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Fig. 17.1 Abdominal aortic aneurysm classication. AAAs include suprarenal, pararenal, juxtarenal, and infrarenal aneurysms, the latter of which
is most amenable to endovascular therapy
A. Lee and M. D. Dake
Thoracic Aortic Aneurysm (TAA)
Similar to the abdomen, a thoracic aortic aneurysm is a dila­tion of the vessel diameter wall greater than 50% of the normal expected size. The extent of the aneurysm can involve the aor­tic root, ascending aorta, aortic arch, and descending aorta, including distal extension into the thoracoabdominal region. Approximately 13% of patients who have had a previously treated aneurysm were found to have aneurysmal involvement of other levels of the aorta. More than half of those with tho­racic aneurysms had other vascular abnormalities, and 12% of those with abdominal aneurysms have thoracic aneurysms [28]. Overall, there is a notable increase in the incidence of TAAs over the past several decades, likely attributed to vastly improved imaging and screening [29, 30]. At the same time, there is an increased incidence of ruptured TAA due to our aging population [31]. Treatment of TAAs involves under­standing the various etiologies and risk factors of the disease process in order to provide optimal management.
The etiologies and pathogenesis differ between ascending and descending aortic aneurysms. Some studies indicate that these differences between ascending and descending aneu­rysms may be related to the differing embryologic origins of ascending aorta (neural crest cells) and descending aorta (paraxial mesoderm) smooth muscle cells [32]. Each cellular origin is predisposed to its own proteolytic factors, which initiate an inammatory cascade that converge to inltrate the vessel wall and modify the structural integrity of the aor­tic wall. Ascending aortic aneurysms most often result from medial degeneration which appears histologically as smooth muscle cell dropout and elastic ber degeneration [10]. This process leads to overall weakening of the vessel wall, leaving it susceptible to aneurysmal expansion. This is in contrast to the descending thoracic aortic in which atherosclerosis is the major contributor to aneurysm formation.
Other risk factors for TAA include risk factors for athero­sclerotic disease (hypertension and smoking), prior aortic dissection, trauma, infection, connective tissue disorders (Marfan syndrome, Loeys-Dietz syndrome, Turner syn­drome), aortic vasculitides (giant cell arteritis, Takayasu arteritis), bicuspid aortic valve, and familial thoracic aortic aneurysm syndrome.
Aneurysms of the thoracic aorta should be categorized into one of four categories based on their anatomic characteristics: ascending, arch, descending, and thoracoabdominal aneu­rysms. Ascending aneurysms arise between the aortic valve and innominate artery. Arch aneurysms include any aneurysm that involves the brachiocephalic vessels. Descending aneu­rysms arise distal to the left subclavian artery. Descending aneurysms may have a proximal extension in the arch and are classied on a zone system which is useful for treatment plan­ning (Fig.17.2). Descriptions of the specics of aortic arch interventions are beyond the scope of this chapter.
Thoracoabdominal aneurysms affect both the thoracic and abdominal aorta and are further categorized according to the Crawford classication which was modied by Sa [33]. Thoracoabdominal aortic aneurysms are categorized into ve types based on aneurysm location and extent (Fig.17.3).

Clinical Indication

Abdominal Aortic Aneurysm
Patients with AAAs are predominantly asymptomatic; the aneurysm is frequently discovered incidentally during routine physical exams and imaging studies for unrelated issues or in an AAA screening program. On physical exam, AAAs can present as a pulsatile abdominal mass. Symptomatic AAA is characterized by nonspecic abdominal, back, and/or ank
17 Abdominal andThoracic Aortic Aneurysms
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pain that can be often difcult for patients to localize. Depending on the proximal or distal extent of the aneurysm, pain can be localized to the position of the aneurysm. Patients can present with limb ischemia since the aneurysm can act as a nidus for thrombus formation and subsequent distal emboli­zation. Regardless of baseline symptoms, AAA rupture can present with severe abdominal pain and hemodynamic instability.
Elective AAA repair is the standard of care for prevention of rupture, but the risk of rupture must be balanced against potential procedural risks and postoperative complications. The primary determinant of rupture risk is maximum aneu­rysm diameter with larger aneurysms carrying the greatest risks [1316]. The observed rate of rupture for AAA <5cm is less than 5% which increases with size reaching nearly 50% with those over 8cm. The decision on when to treat and man­age asymptomatic AAA has been the subject of debate espe­cially for patient presenting with AAAs between 4.0cm and
5.4cm [12]. Data from two randomized trials clearly demon­strated no survival advantage to early repair for small AAA as compared to surveillance in participants with asymptomatic aneurysms sized 4.0–5.5 cm [1719]. For asymptomatic patients, several randomized trials comparing observation with either open or endovascular AAA repair have found that the risk of AAA rupture generally does not exceed the risk associated with AAA repair until aneurysm diameter exceeds
5.5cm [18, 2023]. These collective results from randomized trials built the foundation for the current guidelines from the Society for Vascular Surgery to offer AAA repair when diam­eter exceeds 5.5cm or if symptomatic regardless of size.
Fig. 17.2 Aortic arch zonal anatomy. Descending aortic aneurysms
can extend into the aortic arch. This extension is classied into a zone system which aids in treatment planning
Key Point
Society for Vascular Surgery guidelines for AAA repair:
• Diameter 5.5cm in men, 5.0in women
• Rapid enlargement, >0.5 cm/6 month period or >1cm/year
• Symptomatic
• Rupture
Fig. 17.3 Thoracoabdominal aortic aneurysm Crawford classication,
modied by Sa. Type I arises near the left subclavian artery and extends to the abdomen but not past the renals. Type II arises near the left subclavian and extends beyond the renals, frequently to the aortic bifurcation. This may additionally include an ascending aortic aneu-
rysm. Type III originates in the distal half of the descending aorta extending beyond the renals. Type IV extends from the diaphragmatic hiatus to the aortic bifurcation, differentiating it from a suprarenal AAA.Type V arises from the distal descending thoracic aorta and does not extend past the renals
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In addition to overall aneurysm size, the expansion rate of aortic aneurysms serves as an alternative predictor of rupture and supports the role for early intervention. Observational studies demonstrate that rapid expansion is independently associated with advanced age, smoking, severe cardiac dis­ease, and stroke [24, 25]. These patients are typically symp­tomatic which can produce vague and nonspecic abdominal discomfort. Regardless of initial diameter, these patients may benet from early repair if the aneurysm expands by >0.5cm within 6months or 1cm per year on serial imaging studies.
Based on randomized cohort data, females present with a rate of AAA rupture that is three times higher than in men after adjustment for age, body size, and initial AAA diame­ter. The mean AAA diameter preceding rupture was 6.0cm in men but only 5.0 cm in women [26, 27]. Although the impact on overall and long-term survival remains uncertain, it is reasonable to offer elective AAA repair to women with AAA of 5cm and men with AAA of 5.5cm with accept­able procedure risk.
Thoracic Aortic Aneurysm
In general, thoracic aneurysms typically exhibit no clinical symptoms. Whether by plain chest X-ray or CT imaging, they are frequently encountered when imaging for another reason. Symptoms, when they do occur, are secondary to mass effect which can include compression upon the recur­rent laryngeal nerve, tracheobronchial tree, or central veins. Aneurysm rupture and dissection can present with acute severe chest and back pain. This condition can be fatal if not identied rapidly.
When considering TAA repair, the operator should weigh the long-term benet of repair with the potential procedural risks. All societal guidelines support repair of TAAs when symptomatic, rapidly expanding, and dissecting and/or after rupture. Thoracic aortic aneurysms occur as an indolent pro­cess and tend to grow slowly at 0.1–1.0cm/year depending on the etiology; however expansion rates can exhibit vari­ability [34]. The rate of growth was noted to be greater for descending versus ascending aortic aneurysms and dissected versus non-dissected aneurysms and for those with systemic connective tissue disorders [10]. The risk for dissection and rupture correlate directly with aortic diameters. Likewise, the presence of acute symptoms, concomitant bicuspid aortic valve, connective tissue disease, or a rapidly expanding aor­tic diameter also increase the risk for potential rupture and complications [35].
The annual risk of rupture or dissection is <2% for TAAs between 4.0 and 4.9 cm with increased risk as the size increases to nearly 7% for TAAs >6.0 cm [36]. There is a signicant increase in the risk of rupture or dissection with a
diameter greater than 6.0 cm for an ascending TAA and
7.0cm for a descending TAA [37]. With aneurysm pathol­ogy, the aorta loses its inherent natural elasticity and becomes less able to withstand distention. The mechanical properties of the aneurysmal aorta deteriorate dramatically as the aorta enlarges, reaching critical levels associated with rupture by a diameter of 6cm.
For asymptomatic ascending TAA, recommendations for repair are based on an end-diastolic aortic diameter of 5–6 cm. For patients with systemic vascular disorders, a lower threshold for repair could be offered starting at 4.5cm. Similarly, for the descending aorta, repair is indicated for diameters >6cm and >5cm for those with genetically dis­posed risk factors. Other acceptable indications include rapid expansion 5–10 mm per year for aneurysms <5 cm in diameter while factoring in their etiology [38, 39].
Key Point
Guidelines for TAA repair:
• Ascending diameter >5–6cm
• Ascending diameter >4.5cm for those with vascu­lar disorders
• Descending diameter >6cm
• Descending diameter >5cm for those with vascular disorders
• Rapid enlargement >5–10mm/year
• Symptomatic
• Dissecting
• Rupture

Conventional Therapy

Abdominal Aortic Aneurysm
Before deciding on the type of intervention (medical, endo­vascular, open, or hybrid), it is important to consider the patient’s aneurysm size and location, overall clinical condi­tion, comorbidities, and functional status to determine peri­procedural risk [40]. Operator experience and hospital-related variables are known to have a profound impact on procedural outcome [41, 42].
Medical therapy is focused on preventing aortic expan­sion for aneurysms that do not meet size or growth criteria for treatment through cardiovascular risk reduction and smoking cessation. Smoking cessation should be promoted in all clinical settings to improve patient survival including improved outcomes associated with aortic repair. Likewise,
17 Abdominal andThoracic Aortic Aneurysms
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unless contraindicated, recommending a regimen of exercise, antiplatelet, statin, and antihypertensive therapies (goal SBP <120 mmHg) optimizes cardiovascular health which conse­quently improves all outcomes associated with aortic aneu­rysm repair. Other medications such as beta-blockers, angiotensin receptor blockers or angiotensin-converting enzyme inhibitors, antibiotics, and anti- inammatory agents have shown protective effects to aneurysm expansion in ret­rospective reviews and animal models, but their overall clin­ical efcacy has yet to be proven.
Open AAA repair involves replacement of the diseased aorta with prosthetic graft such as polyester (Dacron) or polytetrauoroethylene (PTFE), autogenous vein, or cadav­eric allograft. The graft diameter should complement the diameter of the native aorta to minimize size mismatch. The distal aspect of the repair depends on the distal extension of the aneurysm. If conned to the aorta, a tube graft is often used for distal anastomosis to the non-aneurysmal distal aorta; if the aneurysm extends to the iliac arteries, a bifur­cated graft can be sewn to the external iliac or femoral arter­ies. The technique has been consistently performed since it was rst described in 1952 [43].
In general, exposure to the aorta can be performed through a transabdominal or retroperitoneal approach. By utilizing a retroperitoneal incision, the suprarenal aorta can be approached with an option to extend above the celiac artery by dividing the diaphragm. Based primarily on surgeon pref­erence, this exposure also avoids previous abdominal inci­sions while lowering rates of postoperative complications and enabling quicker recovery. The transabdominal incision provides adequate exposure of pelvic vasculature including iliac arteries. Approach is frequently provider and patient specic; there are no overall noteworthy differences to either approach in affecting perioperative mortality.
Thoracic Aortic Aneurysm
The earliest report of open thoracic aneurysm repair dates back to 1951 when Lam and Aram reported the resection of a descending thoracic aneurysm with allograft replacement [44]. Similar to AAA management, a thorough preoperative risk assessment including clinical status, comorbidities, and functional status should be evaluated. Evaluation may include pulmonary function testing, echocardiogram with valvular and left ventricular function, and cardiac catheter­ization for staging of coronary artery disease [45].
The surgical approach is dependent entirely on the extent of aneurysm involvement and the presence of healthy native tissue. Exposure can be gained via a sternotomy or left poste­rior lateral approach. TAA repair typically requires placing the patient on cardiopulmonary bypass often with a cardiople­gia-arrested heart. There is expected organ ischemic time depending on which visceral branches are involved. Selective shunts along with circulatory arrest and hypothermic (32°C) conditions can minimize interruption of ow and tissue injury. The diseased aorta is replaced, while the visceral branches are sewn to a Dacron conduit. The aortic cross clamp is sequen­tially advanced distally after each reimplantation.

Interventional Therapy

Abdominal Aortic Aneurysm
Endovascular AAA repair (EVAR) has been a revolutionary advancement in the treatment of AAA (Fig. 17.4). First reported by Parodi etal., this less invasive and modular aortic repair system involves delivering stent grafts from the access vessel(s), usually from the common femoral artery [46].
Fig. 17.4 Infrarenal AAA measuring 5.6cm. (a) 3-D reformatting of
CT angiography with TeraRecon software shows a 3-D rendering of the infrarenal AAA (top left). The largest aneurysmal dimension measures
5.6cm (bottom left). TeraRecon reformatting straightens the tortuosity of the vessels using a center line to aid in graft measurements and branch vessel visualization (right). (b) Aortogram with Endurant (Medtronic) stent graft in position via the right iliac limb. A marking
pigtail can be seen advanced through the left iliac limb. (c) After deployment of the stent graft, proximal balloon molding with a Coda balloon (Cook Medical, Bloomington, IN) is performed to better appose stent graft to aortic wall. (d) Completion aortogram showing patent renal and internal iliac arteries status post endograft placement. No endoleak can be seen
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Deployment of the stent creates a conduit within the aorta using a stent covered in low-porosity graft material, sealed by outward force at the proximal and distal contact points in order to completely exclude blood ow to the aneurysmal sac. The use of EVAR compared to open repair has been stud­ied across three randomized trials; EVAR clearly exhibited lower perioperative and short-term (<30days) morbidity and mortality than open surgical repair [47]. Despite the lower initial complication rate, EVAR does require far more sec­ondary procedures during the lifetime of the graft; the major­ity of these procedures can be performed by endovascular approaches. Since the introduction of endovascular repair, the annual number of deaths from ruptured AAA has also signi­cantly decreased, coinciding with an increase in intact treated AAAs and a decrease in ruptured AAA diagnoses [48]. Although an appealing and relatively safe option for AAA repair, the drawback of EVAR is the strict anatomic criterion that is required to yield the most optimal outcome (Table17.1).
Table 17.1 Aortoiliac anatomical conditions for endovascular AAA
repair [51]
Structure Parameters and range Aortic neck Diameter 18–32mm Length >10–15mm Angulation <45–60° Common iliac artery Length >20mm Diameter 8–22mm Minimal calcication and tortuosity External iliac artery Diameter >7mm Minimal calcication and tortuosity
This emphasizes the importance of preoperative planning and understanding the relationship between the anatomical char­acteristic of the aorta, technical limits, and properties of the endograft.
Thoracic Aortic Aneurysm
The availability of minimal invasive treatment for thoracic aortic aneurysms has gained wide recognition because of the observed improvement in patient outcomes, particularly in the high-risk cohort (Fig.17.5). As early as 1994, Dake et al. rst reported the use of thoracic stent grafts for the treatment of descending thoracic aortic aneurysms in patients who were believed to be at excessive risk for con­ventional open surgery [49]. Current data from nonrandom­ized studies suggest that endovascular repair reduces perioperative mortality, neurological morbidity, renal insuf­ciency, and cardiac complications compared to open sur­gery [50, 51]. With fewer overall complications, primary technical success was highly achievable across many reported series. Despite the promising results, endoleaks (6–9%) and re-interventions (2%) are higher in the endovas­cular group versus open surgical repair group up to 2years posttreatment [52]. In an early series of 84 patients, major procedure-related or device-related complications occurred in 38%, including proximal attachment failure (8%), distal attachment failure (6%), mechanical device failure (3%), periprocedural death (6%), and late aneurysm rupture (6%) [53]. With various commercially available endovascular grafts, each stent carries their own respective advantages in regard to prole and ease of delivery, accuracy of deploy­ment, and exible conformation; despite this, there is no
Fig. 17.5 Descending TAA measuring 5.5 cm aneurysm. (a) 3-D
reformatting of CT angiography with TeraRecon software shows a short descending aortic aneurysm (top left). The largest aneurysmal dimen­sion measures 5.5cm (bottom left). With assistance of center line mea­surements, precise lengths of stent graft can be obtained while
accounting for visceral branches (right). (b) With device in place, left anterior oblique aortogram delineates the aneurysm and proximal and distal landing zone. (c) The Zenith Alpha (Cook Medical) thoracic stent graft was deployed across the aneurysm. Post-deployment angiogram demonstrates no evidence of endoleak and a preserved celiac artery
17 Abdominal andThoracic Aortic Aneurysms
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clear advantage between available devices. Compared with open surgery, thoracic aortic endovascular repair (TEVAR) provides much lower perioperative morbidity and mortality rates, but clearly, technical renements need to be made before it can become a routine treatment for TAA extending into the aortic arch or the abdominal viscera [10]. Graft sur­veillance is also important during the postoperative period to monitor stent behavior and progression of the patients’ underlying disease to prevent complications.
Planning andKey Concepts forEndovascular Repair
• Upon initial evaluation, most interventionalists advocate for dedicated high-quality aortic CT arteriography (CTA) imaging of the torso at <2.5mm slices to better delineate the aortic anatomy for specications and device selection. Additionally, three-dimensional imaging with specialized software (TeraRecon) processing can provide exact iden­tication of visceral or side branches, angulation, extent of vessel calcication, presence of intraluminal thrombus, and vessel diameters. The access sites including the iliac and femoral arteries need to be evaluated to determine safety of stent delivery and avoid iliac rupture or disrup­tion. At times, endovascular or surgical conduits are needed when iliac arteries are too diseased for safe deliv­ery of endografts.
• The proximal and distal landing zones for the stent must be thoroughly interrogated to ensure adequate stent cov­erage for full aneurysm exclusion. In general, choosing an aortic graft with approximately 15–20% oversizing to the aortic diameter is recommended to ensure coverage and enough outward radial force to prevent stent migration. Signicant oversizing (>20%) can cause excessive stent material fabric to kink and blood can leak around the graft, incompletely excluding the aneurysm and increas­ing the risk of retrograde aortic dissection. Undersizing will yield an inferior repair and increased risk of stent migration, endoleak, and need for additional and unnec­essary interventions.
– For AAA, stent coverage should include the entire aor-
toiliac region from below the renal arteries to the iliac bifurcation.
– For TEVAR, the stent graft should span the aneurysm
while obtaining approximately a 2-cm seal at the prox­imal and distal end points. Depending on aneurysmal location, bypassing supraaortic or visceral branching vessels may need to be performed as a staged proce­dure before endovascular treatment.
• With continued advancements in technological devices, it is important to understand the anatomical indications and be reasonably comfortable with using a particular stent
graft during endovascular aneurysm repair. Each endo­graft has its own individual advantage depending on spe­cic patient anatomic situations and operator preference. The instructions for use (IFU) are published parameters that are set forth by the device company and designed for optimal graft usage. Careful preoperative sizing and plan­ning with adherence to device design specications will yield the best technical and patient outcomes [54].
• These cases are typically performed with general anesthe­sia to allow for continuous hemodynamic monitoring.
The How To
1. Preoperative imaging will determine whether per-
cutaneous or open femoral access is optimal. Percutaneous access should be obtained at the level of the femoral head which can be marked
­ral artery is accessed via the Seldinger technique, frequently using ultrasound guidance. Alternatively, open exposure of the femoral arter­ies can be performed, puncture is then performed under direct visualization, and a 0.035” guidewire is advanced into the aorta.
2. If percutaneous access is possible, a pre-closure technique using ProGlide Suture-Mediated Closure System (Abbott, Abbott Park, IL) is placed at the initiation of the procedure to facili­tate closure of the arteriotomy sites after the case. Typically for larger sheaths (
8F), two ProGlide devices will be placed to close the arteriotomy safely. The process is repeated for the contralateral access site depending on anticipated sheath size.
3. Throughout the procedure the patient should be adequately heparinized to minimize the risk of thrombosis. Typically, an intravenous bolus of 80–100 units per kg is given after arterial access is safely obtained and additional doses are given to
4. The preoperative CTA is used to determine which femoral artery will be the primary device side. The contralateral side will initially hold the pigtail or similar multi-side-hole injection catheter.
5. The existing guidewire on the primary device side should be exchanged for a stiff working wire to facilitate passage of large bore sheaths and devices.
6. An aortogram is performed through a contralateral side pigtail or Omni Flush catheter for procedural
7. Device advancement and positioning:
(continued)
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A. Lee and M. D. Dake
(a) For EVAR, place an Omni Flush catheter
from the contralateral groin at the L1 region of the vertebral spine, and position the image
undeployed endograft and renal arteries.
(b)For TEVAR, change the angle of the detector
end of the endograft and best visualize arch vessels.
8. Aortogram: (a)For EVAR, identify the renal arteries and
position graft just distal to the lowest renal artery. Sometimes accessory renal arteries will intentionally be covered to allow ade­quate proximal seal zone.
(b) For TEVAR, identify location of the aneurysm
and position graft for optimal seal. Depending on the length of the aneurysm, additional grafts may be overlapped to extend coverage distally
9. Device deployment EVAR: (a) Deploy main body until contralateral gate is
opened. Hold device in place.
(b) Cannulate the contralateral gate from contra-
lateral femoral access with an appropriately
main body and not behind or in front of it by
trast, or spinning a pigtail catheter.
(c) Perform a retrograde arteriogram from contra-
lateral femoral introducer sheath with catheter containing 1-centimeter markings to measure the length of the iliac limb, accounting for
required due to differences in the diameter of the proximal and distal landing zones.
(b)
of this chapter.
11. Balloon molding with a compliant balloon is performed on the proximal aortic seal zone, over­lapping regions, and distal end points.
12. Completion aortogram is performed to evaluate for endoleak (refer to Chap. 19 for more informa­tion on endoleaks).
13. Percutaneous closure of groin sites with ProGlide devices.
Common Complications
Key Point
Pearls to minimize post-procedural complications:
1. Identify and evaluate site of access to decide on
need for open or endovascular conduits.
2. Always ensure adequate anticoagulation during the
procedure to prevent thrombotic events.
3. Always maintain wire access with good wire
-
hygiene during catheter or wire exchanges. This can avoid unnecessary radiation and contrast use.
4. Have different sizes available in case of unforeseen
events that will require additional pieces.
5. Always check distal pulses at the end of the case.
divider.
(d) Position the iliac limb into the aortic main
body graft with deployment extending just proximal to the internal iliac artery.
(e) Complete deployment of aortic main body
graft and ipsilateral iliac limb. This limb is often short of the internal iliac artery. Sometimes the internal iliac artery will be intentionally covered to ensure adequate seal.
(f)
limb with retrograde arteriogram to identify iliac bifurcation. Determine length of iliac limb extension for appropriate overlap and dis­tal seal while preserving the hypogastric artery.
10. Device deployment TEVAR: (a)Device planning often includes multiple-sized
devices and sometimes tapered devices. Careful planning to deliver multiple devices is
Access
Compared to open surgical repair, endovascular approaches are associated with high technical success with lower com­plication rates. The majority of early complications result from access-related issues including hematoma, pseudoaneu­rysm or arteriovenous stula formation, thrombosis, and dis­section. Atherosclerotic vessels cannot tolerate the driving force of these large sheaths, which can cause signicant ves­sel trauma and rupture. Severely diseased iliac and femoral arteries may require adjunctive interventions such as angio­plasty, stenting, or endovascular or surgical graft conduits to allow safe passage of larger bore sheaths. Radial expanding sheaths can also be used in undersized iliac artery to prevent iliac artery trauma. Based on preoperative imaging, these interventions can be anticipated and planned ahead.
Access-related bleeding can also present in a delayed fashion and lead to hemorrhagic shock from retroperitoneal hemorrhage. This can be mitigated by accessing at the level of the femoral head so that appropriate pressure can be held
17 Abdominal andThoracic Aortic Aneurysms
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following the procedure. From a systematic review, access­related complications occurred in 4.4% of patients, a rate that was signicantly lower compared with open femoral access (relative risk [RR] 0.47, 95% CI 0.28–0.78) [55]. This emphasizes the importance of preoperative planning and appropriate patient selection.
Endoleaks (Refer toChap. 19 forMore Information)
Endoleaks occur when there is persistent blood ow into the aneurysmal sac despite endovascular coverage.
Contrast Nephropathy
Renal complications after TAA and AAA repair have been linked to increased patient morbidity and mortality. Prior to any intervention whether open or endovascular, it is impor­tant to identify those patients at risk by assessing preopera­tive renal function. Although clinical utility remains unclear, it still remains common practice to be conservative in patients with borderline renal function or a preoperative GFR<60mL/ min/1.73m
2
. Home medications that can be nephrotoxic or vasoconstrictive should be held preoperatively. These patients can be treated with hydration, bicarbonate infusion, and/or Mucomyst prior to their procedure for renal protec­tion. Overall contrast volume should be minimized and iso­osmolar contrast agents can be utilized [56]. Further studies noted that deterioration of renal function was independently associated with age >70years in all patients (RR 2.92) dur­ing long-term follow-up of 23.2months [57]. Retrospective studies have shown that renal complications were strongly associated with 30-day mortality [58].
Spinal Cord Ischemia
This complication is almost exclusively associated with TEVAR rather than EVAR.Although both open and endo­vascular thoracic aneurysm repair exhibit a risk for spinal cord ischemia, studies have demonstrated lower rates with TEVAR.Across the literature, rates of spinal cord ischemia following thoracic aortic surgery have been reported to be as high as 29% but average 10–11% [59]. In the periopera­tive setting, the spinal cord is extremely sensitive to uctua­tions in blood pressure. Any decreases in blood pressure can affect perfusion to the spinal and intercostal arteries because of graft coverage, ligation, or embolization. Additional risk factors include advanced age, aortic rupture, prior aortic surgery, postoperative bleeding, intraoperative hypotension, and renal insufciency [60, 61]. To mitigate this risk, place­ment of somatosensory evoked potential monitoring and a lumbar drain allow for perioperative monitoring and increased spinal cord perfusion. During TEVAR, the extent of aortic coverage is the major risk factor for spinal cord ischemia. Interventions directed at increasing spinal cord perfusion by increasing systemic blood pressure and
decreasing CSF pressure were effective for the reversal of delayed onset of paraplegia after thoracic aneurysm repair, resulting in an overall 3% incidence of permanent paraple­gia and 3% incidence of residual paraparesis for endovascu­lar cases [62].
Postoperative Monitoring
Following uncomplicated endovascular repair, patients are frequently discharged after 24h. Fluids are typically contin­ued to counter contrast nephropathy. Diets can be safely resumed and advanced as tolerated. Peripheral pulses are checked throughout the hospital course to evaluate for distal perfusion. Routine postoperative surveillance is important to both monitor the graft as well as the excluded aneurysmal sac. A multiphase CTA is performed at 1month to evaluate for endoleak or other device- related complications. Depending on the imaging results, subsequent intervention or additional follow- up surveillance imaging can then be arranged. Imaging follow-up is provider specic but fre­quently performed at 1, 3, 6, and 12months post-procedur­ally followed by annually thereafter. To minimize costs, aortic ultrasound is an acceptable replacement for CTA but is highly technician dependent. It is important for patients to continue their antiplatelet and statin medications as part of their regimen to promote cardiovascular health.

References

1. Johnston KW, Rutherford RB, Tilson MD, Shah DM, Hollier L, Stanley JC. Suggested standards for reporting on arterial aneu­rysms. Subcommittee on reporting standards for arterial aneu­rysms, Ad Hoc committee on reporting standards, Society for vascular surgery and North American chapter, International society for cardiovascular surgery. JVasc Surg. 1991;13:452.
2. Brown PM, Pattenden R, Vernooy C, Zelt DT, Gutelius JR.Selective management of abdominal aortic aneurysms in a prospective mea­surement program. JVasc Surg. 1996;23(2):213–20.
3. Bown MJ, Sutton AJ, Bell PR, Sayers RDA.Meta-analysis of 50 years of ruptured abdominal aortic aneurysm repair. Br J Surg. 2002;89:714.
4. Hoornweg LL, Storm-Versloot MN, Ubbink DT, Koelemay MJ, Legemate DA, Balm R.Meta-analysis on mortality of rup­tured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg. 2008;35:558.
5. Parkinson F, Ferguson S, Lewis P, Williams IM, Twine CP.South East Wales vascular network. Rupture rates of untreated large abdominal aortic aneurysms in patients unt for elective repair. J Vasc Surg. 2015;61(6):1606–12. https://doi.org/10.1016/j.
jvs.2014.10.023. Epub 2015 Feb 7. Review.
6. Karrowni W, Dughman S, Hajj GP, Miller FJ Jr. Statin therapy reduces growth of abdominal aortic aneurysms. J Investig Med. 2011;59(8):1239–43.
7. Golledge J, Muller J, Daugherty A, Norman P. Abdominal aor­tic aneurysm: pathogenesis and implications for management. Arterioscler Thromb Vasc Biol. 2006;26(12):2605–13. Epub 2006 Sep 14. Review.
8. Kotze CW, Ahmed IG. “Etiology, pathogenesis and pathophysi­ology of aortic aneurysms.” Etiology and pathogenesis of aortic
206
A. Lee and M. D. Dake
aneurysms, and aneurysm rupture edited by Reinhart Grundmann, Intech, 2011, 1–22. www.intechopen.com.
9. Xu J, Shi GP.Vascular wall extracellular matrix proteins and vas­cular diseases. Biochem Biophys Acta. 2014;1842(11):2106–19.
https://doi.org/10.1016/j.bbadis.2014.07.008. Epub 2014 Jul 18.
10. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation. 2005;111(6):816–28.
11. Lee AM, Chaikof EL.Is the abdominal aortic aneurysm rupture rate decreasing? Adv Surg. 2013;47:271–86.
12. Chaikof EL, Brewster DC, Dalman RL, Makaroun MS, Illig KA, Sicard GA, etal. Society for vascular surgery. The care of patients with an abdominal aortic aneurysm: the society for vascular surgery practice guidelines. JVasc Surg. 2009;50(4 Suppl):S2–49.
13. Baxter BT, Terrin MC, Dalman RL.Medical management of small abdominal aortic aneurysms. Circulation. 2008;117(14):1883–9.
14. Evans GH, Stansby G, Hamilton G.Suggested standards for report­ing on arterial aneurysms. JVasc Surg. 1992;15(2):456.
15. Fillinger M. Who should we operate on and how do we decide: predicting rupture and survival in patients with aortic aneurysm. Semin Vasc Surg. 2007;20(2):121–7.
16. Darling RC.Ruptured arteriosclerotic abdominal aortic aneurysms. A pathologic and clinical study. Am JSurg. 1970;119(4):397–401.
17. Lall P, Gloviczki P, Agarwal G, Duncan AA, Kalra M, Hoskin T, etal. Comparison of EVAR and open repair in patients with small abdominal aortic aneurysms: can we predict results of the PIVOTAL trial? JVasc Surg. 2009;49(1):52–9.
18. Cao P, De Rango P, Verzini F, Parlani G, Romano L, Cieri E, CAESAR Trial Group. Comparison of surveillance versus aortic endografting for small aneurysm repair (CAESAR): results from a randomised trial. Eur JVasc Endovasc Surg. 2011;41(1):13–25.
19. Filardo G, Powell JT, Martinez MA, Ballard DJ.Surgery for small asymptomatic abdominal aortic aneurysms. Cochrane Database Syst Rev. 2012;3:CD001835.
20. UK Small Aneurysm Trial Participants. Mortality results for ran­domised controlled trial of early elective surgery or ultrasono­graphic surveillance for small abdominal aortic aneurysms. Lancet. 1998;352:1649.
21. Lederle FA, Wilson SE, Johnson GR, Reinke DB, Littooy FN, Acher CW, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl JMed. 2002;346:1437.
22. Ouriel K, Clair DG, Kent KC, Zarins CK. Positive impact of endovascular options for treating aneurysms early (PIVOTAL) investigators. Endovascular repair compared with surveillance for patients with small abdominal aortic aneurysms. JVasc Surg. 2010;51:1081.
23. United Kingdom EVAR Trial Investigators, Greenhalgh RM, Brown LC, et al. Endovascular repair of aortic aneurysm in patients physically ineligible for open repair. N Engl J Med. 2010;362:1872.
24. Brewster DC, Cronenwett JL, Hallett JW Jr, Johnston KW, Krupski WC, Matsumura JS, Joint Council of the American Association for Vascular Surgery and Society for Vascular Surgery, et al. Guidelines for the treatment of abdominal aortic aneurysms. Report of a subcommittee of the joint council of the American association for vascular surgery and society for vascular surgery. JVasc Surg. 2003;37(5):1106–17.
25. Chang JB, Stein TA, Liu JP, Dunn ME. Risk factors associated with rapid growth of small abdominal aortic aneurysms. Surgery. 1997;121(2):117–22.
26. Brown LC, Powell JT, UK Small Aneurysm Trial Participants. Risk factors for aneurysm rupture in patients kept under ultrasound sur­veillance. Ann Surg. 1999;230(3):289–96.
27. Lederle FA.Should abdominal aortic aneurysm be managed differ­ently in women? Scand JSurg. 2008;97(2):125–7.
28. Crawford ES, Cohen ES. Aortic aneurysm: a multifocal disease. Presidential address. Arch Surg. 1982;117(11):1393–400.
29. Elefteriades JA. Indications for aortic replacement. J Thorac Cardiovasc Surg. 2010;140(6 Suppl):S5–9.; discussion S45-51.
https://doi.org/10.1016/j.jtcvs.2010.10.001.
30. von Allmen RS, Anjum A, Powell JT.Incidence of descending aor­tic pathology and evaluation of the impact of thoracic endovascu­lar aortic repair: a population-based study in England and Wales from 1999 to 2010. Eur JVasc Endovasc Surg. 2013;45(2):154–9.
https://doi.org/10.1016/j.ejvs.2012.12.007. Epub 2012 Dec 29.
31. Acosta S, Ogren M, Bengtsson H, Bergqvist D, Lindblad B, Zdanowski Z. Increasing incidence of ruptured abdomi­nal aortic aneurysm: a population-based study. J Vasc Surg. 2006;44(2):237–43.
32. Tsamis A, Krawiec JT, Vorp DA.Elastin and collagen bre micro­structure of the human aorta in aging and disease: a review. JR Soc Interface. 2013;10:20121004.
33. Sa HJ, Winnerkvist A, Miller CC 3rd, Iliopoulos DC, Reardon MJ, Espada R, Baldwin JC.Effect of extended cross-clamp time during thoracoabdominal aortic aneurysm repair. Ann Thorac Surg. 1998;66(4):1204–9.
34. Elefteriades JA, Farkas EA. Thoracic aortic aneurysm clinically pertinent controversies and uncertainties. J Am Coll Cardiol. 2010;55(9):841–57. https://doi.org/10.1016/j.jacc.2009.08.084.
35. Davies RR, Gallo A, Coady MA, Tellides G, Botta DM, Burke B, etal. Novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg. 2006;81:169.
36. Davies RR, Goldstein LJ, Coady MA, Tittle SL, Rizzo JA, Kopf GS, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg. 2002;73:17.
37. Coady MA, Rizzo JA, Hammond GL, Mandapati D, Darr U, Kopf GS, etal. What is the appropriate size criterion for resection of tho­racic aortic aneurysms? JThorac Cardiovasc Surg. 1997;113:476.
38. Hiratzka LF, Creager MA, etal. Surgery for aortic dilatation in patients with bicuspid aortic valves: A statement of clarifi­cation from the American college of cardiology/american heart association task force on clinical practice guidelines. J Am Coll Cardiol. 2016;133:680. 2010 ACCF/AHA/AATS/ACR/ ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients with Thoracic Aortic Disease Representative Members*.
39. Lobato AC, Puech-Leão P.Predictive factors for rupture of thora­coabdominal aortic aneurysm. JVasc Surg. 1998;27:446.
40. Tambyraja AL, Murie JA, Chalmers RT.Prediction of outcome after abdominal aortic aneurysm rupture. JVasc Surg. 2008;47(1):222–
30. Epub 2007 Oct 24.
41. Dueck AD, Kucey DS, Johnston KW, Alter D, Laupacis A.Survival after ruptured abdominal aortic aneurysm: effect of patient, sur­geon, and hospital factors. JVasc Surg. 2004;39:1253–60.
42. Lovricevic I, Despot I, DeSyo D, etal. Ruptured abdominal aortic aneurysms–Ten-year experience: review of results and prognostic factors. Acta Clin Croat. 2000;39:33–9.
43. Dubost C, Allary M, Oeconomos N.Resection of an aneurysm of the abdominal aorta: reestablishment of the continuity by a pre­served human arterial graft, with result after ve months. AMA Arch Surg. 1952;64(3):405–8.
44. Lam CR, Aram HH. Resection of the descending thoracic aorta for aneurysm; a report of the use of a homograft in a case and an experimental study. Ann Surg. 1951;134(4):743–52.
45. Mastroroberto P, Chello M. Emergency thoracoabdominal aor­tic aneurysm repair: clinical outcome. JThorac Cardiovasc Surg. 1999;118(3):477–81. discussion 481-2.
46. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg. 1991;5(6):491–9.
47. Schermerhorn ML, Bensley RP, Giles KA, Hurks R, Oʼmalley AJ, Cotterill P, et al. Changes in abdominal aortic aneurysm rupture
17 Abdominal andThoracic Aortic Aneurysms
207
and short-term mortality, 1995-2008: a retrospective observational study. Ann Surg. 2012;256(4):651–8.
48. Giles KA, Hamdan AD, Pomposelli FB, Wyers MC, Dahlberg SE, Schermerhorn ML. Population-based outcomes following endo­vascular and open repair of ruptured abdominal aortic aneurysms. JEndovasc Ther. 2009;16(5):554–64.
49. Dake MD, Miller DC, Semba CP, Mitchell RS, Walker PJ, Liddell RP. Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl JMed. 1994;331(26):1729–34.
50. Walsh SR, Tang TY, Sadat U, Naik J, Gaunt ME, Boyle JR, etal. Endovascular stenting versus open surgery for thoracic aortic dis­ease: systematic review and meta-analysis of perioperative results. JVasc Surg. 2008;47:1094.
51. Cheng D, Martin J, Shennib H, Dunning J, Muneretto C, Schueler S, etal. Endovascular aortic repair versus open surgical repair for descending thoracic aortic disease a systematic review and meta­analysis of comparative studies. JAm Coll Cardiol. 2010;55:986.
52. Bavaria JE, Appoo JJ, Makaroun MS, Verter J, ZF Y, Mitchell RS, Gore TAG Investigators. Endovascular stent grafting versus open surgical repair of descending thoracic aortic aneurysms in low-risk patients: a multicenter comparative trial. JThorac Cardiovasc Surg. 2007;133:369.
53. Ellozy SH, Carroccio A, Minor M, Jacobs T, Chae K, Cha A, etal. Challenges of endovascular tube graft repair of thoracic aortic aneurysm: midterm follow-up and lessons learned. J Vasc Surg. 2003;38(4):676–83.
54. Schanzer A, Greenberg RK, Hevelone N, Robinson WP, Eslami MH, Goldberg RJ, et al. Predictors of abdominal aor­tic aneurysm sac enlargement after endovascular repair. Circulation. 2011;123(24):2848–55. https://doi.org/10.1161/
CIRCULATIONAHA.110.014902. Epub 2011 Apr 10. Erratum in:
Circulation. 2012 Jan 17;125(2):e266.
55. Malkawi AH, Hinchliffe RJ, Holt PJ, Loftus IM, Thompson MM. Percutaneous access for endovascular aneurysm repair: a systematic review. Eur JVasc Endovasc Surg. 2010;39(6):676–82.
https://doi.org/10.1016/j.ejvs.2010.02.001. Epub 2010 Feb 24.
56. Surowiec SM, Davies MG, Fegley AJ, Tanski WJ, Pamoukian VN, Sternbach Y, etal. Relationship of proximal xation to postopera­tive renal dysfunction in patients with normal serum creatinine con­centration. JVasc Surg. 2004;39(4):804–10.
57. Mills JL, Duong ST, Leon LR Jr, Goshima KR, Ihnat DM, Wendel CS, etal. Comparison of the effects of open and endovascular aortic aneurysm repair on long-term renal function using chronic kidney disease staging based on glomerular ltration rate. J Vasc Surg. 2008;47(6):1141–9. https://doi.org/10.1016/j.jvs.2008.01.039.
58. Zettervall SL, Ultee KH, Soden PA, Deery SE, Shean KE, Pothof AB, et al. Predictors of renal dysfunction after endovascular and open repair of abdominal aortic aneurysms. J Vasc Surg. 2017;65(4):991–6. https://doi.org/10.1016/j.jvs.2016.06.113. Epub 2016 Sep 26.
59. Messé SR, Bavaria JE, Mullen M, Cheung AT, Davis R, Augoustides JG, etal. Neurologic outcomes from high risk descending thoracic and thoracoabdominal aortic operations in the era of endovascular repair. Neurocrit Care. 2008;9(3):344–51. https://doi.org/10.1007/
s12028-008-9104-9.
60. Cambria RP, Clouse WD, Davison JK, Dunn PF, Corey M, Dorer D.Thoracoabdominal aneurysm repair: results with 337 operations performed over a 15-year interval. Ann Surg. 2002;236:471.
61. McGarvey ML, Cheung AT, Szeto W, Messe SR. Management of neurologic complications of thoracic aortic surgery. J Clin Neurophysiol. 2007;24:336.
62. Cheung AT, Weiss SJ, McGarvey ML, Stecker MM, Hogan MS, et al. Interventions for reversing delayed- onset postoperative paraplegia after thoracic aortic reconstruction. Ann Thorac Surg. 2002;74:413.