66. Thoracoabdominal Aortic Aneurysms- Indications and Guidelines

Jarot J. Guerra MD, Akiko Tanaka MD PhD, Hazim J. Safi MD, Anthony L. Estrera MD

McGovern Medical School at UTHealth Houston

August 1^st, 2024

Abbreviations & Definitions

AKI – Acute kidney injury
B/FEVAR – Branched and/or fenestrated endovascular aortic repair
CPB – Cardiopulmonary bypass
CMD – Custom-made devices
CSF – Cerebrospinal fluid
CTA – Computed tomography angiography
HTAD – Heritable thoracic aortic disease
LVEF – Left ventricular ejection fraction
PMEGs – Physician-modified endovascular grafts
SCI – Spinal cord ischemia
TAA – Thoracic aortic aneurysm
TAAA – Thoracoabdominal aortic aneurysm
TEVAR – Thoracic endovascular aortic repair

Indications & Guidelines for Management by Grade/Stage of Disease

Thoracoabdominal aortic aneurysm (TAAA) repair is one of the most invasive surgical procedures as it anatomically and physiologically involves all major organs. Since the first successful report of TAAA in the 1950s, operative techniques and approaches have evolved to conquer the challenges, including spinal cord ischemia (SCI), acute kidney injury (AKI), respiratory failure, and bleeding.¹ In this chapter, we describe various aspects of TAAA repair to optimize postoperative outcomes.

Classification of TAAA

The classification is important for proper perioperative planning and management. The original Crawford classification of TAAA was modified by Safi and colleagues to stratify the risk of SCI,² in which they added Extent V (Figure 1). The classification includes Extent I, distal to the left subclavian to above the renal arteries; II, distal to the left subclavian artery and extending below the renal arteries; III, distal to T6 and extending below the renal arteries; IV, below the diaphragm and extending below the renal arteries; and V, distal to T6 to above the renal arteries. Extents II and III carry the highest risks for SCI.^3,4 In addition, significant disabling complications (a composite of mortality, stroke, SCI, and dialysis) have a clear correlation with the extent of repair using the modified classification.⁵

Figure 1: Classification of thoracoabdominal aortic aneurysm.

Diagnosis

Computed tomography angiography (CTA) is the gold standard for diagnosing and evaluating TAAAs. CTA allows for visualization of the aortic wall, aneurysm size, presence or absence of clot formation, intercostal arteries, and effects on the surrounding tissues. Intravascular ultrasound allows for precise assessment of the aortic wall pathologies, especially in aortic dissection or traumatic aortic injury.⁶ This modality allows for high-resolution imaging of the aortic wall, dynamic visualization of intimal lesions, and delineation of branch vessel involvement. The drawback is that it is operator-dependent, requires invasive intra-arterial access, and adds additional cost.

Indications for TAAA Repair

Indications and perioperative recommendations for TAAA repair are listed in Tables 1 and 2. ACC/AHA⁷ and EACTS/STS⁸ guidelines use different cut-off sizes for TAAA repair. High-risk TAAAs include aneurysms with rapid growth (>0.5 cm/yr), pain, change in appearance, saccular, associated penetrating atherosclerotic ulcers, and the presence of heritable thoracic aortic disease (HTAD).

Table 1: Recommendations from AHA/ACC 2022 Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines.⁷

Open Surgical Repair of TAAA	COR	LOE
In patients with intact degenerative TAAA, repair is recommended when diameter is ≥6.0 cm.	I	B-NR
In patients with intact degenerative TAAA, repair is reasonable when the diameter is ≥5.5 cm and is performed by experienced surgeons in a Multidisciplinary Aortic Team.	IIa	B-NR
In patients with intact degenerative TAAA who have features associated with an increased risk of rupture, repair is reasonable when the diameter is <5.5 cm.	IIa	B-NR

Table 2: Recommendations from EACTS/STS 2024 Guidelines for Diagnosing and Treating Acute and Chronic Syndromes of the Aortic Organ (with permission).⁸

Recommendation	COR	LOE
It is recommended to view, interpret, and treat the aorta in the context of an organ, whereby diagnosis, treatment, and surveillance should be approached with this perspective.	I	C
In asymptomatic patients with TAAA, repair is recommended at ≥55 mm in diameter.	I	C
In asymptomatic patients with TAAA and high-risk features, repair is recommended at <55 mm in diameter.	IIa	C
In patients with low-to-moderate perioperative risk, open repair as well as endovascular treatment of pararenal and TAAA should be considered.	IIa	C
B/FEVAR procedure should be considered the first-line treatment for patients unfit for open repair.	IIa	B
A hybrid approach may be considered for patients unfit for open repair and anatomically unsuitable for B/FEVAR procedure.	IIb	C
In patients at high-risk of SCI undergoing endovascular treatment of type I, II, III, or V TAAA repair, a staged TEVAR-B/FEVAR approach should be considered.	IIa	C
In open TAAA repair, proximal clamping before the full establishment of CPB to avoid retrograde embolization of parietal thrombi should be considered.	IIa	C
Left heart bypass or partial femoral-femoral bypass for TAAA repair should be considered based on surgical and institutional experience.	IIa	C
In patients undergoing open descending or TAAA repair, cryoablation of multiple intercostal spaces may be considered for pain control as an adjuvant strategy.	IIb	C
Monitoring End-Organ Function and How to Avoid End-Organ Injury
Multiple arterial pressure monitoring lines (upper and lower body) are recommended for TAAA repair. A femoral arterial line should be used for lower body perfusion-pressure monitoring.	I	C
CSF drainage for spinal cord protection is recommended in open TAAA repair.	I	B
Selective visceral and renal perfusion is recommended in open TAAA repair.	I	B
Prevention of steal in particular from segmental arteries to avoid SCI is recommended.	I	C
In TAAA surgery, maintenance of lower limb perfusion to avoid rhabdomyolysis and AKI is recommended.	I	C
In patients at an increased risk of SCI undergoing endovascular treatment of TAA or TAAA disease, prophylactic CSF drainage should be considered.	IIa	C
The 4-territory concept should be considered during planning to reduce procedure-induced deprivation of antegrade arterial spinal cord supply to a minimum.	IIa	C
A critical appraisal of the contribution of thoracic and lumbar segmental arteries to spinal cord perfusion should be considered before surgery to determine the need for reimplantation.	IIa	C
Deep hypothermic circulatory arrest should be considered in patients undergoing open TAAA repair based on surgical and institutional experience.	IIa	C

Supporting Evidence for Current Indications & Guidelines

Recommendations from:

• AHA/ACC 2022 Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines
• EACTS/STS 2024 Guidelines for Diagnosing and Treating Acute and Chronic Syndromes of the Aortic Organ (with permission)

Preoperative Workup

A systematic preoperative evaluation is mandatory for TAAA repair. A thorough history-taking is important to decide on the extent of repair and determine the size of the aneurysm to intervene. The patient may not report an aortic family history but may report sudden death, which could be an unidentified aortic death. We consider patients with PaCO₂ >45 mmHg and FEV₁ <0.8 L to be high risk. In addition, reduced LVEF is a predictor of mortality.⁹ Echocardiography also assists in stratifying operative risk and helps determine the need for additional cardiac testing. It is unclear whether preoperative coronary or carotid artery revascularization is beneficial in reducing perioperative heart attack and stroke.¹⁰ Renal function must be evaluated with an estimation of the glomerular filtration rate (GFR): 30-day mortality after open TAAA repair ranges from 5% for patients with a normal GFR to 27% for patients with a GFR <49 mL/min.¹¹

Spinal Cord Ischemia (SCI)

SCI occurs because of cessation of blood flow to intercostal arteries, inadequate collateral circulation, reperfusion injury, and decreased cerebrospinal perfusion pressure. The Adamkiewicz artery (AKA) is often the largest anterior medullary artery¹² and is the main source for the distal two-thirds of the spinal cord’s perfusion. In the 1990s, Safi and colleagues showed that reconstruction of the T8-T12 segmental arteries was associated with a reduction in SCI.¹³ Imaging studies verified that the AKA was often located within T7-L1 and on the left (>80%).¹⁴ Important collaterals to the spinal cord are the vertebral and internal iliac arteries,¹⁵ connected by the small arteries in the spinal canal, perivertebral tissues, and paraspinous muscles. Thus, higher systemic pressures help to maintain the flow through the small caliber “collateral network.” The risk of delayed SCI doubles in patients with T8-T12 ligations, regardless of intact intraoperative monitoring.¹⁶ Without reattachment of segmental arteries, the spinal perfusion solely depends on the collateral network and is vulnerable to hypotension. Thus, reattachment of the patent T8-T12 segmental arteries should be performed for spinal cord protection. In addition, embolic SCI is not uncommon (80% of SCI in a series by Tanaka and colleagues);¹⁷ thus, care must be taken when handling. Several techniques minimize SCI during aortic clamping and after reconstruction, including intercostal artery reattachment, distal aortic perfusion, cardiopulmonary bypass, regional or systemic hypothermia,¹⁸ and cerebrospinal fluid (CSF) drainage. Our team’s spinal protective adjuncts are CSF drainage, mild passive hypothermia, and left heart bypass.¹⁹

The proposed effect of CSF drainage is to lower spinal fluid pressure and, thereby, reduce resistance to perfusion and increase blood perfusion pressure.²⁰ It is typical to drain 400-500 mL over 3 days intraoperatively and postoperatively. While post-spinal headaches are common after CSF drainage (8%), intracranial hemorrhage with CSF drainage use is rarely seen, with an incidence of 0-0.3% when the intrathecal pressure is targeted to 10 mmHg.^14,21 However, when targeted below 5 mmHg, the incidence can increase to 8%.²²

Surgical Technique

We routinely use a double-lumen endotracheal tube for selective right lung ventilation, a pulmonary arterial catheter, and motor evoked and somatosensory evoked potentials. The patient is then turned to the right lateral decubitus position for placement of the CSF drain, with a goal CSF pressure <10 mmHg. This CSF drain is maintained intraoperatively and for 3 days postoperatively, as discussed later in this chapter.

The shoulders are positioned perpendicular to the table, and the hips are rotated 30 degrees posteriorly for left femoral cannulation. A thoracoabdominal incision is tailored to fit the extent of the aneurysm. The incision begins posterosuperior to the tip of the scapula and proceeds medially along the anterolateral margin of the abdominal wall (lateral to rectus sheath), extended inferiorly below the level of the umbilicus. Next, the latissimus dorsi is divided, and the serratus anterior muscle is mobilized. After the left lung is deflated, the left chest is entered, usually through the sixth intercostal space. The 5th or 6th rib is shingled at the posterior end to gain more exposure. The costal cartilage is cut, the retroperitoneal space is dissected by the diaphragm, and the anterolateral muscular portion of the left diaphragm is divided. We avoid a full split of the diaphragm to avoid injury to the phrenic nerve and preserve the pulmonary function. The abdominal contents are retracted medially to the right of the abdominal aorta, including the left kidney. The dissection is carried out enough to gain access to the distal end of TAAA. The left crus and the median arcuate ligament are divided to expose the aortic hiatus and make space for the graft to pass through.

Dissection of the visceral and renal branches is not needed. The lumbar branch of the left renal vein is tied with silk and divided. Preoperative imaging should be carefully reviewed for the left renal vein, as a retroaortic renal vein is present in 2% of patients, which can be mistaken for a large lumbar branch. We use a self-retaining retractor to aid in exposure, typically the Omni-Tract® (Integra Lifesciences Corporation, Princeton, NJ) system. First, we place the Wishbone® Frame parallel to the incision. The Mayo Swivel Retractors are placed on the 6^th rib and the lower cut edge of the costal cartilage for the basic exposure. Then, a Deaver or Splanchnic Swivel is placed to retract the viscera (spleen and left kidney), and a Malleable Slotted Swivel for retraction of the gut. At this point, a needle temperature probe is placed in the left kidney.

In the chest, we divide the inferior pulmonary ligament and open the pericardium posteriorly to the phrenic nerve to expose the left inferior pulmonary vein. The ligamentum arteriosum is divided after identification and preservation of the recurrent laryngeal nerve.

We use left heart bypass to unload the heart and maintain distal perfusion for organ protection, especially the spinal cord. The patient’s core temperature can passively drift to 33-34° C but not lower to avoid ventricular fibrillation. During the aortic reconstruction, we use the cell-saver system for rapid transfusion.²³ Cannulas are placed for distal aortic perfusion. A purse-string suture is placed in the left inferior pulmonary vein and the left common femoral artery. If the common femoral artery is smaller than a 17-18 Fr cannula, we recommend suturing an 8 mm Dacron graft in a side-to-end fashion to avoid limb ischemia and resultant renal injury.²⁴ Systemic heparin is given at 1 mg/kg, and the left inferior pulmonary vein is then cannulated with the catheter tip directed toward the left atrium. The femoral artery is directly cannulated using the Seldinger technique, or a return circuit connected to the graft. Profound hypothermia, although seldom employed, is a useful adjunct for very large aneurysms, severe atheromatous plaques at the distal arch, when the proximal descending thoracic aorta precludes proximal aortic control, or in cases of rupture at those locations. A segmental clamp is applied to the proximal descending thoracic aorta and the mid-thoracic aorta before transecting the aorta. After opening the upper thoracic aorta, intercostal arteries within this segment are ligated to prevent the steal phenomenon of spinal perfusion and control blood loss from the back bleed.

The proximal aorta is divided completely and separated from the underlying esophagus to mitigate the risk of graft-esophageal fistula. A commercially available collagen or gelatin-impregnated woven Dacron graft is sutured end-to-end with polypropylene suture. A 2-0 polypropylene suture is preferred if the anastomosis incorporates a calcified artery or a previously placed stent graft. In cases of fragile tissues, such as in acute aortic dissections, 4-0 polypropylene sutures are preferred. After completion of the proximal anastomosis, the clamp is moved distally to the celiac axis. In cases of young patients, proximal aortic disease, or dissection in the aortic arch, the reversed elephant trunk technique is used to prepare for possible future proximal intervention.

Lower thoracic intercostal arteries (i.e., T8 to T12) are temporarily occluded with balloon-tipped catheters for back bleed control and to preserve for reconstruction. The extent and timing of lower intercostal artery reattachment depend on intraoperative neuromonitoring results. Patent intercostal arteries from T8-T12 can be reattached, either as an opening in the graft or as an end-to-side graft. The graft is tunneled from the chest to the abdomen through the aortic hiatus. The distal aortic clamp above the celiac artery is moved to the infrarenal abdominal aorta. The upper abdominal aorta is opened, and the celiac and superior mesenteric arteries are perfused via balloon-tipped catheters with tepid blood (34° C) from the centrifugal pump.

The kidneys are similarly perfused with a bolus of cold crystalloid (Houston solution: Ringer’s lactate 1000 mL, K+ 10 mEq, furosemide 5 mg, mannitol 8.5 g) to maintain a renal temperature of 20°C. The viscera are usually attached as a patch. In cases of Marfan syndrome or other HTAD, patients <60 years of age, or ostial separation of >3 cm, a pre-manufactured side-branched thoracoabdominal aortic graft is used with separate bypasses to each of the vessels. The distal anastomosis can be performed either before or after pulsatile flow is restored to the viscera and renal arteries. After completion of the distal anastomosis, the graft is de-aired, and the clamps are released.

The anastomoses are checked for hemostasis, and the distal aortic perfusion cannulas are removed once the nasopharyngeal temperature reaches 35.5-36°C. Anticoagulation is reversed with protamine sulfate and blood products, as necessary. When the cell salvage exceeds more than 30-40 units, the coagulopathy needs to be proactively corrected without waiting for the labs to come back. All mural thrombi in the aorta should be removed to search for intercostal arteries or small branches with patent orifices and ligated. The cut aortic wall edge should be cauterized.

Intercostal nerve block using a cryoablation probe is performed to T4-T8 for postoperative pain management (or to T10, according to the incision level) while packing and obtaining hemostasis.²⁵ The use of electromyography during cryoanalgesia is recommended to confirm the completeness of the nerve block.

The muscular portion of the diaphragm is reapproximated with a running horizontal mattress #1 polypropylene suture. Two or three chest tubes (straight chest tubes anteriorly and posteriorly to the left lung and one right-angled chest tube on the diaphragm) are placed. The left lung is reinflated, and the chest is closed by reapproximating ribs with figure-of-8 #2 polyglactin 910 sutures (ETHICON, Johnson & Johnson MedTech). The 7^th rib is drilled to allow for the suture to pass directly through the rib so that the intercostal nerve is not caught with the rib approximation sutures. The cut costal cartilage edges are hard to stabilize and may cause uncomfortable clicking later. Thus, we cut back by 1-2 cm before the closure. The remainder of the chest and abdomen are closed in standard fashion. The double-lumen endotracheal tube is usually exchanged for a single-lumen tube before transfer unless there is significant airway edema.

Postoperative Care

Patients are managed in the intensive care unit. Monitoring for spinal cord function is critical after TAAA repair. Postoperatively, patients should be awakened as soon as possible to ascertain neurologic status. Half of SCI may resolve with treatment; thus, strict monitoring and early detection of neurological status are critical.

The goal for systolic blood pressure is >130 mmHg²² (or mean arterial pressure >80 mmHg), and the CSF pressure goal is <10 mmHg. We recently shifted the target parameter for blood pressure from the mean to the systolic arterial pressure, as we found more correlation between systolic pressure and the incidence of delayed SCI. A limit of 15 mL of CSF fluid is drained each hour to prevent intracranial hypotension and hemorrhage. If blood is noted in the effluent, the drain is capped, and any coagulopathy is corrected. The mean onset of delayed SCI is 1.8 days, with a median duration of 1 day (interquartile range 1-2 days). Thus, the drain is usually removed on the third postoperative day if the patient is neurologically intact.

Outcomes in High-Volume Centers (>10 Cases/Year)

In-hospital mortality after open TAAA repair in high-volume centers is less than 15% (30-day mortality <10%). Extents II and III have the highest mortality rates of 5-30% and 8-21%, respectively.^26-37 The predictors of mortality are Extent II/III repairs, older age, and emergent repair. SCI is reported in up to 11%, but half of the cases have functional recovery in high-volume centers (permanent <5%). Extents II and III also carry the highest risks for SCI.^19,26 Respiratory and renal complications remain common, with tracheostomy required in 6-31% and new dialysis seen in 3-29%. Gastrointestinal complications are rare, and bowel ischemia is seen in less than 2%. Of note, vocal paralysis is seen in 3-15%.

Ongoing Trial(s)/Recent Publications

To the authors’ knowledge, there are no ongoing trials at this time.

Expert Commentary

TAAAs are a life-threatening condition that necessitates the expertise of a multidisciplinary aortic team for effective management. Although TAAAs account for 10% of all aortic aneurysms, their postoperative morbidity and mortality are higher than those of any other aortic aneurysm. A systematic workup is mandatory before TAAA repair. Advanced COPD and decreased renal function are major predictors of morbidity and mortality. The presence of HTAD will dictate a more aggressive surgical plan. Since Dr. Crawford’s description of TAAA repair using the “clamp and go” technique in the 1950s, major challenges remain, particularly in preventing SCI, renal or respiratory failure, and bleeding.

The Crawford classification of TAAA, modified by Safi et al., helps categorize the extent of repair and the risk of SCI. Regardless of size or anatomical extent, all symptomatic aortic aneurysms should be addressed and urgently repaired. Present guidelines indicate that elective repair is recommended for intact TAAA at a diameter of ≥6 cm. It is reasonable to perform TAAA repair if the diameter is >5.5 cm and an experienced multidisciplinary aortic team conducts it. TAAAs with high-risk factors for rupture, such as rapid growth >0.5 cm/year, saccular appearance, changes in aneurysm appearance, or those that are symptomatic or associated with penetrated aortic ulcers, warrant repair even if the diameter is <5.5 cm. For patients with HTAD, a threshold between 5 and 5.5 cm is considered reasonable, given the aggressiveness of the affected genetic variant. The thresholds recommended by guidelines for elective surgical repair can reduce the risk of rupture, but do not alleviate the risk of dissection. The size threshold continues to be a topic of extensive debate. Patients with TAAA need to be closely monitored in the outpatient setting, and their hypertension and other modifiable risk factors, such as smoking cessation and lipid management, are major factors to be optimized.

Open repair has been the gold standard for decades, providing definitive and durable repair for TAAA. Our technique is described earlier in the chapter. It is preferred in younger patients, chronic dissections, HTAD, and those with good cardiopulmonary reserve. Long-term durability is well established, with a freedom from repair failure rate of 95% at 10 years and 94% at 15 years. Endovascular repair continues to evolve. Historically, it is preferred for older patients, those with suitable landing zones, as well as for individuals with poor cardiopulmonary reserve and severe comorbidities. However, data from specialized centers using custom-made devices (CMD) or physician-modified endografts (PMEGs) have shown promising results even in low-risk patients. Endovascular repair is associated with lower operative mortality, renal failure, and shorter hospital stays, but carries a higher risk of mesenteric ischemia, paraplegia, and branched vessel occlusion. The need for secondary procedures is also more common in the endovascular group compared to the open repair approach. Regardless of the repair method, both open and endovascular techniques have a steep learning curve and require highly specialized skills. They are best performed by high-volume surgeons in high-volume centers.

Strategies for spinal cord and end-organ protection are paramount in any TAAA repair strategy. Our strategies for preventing SCI are highlighted in this chapter. Reattaching patent segmental arteries T8-T12 decreases both immediate and delayed SCI. Over 50% of SCI occurs in a delayed fashion. Postoperative hypotension is associated with delayed SCI. Since the 1990s, we have implemented distal aortic perfusion, hypothermia, and CSF drainage as our strategy for SCI prevention, especially in Extent II and III repairs. Cardiopulmonary bypass or left heart bypass is used during TAAA repair to maintain the distal aortic pressure and unload the heart during aortic cross-clamping. We typically cool to mild hypothermia, 24-32℃. A systemic temperature drop of 5℃ can increase an additional 30 minutes to the ischemic tolerance of the spinal cord. We routinely place CSF drains. CSF drains decrease intrathecal pressure and lower resistance to spinal cord perfusion. Other adjuncts include sequential segmental clamping of the aorta and prevention of steal syndrome. This minimizes organ ischemic time and allows for the collaterals to perfuse. We also routinely use somatosensory (SSEP) and motor evoked potential (MEP) monitoring. Immediate MEP/SSEP signal loss after aortic clamping suggests that the major supply to the spinal cord exists within the clamped segment and that collateral flow is poor. There is no single measure to improve outcomes after open TAAA repair. Functional recovery is observed in nearly 50% of patients with SCI, and permanent paraplegia is reported in <5%. If patients are stable, a referral to large, high-volume aortic centers for complex cases may be considered. Minimizing the ischemic insults to organs, optimizing spinal cord perfusion, and minimizing intraoperative bleeding are crucial in obtaining optimal outcomes after TAAA repair.

In conclusion, open TAAA repair is associated with a higher morbidity and mortality when compared to endovascular repair. Nevertheless, open repair is durable, and the need for secondary interventions is minimal. Elective endovascular repair has progressed with the utilization of CMD and PMEGs. Emergent endovascular repair is feasible with off-the-shelf devices. According to recent large studies on endovascular TAAA repair, it is linked to a slightly lower rate of early adverse events and similar long-term survival rates to those of the open approach. Reinterventions are much more prevalent than in the open repair strategy. Long-term follow-up with surveillance imaging is essential for all patients after TAAA repair, especially for younger individuals with connective tissue disorders and those with chronic dissection who are susceptible to subsequent aortic degeneration and aneurysm formation. Overall, imaging should be conducted early in the postoperative period and annually for the first few years in both open and endovascular procedures. Magnetic resonance imaging may be advantageous for young patients needing lifelong surveillance. Long-term survival following either open or endovascular TAAA repair is significantly lower than that of the general population.

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