Natural History

An AAA is usually asymptomatic and is most commonly discovered as an incidental finding on a radiological examination. The prevalence of AAA increases with age, and the incidence in patients 45 to 54 years is 2.6% in men and 0.5% in women. In the older population (age 75 to 84 years), the incidence of AAA is 19.8% in men and 5.2% in women. The overall prevalence of AAA varies from 5% to 7% in patients over 65 years of age, and men are affected 4 to 6 times more often than women. A variety of cardiovascular and noncardiovascular co-morbidities, such as hypertension, coronary artery disease, cerebrovascular disease, and malignancy, co-exist with AAA. In patients with AAA, coronary artery disease and cerebrovascular disease are noted in 40% and 25%, respectively. Hypertension is present in more than half (55%) of patients with AAA; while malignancy is noted in 23% and claudication in 28%. Approximately two thirds (66%) of AAA patients die from cardiovascular etiologies.

Most aortic aneurysms increase at a rate of 0.2 to 0.3 cm/yr when the size is less than 5.5 cm. However, once the aneurysm reaches 5 to 6 cm, there is a rapid increase of up to 3 cm/yr. A rapid growth in an AAA is usually seen in smokers and females. The devastating sequela of an enlarging AAA is catastrophic rupture and death. Ruptured AAA accounts for 1% of all deaths and it is the tenth leading cause of death in patients over 50 years in age. Another clinical manifestation of AAA is distal embolization, resulting in acute limb ischemia, gangrene, blue toe syndrome, and limb loss.

Risk Factors

The risk factors for AAA are similar to those for atherosclerosis: male gender, age over 65 years, a history of ever smoking (>100 cigarettes in a person’s lifetime), hypertension, hypercholesterolemia, and genetic predisposition. One of the potential risk factors is a family history of AAA and surgical interventions for AAA in a family member. Five percent of patients with AAA have associated thoracic aneurysms, and approximately 15% have associated femoral or popliteal aneurysms.

Inflammatory aneurysms are a unique subset (5%) of AAA and usually present with vague flank pain, abdominal discomfort, and fever. A computerized tomography (CT) scan or magnetic resonance imaging (MRI) usually demonstrate concentric thickening around the abdominal wall. The inflammatory process in the retroperitonium is extensive and often involves the inferior vena cava, ureters, renal vein, and duodenum. When such an AAA reaches 5.5 cm, the endovascular approach may be optimal.

A minority of AAAs are associated with a nonatherosclerotic degenerative connective tissue disease, such as Ehlers-Danlos syndrome, Marfan syndrome, and Loeys-Dietz syndrome. Mycotic aneurysms are rare, but can cause pseudoaneurysms; and the most common etiologies are Salmonella and Staphylococcal aureus . Surgical options include resection and extra-anatomic bypass or aorta bi-femoral bypass using the deep femoral veins. Patients with mycotic aneurysms commonly have co-morbidities and, therefore, the surgical approach may be prohibitive. Endovascular aneurysm repair (EVAR) for treatment of abdominal mycotic aneurysms may be a short-term solution to avoid catastrophic rupture. A rare complication of AAA is aortoenteric fistula and case reports have successfully excluded these using an endograft.

Laplace Law

Laplace law indicates that wall tension of a symmetric shape is directly proportional to the intraluminal pressure and inversely proportional to the wall thickness. However, in reality, AAAs are not symmetrical in shape and have variations in wall thickness and strength.

Predictors of Rupture

The maximum AAA diameter is the most extensively accepted single parameter that predicts the risk of rupture. The risk of rupture increases when the AAA size is greater than 5.5 cm in men and women. The expansion rate is also an important determinant of risk of rupture. Rapidly enlarging AAAs, defined as a growth of 0.5 cm every 6 months, are also considered to be at high risk for rupture. Continued smoking and lifting heavy weights can cause a rupture in patients with aneurysms.

Physical Exam

Despite the novelty and importance of a physical exam, the only reliable finding is a widened palpable or pulsatile aorta above the umbilicus. Only 30% of these asymptomatic AAAs are detected on routine physical examination as a pulsatile abdominal mass. Auscultation of the aneurysm is useful, as the presence of a bruit may indicate associated aortic or mesenteric artery occlusive disease. Occasionally, a machinery murmur over the aneurysm may indicate an aortocaval fistula. The physical examination is dependent on the clinician’s experience and the patient’s body habitus. A large aneurysm in a thin individual is detected easily, while accuracy of physical examination is reduced by an obese body habitus. The overall sensitivity is approximately 29%, but can reach 96% in patients with an aneurysm ≥5.0 cm. The absence of a widened or palpable aorta does not exclude the presence of an AAA. Concomitant aneurysms, such as femoral and popliteal aneurysms, can be more easily diagnosed, yet continue to be under diagnosed. Other physical exam findings can be distal arterial embolization, blue toe syndrome, or livedo reticularis, and diminished distal pulses.

Abdominal Ultrasound

This is a safe, cost-effective, and simple test of choice for screening patients with AAA. The sensitivity and specificity of ultrasound, when performed by trained personnel, is close to 96% and 100%, respectively, for detection of infrarenal AAA. Ultrasound can serve as an excellent tool for the diagnosis and follow-up of AAA. Poor imaging quality, due to patient body habitus and variations in interpretations, are a few of the notable limitations.

Magnetic Resonance Angiography

Magnetic resonance angiography (MRA) is a noninvasive nonradiation test used to diagnose and evaluate the size of the AAA; however, MRA cannot usually be performed on patients with metallic implants, such as pacemakers.

Computerized Tomography

Computerized tomography (CT) scans can not only confirm the precise size, they can also delineate thrombus, occlusion, or stenosis. CT scanning plays a pivotal role in planning EVAR versus open repair and follow-up for shrinkage of size and endoleaks. The details of utilization of CT scan in preplanning an EVAR will be described later in this chapter.

Symptomatic Patients

When an AAA becomes symptomatic it can be categorized into the following:

• 1.
  

  Impending rupture

  
  
• 2.
  

  Embolic or thrombotic complications

  
  
• 3.
  

  Mass effect

Symptomatic AAA patients usually present with abdominal pain, low back pain, and flank pain. A sudden onset of back pain or abdominal pain, hypotension, and a palpable abdominal mass are the classic triad of symptoms for a ruptured AAA. However, a clinical diagnosis for ruptured AAA requires a high index of suspicion and misdiagnosis that includes renal colic, perforated viscus, abdominal wall hernia, diverticulitis, and ischemic bowel.

Thromboembolic symptoms from AAA can cause acute limb ischemia, gangrene, and limb loss. Baxter et al. identified 15 patients, among a review of 302 patients undergoing open AAA repair, to have distal embolization as the first manifestation. Among these patients, only two had an AAA size greater than 5 cm, which is suggestive of the potentially dangerous nature of small AAAs that are more likely to present with thromboembolic symptoms ( Figure 23-1 ). Large AAAs may cause vague symptoms, such as back pain, early satiety, ureteral compression, and venous thrombosis due to iliocaval compression.

76-year-old patient with (A) blue toe syndrome from a (B) 3.5-cm abdominal aortic aneurysm (AAA).

Asymptomatic Aneurysms

AAA patients are generally asymptomatic and are found during incidental radiological tests, such as x-ray, ultrasound, CT scan, MRI, and positron emission tomography (PET) scan. The maximum diameter of the AAA is the best indicator of rupture. The generally accepted indications are that men and women with an AAA greater than 5.0 to 5.5 cm require revascularization due to an increased risk of rupture. Rapidly growing aneurysms, defined by a growth rate greater than 0.5 cm in 6 months or 1.0 cm in 1 year, also need revascularization. Factors which should be considered include estimated risk of rupture under observation, the operative risk involved, life expectancy of the patient, and the patient’s personal preferences.

Initial Comparisons of Open Surgical Repair Versus Endovascular AAA Repair

The widespread use of EVAR to treat AAA followed the Food and Drug Administration (FDA) approval of second generation abdominal aortic endograft in 1999. The early EVAR outcomes noted in nonrandomized trials, registries, and single-center trials demonstrated lower rates of mortality and morbidity. A comparison of endoluminal versus open repair in the treatment of AAAs was analyzed in 303 patients. Open repair was performed in 195 patients and endovascular repair in 108 patients. The perioperative mortality rates were 5.6% each in the open repair group and the endovascular group. The advantages of endovascular repair were lower blood loss, shorter intensive care unit (ICU) stay, and reduced neurological complications. However, the Achilles heel for EVAR continued to be late complications such as endoleak and migration.

After 15 years of initial EVAR, by 2006 in the United States 21,725 endovascular exclusion of AAA procedures were performed, and thus EVAR numbers exceeded the number of open surgical AAA revascularization. The recent developments in catheter-based, endovascular techniques led to a substantial increase in the proportion of AAAs managed electively with EVAR. As of 2012, more than 70% of all infrarenal AAA was being treated with EVAR in the United States. ^.

Randomized Controlled Trials of EVAR Versus Open Surgical Repair

The landmark trials that demonstrated the safety, efficacy, and long-term results of EVAR versus open surgical repair for AAA were the Dutch randomized endovascular aneurysm management (DREAM) trial, EVAR I, EVAR 2, and OVER trial ( Table 23-1 ).

Preoperative Imaging

Multiple modalities such as CT angiogram, MRA, intravascular ultrasound (IVUS), and angiogram are available to image AAA. A contrasted CT scan using the thin slices (0.9 to 3 mm) is the imaging modality of choice for preoperative evaluation of AAA prior to EVAR. In patients with significant renal insufficiency CT scan without contrast and MRA without gadolinium may be used. Such alternative techniques may miss important anatomical information such as: laminated thrombus, patent inferior mesenteric artery (IMA), and severe iliofemoral occlusive disease. Besides the axial cuts, a review of sagittal, coronal, and three-dimensional (3D) reconstructions is necessary to fully understand the aneurysm anatomy, including its angulation ( Table 23-2 ). IVUS can be used to size the aortic and iliac artery seal zones, and evaluate potential eccentric thrombus in the aortic neck and the external iliac artery for occlusive disease ( Figures 23-2 and 23-3 ).

Computed tomography (CT) scan for pre-EVAR planning: A, center line measurements for infrarenal neck length and diameter. B, Infrarenal neck measured at 1 mm, 13 mm, and 16 mm below the lowest renal artery. C, 3D image reconstruction of EVAR graft superimposed on the abdominal aortic aneurysm (AAA).

Shows magnetic resonance angiography (MRA) for pre-EVAR planning. A, Neck length. B, Diameter. C, External iliac diameter.

Anesthesia

All patients scheduled for elective EVAR should undergo appropriate preoperative risk stratification according to American College of Cardiology (ACC)/American Heart Association (AHA) guidelines. Patients who are considered inoperable for open surgical repair of AAA carry a risk of 18% to 43% perioperative cardiovascular events if primary conversion of EVAR to surgical open repair becomes necessary. Initially, the majority of patients received general anesthesia for EVAR. The smaller sheath size and closure devices have enabled patients to undergo EVAR with monitored anesthesia care (MAC). EVAR operators should coordinate and plan the procedure with the anesthesia for procedure safety and reduce complications.

Strategic Planning and Multispecialty Team

A careful and well thought out strategic plan of EVAR is essential for optimal outcomes. The planning should include a physical examination and detailed history and a thorough explanation of natural history of AAA to the patient and family. The multispecialty (vascular surgeon, cardiologist, and/or radiologist) discussion should include all treatment options for AAA revascularization, and risk benefit and alternatives of EVAR. Each EVAR case should be preferably planned with a vascular surgeon and anesthesiologist in a team-based approach. Recent advances in CT software technology include availability of 3D measurements to assist in intraoperative navigation techniques. All high-risk patients should have risk factor reduction by appropriate treatment with aspirin, beta blockers, ACE inhibitors, and statins prior to EVAR. Baseline pulmonary functions test and lab works such as blood urea nitrogen (BUN), creatinine, hemoglobin levels, and prothrombin time should be known prior to surgery. Anticoagulants such as warfarin or newer ones should be held in advance and, if needed, bridged with heparin. A type and screen of blood type rather than type and cross can reduce the number of transfusions. All the devices and auxiliary equipment such as snares, covered stents, and a Palmaz stent (Cordis corp., Miami Lakes, Florida) should be available before the start of the case.

EVAR is performed by various specialists who have proficiency in the procedure and follow-up. The multispecialty team usually should include vascular surgery, cardiology or radiology, and anesthesia. Despite the ability of a nonvascular surgery physician to perform EVAR, it is highly recommended to have a team approach with vascular surgery. Such a team approach plays a vital role in endovascular management of ruptured AAA. Acute complications such as vessel rupture, distal embolization, requirement for a surgical cut down for vessel access and repair, or emergent conversion to open repair will need vascular surgery expertise.

Anatomic Considerations

Anatomical considerations that are important for AAA suitability for EVAR are as follows:

• •
  

  Proximal and distal attachment site

  
  
• •
  

  Diameter and characteristics of access vessels

  
  
• •
  

  Percutaneous access for EVAR

  
  
• •
  

  Aorto iliac artery side branches with potential for exclusion during EVAR: hypogastric artery, accessory or anomalous origin of renal artery, and patent inferior mesenteric artery

Proximal and Distal Attachment Sites

One of the most important anatomical factors that predicts the suitability for EVAR is the character of aortic neck. Important measurements and characteristics include length, diameter, angulations, presence of thrombus, reverse taper, and calcification. The majority of the endovascular grafts have prespecified instructions for use (IFU)—the infrarenal neck length should be at least 10 mm in length and less than 32 mm in diameter with infrarenal angulations less than 90° ( Figures 23-4 and 23-5 ).

Case example of aortic neck characteristics that are ideal for EVAR. A, 1, Length of the aneurysmal neck; D1, Diameter of the proximal neck; D2, Diameter of the distal neck; 2, Angulation of the neck. B and C, Reverse taper of the aortic neck.

Angiographic confirmation of aortic neck measurements. A, Infrarenal neck angulation. B, Infrarenal neck length.

Aortic Neck: Diameter, Length, Angulation, Taper, Reverse Taper, and Thrombus

Aortic neck diameters that can be treated can range from 18 to 32 mm. Most measurements are based on the CT scan outer wall to outer wall except for Gore (W.L. Gore and associates, Inc., Flagstaff, Arizona), which measures inner to inner wall. The two important dimensions of the infrarenal neck of the AAA are measured as D1 and D2. D1 is the first image of the infrarenal aorta measured outer to outer wall in the short axis. D2 is the diameter below D1 at 10 mm or 15 mm distal based the graft. The length of the aortic neck is determined by counting the number of images from lower renal artery to the start of the aneurysm based on the CT scan slices at the time of imaging (0.9 to 5 mm).

The distal attachment site is equally important to ensure adequate seal and prevent endoleak (discussed later). The distal landing zone is preferable in the common iliac artery and allows perfusion of the hypogastric artery. In patients with common iliac artery (CIA) aneurysms, the endovascular approach can be performed with low morbidity, blood loss, hospital stay, and short-term mortality. The mid-term durability and survival from endovascular approach offers the advantage of first-line treatment option for patients with iliac artery aneurysms ( Figure 23-6 ). The diameter of the CIA and morphology such as calcification, thrombus, and stenosis should be evaluated. CIA diameters up to 25 mm can be treated with endograft using a flared 28-mm limb available with Endurant stent graft system (Medtronic Inc., Santa Rosa, California).

Common iliac artery with a good landing zone in a patient evaluated for EVAR. A, Angiography. B and C, Computed tomography (CT) scan.

The two main issues of obliteration of hypogastric arteries are pelvic ischemia and Type II endoleak (explained later). A large series of EVAR patients who underwent hypogastric embolization had persistent buttock claudication in 12% of unilateral and 11% of bilateral hypogastric artery interruptions. Erectile dysfunction occurred in 9% of unilateral and 13% of bilateral hypogastric occlusions. The dreaded complication of ischemic colitis develops in less than 2% of EVAR cases. The risk for colon necrosis increases in EVAR patients who have an occlusive disease of all three mesenteric vessels, or if previous colon surgery has interrupted the mesenteric collateral pathways. Colon ischemia is more likely to result from atheroembolism to the pelvic circulation rather than hypogastric artery occlusion.

The characteristics of the common iliac artery can determine the following options that are available to manage the distal landing zone during EVAR ( Figure 23-7 ).

• 1.
  

  If the internal iliac artery is not aneurysmal, coil embolization of the internal iliac artery is performed at its origin to reduce the postprocedure rates of buttock claudication. The patency of branches of internal iliac artery may help in reducing the buttock postprocedure. The limb can be further extended across the embolized hypogastric artery into the external iliac artery (EIA) to obtain adequate seal.

  
  
• 2.
  

  If flow to the internal iliac artery has to be preserved then a surgical bypass from internal iliac artery to the external iliac artery can be performed. This hybrid technique has demonstrated good mid- and long-term patency. However, the operative times, length of hospital stay, and blood loss are increased.

  
  
• 3.
  

  If the hypogastric artery needs to be preserved, a double-barrel stenting can preserve the flow to the internal iliac artery and obtain adequate seal at the common iliac artery. In this technique one covered stent is placed from the CIA into the hypogastric artery and a simultaneous limb of the EVAR graft will extend from CIA to the EIA ( Figure 23-8 ).

  
  

  
  

  
  

  

  
  

  
  

  A case of sandwich technique during EVAR to maintain hypogastric artery patency. A, The left hypogastric artery shows severe ostial stenosis. B, Simultaneous stenting of left hypogastric artery and left external iliac artery (EIA). C, Final angiogram to show preservation of the left hypogastric artery and the left external iliac artery (EIA).

  
  
  
  
• 4.
  

  If the common iliac artery is occluded then a uni-aortic limb placement with femoral-femoral bypass is performed. A contralateral placement of flexible covered stent from external iliac artery to internal iliac artery will allow retrograde perfusion.

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