Management of Thoracoabdominal Aortic Aneurysms

Chapter Management of Thoracoabdominal Aortic Aneurysms Yuki Ikeno, Akiko Tanaka and Anthony L. Estrera Abstract Thoracoabdominal aortic aneurysms (TAAA) represent a unique pathology that is associated with significant mortality if left untreated. TAAA most commonly present in combination wit...

Chapter Management of Thoracoabdominal Aortic Aneurysms Yuki Ikeno, Akiko Tanaka and Anthony L. Estrera Abstract Thoracoabdominal aortic aneurysms (TAAA) represent a unique pathology that is associated with significant mortality if left untreated. TAAA most commonly present in combination with multiple comorbidities of the heart, kidneys, and peripheral vascular systems. Optimal treatment of TAAA remains a complex challenge, with ultimate success requiring a coordinated effort from a multidisciplinary team. This chapter provides a comprehensive approach to the diagnosis and management of TAAA, as well as insight into the recent surgical paradigms and advances in organ protection, spotlighting the latest surgical outcomes and the evolution of techniques that have markedly improved patient care in this complex field. Keywords: thoracoabdominal aortic aneurysms, TAAA, CSF drainage, endovascular, aortic surgery, Crawford classification 1. Introduction A landmark in aortic surgery was achieved by Etheredge and colleagues in 1955 with the first successful repair of a thoracoabdominal aortic aneurysm (TAAA) using a homograft tube. The following year, another groundbreaking development was achieved when DeBakey and his team employed a Dacron tube graft for the replace- ment of the descending thoracic aorta and infrarenal abdominal aorta. Later, Crawford and associates introduced a method subsequently known as the clamp-and- go technique. This approach encapsulated three basic principles of aortic surgery: the inclusion technique; the utilization of a Dacron tube graft as a conduit; and reimplan- tation of visceral and renal arteries. Historically, TAAA repair necessitated rapid execution to mitigate prolonged organ ischemia. Over time, TAAA surgery has been transformed with the use of adjuncts aimed at enhancing organ protection and improving overall outcomes. As a result, the surgical outcomes for TAAA repair have improved dramatically, ensuring favorable long-term survival compared to the untreated cohort (Figure 1). These pioneering efforts have significantly shaped the landscape of aortic surgery, provid- ing a robust framework for the management and surgical correction of complex aortic aneurysms. However, further enhancements of these surgical outcomes remain. 1 Aortic Aneurysms – Screening, Diagnostics and Management Figure 1. Thoracoabdominal aortic aneurysm: comparison of survival rates in untreated patients versus surgically treated patients. 2. Natural history Aortic aneurysm disease remains a significant cause of death in the United States. Advancement in diagnostic imaging modalities, aging population, and overall heightened awareness all contribute to an apparent increase in the prevalence of aortic aneurysms. Nevertheless, the annual repair rate of TAAAs, which involve both the thoracic and abdominal aorta, is less than 1000 cases, compared to approximately 50,000 repairs for infrarenal abdominal aortic aneurysms. The prevalence of abdomi- nal aortic aneurysms is estimated to range from 2.3% to 10.7%, with this variation contingent upon the demographic characteristics of the studied population and the criteria defining aneurysm size [4, 5]. On the other hand, the incidence rate of TAAAs is approximately 10.4 cases per 100,000 person-years. Furthermore, the average age of patients diagnosed with TAAA ranges from 59 to 69 years, exhibiting a male- to-female predominance ratio ranging from 2:1 to 4:1 [7 ]. Aneurysm disease occurs in more than one part of the aorta in approximately 20% of cases. The so-called “mega” aorta is an “extensive” aortic aneurysm involving the ascending, transverse arch, and entire thoracoabdominal aorta. Less than 40% of individuals with untreated TAAA survive more than 5 years, with the majority of these deaths attributable to aneurysm rupture. Studies focus- ing on TAAAs have demonstrated an increased likelihood of rupture in aneurysms exceeding 5 cm in diameter, with the risk of rupture escalating in proportion to the size of the aneurysm [8, 9]. The median diameter at which TAAAs typically rupture is approximately 7 cm. Aneurysms that are 8 cm or larger carry an 80% risk of rupturing within a year of their diagnosis. The lifetime risk of rupture for any untreated aortic aneurysm is estimated to be between 75 and 80%. The average rate of growth for TAAAs is noted to be between 0.10 and 0.42 cm annually, with aneurysms larger than 5 cm exhibiting an exponential increase in growth rate [12, 13]. 3. Pathogenesis An aortic aneurysm is delineated as a localized or diffuse enlargement exceed- ing 50% of the normal diameter of the aorta. Predominantly, TAAAs are of a 2 Management of Thoracoabdominal Aortic Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.1005225 degenerative nature, sharing similar pathologies with the more frequently encoun- tered infrarenal abdominal aortic aneurysms. Historically, arteriosclerosis has been implicated in the etiology of aortic aneurysm formation. Nonetheless, arterioscle- rosis predominantly influences the intimal layer, often leading to occlusive disease, whereas aneurysm pathogenesis typically involves the medial and adventitial layers. From a histological perspective, degenerative aortic aneurysms are characterized by medial thinning, disruption of smooth muscle cells and elastin, infiltration by inflammatory cells, and neovascularization [14–16]. A consistent histological feature is a chronic inflammatory infiltrate in the aneurysm wall’s outer layer, comprising macrophages, T cells, and B cells. The extent of this inflammation varies, and the catalyst for cellular migration remains elusive. These inflammatory cells, particularly macrophages, secrete proteases and elastase, which contribute to the degradation of the aortic wall. Elastin degradation products may further act as chemotactic agents, attracting additional inflammatory cells. The role of matrix metalloproteinases (MMPs), particularly elastases such as MMP2, MMP9, and MMP12, in the develop- ment of aortic aneurysms, has been corroborated by both clinical and experimental research. These elastases have been identified in increased concentrations in the tissue of aortic aneurysms, suggesting their significant involvement in aneurysm pathogenesis [14, 17–19]. Approximately 25% of TAAAs are associated with chronic aortic dissection. An estimated 20–40% of patients will develop aneurysms in the thoracoabdominal aorta within 2–5 years following acute aortic dissection [20–22]. There is a notable familial aggregation in aortic dissections, as evidenced by the fact that up to 20% of individu- als with ascending thoracic aortic aneurysms—a precursor to aortic dissections—have at least one first-degree relative similarly afflicted [23–25]. Marfan syndrome, typi- fied by a constellation of skeletal, ocular, and cardiovascular anomalies, stands as the predominant hereditary connective tissue disorder associated with aortic aneurysm and dissection. This syndrome manifests globally at an incidence rate of approxi- mately 1 in 5000–10,000 individuals. The aortic dilatation noted in Marfan patients is often attributed to mutations in the fibrillin-1 protein, which is encoded by the FBN1 gene. Several other genetic syndromes predisposing individuals to TAAA and dissec- tion have been recognized, including Loeys-Dietz syndrome, Ehlers-Danlos syn- drome, Turner syndrome, and polycystic kidney disease [26–28]. To date, four genes have been identified as contributing to familial thoracic aortic aneurysms and dissec- tions, accounting for approximately 20% of these familial conditions. Mutations in the smooth muscle isoform of alpha-actin, encoded by the ACTA2 gene, are impli- cated in about 15% of familial aortic diseases. Other genes, each accountable for less than 2% of cases, include MYH11, TGFBR2, and TGFBR1 [30–32]. Other rare causes of thoracic aortic disease are inflammatory diseases, such as Takayasu arteritis, Behçet disease, and giant cell arteritis. Infection from Staphylococcus aureus, Staphylococcus epidermidis, Salmonella, and Streptococcus species, can cause primary infected aortic aneurysms [34, 35]. A false aneurysm can develop due to trauma or at the site of surgical anastomoses. 4. Clinical presentations Many patients with aneurysms are asymptomatic. Patients with TAAA may present with chronic back pain, although discomfort may also be experienced in the chest, flank, or epigastrium. Acute changes in pain characteristics and intensity may 3 Aortic Aneurysms – Screening, Diagnostics and Management be indicative of rapid expansion or imminent rupture of the aorta. Hoarseness, a consequence of vocal cord paralysis due to compression of the left recurrent laryngeal or vagus nerves, and dyspnea secondary to compression on the tracheobronchial tree, may be observed in patients with large proximal descending thoracic aortic aneu- rysms. Direct erosion of the aneurysm into the adjacent tracheobronchial tree or esophagus can cause life-threatening hemorrhaging, presenting as massive hemop- tysis or hematemesis, respectively. In rare instances, paraplegia or paraparesis may arise in patients with TAAAs, due to acute occlusion of intercostal or spinal arteries, a scenario typically associated with acute aortic dissection or thromboembolism. While most aneurysms exhibit varying degrees of mural thrombus, distal embolization resulting in acute mesenteric, renal, or lower extremity ischemia is relatively rare. Rupture is estimated to be the initial clinical manifestation in approximately 5% of TAAA cases. The sudden onset of pain with hypotension is a critical indicator of a ruptured aneurysm. Patients with ruptured TAAA, who make it to the hospital alive usually have ruptured TAAA contained within the pleural or retro- peritoneal space, and may present hours and days after the onset of free rupture, which is associated with severe hypotension and often results in instant death and prehospital mortality. 5. Classifications The Crawford classification and its modified version are used to categorize TAAAs based on their anatomical location and extent. These classifications are crucial for planning surgical interventions and understanding the prognosis of patients with TAAAs. The original Crawford classification divides TAAAs into four types, based on the segments of the aorta affected : Extent I: involves the descending thoracic aorta from just distal to the left subcla- vian artery down to the abdominal aorta above the renal arteries. Extent II: involves the descending thoracic aorta from just distal to the left subclavian artery and extending into the abdominal aorta, including the segment where the renal arteries originate, or extending down to the aortic bifurcation. Extent III: originates in the descending thoracic aorta from distal to the sixth rib and extends into the abdominal aorta, including the segment where the renal arteries originate, or extending down to the aortic bifurcation. Extent IV: starts from the level of the twelfth rib to the aortic bifurcation. The modified Crawford classification, also known as the Safi classification, expands the original system to better categorize the aneurysms based on their anatomical extent and to aid in surgical planning. It introduces one additional type: Extent V, which involves the descending thoracic aorta distal to the sixth rib down to the level just above the renal arteries, without extending into the segment where the renal arteries originate (Figure 2). 4 Management of Thoracoabdominal Aortic Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.1005225 Figure 2. Thoracoabdominal aortic aneurysm classification. Extent I, distal to the left subclavian artery to above the renal arteries. Extent II, distal to the left subclavian artery to below the renal arteries. Extent III, from the sixth intercostal space to below the renal arteries. Extent IV, the twelfth intercostal space to the iliac bifurcation (total abdominal aortic aneurysm). Extent V, below the sixth intercostal space to just above the renal arteries. These classifications are essential for determining the surgical approach, which can range from open repair to endovascular procedures, and for predicting potential complications and substantial surgical risks associated with the aneurysm extent. 6. Imaging The diagnosis of TAAA is achieved through various imaging techniques, with computed tomography angiography (CTA) being the gold standard. In scenarios of compromised renal function, intravenous iodinated contrast can be omitted, as it is not essential for the basic sizing of TAAA. CTA facilitates measurements of the aortic diameter from the ascending segment to its bifurcation across different levels. The reformatted coronal/sagittal views or three-dimensional reconstructions offer supplementary information for surgical planning, such as clamp sites. Magnetic resonance angiography (MRA) has gained widespread acceptance as a screening modality for aortic diseases and their branches. The primary advantage of MRA over CTA lies in its non-reliance on intravenous iodinated contrast, render- ing it safer for individuals with renal impairment. Moreover, MRA circumvents the exposure to radiation associated with CT, making it preferable for patients requiring sequential monitoring. The downside of MRA is longer imaging acquisition time (not amenable for people with claustrophobia), lower spatial resolution, and higher cost compared to CTA. Furthermore, CT exhibits a greater efficacy in evaluation for calcification and intramural thrombus compared to MRA. Intravascular ultrasound has emerged as a significant diagnostic tool for thoracic aortic disease, offering detailed insights into intraluminal relationships, particularly in aortic dissection during endovascular aortic repair. Epiaortic ultrasound is help- ful in deciding where to cannulate or clamp patients with atheromatous plaque and elephant trunk. 5 Aortic Aneurysms – Screening, Diagnostics and Management 7. Surgical indications The surgical indications of TAAA are determined by the balance of surgical risks and the expected adverse events. Guidelines suggest optimal treatment options for each condition [39–41]. American Heart Association (AHA) guidelines in 2022 recommend open surgical repair for TAAA when the diameter is ≧ 6.0 cm. As a class IIa recommendation, open repair is reasonable when the diameter is ≧ 5.5 cm and the repair is performed by experienced surgeons in a multidisciplinary aortic team. Open repair is also reasonable in patients who have features associated with an increased risk of rupture, including rapid growth ≧ 0.5 cm/year, symptomatic aneurysm, significant change in aneurysm appearance, and saccular aneurysm or presence of penetrating atherosclerotic ulcers. Patients who have ruptured aneurysm are indicated for emergent/urgent surgical repair due to its lethal nature. In patients with acute type B dissection, interventions should be recommended when patients have organ malperfusion, the progression of dissection, aneurysm expansion, or uncontrolled hypertension (complicated type B dissection). 8. Preoperative evaluation The initial consultation with TAAA patients primarily emphasizes a comprehen- sive history and physical examination aimed at identifying comorbid conditions, given the aneurysm typically presents with minimal symptoms or physical manifes- tations. The delineation of the aneurysm’s scope is accomplished through imaging modalities. Subsequent assessments focus on evaluating associated risk factors, with the inclusion of consultations from cardiologists, pulmonologists, or nephrologists, as necessary, for a more refined risk stratification. Ischemic heart disease emerges as a prevalent condition within this patient cohort, representing the leading mortality cause among those afflicted with TAAA. Transesophageal echocardiogram (TEE) serves as a pivotal tool for accurate cardiac function assessment. In cases of critically narrowed coronary artery disease, coronary artery revascularization via percutaneous interventions, such as balloon angioplasty or stenting, or surgical bypass, might be indicated prior to undertaking TAAA sur- gery. However, the imminent risk of aneurysmal rupture must be judiciously balanced against the coronary intervention risks and the potential delay introduced by such procedures. 9. O  perative techniques The patient is first placed in the supine position on the operating table. Following the induction of general anesthesia, endotracheal intubation is established utiliz- ing a double-lumen tube to facilitate selective ventilation of a single lung during the procedure. A sheath is inserted into the internal jugular vein, and a pulmonary balloon-tipped catheter is navigated into the pulmonary artery for cardiac monitoring and rapid infusion. Large bore peripheral venous lines are placed for the administra- tion of fluids and blood products. Temperature probes are positioned in the naso- pharynx and bladder. Electrodes for electroencephalographic monitoring and motor and somatosensory evoked potentials are fixed for assessing the functionality of the 6 Management of Thoracoabdominal Aortic Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.1005225 central nervous system and spinal cord, respectively (Figure 3). Subsequently, the patient is repositioned into a right lateral decubitus posture and a lumbar catheter is inserted into the third or fourth lumbar interspace for the monitoring and drainage of cerebrospinal fluid (CSF), maintaining the CSF pressure at or below 10 mmHg (Figure 4). The patient is then adjusted to a modified right lateral decubitus position, with a slight rotation of the hips to provide access to both groin areas. The surgical area is then sterilized and draped. The incision is tailored to accommodate the extent of the aneurysm (Figure 5). A comprehensive thoracoabdominal incision is commenced posteriorly between the tip of the scapula and the spinous process, arcing along the sixth intercostal space to the costal cartilage, and then extending obliquely toward the umbilicus. The latis- simus dorsi muscle is sectioned, and the insertion of the serratus anterior muscle is mobilized. Deflation of the left lung permits entry into the left thoracic cavity, which is typically required for extents II, III, and IV TAAAs. A modified thoracoabdominal incision, similar in initiation but terminating at the costal cartilage, offers optimal exposure for surgeries involving the descending thoracic aorta, particularly for Figure 3. Somatosensory and motor evoked potentials are recorded at three sites: the popliteal fossa (A, B), C5 (C) and the vertex (D). extents I and V TAAAs, in which the aneurysm concludes above the renal arteries. Figure 4. Placement of the lumbar catheter in the third or fourth lumbar space to provide cerebrospinal fluid drainage and pressure monitoring. 7 Aortic Aneurysms – Screening, Diagnostics and Management Figure 5. Tailoring of thoracoabdominal incisions for aneurysm extent. DTAA = descending thoracic aortic aneurysms; TAAA = thoracoabdominal aortic aneurysm; SMA = superior mesenteric artery. A self-retaining retractor is deployed to ensure uninterrupted exposure of the tho- racic and abdominal regions during the operation. Dissection is initiated at the lung hilum level, proceeding cephalad to the proximal descending thoracic aorta. The ligamentum arteriosum is identified and sectioned, with caution to avert damage to the left recurrent laryngeal nerve. The distal extent of the abdominal aneurysm is evaluated. The diaphragm’s muscular component alone is divided, ensuring preservation of the left phrenic nerve (Figure 6). A retroperitoneal approach is then established, facilitating the medial visceral rota- tion of the spleen, bowel, and left kidney to the right side of the abdominal aorta. Anticoagulation is achieved with intravenous heparin (0.5–1 mg/kg body weight) in anticipation of distal aortic perfusion. An incision in the pericardium, posterior to the left phrenic nerve, permits direct observation of the pulmonary veins and left atrium. Cannulation is performed on the left inferior pulmonary vein. A centrifugal pump, equipped with an inline heat exchanger, is connected to the outflow cannula, and arterial inflow is established through the left common femoral artery via a Dacron graft sutured in an end-to-side manner, or through the descending thoracic aorta, if the femoral artery is not accessible, to commence distal aortic perfusion (Figure 7). Protective clamps are positioned on the proximal segment of the descending thoracic aorta, immediately beyond the left subclavian artery and at the mid-thoracic region. In scenarios in which the aneurysm’s initial segment is in close proximity to the left subclavian artery, the aortic segment lying between the left common and left subclavian arteries is subjected to clamping. The left subclavian artery undergoes individual clamping. Due to the risk associated with the graft-esophageal fistulas, the proximal anastomosis no longer employs the inclusion technique. Instead, the aorta is sectioned to detach it from the underlying esophagus (Figure 8A). A preference is shown for a woven Dacron graft, which has been treated with collagen or gelatin, 8 Management of Thoracoabdominal Aortic Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.1005225 Figure 6. In previous surgical practice, the diaphragm (1) was divided (2). Currently, only the muscular portion of the diaphragm is cut (3). for the purpose of replacement. This graft is then sutured directly to the descending thoracic aorta in an end-to-end manner, employing a continuous 2-0 or 3-0 monofila- ment polypropylene suture. The integrity of the anastomosis is verified for any signs of hemorrhage. If needed, reinforced pledgeted sutures are placed for additional security. A sequential clamping method is implemented across all TAAAs. Upon the completion of the proximal anastomosis, the clamp on the mid-descending aorta is relocated distally toward the abdominal aorta at the level of the celiac axis to facili- tate the reattachment of intercostal arteries, specifically those between the T8-T12 levels, except in circumstances involving occluded arteries, a significantly calcified aorta, or an acute aortic dissection. This process is conducted under the guidance of neuromonitoring techniques, such as motor and somatosensory evoked potentials. The absence of alterations in the neuromonitoring data pertaining to spinal cord function permits the team to proceed with distal anastomosis prior to reattaching the intercostal arteries without the risk of spinal cord damage. The distal clamp is then advanced to the infrarenal aorta, the abdominal aorta is incised, and the graft is threaded through the aortic hiatus. The celiac, superior mesenteric, and renal 9 Aortic Aneurysms – Screening, Diagnostics and Management Figure 7. Distal aortic perfusion from the left inferior pulmonary vein to the left common femoral artery. Figure 8. Sequential clamping and graft replacement. Padded clamps are placed on the proximal and mid-distal descending thoracic aorta. A: the proximal part of the aneurysm is opened. The aortic neck is completely transected and separated from the esophagus. The proximal anastomosis is fashioned. Subsequently, the patent lower intercostal arteries are reattached via an elliptical hole in the graft. B: the proximal clamp is then moved onto the graft to restore pulsatile flow to the intercostal arteries, and the graft is pulled through the hiatus into the abdomen. The distal clamp is reapplied onto the infrarenal aorta. The remainder of the aneurysm is opened. Balloon-tipped catheters are inserted into the celiac, superior mesenteric, and renal arteries to permit perfusion. C: an elliptical hole is made in the graft for reimplantation of the visceral and renal arteries. arteries are identified and cannulated for perfusion using balloon-tipped catheters of either 9- or 12-Fr, chosen based on the ostia’s dimensions (Figure 8B). The delivery of cold perfusate at 4°C to the visceral organs is adjusted based on the proximal aortic 10 Management of Thoracoabdominal Aortic Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.1005225 pressure, maintained within a range of 300–600 mL/min. The renal temperature is closely monitored and maintained at an approximate 15°C. Typically, visceral vessels are reattached employing the inclusion technique. Following the completion of this anastomosis, the proximal clamp is advanced beyond the visceral patch, restoring pulsatile circulation to the visceral organs and kidneys. The terminal graft anastomo- sis is finalized at the aortic bifurcation. Generally, an island patch is utilized for the reattachment of the celiac, superior mesenteric, and both renal arteries. In instances in which either the right or left renal artery is situated at a considerable distance from the other arteries, a separate interposition bypass graft is necessitated for its reattachment. For patients diagnosed with connective tissue disease (e.g., Marfan syndrome), or those younger than 60 years, the use of a visceral patch is discontinued, due to the elevated risk of recurrent patch aneurysms. Instead, a commercially available woven Dacron graft with side-arm grafts measuring 10 mm and 12 mm is employed for the independent attachment of the celiac, superior mesenteric, and left and right renal arteries. Should intercostal reattachment be executed, reinstating pulsatile blood flow to the reattached intercostal arteries, an end graft or loop graft has superseded the island patch for the reattachment of intercostal arteries (Figure 8C). The patient is gradually withdrawn from partial bypass as the core body or nasopharyngeal temperature reaches 36°C. Protamine sulfate is administered in a dosage of 1 mg per 1 mg of heparin used, and both the atrial and femoral cannula are removed. Following the achievement of hemostasis, two or three 36-Fr chest tubes are placed within the left pleural cavity. The diaphragm is sutured together using a running 1-0 polypropylene stitch. The left lung is re-expanded. The surgical incision is closed following standard procedures. The patient is then placed in the supine posi- tion and a single-lumen endotracheal tube is exchanged for the double-lumen tube. If the vocal cords are swollen, the double-lumen tube is kept in place until the swelling resolves. The patient is then transferred to the intensive care unit (ICU). 10. Postoperative management Efforts are made to expedite the patient’s awakening to assess neurological func- tion. Most patients are candidates for extubation within a few hours postadmission to the ICU. Replacement of blood loss is generously undertaken and maintain hemo- globin above 8–9 g/dL. The patient’s systolic arterial pressure is maintained within the range of 130–160 mmHg to ensure sufficient perfusion of organs, with particular attention to the spinal cord. CSF pressure is measured and drained with a maximum of 15 mL/h to maintain a pressure of 10 mmHg or below. The goal is to wean the patient from mechanical ventilation by the first day following surgery. Resumption of an oral diet is advised upon the patient’s extubation. Following recovery from anesthesia, neurological evaluation is performed hourly to detect potential delayed neurological deficits. Indicators of concern for such deficits include unstable arterial blood pressure, hypoxemia, low hemoglobin levels (below 10 g/dL), or elevated CSF pressure (exceeding 15 mmHg). CSF drainage is terminated on the third day after surgery if the patient remains neurologically intact. The duration of ICU stay typically ranges from 3 to 4 days, contingent upon the patient’s neurological and pulmonary status, after which the patient is transferred to a telemetry unit. Initiation of physical therapy begins in the ICU and is maintained throughout the duration of the hospital stay. 11 Aortic Aneurysms – Screening, Diagnostics and Management Annual CT scans are advocated to monitor for the emergence of new aneurysms or the formation of graft-related pseudoaneurysms. The interval of follow-up visits or CT scans is adjusted based on the etiology of TAAA. For instance, patients with residual unoperated aortic dissection, connective tissue disorders (such as Marfan syndrome), a familial history of aortic aneurysms, or concurrent aneurysms may require more frequent surveillance. 11. Surgical outcomes Mortality rates for patients undergoing TAAA repair and descending thoracic aortic aneurysms fluctuate significantly, observed within a range of 4–21% [9, 42–44]. This variation in outcomes can be attributed to the diversity within the patient demographics and the varying levels of expertise among the medical teams. According to aggregated data collected by the authors over the period from January 1991 to July 2012, a cohort of 1511 individuals underwent procedures for the repair of TAAA and descending thoracic aortic aneurysms. Within this group, males con- stituted 64%, with a median age of 67 years, and ages ranging from 8 to 91 years. Notably, approximately 7% of these surgeries were conducted as emergency interven- tions in response to either free or contained ruptures of the TAAA or descending thoracic aortic aneurysms. The current data indicate that the 30-day postoperative mortality rate is roughly 15%. However, in patients demonstrating normal renal func- tion, as evidenced by a glomerular filtration rate greater than 90 mL/min/1.73 m2, the early mortality rate is significantly lower, recorded at 5.9%. Multivariable analysis has facilitated the identification of advanced age, renal failure, and paraplegia as significant predictors of mortality risk. Despite these risks, it is noteworthy that approximately 70% of patients experience recovery from TAAA surgeries without encountering severe postoperative complications. The 5-year survival rate post- TAAA repair is estimated between 60% and 70%. Further analysis has illuminated several factors that negatively impact long-term survival, including advanced age, the presence of extent II TAAA, renal failure, the requirement for emergency surgical intervention, cerebrovascular disease, and active tobacco smoking. 11.1 N  eurological outcomes The occurrence of postoperative neurologic deficits constitutes the most severe complication following TAAA repair. Cross-clamping the descending thoracic aorta pre- cipitates immediate ischemia of the spinal cord, primarily due to the abrupt cessation of perfusion to this region coupled with a consequent rise in CSF pressure. Historically, in the era characterized by the “cross-clamp-and-go” approach, the duration of clamp application emerged as the principal determinant of neurologic deficits. The current strategy for mitigating such risks includes enhancing spinal cord perfusion pressure directly through distal aortic perfusion and indirectly by minimizing CSF pressure to 10 mmHg or below. Evidence from both animal and human studies has substantiated that the drainage of CSF effectively lowers CSF pressure, thereby, facilitating improved perfusion of the spinal cord during periods of aortic cross-clamping [45, 47, 48]. In this comprehensive analysis, adjunctive strategies comprising distal aortic per- fusion and CSF drainage, along with moderate hypothermia, were employed in 76% of the patient cohort, totaling 1155 out of 1511 patients. The implementation of these combined adjunctive measures has been correlated with a substantial 44% reduction 12 Management of Thoracoabdominal Aortic Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.1005225 in the likelihood of neurologic deficits across all extents of aneurysm. Specifically, the overall incidence of neurologic deficits in patients not receiving adjunctive care was documented at 4.5%, compared to a reduced rate of 2.5% in those who did. Despite the duration of aortic cross-clamp application continuing to be a significant indicator of paraplegia risk, the introduction of adjunctive measures has effectively extended ischemic tolerance. For patients with high-risk extent II aneurysms, the employment of these adjuncts decreased the incidence of neurological deficits from 30% to 9% at an average aortic cross-clamp duration of 75 minutes (Figure 9). When analyzing all aneurysm extents collectively and excluding cases without adjunctive measures, the use of adjuncts has significantly lowered neurologic deficit rates to a range of 1–5%, simultaneously enhancing tolerance to clamp times. Since 1991, the adjunctive use of distal aortic perfusion, CSF drainage, and reim- plantation of segmental arteries has been a standard practice for patients undergoing elective TAAA repair. Among a subset of 1004 patients, immediate postoperative neurologic deficits, including paraplegia or paraparesis upon emergence from anesthe- sia, were observed in 2.4% of patients treated with adjuncts, compared to 6.8% of those without. This strategic combination has effectively reduced the cumulative inci- dence of neurologic deficits to 3.3% for TAAA repairs. Historically, the repair of extent II TAAAs was associated with the highest rate of neurologic deficits, reaching 30–40% in the pre-adjunct era. With the introduction of adjunctive measures, the incidence of immediate neurologic deficits for extent II TAAA repairs has been reduced to 7.2%. In addition to aneurysm extent, other perioperative risk factors for immediate neurologic deficits include advanced age, emergency surgery, renal dysfunction, active tobacco use, and cerebrovascular disease. The combined application of intraoperative distal aor- tic perfusion and perioperative CSF drainage effectively prevents 1 neurologic deficit in every 20 cases across all patient groups, and 1 in 5 for patients with extent II TAAA. The advancements in protective measures for the spinal cord during TAAA repair have significantly reduced the occurrence of neurologic complications, thereby highlighting the emergence of delayed onset neurologic deficit (DND) as a pivotal clinical concern (Figure 10). The precise mechanisms contributing to the develop- ment of DND remain elusive. It is hypothesized that DND following TAAA repair may be attributed to a “second hit” phenomenon. While intraoperative adjuncts are Figure 9. In extent II aneurysms, the probability of developing neurologic deficits increases with increasing clamp time, but the use of adjunct distal aortic perfusion and CSF drainage reduces the chances of neurologic deficit by prolonging ischemic tolerance. 13 Aortic Aneurysms – Screening, Diagnostics and Management effective in safeguarding the spinal cord and diminishing the incidence of immediate neurologic deficits, the spinal cord continues to be susceptible to injury in the early postoperative phase. Potential additional ischemic events, triggered by hemodynamic fluctuations, any elevation in CSF pressure, or a combination of both, may serve as the “second hit” leading to DND. Consequently, in instances of DND development, CSF is actively drained to mitigate the compartment pressure. To enhance postoperative spinal cord perfusion and oxygenation, strategies involve maintaining the mean arterial pressure above 90–100 mmHg, ensuring hemoglobin levels exceed 10 mg/dL, and sustaining a cardiac index above 2.0 L/min/m2. Upon the onset of DND, interventions aimed at augmenting spinal cord perfusion are promptly implemented. CSF pressure is reduced to below 10 mmHg. For individuals diag- nosed with DND, CSF drainage is maintained for a minimum duration of 72 hours. Employing this comprehensive management strategy for DND has resulted in a noted improvement in neurologic function in 57% of affected patients. Specifically, functional recovery was observed in 75% of patients when the CSF drain was intact at the time DND was identified, compared to a 43% recovery rate in patients requiring CSF drain reinsertion subsequent to DND manifestation. 11.2 Renal failure Acute postoperative renal failure is characterized by a daily increase in serum cre- atinine levels by 1 mg/dL over two consecutive days or the necessity for hemodialysis intervention. The incidence of acute renal failure among patients undergoing TAAA repairs is reported between 5% and 40%, correlating with mortality rates reaching up to 70%. The prognosis for long-term survival among patients undergoing hemodialysis is notably poor. Known predictors for acute postoperative renal failure include preexisting chronic renal insufficiency and ruptured aneurysms. While it has been posited that patients with extensive Type II TAAA are at elevated risk for postoperative renal failure, the extent of TAAA has not been definitively proven as a significant prognostic factor and the high incidence of postoperative renal failure remains a significant concern. The search for an optimal renal protection strategy continues to be of paramount importance. Figure 10. Odds of delayed neurologic deficit by lowest postoperative mean arterial blood pressure, with or without cerebrospinal fluid drain complication. Odds are referenced to one. For example, a patient with a mean arterial blood pressure of 40 mmHg and a cerebrospinal fluid drain complication would have 40:1 odds of delayed neurologic deficit. 14 Management of Thoracoabdominal Aortic Aneurysms DOI: http://dx.doi.org/10.5772/intechopen.1005225 11.3 E  ndovascular repair Since the inaugural success of thoracic stent graft repair documented in 1994 , the endovascular treatment of thoracic aortic diseases has rapidly advanced. The first device, developed by WL Gore in Flagstaff, AZ, was the initial thoracic aortic device to be granted approval by the United States Food and Drug Administration in 2005. Endovascular therapy offers the advantages of reduced morbidity and mortality when contrasted with traditional open surgical approaches. The endovascular manage- ment of TAAA necessitates the revascularization of visceral and renal vessels and is presently conducted via three distinct methodologies: hybrid repair; employment of parallel grafts; and utilization of bespoke branched and fenestrated devices. The hybrid method integrates open debranching of the aorta with the subsequent endovascular exclusion of the aneurysmal segment, involving the bypass of visceral and renal arteries from an iliac artery. This approach circumvents the need for open thoracotomy, aortic cross-clamping, and single-lung ventilation [52–54]. Despite its technical feasibility, the associated risks of morbidity and mortality are significantly high. Recent scholarly works have indicated no substantial difference in outcomes between hybrid and open TAAA repairs, suggesting that the application of hybrid repair may be confined to individuals ineligible for open repair or other endovascular techniques due to anatomical constraints or the urgency of the situation [55–57]. An alternative strategy involves the use of parallel grafts, also known as chimneys, periscopes, or snorkels (collectively referred to as CHIMPS), to maintain perfusion to branch vessels. This method has been prominently advocated by Lobato et al. in Brazil, demonstrating a high rate of technical success and primary patency with a relatively low mortality rate. The advantages of parallel stent grafts include their modularity and adaptability to diverse anatomical configurations, making them par- ticularly beneficial for patients with challenging vessel characteristics. However, this technique is not without drawbacks, such as the potential for endoleaks through the gutters, which may lead to aneurysm sac pressurization. A recent systematic review of the chimney graft technique included 75 patients and a total of 96 branches, with a reported 98.9% early success rate with a perioperative mortality rate of 4%. Total endovascular repair of TAAA, employing custom-made branched and/or fenestrated devices, represents the culmination of these approaches. Significant series and multicenter prospective studies have reported varying rates of perioperative mortality (2.5–12.5%) and complications, underscoring the need for continued inno- vation to enhance outcomes [60, 61]. The largest series by Dias-Neto et al. on their experience with 1947 patients reported a perioperative mortality and/or permanent paraplegia rate occurred in 14% of the single-stage approach and 6% of multi-stage approach. Despite considerable advancements, the evolution of endovascular technologies for TAAA repair persists, with the future likely to see the development of modu- lar, off-the-shelf devices capable of accommodating a broad spectrum of clinical scenarios. Disclosures Dr. Estrera is a consultant for WL Gore, CryoLife, Edwards Lifesciences, and Terumo Aortic. The other authors have no conflicts of interest. No outside funding was provided for this report. 15 Aortic Aneurysms – Screening, Diagnostics and Management Author details Yuki Ikeno, Akiko Tanaka and Anthony L. Estrera* Department of Cardiothoracic and Vascular Surgery, McGovern Medical School at UTHealth Houston, Houston, TX, USA *Address all correspondence to: [email protected] © 2024 The Author(s). Licensee IntechOpen. 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