Examine a serum lipid profile that includes total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides (TG). Furthermore, in younger patients or those with a strong family history of atherosclerosis at any early age, lipoprotein (a) and homocysteine levels should be determined.

If a history of diabetes exists, a glycosylated hemoglobin level (HbA1c) should be checked. Excellent control of diabetes reduces long-term complications, and the American Diabetes Association (ADA) currently recommends that the HbA1c be below 7%.[10]

If a patient has a history of thrombosis in any venous or arterial segment or a family history of a clotting disorder, an evaluation for hypercoagulability is necessary. Tests include routine prothrombin time (PT), activated partial thromboplastin time (aPTT), platelet count, factor V Leiden, factor II (prothrombin) C-20210a, anticardiolipin antibody, protein C, protein S, and antithrombin III.

Imaging Studies

Contrast aortography is not always required, unless interventional therapy (percutaneous transluminal angioplasty [PTA]/stenting or surgical revascularization) is planned. Serum creatinine is checked to validate a baseline level prior to the use of contrast agents that may be nephrotoxic.

Computed tomography (CT) angiography (CTA) is an excellent modality for planning operative or endovascular treatments.[11] It has the advantage of producing three-dimensional images of the arterial system that are as accurate as those achieved with conventional catheter arteriography. However, the use of an iodinated contrast agent is still required to obtain the images in CTA, though direct arterial cannulation is not needed.

As an alternative to conventional angiography, the surgeon may consider magnetic resonance angiography (MRA) or arterial duplex mapping as definitive imaging studies for planning surgery. MRA is overly sensitive and may suggest significant arterial stenoses that are simply not present.

Ankle-Brachial Index and Pulse Volume Recording

At least half of patients with peripheral arterial disease (PAD) are asymptomatic and are diagnosed only by physical examination, Doppler-derived measurement of the ankle-brachial index (ABI), or both.

An ABI lower than 0.9 clearly is abnormal and confirms the diagnosis of PAD. An abnormal ABI should alert the clinician to the fact that this group of patients is at risk for early mortality from cardiovascular causes (eg, myocardial infarction, stroke, other vascular death). The ABI also can grade the severity of PAD. Note that Doppler-derived segmental arterial pressures do not accurately reflect the severity of aortoiliac occlusive disease (AIOD).

In addition, the ABI is not very sensitive in identifying patients with mild occlusive lesions in the aortoiliac segment. A treadmill exercise stress test should be recommended for those patients with mild iliac occlusive disease who have symptoms suggestive of claudication even though the ABI is normal at rest. After exercise, the blood flow through stenotic vessels increases and the pressure decline across these lesions is augmented.

Moreover, if the blood pressure cuff is unable to compress the vessels adequately, the Doppler-derived pressures may be falsely elevated. This may occur in patients with diabetes or end-stage renal disease. In the event that supranormal (falsely elevated) Doppler-derived pressures are encountered, pulse volume recording (PVR) may be useful in evaluating leg perfusion.

The PVR waveform reflects the volume of blood in the leg during an individual cardiac cycle. A normal waveform demonstrates a brisk upstroke, a sharp systolic peak, and a downstroke with a dicrotic notch. With significant PAD, the dicrotic notch is lost, the slope of the upstroke and downstroke decline, the amplitude of the waveform is reduced, and the contour of the systolic peak is more rounded.

Other Tests

Because an association with coronary disease in patients with PAD exists, electrocardiography (ECG) should be performed even in patients without cardiac history.

For those patients being considered for an intra-abdominal aortic procedure, pulmonary function tests are important if a history of obstructive pulmonary disease or dyspnea is present. Often, the results of this preoperative evaluation signal a need to alter the surgical approach.

An intensive preoperative cardiac evaluation is reserved for patients with newly onset angina pectoris, unstable angina pectoris, or evidence of ventricular dysfunction on dobutamine stress echocardiography. Adenosine thallium perfusion tests are not routinely performed, because of the high sensitivity and low specificity.

 

Treatment

Approach Considerations

Treatment of patients with peripheral arterial disease (PAD) has two goals. The first and foremost goal is to reduce the risk of vascular events (myocardial infarction [MI], stroke, vascular death) that occur at an alarmingly high rate in patients with PAD. About 30% of patients with PAD die within 5 years, and death is usually due to an ischemic coronary event.

The second goal of treatment is to improve symptoms in those patients with claudication and prevent amputation in patients with critical limb ischemia (CLI). CLI is present when patients have symptoms of ischemic rest pain, nonhealing foot ulcers, or gangrene, and its presence mandates urgent evaluation with aortography and endovascular and/or surgical revascularization to prevent limb loss.

At least 50% of patients with PAD may be asymptomatic. Because natural history data are poor for iliac stenosis, surgical or endovascular intervention should not be considered if patients truly are asymptomatic. Surgical intervention for limb-threatening ischemia is accepted universally, unless the limb is deemed nonviable. Determining whether or not to intervene in a patient with mild claudication may not be as straightforward.

The Practice Guidelines Committee of the Society for Vascular Surgery (SVS) has developed specific practice recommendations for the treatment of asymptomatic PAD and intermittent claudication in patients with atherosclerotic disease of the lower extremities.[12]  (See Guidelines.)

No controversy exists regarding the appropriate surgical procedure to treat aortoiliac occlusive disease (AIOD). Use thromboendarterectomy (TEA) only in cases of type I atherosclerosis. TEA also is an excellent option for those patients with blue toe syndrome from severe ulcerogenic aortoiliac atherosclerosis that involves only the infrarenal aorta and common iliac arteries. Some authors have advocated performing the aortic procedure through a retroperitoneal rather than an intra-abdominal approach. Despite some excellent work in this area, outcomes have generally been similar whether the procedure is performed in a retroperitoneal or a transabdominal fashion.

An important role exists for conservative therapy in patients with AIOD. Although surgical therapy usually alleviates symptoms, the patient must be apprised of the operative risk of mortality (2-3%), as well as anticipated outcomes over time. Since the advent of catheter-based treatments for AIOD, asymptomatic patients are often treated prophylactically with either angioplasty or stenting of iliac arterial lesions that are discovered during coronary angiography. This practice of drive-by angioplasty should not be recommended.

Controversy remains regarding the appropriate place for minimally invasive treatment of AIOD.[13] Laparoscopically assisted aortofemoral bypasses (AFBs) have been performed in both animals and humans with satisfactory results. However, a significant learning curve seems to be involved, and no long-term follow-up data are available for review.

Medical Therapy

Three fundamental principles are involved in the treatment of symptomatic PAD due to AIOD.

First, the risk factors must be identified and aggressively treated. The two most important risk factors for PAD are cigarette smoking and diabetes. Complete cessation of smoking is mandatory. Carefully regulate serum glucose; the goal is a glycosylated hemoglobin (HbA1c) level below 7%. The goal of hypertension control should be blood pressures lower than 140/90 mm Hg. The low-density lipoprotein (LDL) cholesterol level should be reduced to less than 100 mg/dL, usually with hepatic 3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins).

In addition to modification of risk factors, patients with AIOD should receive lifelong antiplatelet therapy to reduce the risk of MI, stroke, and vascular death.

Second, initiate a walking exercise program. Numerous prospective randomized clinical trials have attested to the efficacy of walking exercise to treat claudication.[14, 15] Every trial has demonstrated improvements of 180-340% in walking distance. Supervised walking programs usually produce better results than unsupervised exercise does. Walking exercise has even been compared to angioplasty and found to produce superior results. Walking exercise improves symptoms of claudication because the muscle enzymes involved in oxygen extraction and utilization become more efficient over time.

Finally, two pharmacologic agents approved by the US Food and Drug Administration (FDA), pentoxifylline and cilostazol, may alleviate the symptoms of claudication caused by lower-extremity arterial occlusive disease. Pentoxifylline is a methylxanthine derivative that acts as a hemorheologic agent, lowering blood viscosity. Unfortunately, it is effective in only 30-40% of patients and must be taken three times daily. If it is effective, walking distances only improve modestly.

Cilostazol, a phosphodiesterase III inhibitor, has been shown to be more effective than either pentoxifylline or placebo. Its mechanism of action is not well understood. Adverse effects may include headache and loose stools, but the medication generally is well tolerated. It should not be used in patients with significant congestive heart failure.

Surgical Therapy

Choice of surgical procedure

Direct arterial reconstruction on the diseased aortoiliac arterial segment is well established. Aortoiliac TEA and AFB are the two traditional means of surgically treating AIOD. The two procedures have similar risks and results, and the outcomes have stood the test of time. In 1966, Blaisdell introduced axillofemoral bypass as an extra-anatomic technique for improving inflow to the lower extremities without the need for an abdominal procedure.[16] Since then, with the advent of arterial stents, endovascular repair of aortoiliac lesions has become a reasonable alternative to consider if the pathologic anatomy is suitable.[17, 18]

Thromboendarterectomy

TEA of the aorta and iliac arteries was the first reconstructive procedure performed for AIOD. The concept is simple. A dissection plane exists between the arterial media and the obstructing plaque. When the appropriate plane is entered, the arterial intima, plaque, and internal elastic lamina of the media are removed as a single specimen.

Early on, surgeons were concerned that the remaining portion of arterial wall was not sturdy enough to hold blood under arterial pressure. With more experience, however, it became clear that the remaining portion of the vessel (external elastic lamina of the media and adventitia) following TEA provided a secure and durable conduit with excellent long-term patency. When aortoiliac TEA is used to treat type I atherosclerotic occlusive disease, patency rates are excellent. However, the results are not as good when TEA is applied to patients with more extensive distal occlusive lesions in the external iliac and femoral arteries.

Today, aortoiliac TEA is not used as commonly as AFB is, primarily because the procedure is best suited for patients who have type I atherosclerosis with occlusive disease limited to the infrarenal aorta and common iliac arteries (see the image below). Patients with type 1 atherosclerosis represent a minority of patients with PAD. Furthermore, younger surgeons may not have had proper exposure to the technique of aortoiliac TEA during their training and therefore may not have appropriate experience using the procedure to treat AIOD.

Type I atherosclerosis with occlusive disease limi Type I atherosclerosis with occlusive disease limited to the infrarenal aorta and common iliac arteries.

The main advantage of aortoiliac TEA over conventional AFB for the treatment of AIOD is that prosthetic material is not needed to perform the arterial reconstruction. Even for the most experienced surgeons, aortic prosthetic graft infections occur in 0.5-3% of patients after AFB.

Many patients undergo aortoiliac TEA not for removal of the plaques that obstruct blood flow but, rather, for removal of the source of atheroembolism causing blue toe syndrome. Aortoiliac TEA is ideally suited for this indication because the offending degenerated atheroma is removed, leaving a clean, glistening surface that is soon covered by new functional endothelium.

The only significant disadvantage of TEA as compared with AFB is that a larger, more meticulous dissection is required to expose and control the branches of the infrarenal aorta.

Finally, aortoiliac TEA should not be performed if occlusive plaques involve the more distal external iliac and femoral arteries. The "tail" of the atheroma in the common iliac artery may extend into the orifice of the external iliac artery, and this tongue usually is removed easily during the course of the procedure. However, if diffuse disease exists in the more distal external iliac and femoral arteries, AFB is a more suitable alternative.

Aortobifemoral bypass

AFB is the most common open surgical alternative used to treat AIOD. In the early experience of aortic surgery, unilateral AFB or even aortoiliac bypass (AIB) often was performed to limit the extent of the procedure. However, as more experience was gained with these operations, using the common femoral arteries as the outflow target clearly produced better long-term patency results.

Unilateral AFB is performed infrequently today because the extremity that was neglected initially seldom is truly healthy and invariably demonstrates symptoms from progressive atherosclerosis. Therefore, bilateral AFB is appropriate to avoid the need for subsequent inflow operative procedures on the limb that demonstrates less extensive occlusive disease.

The original approach to AFB was transabdominal. As an alternative approach, retroperitoneal exposure of the aorta can be used to avoid entering the peritoneum. Some authors have advocated this approach on the basis of a theoretical advantage of fewer pulmonary problems, more rapid resolution of postoperative ileus, and fewer days in the hospital. Other studies have not supported this proposed benefit.

In some circumstances, a bypass serving both legs can be constructed using a single common iliac artery as the donor site. This procedure can be performed through either a transperitoneal or a retroperitoneal approach.

Extra-anatomic bypass

For higher-risk patients who are less likely to tolerate an abdominal operation, extra-anatomic bypass was developed in the mid 1960s. Axillobifemoral bypass provided an extracavitary means of improving blood flow to the lower extremities. This procedure proved especially useful in the treatment of aortic graft infections. However, the long-term patency of extra-anatomic bypass is distinctly inferior to that of conventional AFB.

Angioplasty and stenting

With the advent of percutaneous transluminal angioplasty (PTA) and stenting, excellent minimally invasive alternatives to conventional open reconstructive surgery now are available.[19, 20]

If applied to the appropriate anatomic problem, the results of iliac angioplasty/stent placement rival open surgical results. For isolated segmental common iliac artery stenoses, angioplasty/stenting rivals open surgical results. For occlusive disease that diffusely involves the aortoiliac segment, direct open surgical repair still offers the best long-term outcome. However, through catheter-based treatments (angioplasty/stenting), patients with significant operative risk due to comorbid diseases can be offered therapy.

Preparation for surgery

Because most patients with AIOD are older than 50 years, finding associated ischemic heart disease is not uncommon, even if classic anginal symptoms are not present. Hertzer et al found that most patients undergoing aortic operations for arterial occlusive disease had diseased coronary arteries when coronary arteriography was performed. Moreover, Porter et al found a significant incidence of occlusive plaques in the carotid arteries in a similar group of patients. Clearly, AIOD does not exist in a vacuum. However, despite the association of coronary and extracranial arterial occlusive disease with PAD, it is clear that not every patient needs an extensive preoperative evaluation before undergoing aortic surgery.

Preoperative cardiac evaluations are reserved for patients who have an abnormal finding on electrocardiography (ECG) or a history of new-onset or unstable angina and for those with symptoms of ventricular dysfunction (orthopnea, dyspnea on exertion). Patients who have had coronary angioplasty or bypass or who have a history of stable angina on appropriate medication probably do not need a preoperative cardiac evaluation, unless a change has occurred in either exercise tolerance or anginal pattern.

Immediately before the induction of anesthesia, the anesthesiologist places an epidural catheter. Although the catheter is not used during the procedure, the analgesic relief provided by instillation of narcotic and local anesthetic agents in the postoperative period is invaluable.

In addition, a systemic dose of a perioperative cephalosporin is administered intravenously before the skin incision is made. The antibiotic is continued postoperatively for 24-28 hours to lower the risk of graft infection.

Operative details

Both TEA and AFB can be performed through either a longitudinal midline or a transverse intra-abdominal incision and even may be performed via a retroperitoneal exposure to the aorta.

More dissection is needed with TEA. Total circumferential mobilization of the infrarenal aorta and common iliac arteries is required in order to perform aortoiliac TEA. The proximal extent of the dissection is the level of the renal arteries as long as the occlusive plaques do not extend proximally and impinge on the orifices of these vessels. If occlusive disease extends cephalad to the renal arteries, the dissection must be carried proximally to the origin of the superior mesenteric artery (SMA) to allow placement of the aortic occluding clamp at the base of this vessel.

An alternative approach for suprarenal control of the aorta is placement of the aortic cross-clamp above the level of the celiac axis, a maneuver that is not difficult and is quite familiar to vascular surgeons. The lumbar, middle sacral, and inferior mesenteric (IMA) arteries must be managed by using vessel loops to control backbleeding when the aorta is opened.

Take care to identify and preserve any accessory renal arterial branches, which may be present in as many as 20% of patients. In addition, the proximal portion of the external iliac and hypogastric arteries should be dissected adequately to allow placement of occluding clamps on these vessels distal enough from the origin to view the proximal portion of the external iliac artery

The difficult portion of the dissection occurs around the distal aorta and proximal common iliac arteries. The inferior vena cava and the common iliac veins may be quite adherent to the arteries at this point, and care must be taken to avoid injury to these veins. After the dissection is completed, 5000 units of intravenous heparin are administered prior to arterial occlusion.

The distal clamps are placed first to reduce the incidence of atheroembolism that may occur following application of the aortic clamp. A longitudinal incision is made in the aorta, extending from 2 cm distal to the aortic occluding clamp proximally to 2 cm proximal to the aortic bifurcation distally. Place the line of incision on the right side of the anterior surface of the aorta to avoid the origin of the IMA.

The endarterectomy plane is easily established where the atheromatous disease is most severe. Grasp the plaque and gently push away the remaining arterial wall. The dissection is continued distally until the bifurcation is reached, and the appropriate plane is continued into the orifice of each common iliac artery.

The iliac artery may be incised longitudinally (if the common iliac is long), or even transversely, directly over the common iliac bifurcation. The author prefers a longitudinal incision extending from the proximal common iliac artery 2 cm from the origin to the iliac bifurcation because it affords the surgeon a better view of the endarterectomized surface and the endarterectomy endpoint. A bridge of arterial wall is preserved between the abdominal aortic incision and the common iliac incisions.

Once the entire plaque is mobilized in the common iliac, the entire specimen may be pulled in a cephalad direction and removed entirely as a single specimen that bears some resemblance to a pair of pants.

Take care to examine the distal endpoint in the iliac artery. A tongue of atheroma may continue into the origin of the external iliac and hypogastric arteries. This tail of atheroma must be excised in a more superficial plane to avoid extending the endarterectomy into the deeper plane used to perform TEA. The plane of the atheroma actually is easy to discern because the atheroma usually is a darker yellow color and has a different consistency than the more normal adherent intima.

After any remaining plaque and/or strands of media are removed, the arteriotomies are closed with continuous polypropylene sutures. If the aorta is small (<2 cm), a prosthetic zero-porosity Dacron patch is used to avoid the narrowing that may occur during primary closure of a longitudinal arteriotomy. Once blood flow has been restored, femoral pulses should be palpated to confirm the presence of adequate inflow.

A similar aortic exposure is used to perform AFB. In addition, the common femoral artery, the proximal superficial femoral artery (SFA), and the proximal deep femoral (profunda femoris) artery are mobilized through longitudinal groin incisions that are made just lateral to the femoral pulse. If the pulse is not present, the proper line of incision is found by measuring 3-4 fingerbreadths lateral to the pubic tubercle.

Cover the skin in a povidone-iodine–impregnated plastic drape to help avoid skin contact with the prosthetic graft. The infrarenal aorta immediately adjacent to the renal arteries is mobilized. Circumferential mobilization of the aorta is not necessary. The common femoral artery and its branches are mobilized from the inguinal ligament to the bifurcation, exposing enough of the SFA and the deep femoral artery to allow placement of an arterial occluding clamp.

The aortic anastomosis may be performed in either an end-to-end or an end-to-side configuration using continuous polypropylene suture. Although partially occluding aortic clamps have been used in performing end-to-side anastomoses, a better view of the aortic lumen is obtained with the use of proximal and distal clamps that totally occlude the aorta.

If the aorta is filled with atherosclerotic debris that appears loose and may embolize when flow is restored, perform an end-to-end aortic anastomosis and oversew the distal aorta. The configuration of the proximal anastomosis is not as important as its location. The anastomosis to the aorta must be placed near the renal arteries to help avoid recurrent atheromatous and/or aneurysmal disease that may involve infrarenal aorta that remains proximal to the aortic anastomosis.

Once the proximal anastomosis is completed and no bleeding is present, the limbs of the prosthetic graft are passed carefully through retroperitoneal tunnels that were made before the patient received intravenous heparin. The tunnels are made directly anterior to the iliac arteries and posterior to the ureters. The circumflex iliac veins must be avoided during creation of the tunnel and passage of the graft limbs. Partial incision of the inguinal ligament may aid in constructing the tunnel and identifying these large troublesome veins.

The common femoral artery is incised longitudinally, and a conventional end-to-side femoral anastomosis is created with continuous polypropylene suture. Take care to examine the origins of the two outflow branches of the common femoral artery (ie, the SFA and the deep femoral artery). Not uncommonly, the SFA has significant occlusive disease. If the SFA is occluded, any stenosis in the proximal portion of the deep femoral artery must be repaired to insure adequate long-term patency of the aortic graft limb. If the common femoral artery is severely diseased, limited local TEA may have to be performed to facilitate an adequate femoral anastomosis.

Endovascular Reconstruction

Endovascular interventions for AIOD have become commonplace since the first report of kissing iliac stents as an alternative to open surgical reconstruction.[21]  This technique employs the use of two stents, typically balloon-expandable, placed into the aortic bifurcation and simultaneously deployed.

One meta-analysis reported a 12-month primary patency of 89.3%, with primary assisted and secondary patency being 92.3% and 92.3%, respectively.[22]  Of note, this review included both self-expanding and balloon expandable stents. The COBEST trial showed that covered balloon expandable stents had superior patency and outcome at 24 months as compared with bare metal stents.[23]

Groot Jebbink et al evaluated the geometry of kissing stents for recreating the aortic bifurcation and suggested that the discrepancy between the stented lumen and the aortic lumen might affect patency.[24]  They felt that this radial mismatch could cause flow disturbances and give rise to thrombus formation. Their findings support the use of the Covered Endovascular Reconstruction of the Aortic Bifurcation (CERAB) technique to recreate the bifurcation.

The CERAB technique reconstructs the aortic bifurcation in a more anatomic way so as to reduce the mismatch that can occur with traditional kissing stents. In this technique, a covered stent is placed approximately 15-20 mm above the aortic bifurcation, and a large balloon is used to oppose this stent to the aortic wall. The proximal extent of the stent is gently overdilated so as to create a funnel within the aorta. Next, the common iliac covered stents are placed into the distal end of the aortic funnel and simultaneously inflated.

Another endovascular treatment of AIOD involves the use of a unibody low-profile stent graft that preserves the aortic bifurcation. This is an off-label application of the Endologix AFX aortic endoprosthesis. In 2016, Maldonado et al published a study of the largest patient cohort with AIOD treated by means of this modality.[25]  They retrospectively evaluated 91 patients with AIOD and reported a primary patency rate higher than 90%, a primary assisted patency rate higher than 98%. and a secondary patency rate of 100% at 2 years. Notably, 82% were patients with TASC D lesions.

One limitation of this technique is that the AFX stent graft lacks sufficient radial force for heavily calcified lesions; consequently, 59% of patients in this study required adjunct stenting with balloon-expandable stents. Even with this limitation, this is a reasonable technique to employ in patients who cannot undergo more traditional aorta-based surgery. 

Postoperative Care

In the past, all patients were monitored in an intensive care unit (ICU) for the first 24-48 hours following an aortic operation. Over the past decade, it has become increasingly common for patients undergoing operations for occlusive disease to avoid the ICU and receive their postoperative care on a regular surgical floor.

For patients with hemodynamic concerns, systemic arterial paressure and pulmonary capillary wedge pressure (PCWP) are helpful guides for planning intravenous fluid requirements. In addition, hourly urinary output through a bladder catheter is recorded. Although significant blood loss is not common, the hematocrit is monitored every 6-12 hours during the first 24 hours.

If the operation has proceeded smoothly, perform extubation at the end of the procedure. Preoperative pulmonary function tests help to predict which patients are likely to develop postoperative respiratory problems. When the forced expiratory volume in 1 second (FEV1) is less than 1 L, one can anticipate difficult respiratory problems associated with conventional aortic surgical approaches through midline incisions. For such cases, a transverse intra-abdominal or retroperitoneal incision may help to reduce postoperative respiratory complications.

Most large fluid shifts occur following aortic surgery and are related to the size of the dissection and the length of the operation, as well as the amount of intraoperative blood loss. Patients tend to gain significant "wet weight" during the first 48 hours postoperatively. By the beginning of postoperative day 3, mobilization of the excess water back into the intravascular compartment begins to occur. Urine output increases, PCWP rises, and hematocrit may drift downward.

Also monitor the perfusion to the lower extremities carefully. If pedal pulses cannot be palpated as a consequence of SFA occlusive disease, monitor Doppler flow as well as the ankle-brachial index (ABI). After successful revascularization, the ABI should increase by at least 15%.

Complications

Several complications are related to both aortoiliac TEA and AFB, and others are associated only with one or the other. Perioperative thrombosis may be a complication of either procedure and generally is related to technical problems. For example, a plaque that dissects, causing restriction in blood flow and subsequent thrombosis, may occur as a complication of either procedure. Visualization of endarterectomy endpoints and suturing of plaques that may elevate when blood flow is restored may help to reduce the risk of dissection and subsequent thrombosis.

Intraoperative atheroembolism is another complication that may occur during surgical dissection and mobilization of the vessels or following release of the occluding clamps during reperfusion. Meticulous dissection during mobilization of the arteries is imperative. Furthermore, placement of the distal occluding clamps before application of the proximal clamps may help to reduce the risk of atheroembolism that is inherent during any aortic operation.

Injury to adjacent structures (ie, duodenum, inferior vena cava, iliac veins, ureters) usually is easy to avoid with careful technique. However, caution must be exercised with mechanical retractors to avoid inadvertent injury to adjacent structures. Care is necessary both in the retroperitoneum and in the groin to avoid injury to nerves adjacent to major vessels.

Careful closure of groin wounds is necessary in order to avoid a lymphocele, which can lead to graft infection.

A specific complication related to the use of prosthetic material for AFB is the development of aortic graft infection, which occurs in 0.5-3% of cases. Usually, presentation of the infection follows the aortic procedure by a significant length of time (20-24 months). Most commonly, a complication of healing in the groin wound is the first sign that a serious life- or limb-threatening problem must be dealt with.

Graft infections can be classified into two groups, depending on the causative pathogen involved. The more virulent organisms (ie, Staphylococcus aureus, gram-negative bacilli) usually are responsible for causing a more severe type of clinical infection. When systemic signs of sepsis occur with graft infection, a virulent organism is present.

On the other hand, a significant number of graft infections are caused by Staphylococcus epidermidis. These infections are much more indolent, and the extent of graft involvement may be harder to determine. Even with the most skilled physician, mortality after treatment of aortic graft infection is 11-27%. Moreover, the risk of amputation following graft infection is almost as high.

Major complication rates associated with catheter-based treatments (PTA/stenting) for AIOD range from 2.3% to 17%. The problem can occur in the target vessel, the access site, or even other arteries that are far removed anatomically (ie, atheroembolism). These complications include dissection, acute thrombosis, atheroembolism, and even arterial perforation. Complications related to the contrast agent (ie, anaphylaxis [rarely] or contrast-induced renal dysfunction) are uncommon.

Long-Term Monitoring

In general, the results of therapy for AIOD are excellent, but patients still need follow-up care at regular intervals. See patients every 3-6 months for the first year and every 6-12 months thereafter. If a prosthetic graft has been implanted, a lifelong risk of graft infection exists that the patient must recognize. Moreover, oral antibiotic prophylaxis is appropriate before dental procedures, urologic instrumentation, sigmoidoscopy, or other gastrointestinal surgical procedures.

 

Guidelines

SVS Guideline for Asymptomatic PAD and Intermittent Claudication

In March 2015, the Practice Guidelines Committee of the Society for Vascular Surgery (SVS) issued specific practice recommendations for the treatment of asymptomatic peripheral artery disease (PAD) and intermittent claudication in patients with atherosclerotic disease of the lower extremities.[12]  Among the recommendations were the following:

  • Emphasis is placed on risk factor modification, medical therapies, and broader use of exercise programs to improve cardiovascular health and functional performance
  • Screening for PAD appears of unproven benefit at present
  • Revascularization for intermittent claudication is appropriate for selected patients with disabling symptoms, after a careful risk-benefit analysis; treatment should be individualized according to comorbid conditions, degree of functional impairment, and anatomic factors
  • Invasive treatments for intermittent claudication should provide predictable functional improvements with reasonable durability (suggested minimum threshold, >50% chance of sustained efficacy for ≥2 years); anatomic patency is considered a prerequisite for sustained efficacy
  • Endovascular approaches are favored for most candidates with aortoiliac disease
  • Caution is warranted with interventions for intermittent claudication when durability is limited (eg, extensive calcification, small-caliber arteries, diffuse infrainguinal disease, poor runoff); in such cases (if patients are otherwise good-risk) and in cases of previous endovascular failure, surgical bypass may be preferred
  • Patients who undergo invasive treatments for intermittent claudication should be monitored regularly in a surveillance program