Advanced Aortic Aneurysm Management: Endovascular Aneurysm Repair—Standard and Emergency Management
Vinit N. Varu
Ronald L. Dalman
DEFINITION
An abdominal aortic aneurysm (AAA) is defined as a localized enlargement of more than 1.5 times the diameter of the most adjacent, proximal uninvolved aorta; by consensus, this represents more than 3.0 cm in most persons. Definitions vary somewhat between men and women, most likely normalized by body surface area or body mass index (BMI).
The most common etiology of AAAs is progressive, transmural degeneration of the aortic wall. The full scope of pathogenetic considerations and relevant mechanisms is beyond the scope of this chapter but, in summary, although aneurysm disease shares many important risk factors for aortic and peripheral vascular occlusive disease, important differences exist, and current thinking regarding pathogenesis recognizes that aneurysmal and occlusive disease of the aorta are distinct pathologic processes. Hence, the colloquial term “atherosclerotic aneurysm,” although in common use, is an inaccurate and potentially misleading characterization of the most common clinical presentation for AAA.
Risk factors for development, expansion, and rupture are multifactorial1 (Table 1). Smoking is the only modifiable risk factor that has been associated with all three.
The risk of AAA rupture increases with progressive diameter enlargement.2 Rupture and subsequent aneurysm-related mortality may be prevented by elective surgical repair, either by open interposition grafting or endovascular aneurysm repair (EVAR).
Table 1: Risk Factors for Aneurysm Development, Expansion, and Rupture
Symptom
Risk Factors
AAA development
• Tobacco use
• Hypercholesterolemia
• Hypertension
• Male gender
• Family history (male predominance)
AAA expansion
• Advanced age
• Severe cardiac disease
• Previous stroke
• Tobacco use
• Cardiac or renal transplant
AAA rupture
• Female gender
• ↓FEV1
• Larger initial AAA diameter
• Higher mean blood pressure
• Current tobacco use (length of time smoking > > amount)
• Cardiac or renal transplant
• Critical wall stress—wall strength relationship
AAA, abdominal aortic aneurysm; FEV1, forced expiratory volume in 1 second. From Chaikof EL, Brewster DC, Dalman RL, et al. The care of patients with an abdominal aortic aneurysm: The Society for Vascular Surgery practice guidelines: executive summary. J Vasc Surg. 2009;50(4):880-896.
EVAR provides similar long-term survival versus traditional open repair, as well as enhanced perioperative survival. The perioperative survival benefit is sustained for several years following surgery.3 EVAR is now the de facto standard of care for both elective and ruptured AAA repair in patients who are anatomically suited to receive currently available devices.
PATIENT HISTORY AND PHYSICAL FINDINGS
Patients may be entirely asymptomatic despite suffering from large, advanced AAAs. Most commonly, AAAs are found incidentally on imaging studies obtained for other reasons. Occasionally, they may be identified by the presence of prominent aortic pulse, proximal to the umbilicus, on physical exam. Less frequently, AAAs may cause distal limb ischemia secondary to embolization, or fulminate congestive heart failure if they rupture into the adjacent inferior vena cava, creating an acute aortocaval fistula. Only 30% to 40% are noted on physical examination, with detection of pulsatile abdominal mass dependent on aneurysm size. As noted by Sir William Osler, prior to the era of ubiquitous availability and use of cross-sectional abdominal imaging in the evaluation of abdominal pain: “There is no disease more conducive to clinical humility than aneurysm of the abdominal aorta.”
Patients with a ruptured AAA may present with moderate or extreme back and abdominal pain, syncope, hypotension, and mottling of the lower extremities, in conjunction with progressive abdominal distension. When sufficiently stable to remain conscious and conversant, pain is reproducibly elicited by direct palpation of the abdominal aorta. Many patients with ruptured AAA present in extremis, others with progressively hemodynamic deterioration and pain of several hours duration. Patients may actually linger for several days with “contained” retroperitoneal hemorrhage following AAA rupture.
A thorough vascular history should be noted and modifiable risk factors, including smoking, hyperlipidemia, and hypertension, addressed in patients with AAAs. Smoking cessation is recommended to reduce the risk of aneurysm growth and rupture, and statins may also be beneficial in this regard.
AAAs occur almost exclusively in the elderly (mean age of repair 72 years of age) and male patients outnumber female by 4 to 6 is to 1.1 When AAA is recognized in younger patients, it is usually in association with hereditary risk, syndromic aortic conditions such as Marfan syndrome, or in the setting of focal aortitis or mycotic aneurysms. The latter tend to occur most frequently in the suprarenal abdominal aorta, at or directly proximal to the origin of the celiac artery, underneath the crus of the diaphragm. Aneurysmal degeneration of the abdominal aorta may also occur late following thoracic and abdominal aortic dissection.
Factors associated with increased risk of rupture include female gender, large initial diameter, low forced expiratory volume in 1 second (FEV1), current smoking history, and elevated mean blood pressure.
IMAGING AND OTHER DIAGNOSTIC STUDIES
Screening decreases aneurysm-related mortality in AAA disease.4 Current guidelines recommend a screening ultrasound for 65- to 75-year-old at-risk individuals, defined as men who have smoked more than 100 cigarettes in their lifetime or men or women with a family history of AAAs.5
Thin-slice computed tomography (CT) imaging, with intravenous contrast injection timed to opacify the abdominal aorta and runoff vessels, remains the standard modality for operative planning. The extent, morphology, and accessibility of the aneurysm via retrograde iliofemoral access determine the suitability for an endovascular repair. Other relevant anatomic considerations include the location and volume of laminar intraluminal thrombus in the region of the “surgical” neck (defined as the length between the lowest renal artery and the start of the aneurysm); angulation of the surgical neck, size and tortuosity of access vessels; presence and significance of anomalous and accessory renal arteries; diameter at the aortic bifurcation; and diameter of the more proximal abdominal aorta (provides useful guidance as to the likely long-term diameter of the surgical neck).
For cases of suspected AAA rupture, bedside transcutaneous ultrasonography may be used to detect the presence of intraor retroperitoneal fluid (or blood) or assess for confounding conditions eliciting abdominal pain. When sufficiently hemodynamically stable, however, CT aortography should be obtained to assess for suitability for endovascular repair.6
SURGICAL MANAGEMENT
Indications
Patients with “symptomatic” AAAs (e.g., pain likely originating from the aneurysm despite absence of retroperitoneal hemorrhage on CT aortography) are at increased risk of rupture and urgent intervention is recommended. Of those AAAs that rupture, more than half will die prior to hospitalization. Of those that undergo attempted operative repair, approximately 50% mortality is to be expected. The latter estimate is highly dependent on hemodynamic conditions, duration of symptoms, and comorbid conditions present at the time of surgery and is not useful in predicting survival of individual patients.1
For asymptomatic AAAs, management is determined by the maximal orthogonal transverse diameter at the time of evaluation or rate of aneurysm enlargement over time. AAAs less than 4.0 cm are at low risk of rupture and should be monitored with serial imaging; those larger than 5.4 cm are at high risk of rupture and should be repaired. Surveillance is recommended for most patients in the range of 4.0 to 5.4 cm, although young healthy patients and especially women may benefit from repair in AAAs between 5.0 and 5.4 cm.1
Preoperative Planning
Anatomic measurement obtained from high-quality CT aortography, preferably reconstructed with millimeter or submillimeter slices, is paramount to successful endovascular repair. Ideally, precise diameter and path length measurements are derived from three-dimensional (3-D) reconstruction of the two-dimensional (2-D) source images (via TeraRecon™, OsiriX™, or similar software).
Precision is most essential in determining diameter throughout the surgical neck and common iliac landing zones proximal to the bilateral iliac bifurcations. Graft oversizing of 10% to 20% is typically used in the region of the surgical neck. Length measurements are obtained from the lowest renal artery to the iliac bifurcation, using path lengths, when available, from image reconstruction software noted earlier.
Multiple aortic endografts are approved for use in the United States at the current time, and device selection should be tailored to individualized anatomic requirements. Contraindications to endovascular repair may include inadequate neck length, diameter, and angulation; thrombus volume and distribution in the neck; insufficient iliac artery diameter, and excessive iliac or aortic tortuosity. It is the responsibility of the operating surgeon to ensure that for each selected device, the instructions for use (IFU) are understood and appropriate for the planned repair. Experienced operators, with careful planning, may knowingly place devices in off-label circumstances, depending on the patient-specific anatomic and physiologic risk assessment, with the expectation of reasonably long-term results. In off-label applications, however, the onus is on the surgeon to confirm that sufficient proximal and distal fixation and sealing zones exist to ensure a reasonable result.7
Femoral access must also be evaluated with ultrasound or CT imaging to determine if the patient is a candidate for percutaneous repair. The “preclose” technique (see the following text) can be used for arteriotomy closure for devices up to 21 French (Fr) in diameter. Contraindications to percutaneous repair include calcification of the anterior femoral artery wall, diameter less than 7 mm, the presence of an aneurysmal femoral artery, and excessive scaring at the access site.
The superior mesenteric artery (SMA) and celiac arteries should be examined for patency and the presence of flowlimiting stenosis or occlusion; if found, revascularization of the SMA and celiac artery should be considered prior to attempted EVAR, or open repair is considered as an alternative approach. In planning for EVAR, attention must be paid to the status of the inferior mesenteric artery and the total visceral vascularity assessed in terms of consequences of obligate inferior mesenteric artery (IMA) coverage during EVAR. Occasionally, depending on anatomic circumstances, custom fenestration or parallel grafting options may be considered as alternatives, allowing for EVAR management despite the presence of significant celiac or SMA disease. The latter options again, however, should only be considered by operators experienced in these techniques or facile with rapid open conversion when indicated to preserve intestinal perfusion.
Facilities are an essential consideration. Fixed imaging is the preferred option for procedural guidance and aortography, preferably when available in a “hybrid” operating room configuration. This is especially true when tolerances are low regarding IFU status and related anatomic considerations. Anesthesia can be either general or local with conscious sedation, depending on the habitus of the patient, their suitability for conscious sedation, and the potential likelihood of open conversion. In our practice, all patients are consented for open conversion, even though in practice this happens in less than 1% of cases.
TECHNIQUES
ENDOVASCULAR ANEURYSM REPAIR STANDARD
Percutaneous Access
Using ultrasound guidance to determine the location of the femoral bifurcation and potential presence of anterior calcified atherosclerotic plaque, bilateral common femoral arteries (CFAs) are accessed with 0.018-in micropuncture kits. Femoral arteriography is performed to confirm suitability of the selected access site within the CFA prior to serial dilation.
A 0.035-in general purpose wire (e.g., Bentson, Cook Medical, Bloomington, IN) is advanced into the aorta through the micropuncture sheath and 11-cm, 7-Fr sheaths are exchanged over the Bentson into the external iliac arteries (EIA) under continuous fluoroscopic guidance. Full intravenous anticoagulation is established with unfractionated heparin (at least 100 units/kg) and confirmed by subsequent determination of activated clotting time (ACT) greater than 250 seconds.
