collateral blood supply to the spinal cord and chest wall.

Although percutaneous coronary intervention may be considered, the use of either bare metal stents

or just balloon angioplasty is preferred over drug-eluting stents since drug-eluting stents require longterm administration of clopidogrel to prevent stent thrombosis. Fortunately, medical management can

be adopted for most cases of mild-to-moderate coronary artery disease and in cases of severe disease

that is asymptomatic with preserved ejection fraction. Patients who develop symptoms from critical

disease, for example, left main or ostial left anterior descending coronary occlusive disease, should

probably have this addressed prior to aneurysm repair. In very rare situations, combined and

simultaneous coronary artery bypass and TAAA repair may be considered.

OPERATIVE TECHNIQUES

The patient is brought to the operating room and placed in the supine position on the operating table

and prepared for surgery. The right radial artery is cannulated for continuous arterial pressure

monitoring. General anesthesia is induced. Endotracheal intubation is established using a double-lumen

tube for selective one-lung ventilation during surgery. A sheath is inserted in the internal jugular vein,

and a pulmonary balloon-tipped catheter is floated into the pulmonary artery for continuous monitoring

of the central venous and pulmonary artery pressures. Large-bore central and peripheral venous lines

are established for fluid and blood replacement therapy. Temperature probes are placed in the patient’s

nasopharynx and bladder. Electrodes are attached to the scalp for electroencephalography and along the

spinal cord for both motor- and somatosensory-evoked potential (MEP and SSEP) to assess the central

nervous system and spinal cord function, respectively (Fig. 95-5). The patient is then positioned on the

right side with the hips and knees flexed to open the intervertebral spaces. A lumbar catheter is placed

in the third or fourth lumbar space to provide cerebrospinal fluid (CSF) pressure monitoring and

drainage (Fig. 95-6). The CSF pressure is kept at 10 mm Hg or less by gravity drainage of CSF

throughout the procedure. The patient is then repositioned in the right lateral decubitus position with

the hips slightly turned to allow access to both groins. The operative field is scrubbed using standard

aseptic solution and draped.

Figure 95-5. Sagittal computed tomography image of an extent II TAAA.

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Figure 95-6. Placement of the lumbar catheter in the third or fourth lumbar space to provide cerebrospinal fluid drainage and

pressure monitoring.

The incision is tailored to complement the extent of the aneurysm (Fig. 95-7). The full

thoracoabdominal incision begins posteriorly between the tip of the scapula and the spinous process,

curving along the sixth intercostal space to the costal cartilage, and then obliquely to the umbilicus. The

latissimus dorsi muscle is divided and the insertion of the serratus anterior muscle is mobilized. The left

lung is deflated and the left thoracic cavity is entered. Usually, a full thoracoabdominal exploration is

necessary for extent II, III, and IV TAAAs. A modified thoracoabdominal incision begins similar to the

full thoracoabdominal incision, but ends at the costal cartilage. The modified thoracoabdominal incision

provides excellent exposure for surgery involving the descending thoracic aorta, extents I and V TAAA

when the aneurysm ends above the renal arteries. A self-retaining retractor is placed firmly on the edges

of the incision to maintain full thoracic and abdominal exposure during the procedure.

The dissection begins at the level of the hilum of the lung cephalad to the proximal descending

thoracic aorta. The ligamentum arteriosum is identified and transected, taking care to avoid injury to

the left recurrent laryngeal nerve. The extent of the distal abdominal aneurysm is assessed. Only the

muscular portion of the diaphragm is divided and the left phrenic nerve preserved (Fig. 95-8). A

retroperitoneal plane is then developed, mobilizing the spleen, bowel, and left kidney to the right side

of the abdominal aorta (medial visceral rotation). To prepare for distal aortic perfusion, the patient is

anticoagulated using intravenous heparin (0.5 to 1 mg/kg body weight). The pericardium is opened

posterior to the left phrenic nerve to allow direct visualization of the pulmonary veins and left atrium.

The left inferior pulmonary vein is cannulated. A centrifugal pump with an inline heat exchanger is

attached to the outflow cannula and the arterial inflow is established through the left common femoral

artery via a Dacron graft sutured to the common femoral artery in an end-to-side fashion, or the

descending thoracic aorta, if the femoral artery is not accessible. The end-to-side fashion prevents

ischemia to the left leg that may be associated with renal dysfunction. Distal aortic perfusion is begun

(Fig. 95-9).

Padded clamps are applied to the proximal descending thoracic aorta just distal to the left subclavian

artery and the midthoracic aorta. When the proximal extent of the aneurysm is too close to the left

subclavian artery, the aorta between the left common and left subclavian arteries is clamped. The left

subclavian artery is clamped separately. Because of the danger of graft–esophageal fistula, the inclusion

technique for the proximal anastomosis is no longer used. Instead, the aorta is transected to separate it

from the underlying esophagus (Fig. 95-10A). A woven Dacron graft impregnated with collagen or

gelatin for replacement is preferred. The graft is sutured in an end-to-end fashion to the descending

thoracic aorta, using a running 2-0 or 3-0 monofilament polypropylene suture. The anastomosis is

checked for bleeding. Pledgeted polypropylene sutures for reinforcement are placed, if necessary.

Sequential clamping is used for all TAAAs. After completion of the proximal anastomosis, the

middescending aortic clamp is moved distally onto the abdominal aorta at the celiac axis to

accommodate intercostal reattachment. Reattachment of patent, lower intercostal arteries (T8 to T12) is

performed, except in cases of occluded arteries, heavily calcified aorta, or acute aortic dissection,

guided by the neuromonitoring, that is, MEPs and SSEPs. If no changes are noted in the

neuromonitoring of the spinal cord, then patent intercostal arteries can be ligated without fear of spinal

cord injury. If intercostal reattachment is performed, the proximal clamp is released from the aorta and

reapplied on the aortic graft beyond the intercostal patch, restoring pulsatile flow to the reattached

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intercostal arteries (Fig. 95-10B). The distal clamp is moved onto the infrarenal aorta, the abdominal

aorta is opened, and the graft is passed through the aortic hiatus. The celiac, superior mesenteric, and

renal arteries are identified and perfused using 9- or 12-Fr balloon-tipped catheters, depending on the

size of the ostia (Fig. 95-10C). The delivery of cold perfusate (4°C) to the viscera depends on the

proximal aortic pressure, which is maintained between 300 and 600 mL/min. Renal temperature is

directly monitored and kept at approximately 15°C. The visceral vessels are usually reattached using the

inclusion technique. On completion of this anastomosis, the proximal clamp is moved beyond the

visceral patch, restoring pulsatile flow to the viscera and kidneys (Fig. 95-10D). The final graft

anastomosis is then completed at the aortic bifurcation. In most cases, an island patch accommodates

reattachment of the celiac, superior mesenteric, and both renal arteries. If the right or left renal artery

is located at too great a distance from other arteries, its reattachment usually requires a separate

interposition bypass graft. A visceral patch is no longer used for patients with connective tissue disease

(Marfan) and in patients younger than 60 years because of the high incidence of recurrent patch

aneurysms in such cases. Instead, a woven Dacron commercially available graft is used with side-arm

grafts of 10 mm and 12 mm for separate attachment of the celiac, superior mesenteric, and the left and

right renal arteries. Similarly, in these patients, a loop graft has replaced the island patch for

reattachment of the intercostal arteries.

Figure 95-7. Tailoring of thoracoabdominal incisions for aneurysm extent. DTAA, descending thoracic aortic aneurysms; TAAA,

thoracoabdominal aortic aneurysm; SMA, superior mesenteric artery.

Figure 95-8. In previous surgical practice, the diaphragm was divided (A); currently, only the muscular portion of the diaphragm is

cut (B).

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Figure 95-9. Distal aortic perfusion from the left inferior pulmonary vein to the left common femoral artery.

Figure 95-10. Sequential clamping and graft replacement. Padded clamps are placed on the proximal and middistal descending

thoracic aorta. A: The proximal part of the aneurysm is opened. The aortic neck is completely transected and separated from the

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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.

The patient is weaned from partial bypass once the core body or nasopharyngeal temperature reaches

36°C. Protamine is administered (1 mg/1 mg heparin), and the atrial and femoral cannulae are

removed. Once hemostasis is achieved, two or three 36-Fr chest tubes are placed in the pleural cavity

for drainage. The diaphragm is reapproximated using running 1-0 polypropylene suture. The left lung is

reinflated. Closure of the incision is done in a standard fashion. The patient is placed in the supine

position 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). Figure 95-11 shows an extent II TAAA before and after

surgery.

Elephant Trunk Technique for Extensive Aortic Aneurysms

Single-stage repair of extensive aneurysms involving the ascending, arch, and thoracoabdominal aorta

greatly increases operative risks. The patient undergoes a lengthy procedure that requires multiple

incisions, a daunting array of protective surgical adjuncts, protracted clamp times, and considerable

blood loss. Staged repair is a practical solution. Prior to the introduction of the elephant trunk technique

by Borst46 in 1983, staged repair was fraught with complications, particularly excessive bleeding from

the pulmonary artery and thoracic aorta in the second-stage repair of the thoracic or thoracoabdominal

aorta. The elephant trunk technique resolves this problem because it allows the surgeon to avoid

surgical manipulation and cross-clamping the proximal native descending thoracic aorta in the second

stage.

The first stage of the elephant trunk technique is performed in a similar fashion to standard surgery of

the ascending aorta and transverse arch, with the exception that either an inverted distal graft or a

commercially available collared graft is inserted distally (Fig. 95-12A). The folded edge of the inverted

graft or the collared portion of the elephant trunk graft is sutured to the descending thoracic aorta just

distal to the left subclavian artery. When the distal anastomosis is completed, the inner portion of the

inverted graft is retrieved. A side hole is made in the graft, and the aortic island containing the great

vessels is reimplanted. The proximal anastomosis to the ascending aorta is completed, and the distal

portion of the graft, or “elephant trunk,” is left dangling in the proximal descending aorta. In the first

stage, cardiopulmonary bypass, profound hypothermia, circulatory arrest, and retrograde cerebral

perfusion provide protection to the brain and guard against stroke.

The second stage of the elephant trunk technique is much like standard TAAA repair, using the

adjuncts distal aortic perfusion and CSF drainage. After initiation of the pump, the distal clamp is

applied at the mid-descending thoracic aorta. The proximal third of the descending thoracic aorta is

opened without a proximal clamp. The elephant trunk portion of the graft, inserted in the descending

thoracic aorta during stage 1, is grasped quickly and clamped (Fig. 95-12B and C). The new graft is

sutured to the “elephant trunk” to replace the remaining aneurysm.

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Figure 95-11. Example of TAAA extent II repair. (A) Preoperative computed tomography showing proximal part of the aneurysm

with chronic dissection. Intraoperative photograph of the thoracoabdominal aortic aneurysm before (B) and after (C) graft

replacement. The proximal anastomosis was just distal to the left subclavian artery; the patent lower intercostal arteries were

reattached; the celiac, superior mesenteric and right renal arteries were reimplanted together; the left renal artery was reimplanted

via an interposition bypass graft; and the distal anastomosis was to the aorta just above the bifurcation. The separate left renal

artery graft was necessary because it was located far away from the remaining visceral arteries.

Figure 95-12. Elephant trunk technique. Illustration of completed stage 1 elephant trunk (A). In stage 2, the proximal aneurysm is

opened and the existing graft is quickly grasped (B) and clamped (C). The remainder of the surgery follows the standard technique

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for thoracoabdominal aortic aneurysm.

POSTOPERATIVE MANAGEMENT

In the ICU, the patient’s hemodynamic status is monitored very closely. The patient is awakened as

quickly as possible to check neurologic status. Most patients may be extubated within hours of arriving

to the ICU assuming swelling is minimal and hemodynamics are stable. Blood loss is liberally replaced

using banked blood products. The patient’s mean arterial pressure is maintained between 80 and 90 mm

Hg to ensure adequate organ perfusion, particularly to the spinal cord. CSF pressure is continuously

monitored. Approximately 10 to 15 mL of CSF is drained hourly to keep CSF pressure at 10 mm Hg or

less. Ideally, the patient is weaned off the ventilator on the first postoperative day. Oral diet is resumed

when the patient is extubated and has bowel sounds.

After the patient recovers from anesthesia and is moving all extremities, potential delayed neurologic

deficit (DND) is monitored. Warning signs for DND include unstable arterial blood pressure,

hypoxemia, low hemoglobin (<10 g/dL), or increased CSF pressure (>15 mm Hg). CSF drainage is

discontinued on the third postoperative day. The length of stay in the ICU is about 3 to 4 days,

depending on the neurologic and pulmonary status of the patient.47 The patient is subsequently

transferred to the telemetry floor. Physical therapy is initiated in the ICU and continued throughout

the patient’s hospital stay.

Annual CT scan follow-up is recommended to screen for the development of new aneurysms or graftrelated pseudoaneurysm formation. The frequency of follow-up visits or CT scans varies based on

TAAA etiology. For example, patients with remaining unoperated aortic dissection, connective tissue

disorders (Marfan syndrome), family history of aortic aneurysm, or concurrent aneurysms may need

closer surveillance.

SURGICAL OUTCOMES

2 Mortality rates for patients undergoing TAAA and descending thoracic aortic aneurysm repair range

between 4% and 21%.12,48–51 The variable success rates are partly related to the heterogeneity of the

patient population and the expertise of the treating team. In the cumulative experience of the authors of

this chapter (January 1991 to July 2012), 1,511 patients underwent TAAA and descending thoracic

aortic aneurysm repair. Of these patients, 64% were men with a median age of 67 years (range, 8 to 91

years). Approximately 7% of patients had emergency surgery for free or contained rupture of TAAA or

descending thoracic aortic aneurysm. Currently, the 30-day mortality rate is approximately 15%, but

patients with normal renal function, that is, with calculated glomerular filtration rate (GFR) >90

mL/min/1.73 m2, the early mortality was 5.9%. Using multivariable analysis, advanced age, renal

failure, and paraplegia have been identified as important risk factors for mortality.52 Overall, 70% of

patients recover from TAAA without significant postoperative complications.53 The 5-year survival for

patients after TAAA is between 60% and 70%. Recently, negative predictors for long-term survival were

found to include advanced age, extent II TAAA, renal failure, emergency surgery, cerebrovascular

disease, and active tobacco smoking.52

Neurologic Outcomes

3 Postoperative neurologic deficit remains the most devastating complication following TAAA repair.

When the descending thoracic aorta is cross-clamped, the spinal cord is quickly rendered ischemic

because of the immediate interruption of perfusion to the spinal cord and consequent increased CSF

pressure. Therefore, in the “cross-clamp-and-go” era, the single most important predictor of neurologic

deficit was the length of clamp time. The rationale for the present method of protection is to increase

the spinal cord perfusion pressure directly with distal aortic perfusion, and indirectly by reducing CSF

pressure to 10 mm Hg or less. Animal and human studies have confirmed that CSF drainage reduces CSF

pressure and can improve spinal cord perfusion during aortic cross-clamping.54–56

The adjuncts, distal aortic perfusion and CSF drainage with moderate hypothermia, were used in 1,155

of 1,511 (76%) patients. In our cumulative experience, the use of combined adjunct distal aortic

perfusion and CSF drainage has been associated with a 44% reduction in the odds of neurologic

deficit across all aneurysm extents. That is, the overall incidence of neurologic deficit for all patients

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without the use of adjunct was 4.5%, whereas it was 2.5% for those with adjunct. While aortic crossclamp time remains a major predictor of paraplegia when plotted on a continuum, the curve has

shifted to the right with longer ischemic tolerance provided by the adjuncts. In high-risk extent II

aneurysms, adjuncts reduced neurologic deficit from 30% to 9% at the average aortic cross-clamp

time of 75 minutes (Fig. 95-13). When all aneurysm extents are modeled together with nonadjunct

cases excluded, use of adjuncts has pushed the rates down to the range of 1% to 5% and vastly

increased clamp time tolerance. This combination of results has made the current statistical models

insensitive to cross-clamp time, so that although the intercept for extent II aneurysms is greater, the

estimates for all extents are flat across clamp time (Fig. 95-14). Clearly, the adoption of adjunct has

impacted the overall incidence of neurologic deficit, and this has led us to recategorize “low” versus

“high” risk, as “extent non-II” versus “extent II.”57

Figure 95-13. 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.

Figure 95-14. For thoracoabdominal aortic aneurysms and all other aneurysms, the use of adjuncts has made the probability of

neurologic deficits low and unrelated to cross-clamp time.

Since 1991, distal aortic perfusion and CSF drainage have been utilized as adjuncts for all patients

undergoing elective repair of TAAA. Overall, in a total of 1,004 patients, immediate postoperative

neurologic deficit (paraplegia or paraparesis that occurs as the patient awakens from anesthesia)

occurred in 2.4% of patients operated with adjuncts, and in 6.8% patients without adjuncts.52 This

combination of adjuncts has reduced the cumulative rate of neurologic deficits to 0.9% for

descending thoracic aortic repair and to 3.3% for thoracoabdominal aortic repair.52 Repair of the

most extensive TAAAs (extent II) has long been known to result in the highest incidence of

neurologic deficits. In the cross-clamp-and-go era, this incidence was as high as 30% to 40%.50 With

the use of adjuncts, the rate of immediate neurologic deficits for extent II TAAA has been reduced to

7.2%52 (Fig. 95-15). In addition to the extent of the aneurysm, other perioperative risk factors for

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immediate neurologic deficits include age, emergency presentation, renal dysfunction, active

smoking, and cerebrovascular disease. The use of intraoperative distal aortic perfusion and

perioperative CSF drainage, in combination, prevents 1 neurologic deficit in 20 cases for all patients,

and 1 in 5 for extent II TAAA.52

Figure 95-15. The probability of neurologic deficit increases with clamp time and is markedly higher in patients undergoing

thoracoabdominal aortic aneurysm surgery without adjuncts.

Also important in spinal cord protection is the reimplantation of intercostal arteries. During the era of

cross-clamp-and-go reimplantation of intercostal arteries was found to be a risk factor for postoperative

neurologic deficit.58 This link was explained by the longer cross-clamp time required to reattach the

intercostal arteries. The level at which the anterior radicular artery, known as the artery of Adamkiewicz

or arteria radicularis magna, originates is known to be variable. Most commonly, this artery branches

from one of the lower intercostal arteries with or without additional collateral branches from nearby

intercostal arteries. The anterior radicular artery is believed to be the major blood supply to the

anterior spinal artery of the spinal cord. The relationship of neurologic deficit to ligation,

reimplantation, and pre-existing occlusion of intercostal arteries in patients undergoing TAAA repair

using adjuncts has been studied. It was found that ligation of patent lower intercostal arteries (T9 to

T12) increased the risk of paraplegia.58 Therefore, all patent lower intercostal arteries from T9 to T12

are reattached, either together as a patch to a side hole made in the Dacron graft or, when the

intercostal arteries are too far apart, separately as buttons or using interposition bypass grafts.

However, if the lower intercostal arteries are occluded, the patent upper intercostal arteries will be

reimplanted, because these are thought to assume a more important role in the collateral system to the

anterior spinal artery in this situation.

Adequate spinal cord perfusion pressure should be maintained with avoidance of hypotension during

and after surgery. Intravenous nitroprusside, in particular, can precipitate systemic hypotension, and has

been shown to cause a paradoxical increase of CSF pressure.59 Therefore, it is no longer used. A detailed

account of the essential anesthetic care during TAAA repair is beyond the scope of this chapter.

However, the importance of adequate maintenance of systemic arterial pressure with judicious blood

transfusion cannot be overemphasized, as organ perfusion greatly depends on the systemic circulation.

Clearly, the era of cross-clamp-and-go is over and the spinal cord must be provided with some form of

protection.

Cord function can be assessed using intraoperative neurophysiologic monitoring with MEPs and SSEPs

as performed routinely in aortic surgery.60,61 For SSEP, probes are placed at the malleolus

bilaterally, stimulating the posterior tibial nerve. Recordings are performed at three sites (Fig. 95-4),

including the popliteal fossa, C5, and the vertex with a positive finding defined as a drop in

amplitude by 50% and/or a change in latency by 10%. For MEP, precentral gyrus is stimulated and

recording is measured at three sites, including the abductor digiti minimi, tibialis anterior, and

abductor hallucis muscle. Compound muscle action potential is monitored with a positive finding

defined as an all-or-none potential. If there are signal changes, as defined earlier, intraoperative

corrective measures are performed, which include increasing the mean central pressure to more than

80 mm Hg, increasing distal aortic perfusion pressure to more than 60 mm Hg, lowering the CSF

pressure, increasing the hemoglobin level, and attaching additional intercostal arteries. With the

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