current use of adjunct therapy and intraoperative SSEP and MEP monitoring, the current rate of

immediate neurologic deficit remains at 3.1%.62

Delayed Neurologic Deficits

DND refers to the onset of paraplegia or paraparesis after a period of observed normal neurologic

function. Delayed-onset neurologic deficit after TAAA repair was first reported in 1988, at which time

the condition was considered irreversible and beyond the surgeon’s control.63 Since then, numerous

reports have described improvements in patients neurologic function by using CSF drainage for delayedonset neurologic deficits.64–66 DND has been observed as early as 2 hours and as late as 2 weeks

following surgery (median, 3 days), in 2.7% of patients.67 No single risk factor is responsible for DND.

However, using multivariable analysis, acute dissection, extent II TAAA, and renal insufficiency were

identified as significant preoperative predictors for delayed-onset neurologic deficit.67 In a subsequent

case-control study, postoperative mean arterial pressure of less than 60 mm Hg and CSF drain

complications were found to be predictors in the development of delayed-onset neurologic deficit,

independent of preoperative predictors (Fig. 95-16).68

Figure 95-16. 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 mm Hg and a cerebrospinal fluid drain complication would have 40:1 odds of delayed neurologic deficit.

As improved spinal cord protection during TAAA surgery has reduced the incidence of neurologic

complications, delayed-onset neurologic deficit has emerged as an important clinical entity. The exact

mechanisms involved in the development of DND remain unknown. It is speculated that DND after

TAAA repair may result from a “second hit” phenomenon. Adjuncts can protect the spinal cord

intraoperatively and reduce the incidence of immediate neurologic deficit, but the spinal cord remains

vulnerable during the early postoperative period. Additional ischemic insults caused by hemodynamic

instability, malfunction of the CSF drainage catheter, or both may constitute a “second hit,” causing

DND. Furthermore, in the rigid, unyielding spinal column, any rise in CSF pressure could lead to an

increase in compartment pressure, with consequent decreased spinal cord perfusion. Hence, CSF is

drained freely when DND develops to relieve the compartment pressure.

To optimize postoperative spinal cord perfusion and oxygen delivery, mean arterial pressure is kept

above 90 to 100 mm Hg, hemoglobin above 10 mg/dL, and cardiac index greater than 2.0 L/min. If

DND occurs, measures to increase spinal cord perfusion are instituted immediately. The patient is placed

flat in the supine position. The patency and function of the drain is ascertained at once. If the drain has

been removed, the CSF drainage catheter is reinserted immediately and CSF is drained freely until the

CSF pressure drops below 10 mm Hg. The systemic arterial pressure is raised, blood transfusion is

liberally infused, and oxygen saturation is increased, as indicated above. CSF drainage is continued for

at least 72 hours for all patients with delayed-onset neurologic deficit. Using this multifaceted approach

to treating delayed-onset neurologic deficit, an improvement in neurologic function is seen in 57% of

patients.67 When the CSF drain was still in place at the onset of DND, 75% of patients recovered

function; 43% recovered neurologic function if the CSF drain had to be reinserted at the time of the

DND. Patients who developed DND but did not have CSF drainage failed to recover function.

Renal Failure

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Acute postoperative renal failure is defined as an increase in serum creatinine of 1 mg/dL per day for 2

consecutive days or by the need for hemodialysis. The reported rate of acute renal failure from large

series of patients undergoing TAAA repair falls within the range of 5% to 40% and is associated with

mortality rates as high as 70%. Patients who develop acute renal failure more frequently sustain

nonrenal complications, such as respiratory failure, central nervous system dysfunction, sepsis, and

gastrointestinal hemorrhage. For patients who develop postoperative renal failure, early continuous

venovenous hemodialysis or daily intermittent hemodialysis is initiated. In the experience of the authors

of this chapter, approximately one-third of patients who develop acute renal failure remain on

hemodialysis and, predictably, these patients have a prolonged length of hospital stay. Long-term

survival for patients on hemodialysis is dismal. Preoperative chronic renal insufficiency and ruptured

aneurysms are known predictors of acute postoperative renal failure. Although the authors of this

chapter have theorized that patients with the most extensive extent II TAAA are at highest risk for the

development of postoperative renal failure, extent of TAAA has not been shown to be a significant

predictor.

The goals of perioperative renal protection are to maintain adequate renal oxygen delivery, reduce

renal oxygen utilization, and reduce direct renal tubular injury. However, good strategies to protect

renal function during surgical TAAA repair remain elusive. The benefit of cold temperatures for

metabolic suppression in organ protection is well known. Local hypothermia has been shown to protect

against renal ischemia and reperfusion injury in laboratory animals, and there is some evidence that

patients with cold visceral perfusion have superior survival and recovery rates. However, this strategy

has not decreased the incidence of acute renal failure. The incidence of postoperative renal failure

remains troublesome and the pursuit of an optimal method of renal protection continues to be a top

priority.

Glomerular Filtration Rate

4 Clinically apparent renal insufficiency is a known predictor of 30-day mortality. The overall 30-day

mortality was 227 of 1,511 (15%), and the 5-year survival rate was 54%. Increasingly, we are finding

that mortality cannot properly be interpreted without knowledge of preoperative GFR. With normal

GFR (>90 mL/min/1.73 m2), 30-day mortality was 6%, whereas 5-year survival was 77%. With a

decline in GFR to the 65 to 90 range, 30-day mortality was 8.9%. Below a GFR of 65, 30-day mortality

increases to 22%. Long-term survival stratified by quartile of GFR is shown in Figure 95-17. The effect

of GFR on both short-term mortality and long-term survival was highly statistically significant (p

<0.0001 for both measures).

Recently, in patients undergoing TAAA repair without apparent renal disease, we have found that

calculated GFR is a much stronger predictor for mortality than serum creatinine.69 We have used and

appraised many different forms of renal protection, including distal aortic perfusion, warm blood

visceral perfusion, antegrade cold blood visceral perfusion, retrograde cold blood perfusion, and the

perioperative use of a renal protective pharmacologic agent, fenoldopam. None of these yielded overly

promising results. Using multivariable analyses, we found that preoperative renal failure (creatinine

>2.8 g/dL), left renal artery reattachment, visceral perfusion, and clamp-and-sew technique are

predictors of acute renal failure.57

Figure 95-17. Long-term survival stratified by quartile of glomerular filtration rate.

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In the past, we had used visceral perfusion without cooling or systemic heparin, and this was likely

the reason for the negative effect of visceral perfusion on renal protection. We recently reviewed the

impact of various adjuncts on renal function. Distal aortic perfusion has emerged as protective but only

for aortic repair that does not directly involve the renal arteries. There is evidence, however, that

patients treated with cold blood visceral perfusion have superior survival and recovery rates, which may

be related to improved liver protection. Thus far, none of the adjuncts evaluated have clearly prevented

acute renal failure. The major predictors of postoperative renal dysfunction remain preoperative renal

function, cross-clamp time, and repair extending to the renal arteries.

Excluding patients who had clinically apparent preoperative renal failure, we found that acute renal

failure occurred in 344 of 1,261 (27.2%) of our patients overall. For patients with preoperative GFR

above 90, renal failure was 62 of 367 (17%). When GFR was between 65 and 90, postoperative renal

failure was 70 of 310 (23%). At GFRs below 65, renal failure was 212 of 584 (36%). Thirty-day

mortality among patients with acute renal failure was 34% compared to 10% mortality for all other

patients. Aneurysms involving the visceral vessels (extents II, III, and IV) were much more likely to

produce renal failure postoperatively (39 vs. 17%, p <0.0001). Approximately one-third of our patients

who developed acute renal failure remained on hemodialysis, and long-term survival for patients on

hemodialysis has been dismal.

Complications

A summary of complications is shown in Table 95-1. These figures are compiled from a collection of

sources.70–80

Elephant Trunk Technique

The authors of this chapter have performed the two-staged elephant trunk procedure in 348 patients

with extensive aortic aneurysms.81 Mortality rates range from 5% to 10% after stage one and 5% to

15% for stage two, depending on renal function. For patients with normal kidneys (GFR >90),

mortality for each stage was 5%. During the interval between the two stages (approximately 31 days

and 6 weeks), mortality has averaged around 6.5%, ranging from 4% to 17%, depending on why the

second stage was not completed. When a 5-year follow-up of patients who failed to return for secondstage repair was performed, 32% had died. Although we were unable to determine the exact cause of

death for many of these patients, it is likely that a significant number of deaths were a result of

aneurysm rupture. Major complications for both stages have been relatively low, with stroke rates of

2% in the first stage and no neurologic deficits in the second. Determining the optimum length of

recovery time between stages has been difficult. Because these patients are vulnerable to rupture, it is

currently recommended that the second-stage repair be performed after a 4- to 6-week period of

recovery.

COMPLICATIONS

Table 95-1 Complications of Open TAAA Repair

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Impact of Aortic Dissection

Aortic dissection has long been considered a risk factor for neurologic deficit in patients undergoing

repair of descending thoracic and TAAAs, particularly during the clamp-and-go era.82–85 However, in a

series of 729 patients operated on for descending thoracic and TAAAs, no differences were reported in

neurologic outcome between those patients with and without chronic dissection. The rate of paraplegia

was 3.6% with dissection versus 4.7% without dissection.86 Several factors are likely responsible for the

good neurologic outcome of patients with chronic dissection, including better surgical techniques and

anesthetic care, moderate hypothermia, and reimplantation of intercostal arteries. The key element in

the improved spinal cord protection; however, has been the use of the adjuncts distal aortic perfusion

and CSF drainage.

In acute aortic dissection, the risk of paraplegia following graft replacement of the descending

thoracic or thoracoabdominal aorta remains substantial with a neurologic deficit rate of 32%.87

Nevertheless, acute dissection aneurysm patients are usually critically ill, undergoing surgery

emergently with little time for preparation. The method of spinal cord protection employed during

surgery for acute dissection is often not optimal. In particular, reimplantation of intercostal arteries is

ill-advised because of the risk of catastrophic bleeding from the friable dissected tissues, and the use of

the adjuncts distal aortic perfusion and CSF drainage may not be possible in the presence of

hemodynamic instability.

Endovascular Repair

Since the first successful reported thoracic stent graft repair in 1994,88 endovascular management of

thoracic aortic pathology has evolved at a rapid pace. The first thoracic aortic device to receive US Food

and Drug Administration (FDA) approval in the United States was the GORE TAG (WL Gore, Flagstaff,

AZ) device in 2005. Since then, three additional devices, including the Valiant Thoracic (Medtronic,

Santa Rosa, CA), the Zenith TX2 (Cook, Bloomington, IN), and the Relay (Bolton Medical, Sunrise, FL,

USA) have received FDA approval. The benefits of endovascular therapy include decreased morbidity

and mortality compared with conventional open surgery. Endovascular treatment of a TAAA would

require revascularization of visceral and renal vessels. Endovascular repair is currently being performed

using three different approaches, including “hybrid repair,” use of parallel grafts, and custom-made

branched and fenestrated devices.

The hybrid approach requires combined open debranching of the aorta with subsequent endovascular

coverage of the aneurysmal segment.89 The debranching procedures entail an open retroperitoneal

or transperitoneal approach for extra-anatomical bypassing of the visceral and renal arteries from

either iliac artery. This is subsequently followed by exclusion of the thoracoabdominal aorta with

stent grafts. The potential benefits of hybrid repair include the avoidance of open thoracotomy,

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aortic cross-clamping, and single-lung ventilation. 90–92 Although this approach is technically

feasible, the risk of morbidity and mortality remains discouragingly high. More recent literature has

suggested that the hybrid repair has no significant difference in outcomes compared to open TAAA

repair.93–95 Indications for this approach will likely be limited to patients with TAAA who are unfit

for open repair and those who are not candidates for other endovascular repair techniques (i.e.,

those with tortuous or inaccessible vessels, or insufficient time to order a customized stent graft).

Another approach involves the use of parallel grafts (chimneys, periscopes, or snorkels, commonly

referred to as CHIMPS) to preserve blood flow to branch vessels. This technique was championed by

Lobato et al. from Brazil, who reported their experience with 78 patients, 15 of whom had a TAAA.96

Overall, they reported a technical success rate of 98.7%. Over a mean follow-up period of 17

months, the primary patency was 96.7% and early mortality was 5.1% (late: 1.3%). The reported

advantages of the parallel stent grafts include the availability of a modular, off-the-shelf option that

can be tailored to any anatomy.97 This is especially useful in patients who have small and/or

tortuous vessels, history of dissection, or a significant thrombus burden in the paravisceral aorta.

The inherent disadvantages to this approach include potential endoleaks from the “gutters” that can

lead to pressurization of the aneurysm sac. 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%.98

Finally, total endovascular TAAA repair can be performed using custom-made branched and/or

fenestrated devices. The largest series by Greenberg et al. on their experience with 406 patients

reported a perioperative mortality of 2.3% for extent IV, 5.2% for extent II and III, and 12.5% for

extent I aneurysms.99 The estimated 24-month survival was 82%, 74%, and 70% for extents IV, II

and III, and I, respectively. Late complications included rupture in two patients. In a multicenter

prospective study of 268 patients undergoing endovascular fenestrated and/or branched repair for

juxtarenal, pararenal, and TAAA, Marzelle et al. reported 30-day mortality, inhospital mortality

(IM), and combined mortality and severe complications (CMSC) rates of 6.7%, 10.1%, and 22.0%,

respectively.100 The authors concluded that due to the significant rate of mortality and

complications, new strategies should be investigated to improve outcomes. Although significant

progress has been made, the endovascular technologies continue to mature at a rapid pace.

Ultimately, endovascular repair of TAAA will require modular, off-the-shelf devices that can be

tailored to the variety of clinical circumstances.

ACKNOWLEDGMENTS

The authors of this chapter are grateful to G. Ken Goodrick, editor, and to Chris Akers for assistance

with the illustrations.

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