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Volume 45, Issue 4, Pages 667-676 (April 2007)


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Contemporary results of open repair of ruptured descending thoracic and thoracoabdominal aortic aneurysms

Presented at the Twentieth Annual Meeting of the Eastern Vascular Society, Washington, DC, Sept 28-30, 2006.

Joel E. Barbato, MD, Jang Yong Kim, MD, Mazen Zenati, MD, PhD, Ghassan Abu-Hamad, MD, Robert Y. Rhee, MD, Michel S. Makaroun, MD, Jae-Sung Cho, MDCorresponding Author Informationemail address

Received 17 October 2006; accepted 13 December 2006.

Objective

The purpose of this study was to evaluate the results of open repair for ruptured descending thoracic and thoracoabdominal aortic aneurysm (RDTAA).

Methods

A retrospective review identified 41 consecutive cases of open surgical repair in 40 patients presenting with nontraumatic, atherosclerotic RDTAA from 1996 to 2006. Patients with traumatic injuries or complicated dissections were excluded. Patient characteristics and preoperative, intraoperative, and postoperative variables were collected from the medical record. Univariate and logistic regression were used to identify factors contributing to mortality and morbidity in these patients.

Results

The operative mortality rate was 26.8% (11/41). All but two deaths occurred within 24 hours of operation; seven were intraoperative. Overall actuarial survival rates at 1 and 2 years were 53.7% and 47.1%, respectively. For those who survived to hospital discharge, the respective numbers were 73.3% and 64.4%. Intraoperative hypotension and blood transfusion requirements were independent predictors of perioperative death. Octogenarians had a mortality rate equivalent to that of the younger population (25% vs 27.6%; not significant). There was a strong trend toward an improved outcome in the latter part (2003-2006) compared with the first part (1995-2002; 13.6% vs 42.1%, respectively; P = .075).

Conclusions

Direct open repair for RDTAA can be achieved with acceptable mortality and morbidity rates even in elderly patients. Improved outcome can be expected with increased volume and experience. This series should help establish a reference against which the results of endovascular endeavors and hybrid procedures could be compared.

Article Outline

Abstract

Materials and methods

Results

Discussion

Author contributions

Acknowledgment

Appendix

References

Copyright

Repair of descending thoracic aneurysms (DTA) and thoracoabdominal aortic aneurysms (TAAA) continues to present a significant challenge to the surgeon, with high attendant rates of morbidity and mortality. Aneurysms that present with evidence of either free or contained rupture present an even greater challenge because these patients historically have had even higher risks of postoperative complications. These emergency cases may constitute 15% to 20% of all TAAA repairs.1, 2 The literature is relatively sparse with respect to the surgical outcomes, and the published results vary widely. High-volume single-center experiences have reported operative mortality rates of 15% to 20%, whereas statewide and Nationwide Inpatient Sample reviews1, 3 have noted mortality rates of approximately 50%.

This study was conducted to review a contemporary series of direct surgical repair of ruptured DTA and TAAA (RDTAA) in a tertiary referral center to identify prognostic indicators for adverse outcome and to assess mid-term outcome in these patients. This has become increasingly important in the context of broader application of endovascular techniques and development of hybrid procedures to treat more complex aortic pathology.4, 5, 6, 7, 8, 9

Materials and methods 

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A retrospective review of 40 consecutive patients who underwent 41 repairs of RDTAA between July 1995 and June 2006 was performed. All had atherosclerotic aneurysms except one patient who presented with a ruptured perivisceral aneurysm of a visceral patch after previous repair. Excluded were patients who underwent repair for traumatic aortic disruptions or complicated acute aortic dissections. Diagnosis of rupture was made on the basis of preoperative computed tomography findings and confirmed in all patients by intraoperative visualization of blood outside the aneurysm wall, either in the retroperitoneum or mediastinum for a contained rupture or into the abdominal or pleural cavity for a free rupture in all patients. There were an additional 10 patients during the study period who did not receive an operation as a result of either prohibitive medical factors or patient/family refusal.

Operative mortality was defined as death that occurred within 30 days of operation or in-hospital death if later than 30 days. Preoperative shock was defined as systolic blood pressure less than 90 mm Hg or a requirement for preoperative cardiopulmonary resuscitation (CPR). Roughly half (n = 19) of the operations were performed in the first 8 years of our experience and the remaining half in the last 3 years. All the medical records and available radiographic imaging studies were reviewed. Clinical follow-up examination was complemented with review of the medical records and with telephone contact with the patient or family.

Operations were performed by five different surgeons in the division of vascular surgery at the University of Pittsburgh Medical Center. Cerebrospinal fluid (CSF) drainage was performed on the basis of surgeon preference and the stability of the patient. With respect to use of adjunctive techniques for end-organ protection, the clamp-and-sew technique was used routinely for type IV aneurysms. For all others, surgical technique, including the decision to place the patient on left heart bypass, was determined by the hemodynamic stability of the patient at presentation. Intercostal arteries were not routinely reimplanted, except in one case early in our experience, and every effort was made to preserve those near or at the anastomotic site by beveling the anastomoses. All the visible intercostals were ligated before the aneurysm was opened, to minimize backbleeding and spinal cord ischemia. Any patent vessels were then suture-ligated. Single-lung ventilation was used in all patients. Perfusion to the visceral arteries was not used, although cold perfusion to the renals was used when the hemodynamics of the patient permitted. When left heart bypass was instituted, systemic heparin was used, and flows were adjusted to maintain mean arterial pressure between 60 and 70 mm Hg measured via the right femoral arterial catheter. CSF drainage was maintained to keep the pressure less than 10 cm H2O for 2 to 4 days after surgery. Naloxone, when used, was started at the beginning of the operation at 1 μg · kg−1 · h−1 and continued for 1 or 2 days.10

Continuous variables are summarized as mean ± SD, and nominal variables are summarized as counts or percentages. Intergroup comparisons were performed with Wilcoxon signed rank tests for continuous variables or Fisher exact test statistics for nominal variables. Two-year survival rates were calculated by using Kaplan-Meier statistics, and comparisons of time-to-event curves were accomplished with log-rank statistics where appropriate. Multivariable logistic regression was used to assess demographic, clinical, and procedural factors independently associated with in-hospital outcomes and included death, dialysis, need for tracheostomy, paraplegia, and paraparesis. Cox proportional hazards methodology was used to build a model for 2-year mortality. The long-term survival rates were estimated with the Kaplan-Meier method. This study was approved by the University of Pittsburgh Institutional Review Board.

Results 

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The baseline characteristics of the patients in our study are listed in Table I. The extent of the aneurysms was as follows: type I in 8 patients, type II in 3, type III in 11, type IV in 13, and descending thoracic in 6. The time from the onset of symptoms to operation was less than 6 hours in 10 patients, between 6 and 24 hours in 13 patients, and more than 24 hours in 16 patients; this information was not available in 2 patients. The mode of transportation at presentation was by air in 28 cases (68.3%) and by ground transport in 9. Four patients were inpatients at the time of their ruptures; all patients were admitted with symptoms consistent with but had computed tomographic scans that did not demonstrate rupture. They subsequently all had clinical deterioration (three with hypotension) and intraoperative findings consistent with rupture. Those patients with a shorter duration from symptom onset to operative repair were more likely to present in shock requiring CPR with an in-hospital mortality of 50% vs a mortality of 6.7% (P < .05) in those with symptom duration of greater than 24 hours (Appendix Table I, Appendix Table II). Otherwise, the preoperative characteristics and postoperative outcomes were similar between these groups.

Table I.

Baseline characteristics of patients undergoing repair of ruptured DTA and TAAA

VariableData
Age (y)75.5±6.6
Female39.0(16)
White94.9(39)
History of COPD45.0(18)
History of CVA15.0(6)
History of CAD67.5(27)
Smoking38.5(15)
History of diabetes mellitus2.5(1)
Any prior aortic reconstruction36.6(15)
Preoperative characteristics
Symptom onset to OR (h)
<625.6(10)
6-2435.9(14)
>2438.5(15)
Mean time44.9±57.5
Preoperative shock37.5(15)
Preoperative CPR17.1(7)
Aneurysm size and blood chemistry
Mean aneurysm diameter (cm)8.4±2.3
Free rupture26.8(11)
Mycotic7.3(3)
Mean BUN (mg/dL)24.3±10.8
Mean creatinine (mg/dL)1.4±0.7
Mean hemoglobin (g/dL)11.7±4.3
Operative characteristics
After 200253.7(22)
OR time (h)4.4±1.7
OR fluid used4598±2262
Blood units used7.8±5.7
Lowest SBP (mm Hg)72.2±21.7
Intraoperative CPR21.9(9)
Sequential clamp use24.3(9)
Clamp time (min)65.1±19.5
Visceral ischemia time (min)44.3±15.2
Renal ischemia time (min)43.1±23.9
Renal cold perfusion37.1(13)
Renal bypass28.6(10)
Intercostal reimplantation2.9(1)
Left heart bypass41.0(16)
CSF drain55.0(22)
Naloxone22.5(9)

Data are % (n) or mean ± SD.

COPD, Chronic obstructive pulmonary disease; CVA, cerebrovascular accident; CAD, coronary artery disease; OR, operating room; CPR, cardiopulmonary resuscitation; BUN, blood urea nitrogen; SBP, systolic blood pressure; CSF, cerebrospinal fluid.

The mean duration of follow-up for those who survived to hospital discharge was 28.4 ± 26.6 months (range, 1.4-85.6 months). There was one postoperative stroke; this patient died at day 7 after repair. Of the patients surviving to discharge, only 6 patients were discharged home, whereas 24 were discharged either to a skilled nursing facility or rehabilitation center. Four patients required permanent dialysis, one of whom became a long-term survivor.

The operative mortality rate was 26.8% (11/41). All but two deaths occurred within 24 hours of operation. The intraoperative mortality rate was 17% (7/41); 5 of these patients had received preoperative CPR. Four deaths occurred during dissection before the graft could even be implanted. Two other deaths were due to hemorrhagic shock and cardiac arrest shortly after operation. After 24 hours, one death occurred at postoperative day 7 and another at day 31, when the family withdrew support. After hospital discharge, eight additional patients died within 6 months of discharge; the mortality rate at 1 year was 46.3%. Two-year survival curves are represented in Fig 1. The remaining deaths were late deaths, occurring after at least 1 year of survival. Although the cause of death could not be determined in two patients, none of the other deaths was aneurysm related. Factors associated with in-hospital mortality included intraoperative hypotension (P = .007) and a shorter duration from symptom onset to operation (Table II; P = .04). The presence of chronic obstructive pulmonary disease, an increased preoperative blood urea nitrogen, and the presence of type II and III aneurysms were associated with increased mortality after discharge from the hospital (Table III; P < .05).


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Fig 1. Cumulative survival of patients undergoing surgical repair of ruptured descending thoracic and thoracoabdominal aneurysms.


Table II.

Univariate analysis of variables tested for association with in-hospital mortality

VariableIn-hospital mortalityP value
No (n = 30)Yes (n = 11)
Age (y)75.5±6.675.5±6.8.93
History of COPD45.0(12)60.0(6).30
History of CVA13.3(4)20.0(2).63
History of CAD63.3(19)80.0(8).45
Smoking40.0(12)33.3(3)1.0
Any prior aortic reconstruction36.7(11)36.7(4)1.0
Preoperative characteristics
Symptom onset to OR (h) .041
<617.2(5)50.0(5)
6-2434.5(10)40.0(4)
>2448.3(14)10.0(1)
Mean time53.9±62.518.7±28.3.07
Preoperative shock26.7(8)70.0(7).024
Preoperative CPR6.7(2)45.4(5).01
Aneurysm size and blood chemistry
Aneurysm diameter (cm)8.1±1.99.2±3.0.33
Free rupture16.7(5)54.5(6).041
Mycotic3.3(1)18.2(2).17
BUN27.7±11.123.1±10.3.66
Creatinine1.4±0.81.3±0.5.85
Hemoglobin11.3±2.212.8±7.6.92
Operative characteristics
OR time (h)4.9±1.23.3±2.4.08
Excluding intraoperative deaths 5.2±1.4.69
OR fluid used4814±22753902±2199.21
Blood units used6.4±3.812.7±8.2.033
Lowest SBP78.8±13.450.3±29.6.007
Operative CPR3.3(1)72.3(8)<.001
Sequential clamping24.1(7)25.0(2)1.0
Clamp time63.4±18.976.7±22.3.28
Visceral ischemia time42.5±15.154.2±12.7.14
Renal ischemia time38.8±22.471.2±11.1.014
Renal cold perfusion30.0(9)80.0(4).052
Renal bypass26.7(8)40.0(2).61
Intercostal reimplantation3.3(1)0(0)1.0
Left heart bypass46.7(14)22.2(2).26
CSF drain70.0(21)10.0(1).002
Narcan26.7(8)10.0(1).40
Outcomes
Dialysis (any)20.7(6)0(0)1.0
Tracheostomy33.3(10)100.0(1).35
Pneumonia40.0(12)100.0(2).18
Paraplegia/paraparesis13.3(4)50.0(1).29

Data are % (n) or mean±SD.

COPD, Chronic obstructive pulmonary disease; CVA, cerebrovascular accident; CAD, coronary artery disease; OR, operating room; CPR, cardiopulmonary resuscitation; BUN, blood urea nitrogen; SBP, systolic blood pressure; CSF, cerebrospinal fluid.

Table III.

Factors associated with mortality within the first 2 years after discharge from the hospital (Cox proportional hazards methodology)

VariableHazard ratio95% Confidence intervalP value
COPD17.681.47-213.28.024
BUN1.121.03-1.21.005
Extent of repair (vs type IV)
Type I1.320.10-17.49.83
Type II39.281.41-1095.27.031
Type III101.733.62-2856.82.007
Isolated DTA3.510.55-22.58.18

COPD, Chronic obstructive pulmonary disease; BUN, blood urea nitrogen; DTA, descending thoracic aneurysm.

There were 12 octogenarians. Three patients did not survive to hospital discharge, accounting for an operative mortality of 25% as compared with 27.6% in those younger than 80 years (not significant). Three additional patients died within 4 months of hospital discharge, resulting in a 1-year mortality rate of 50%. One additional patient died 22 months later, 1 month before his 90th birthday. The remaining five survivors are alive and well at a mean of 24 months (range, 10-34 months) follow-up. The baseline characteristics and comorbidities, except for age, did not differ between the groups. The only differences observed were lower mean hemoglobin (9.6 ± 1.9 g/dL vs 12.6 ± 4.8 g/dL; P = .005) and shorter mean renal ischemia time (22.4 ± 23.2 minutes vs 49.4 ± 20.7 minutes; P = .02) in those 80 years or older as compared with the younger cohort. Kaplan-Meier survival estimates (Fig 2, A) at 1 and 2 years were 50% and 37.5%, respectively, for octogenarians, whereas the corresponding figures were 55.2% and 50.6% for the younger patients (P = .72).


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Fig 2. Kaplan-Meier analysis of survival after descending thoracic aneurysm and thoracoabdominal aortic aneurysm repair. Survival is analyzed according to age at operation (A) and year of operation (B).


Spinal cord ischemia developed in five (15.6%) of those who survived the operation for more than 24 hours and allowed neurologic evaluation: paraplegia in four patients and paraparesis in one additional patient. The lone patient who developed paraparesis recovered from it without deficits. Paraplegia was delayed in onset in three of four patients, all cases of which were associated with postoperative hypotension. Of the four patients who developed paraplegia, two had intraoperative CSF drainage, and both had delayed paraplegia develop: one while the drain was still in place and the other after its removal. The latter had the drainage reinstituted without benefit. The remaining two patients with paraplegia did not have intraoperative CSF drainage. One of these patients experienced delayed paraplegia and had a lumbar drain placed; no improvement in neurologic function was achieved. Risk factors associated with spinal cord ischemia were extent of the aneurysm, with type II aneurysms having the highest risk for the development of paraplegia (P < .0001; Table IV), and increased aortic cross-clamp time (P = .03).

Table IV.

Factors associated with increased morbidity and mortality with logistic regression analysis

OutcomeOdds ratio95% Confidence intervalP value
Death
Lowest OR blood pressure0.90.82-0.99.037
Need for tracheostomy
Increased aneurysm size (each 1 cm)5.41.12-26.48.036
COPD26.01.57-431.1.023
Paraplegia
Extent of aneurysm <.001
Type II vs I2.0
Type II vs III1.3
Type II vs IV2.0
Type II vs isolated DTA2.0
Clamp time1.11.01-1.16.03
Dialysis
Increased baseline creatinine31.21.6-591.1.02

OR, Operating room; COPD, chronic obstructive pulmonary disease; DTA, descending thoracic aortic aneurysm.

Analysis of variance.

Pulmonary failure requiring tracheostomy developed in 35.5% of patients. Controlling for other operative and patient characteristics, chronic obstructive pulmonary disease (P = .023) and a larger aneurysm were predictive of the need for tracheostomy. For each increase in size of 1 cm, there was more than a fivefold risk for prolonged ventilatory support and progression to tracheostomy (odds ratio, 5.44; P = .036). The incidence of renal failure necessitating either temporary (n = 3) or permanent (n = 4) dialysis was 19.3%. The only identified predictor was increased baseline creatinine (P = .02).

The mortality rate during the first half (19 of 41 cases from 1995 through 2002) of this series was 42.1%, as compared with 13.6% in the latter half of our experience (22 of 41 cases since 2003). Although this did not reach statistical significance, there was a strong trend toward improved survival (Fig 2, B; P = .075). There were no differences in the baseline patient characteristics or preoperative variables (including preoperative shock and the need for CPR) over time, whereas there were significant differences in the intraoperative variables; patients in the latter half of this series had significantly fewer blood transfusions (10.4 vs 5.9 units; P = .037) and a shorter period of renal ischemia (53.5 vs 35.2 minutes; P = .043).

Discussion 

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This study illustrates that repair of RDTAA still poses a daunting challenge to both the surgeon and the patient. It is a highly lethal problem with lasting effects. According to one report, approximately 50% of patients with rupture of a thoracic aortic aneurysm die within 6 hours of the onset of symptoms, and an additional 25% die between 6 and 24 hours, thus allowing little time for surgical repair.11 In this series, the mortality rate was 26.8%, with most deaths (82%) occurring within the first 24 hours after operation and well over half (62%) of late deaths taking place within 4 months of discharge from hospital, thus reflecting a sustained increased risk of mortality even after successful repair and hospital discharge. This corroborates the findings of earlier studies that there is increased age-adjusted mortality throughout the first postoperative year after repair of both ruptured TAAAs and abdominal aortic aneurysms.3, 12 The overall actuarial survival at 1 year was 63.6% and at 2 years was 48.5%. For the hospital survivors, the corresponding figures were 73.3% and 64.4%.

The reason for the high morbidity and mortality is multifactorial and clearly more complex than the hemodynamic instability of the patient at presentation. Previous investigations have shown that advanced age, female sex, type II aneurysms, preoperative renal insufficiency, increased aortic clamp time, preoperative shock, coronary events, and low hospital and surgeon volume increase the risk of adverse outcomes after repair of ruptured or emergent repair of DTA and TAAA.1, 3, 13, 14, 15, 16, 17 Our data confirm that preoperative shock and type II aneurysm portend an increased incidence of mortality and paraplegia, respectively.

A number of earlier reports are difficult to interpret because of the heterogeneous nature of their clinical material. Some included aortic dissections,13, 18, 19, 20, 21 whereas others incorporated symptomatic aneurysms without rupture in their reviews.15, 16 Furthermore, reporting standards for mortality are not uniform across the literature; some report 30-day mortality, and others report in-hospital mortality. The results in this series are within the reported range in the available literature. In a review of statewide experience, Rigberg et al3 reported a 30-day mortality rate of 48.4%, a finding similar to the 53.8% rate in a survey of the Nationwide Inpatient Sample reported by Cowan and associates.1 Smaller institutional series2, 13, 15, 16, 17, 19 have reported mortality rates ranging from 15% to 67%. The mid-term survival rates seen in this series are also in accordance with the findings of earlier reports3, 16, 22 in which 1-year mortality rates have been reported between 47% and 61.5%.

With respect to the effects of age on mortality, a progressive decrease in 1-year survival rates with advanced age, from 44.4% for patients in their 50s to 31.2% for those in their 80s, has been noted.3 Huynh and colleagues23 reported a 50% 30-day mortality rate for “high-risk” octogenarians presenting with rupture, diabetes, or congestive heart failure. In this regard, the results in this report compare favorably; the 1-year survival estimate for octogenarians was 50%, and the 2-year estimate was 37.5%. In our experience, nearly 30% of cases (12/41) were octogenarians, and their mortality did not differ from that of the younger patients. This occurred even though the octogenarians were more anemic at presentation than the younger population; it is of note, however, that they also had a shorter renal ischemic time. Although advanced age has been found to be a predictor of poor acute and long-term outcome,1, 3, 23 our data indicate that age alone is not a major criterion in the decision-making process of whether to offer repair of RDTAAs.

Although adjunctive end-organ protection methods have effectively reduced adverse outcomes in elective settings,24, 25, 26 the time constraints encountered in the life-threatening condition of RDTAA dissuade their routine use. Girardi et al17 used CSF drainage in only 50% of their patients and reported a paraplegia rate of only 5%, similar to their elective data. LeMaire et al19 failed to demonstrate beneficial effects of left heart bypass or intercostal artery attachment against the development of paraplegia in the absence of CSF drainage. In the present study, the efficacy of distal aortic perfusion, CSF drainage, or naloxone could not be demonstrated, largely because it was not routinely used and because relatively few patients had events. The incidence rate of spinal cord ischemia is similar to the rates published in other series of ruptured TAAAs, which almost universally are significantly higher than those seen in elective cases.16, 27 Given the low numbers and lack of randomization, the efficacy of adjunctive measures will likely need to be extrapolated from elective series.

Associations with outcome and hospital volume are somewhat controversial, because some authors found that hospital experience did result in an improvement in mortality in the setting of elective thoracic aneurysm repair.3, 28, 29 In the emergent setting, such an association has not been uniformly observed. Schepens et al22 reported no improvement in mortality with time; Rigberg et al3 found that only low-volume centers (one case per year) were associated with increased mortality at 1 year. The observed superior outcome in the centers of excellence may be in part related to intrinsic factors related to patient presentation and referral patterns. Crawford and colleagues’18 original report of 117 ruptured thoracic and thoracoabdominal aneurysms described an onset of symptoms related to rupture of less than 24 hours in only 16% of their patients, and as many as 34% of patients had symptoms exceeding 1 week. This may represent a selection or referral bias favoring outcomes, because our data would suggest that patients undergoing operation sooner after symptom onset have the highest mortality. In a report by LeMaire and associates,19 97% of their patients were hemodynamically stable at presentation. This is in contrast to the present series, in which 36.6% of patients presented with a systolic blood pressure less than 90 mm Hg. We made every effort to accept all patients from outlying facilities with an intention to repair, unless they were deemed medically inoperable. This is well reflected by the high number of intraoperative (7/11) deaths and deaths within the first 24 hours. These patients were almost universally in extremis at presentation.

Compromised functional status after urgent/emergent TAAA repair has been detailed in a report by Rectenwald et al.16 In that study, a “bad” outcome—defined as nonambulatory status, discharge to a long-term care facility, or death—was noted in 44% of patients surviving to discharge. However, at 1 year, 87% of patients with follow-up were at home and ambulatory. Similarly, only 6 of 30 surviving patients in this series were discharged home, whereas 24 were discharged either to a skilled nursing facility or to a rehabilitation center. Only two of these were in a long-term nursing home at last follow-up, including the lone long-term (3 years) survivor with paraplegia. Despite the high demand for extended care even after hospital discharge, repair of RDTAA seems well justified because it is a uniformly lethal condition without therapy.

The data in this series strongly suggest the pertinence of volume regarding outcome. Our volume has increased in recent years such that the half of our experience was accumulated over the past 3.5 years and has been concentrated on two surgeons. Although it did not reach significance, owing to small number of patients, a strong trend toward improved mortality in the latter part of our experience most likely represents improved efficiency in the management of these patients with enhanced surgeon and institutional experience. This trend was associated with a more conservative approach to fluid management, with approximately half the intraoperative blood transfusion in the second half of our experience despite similar degrees of hemodynamic instability and patient comorbidities. Thus, prompt diagnosis and expeditious intervention or referral to high-volume centers would be desirable to maximize the chance of optimal outcome.

High incidences of adverse outcomes and laborious, complicated postoperative courses have driven the need for alternative methods of repair. With successful application of endovascular technology in the arena of isolated DTA,30 its horizon is being expanded to include treatment of thoracoabdominal and arch lesions using branched graft technology4, 5, 6 and hybrid procedures,7, 8, 9 with promising preliminary results. In a series of 26 TAAAs treated by hybrid procedures, no paraplegia and a mortality rate of 13% were noted in the 23 elective patients, whereas all 3 patients who presented with rupture died.7 In another series, an overall mortality rate of 30% and paraplegia rate of 20% were reported; in two patients who presented with rupture, there was one paraplegia with no death.9 The results with these alternative approaches may improve with further refinement of technology and skills and may be applicable to repair of ruptured aneurysms. Until then, direct surgical repair for RDTAA provides a meaningful way of saving lives. There is still room for improvement, however, and concerted efforts need to be made to improve surgical outcome. Regionalization of this complex aortic surgery to centers of excellence with high volume should be considered. This series contributes to contemporary results of open repair of ruptured thoracic and thoracoabdominal aneurysms and helps provide a standard against which results of future endovascular endeavors should be held.

Author contributions 

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Conception and design: J-SC

Analysis and interpretation: JEB, JYK, GA-H, RYR, MSM, J-SC

Data collection: JEB, J-SC

Writing the article: JEB, J-SC

Critical revision of the article: JEB, J-SC

Final approval of the article: JEB, JYK, MZ, GA-H, RYR, MSM, J-SC

Statistical analysis: JEB, MZ, J-SC

Overall responsibility: J-SC

 

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We thank Faith Selzer, PhD, for her invaluable assistance with statistical analysis.

Appendix 

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Appendix Table I.

Patient, preoperative, and operative characteristics by time from symptom onset in patients undergoing surgery for TAA and TAAA rupture

VariableTime from symptom onsetP value
<6 h (n=10)6-24 h (n=14)>24 h (n=15)
Patient characteristics
Age (y)74.9±7.0(74.5)74.6±7.4(74.0)76.5±5.7(78.0).56
Female30.0(3)28.6(4)46.7(7).54
White87.5(7)100.0(14)93.3(14).68
History of COPD55.6(5)64.3(9)20.0(3).044
History of CVA11.1(1)14.3(2)13.3(2)1.0
History of CAD55.6(5)71.4(10)66.7(10).83
Smoking33.3(3)46.1(6)40.0(6).83
History of diabetes mellitus11.1(1)0(0)4.5(1).24
Any prior aortic reconstruction40.0(4)57.1(8)20.0(3).12
Preoperative characteristics
Transportation mode .43
Air50.0(5)78.6(11)73.3(11)
Ground30.0(3)21.4(3)20.0(3)
In-hospital20.0(2)0(0)6.7(1)
Time (h)3.4±2.0(4.3)13.9±6.0(12.5)101.4±57.8(97.0)<.001
Preoperative shock80.0(8)28.6(4)20.0(3).007
Preoperative CPR50.0(5)14.3(2)0(0).001
Aneurysm size and blood chemistry
AAA diameter (cm)7.8±2.4(7.5)9.0±2.5(8.5)8.3±2.2(7.7).31
Contained AAA60.0(6)28.6(4)0(0).001
Extent .99
Type I20.0(2)21.4(3)13.3(2)
Type II10.0(1)7.1(1)6.7(1)
Type III30.0(3)28.6(4)20.0(3)
Type IV30.0(3)28.6(4)40.0(6)
Type VI10.0(1)14.3(2)20.0(3)
Mycotic20.0(2)0(0)6.7(1).24
BUN (mg/dL)24.9±12.6(22.5)23.5±9.4(24.5)25.9±11.4(23.0).90
Creatinine (mg/dL)1.6±1.1(1.3)1.3±0.6(1.1)1.3±0.6(1.1).70
Hemoglobin (g/dL)13.2±8.1(10.5)11.9±2.4(12.5)10.7±2.5(10.6).27
Hematocrit (%)29.2±7.3(30.3)34.7±6.5(36.2)32.5±7.3(32.4).13
Operative characteristics
After 200250.0(5)42.9(6)66.7(10).42
OR time (h)3.7±2.5(4.8)4.5±1.6(4.4)4.7±1.2(4.7).84
OR fluid used4200±1949(3750)5080±2710(4200)4157±1750(4100).72
Blood units used9.1±6.0(7.0)8.1±7.3(5.5)6.9±4.2(6.0).51
Lowest SBP (mm Hg)63.9±34.8(79.0)68.6±19.3(72.0)82.5±5.6(80.0).032
Operative CRP50.0(5)21.4(3)0(0).007
Sequential clamp use37.5(3)8.3(1)26.7(4).30
Clamp time (min)62.3±9.8(59.0)63.0±15.6(64.5)65.5±24.3(56.0).96
Visceral ischemia time (min)43.7±12.6(44.0)44.7±19.4(45.0)41.9±9.9(40.0).79
Renal ischemia time (min)47.2±13.7(50.0)46.1±26.6(47.5)36.6±23.2(35.0).39
Renal perfusion16.7(1)33.3(4)40.0(6).42
Renal bypass33.3(2)16.7(2)40.0(6).42
Intercostal reimplantation0(0)0(0)6.7(1)1.0
LHB50.0(4)28.6(4)40.0(6).57
CSF drain44.4(4)50.0(7)66.7(10).54
Naloxone22.2(2)14.3(2)33.3(5).56

Data are % (n) or mean ± SD (median).

AAA, Abdominal aortic aneurysm; COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular accident; CAD, coronary artery disease; CPR, cardiopulmonary resuscitation; BUN, blood urea nitrogen; OR, operating room; SBP, systolic blood pressure; CRP, C-reactive protein; CSF, cerebrospinal fluid.

Compared by using the Fisher exact test (categorical variables) or Kruskal-Wallis test (continuous variables).

The sample size for each is as follows (the time from symptom onset to OR was unknown for two patients):

Race, LHB, and lowest systolic blood pressure, n= 8 (<6 h), n= 14 (6-24 h), n= 15 (>24 h)

Smoking: n= 9 (<6 h), n= 13 (6-24 h), n= 15 (>24 h)

COPD, CVA, CAD, diabetes mellitus, naloxone, CSF drain: n = 9 (<6 h), n = 14 (6-24 h), n = 15 (>24 h)

Renal perfusion, renal bypass, intercostal implantation: n = 6 (<6 h), n = 12 (6-24 h), n = 15 (>24 h)

Dialysis: n = 5 (<6 h), n = 11 (6-24 h), n = 15 (>24 h)

Tracheostomy: n = 6 (<6 h), n = 10 (6-24 h), n = 14 (>24 h)

Sequential clamp: n = 8 (<6 h), n = 12 (6-24 h), n = 15 (>24 h)

Pneumonia, paraplegia, paraparesis: n = 6 (<6 h), n = 11 (6-24 h), n = 14 (>24 h)

AAA diameter: n = 8 (<6 h), n = 13 (6-24 h), n = 12 (>24 h)

Clamp time: n = 6 (<6 h), n = 10 (6-24 h), n = 14 (>24 h)

Visceral ischemia time: n = 6 (<6 h), n = 12 (6-24 h), n = 13 (>24 h)

Appendix Table II.

Outcome characteristics by time from symptom onset in patients undergoing repair of ruptured TAA and TAAA

VariableTime from symptom onsetP value
<6 h (n = 10)6-24 h (n = 14)>24 h (n = 15)
Outcomes
Dialysis (any)20.0(1)36.4(4)7.1(1)0.22
Tracheostomy33.3(2)50.0(5)28.6(4)0.62
Pneumonia50.0(3)54.5(6)35.7(5)0.64
Paraplegia (any)16.7(1)9.1(1)21.4(3)0.82
Paraparesis (any)16.7(1)9.1(1)21.4(3)0.82
In-hospital death50.0(5)28.6(4)6.7(1)0.041
Length of stay (discharged only)18.8±17.3(11.0)22.3±18.6(15.0)14.6±9.6(11.5)0.70
Days to in-hospital death6.2±13.9(0)1.7±3.5(0)0(0)0.88

Data are % (n) or mean ± SD (median).

LHB, left heart bypass.

Compared by using the Fisher exact test (categorical variables) or Kruskal-Wallis test (continuous variables).

The sample size for each is as follows (the time from symptom onset to operating room was unknown for two patients):

Race, LHB, and lowest systolic blood pressure: n = 8 (<6 h), n = 14 (6-24 h), n = 15 (>24 h)

Smoking: n = 9 (<6 h), n = 13 (6-24 h), n = 15 (>24 h)

Chronic obstructive pulmonary disease, cerebrovascular accident, coronary artery disease, diabetes mellitus, naloxone, cerebrospinal fluid drain: n = 9 (<6 h), n = 14 (6-24 h), n = 15 (>24 h)

Renal perfusion, renal bypass, intercostal implantation: n = 6 (<6 h), n = 12 (6-24 h), n = 15 (>24 h)

Dialysis: n = 5 (<6 h), n = 11 (6-24 h), n = 15 (>24 h)

Tracheostomy: n = 6 (<6 h), n = 10 (6-24 h), n = 14 (>24 h)

Sequential clamp: n = 8 (<6 h), n = 12 (6-24 h), n = 15 (>24 h)

Pneumonia, paraplegia, paraparesis: n = 6 (<6 h), n = 11 (6-24 h), n = 14 (>24 h)

Abdominal aortic aneurysm diameter: n = 8 (<6 h), n = 13 (6-24 h), n = 12 (>24 h)

Clamp time: n = 6 (<6 h), n = 10 (6-24 h), n = 14 (>24 h)

Visceral ischemia time: n = 6 (<6 h), n = 12 (6-24 h), n = 13 (>24 h)

References 

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Division of Vascular Surgery, University of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, Pa.

Corresponding Author InformationReprint requests: Jae-Sung Cho, MD, University of Pittsburgh Medical Center, 200 Lothrop St, A1011 PUH, Pittsburgh, PA 15213.

 Competition of interest: none.

PII: S0741-5214(06)02305-6

doi:10.1016/j.jvs.2006.12.049


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