| | Experience with 1509 patients undergoing thoracoabdominal aortic operations☆☆☆Presented at the Fortieth Scientific Meeting of the International Society for Cardiovascular Surgery, North American Chapter, Chicago, Ill., June 9-10, 1992. Received 12 June 1992; accepted 1 September 1992. Abstract Purpose: The purpose of this study was to retrospectively identify variables associated with early death and postoperative complications in patients undergoing thoracoabdominal aortic operations. Methods: The data on 1509 patients who underwent 1679 thoracoabdominal aortic repairs between 1960 and 1991 were retrospectively reviewed. The median age was 66 years (range 1.5 years to 86 years), and aortic dissection was present in 276 (18%) patients. The extent of the first repair performed included 378 (25%) type I (proximal descending to upper abdominal aorta), 442 (29%) type II (proximal descending aorta to below the renal arteries), 343 (23%) type III (distal descending and abdominal aorta), and 346 (23%) type IV (most of the abdominal aorta). The median total aortic clamp time was 43 minutes. Results: The 30-day survival rate was 92% (1386/1509) for the 30-year period. On multivariate analysis the preoperative and operative variables associated with death included (p < 0.05) increasing age, preoperative creatinine level, concurrent proximal aortic aneurysms, coronary artery disease, chronic lung disease, and total aortic clamp time. When the postoperative variables were also included in the stepwise logistic regression model, then in addition, cardiac complications, stroke, kidney failure, and gastrointestinal hemorrhage became significant (p < 0.05). The overall incidence of paraplegia or paraparesis was 16% (234/1509). By use of stepwise logistic regression analysis, the significant predictors (p < 0.05) of paraplegia or paraparesis developing were total aortic clamp time, extent of aorta repaired, aortic rupture, patient age, proximal aortic aneurysm, and history of renal dysfunction. Kidney failure (postoperative creatinine level >3 mg/dl or dialysis) occurred in 18% (269/1509) of patients; dialysis was required in 9% (136/1509). Gastrointestinal complications manifested in 7% (101/1509) of patients. Conclusion: Although the survival rate has improved, paraplegia/paraparesis and kidney failure continue to be vexing problems that require further research. (J VASC SURG 1993;17:357-70.)
After the initial reports in 1955 by Etheredge et al.1 and in 1956 by DeBakey et al.2 of the successful repair of thoracoabdominal aortic aneurysms, Crawford,3 in 1965, commenced using the inclusion technique for repair of thoracoabdominal aortic aneurysms.4, 5, 6 Results of thoracoabdominal aortic operations have improved considerably over the ensuing years to the extent that in recent prospective studies, we have reported a 97% 30-day survival rate in 210 consecutive patients who underwent operation over a 13-month period.7, 8 Similarly the results of thoracoabdominal aneurysm operations combined with repairs of occlusive disease of the visceral arteries have been good.9 Nevertheless the postoperative complications of lower extremity neuromuscular deficits,6, 10 kidney failure,11 and lung failure8 have continued to be significant problems.
In this study we retrospectively reviewed 1509 patients who underwent operation by the senior author (E.S.C.) to establish a baseline of results and thus identify the predictors of early death, lower extremity deficits, and kidney failure.
Patients and methods  Between June 20, 1960, and January 31, 1991, the senior author operated on 1509 patients with thoracoabdominal aortic aneurysms who underwent a total of 1679 aortic repairs. For the purpose of statistical analysis, only the first operation was considered. The patient records were abstracted, and the data were entered into a data base and then were checked for accuracy by searching for data point outliers and by randomly checking chart data with data on the computer. In-hospital follow-up was complete for all patients, and 30-day follow-up was complete for 95% (1433/1509) of patients. All 76 patients for whom 30-day follow-up was not obtainable had been discharged from the hospital alive and well within 30 days after undergoing surgery; however, because of distant national or international referral or the patients having undergone operation in the early part of the series, follow-up status was not available. This may have influenced the reported early mortality rate, although deaths occurring after discharge but before 30 days after operation were rare. The median age of the patients was 66 years (range 1.5 years to 86 years). Of these, 985 (65%) were male and 524 (35%) were female. Aortic dissection was present in 18% (276), and 4% (61) had aortic rupture. Concurrent medical problems included evidence of chronic lung disease in 40% (603), history of atherosclerotic heart disease in 31% (470), cerebrovascular disease in 15% (230), and renal insufficiency in 13% (210). Atherosclerotic heart disease was defined as historical evidence of coronary artery disease, including myocardial infarction, angina, changes in electrocardiogram readings, and previous coronary artery bypass. Cerebrovascular disease was defined as a history of previous transient ischemic attacks, amaurosis fugax, cerebrovascular accident, or carotid artery endarterectomy. Renal insufficiency was defined as a history of previous renal dysfunction, either acute or chronic, including kidney failure. The extent of the aortic repair was graded according to the Crawford classification.6 Type I extended from the proximal descending thoracic aorta to the upper abdominal aorta (n = 378 [25%]); type II form the proximal descending thoracic aorta to below the renal arteries (n = 442 [29%]); type III from the distal half of the descending thoracic aorta and into the abdomen (n = 343 [23%]); and type IV involved most of or the entire abdominal aorta (n = 346 [23%]). Other variables are presented in Tables I to III.
Not shown in the tables are that 28 patients had infected aneurysms, 34 had aortitis, 14 had false aneurysms, and 2 had trauma. Preoperative paraplegia was present in 22 patients. The operative technique for the repair of thoracoabdominal aneurysms by use of the inclusion technique has been described previously, including for visceral artery disease and aortic dissection.3, 4, 5, 6, 9, 10, 12 Recent technical modifications that are important are angling of the thoracoabdominal incision more toward the umbilicus to prevent necrosis of the lower skin flap3, 12; the circumferential transection of the proximal aorta so that the esophagus is not included in the anastomosis, and the subsequent risk of an aortoesophageal fistula is avoided3, 12; incorporation of at least all segmental intercostal arteries and lumbar arteries from T8 to and including L1 into the new aortic prosthesis3, 12, 13; and use of our modification of the elephant trunk procedure to stage repairs for extensive aneurysmal disease that involves most of the aorta.12, 13 Operative variables in this study included a median total aortic clamp time (defined as reestablishment of blood flow to the lower limbs) of 43 minutes (range 11 minutes to 197 minutes); clamp time for the visceral vessels of 36 minutes (range 0 to 169 minutes); and the time for appearance of indigo carmine in the urine after aortic unclamping of 20 minutes (range 0 to 185 minutes). Some patients had immediate reappearance of dye in the urine. Lumbar or intercostal arteries were reattached in 45% (684/1509) of patients. Distal aortic perfusion, usually by atriofemoral bypass, was used in 17% (258/1509) of patients. The number of patients with data available and the median number of units of blood and blood product used during operation were red blood cells (n = 719), 7 units (range 1 to 46); fresh-frozen plasma (n = 713), 16 units (range 0 to 132); platelets (n = 709), 20 units (range 0 to 110); cryoprecipitate (n = 432), 0 units (range 0 to 100); and autotransfused cells (n = 710), 8 units (range 0 to 68). In the latter part of the study, most patients received intravenous aminocaproic acid (Amicar). Statistical analysis was performed with the BMDP statistical software program (BMDP Statistical Software, Inc., Los Angeles, Calif.) as described previously.6, 7, 8, 9 Multivariate analysis was performed with stepwise logistic regression analysis. Twenty-five preoperative and operative variables and nine postoperative variables were selected for univariate analysis of their association with 30-day deaths, postoperative paraplegia or paraparesis, and kidney failure. All lower limb neuromuscular lower motor deficits, either immediate or delayed, that occurred in the hospital were defined as paraplegia or paraparesis, even when they were unilateral, unless they were associated with upper limb unilateral deficits. The latter were considered to be strokes unless they were also associated with bilateral paraplegia or paraparesis. Thus all recorded lower limb deficits that occurred in hospital were reported. Kidney failure was defined as the need for postoperative dialysis or a postoperative creatinine serum level exceeding 3 mg/dl. Cardiac complications included myocardial infarction, ventricular tachycardia or fibrillation, supraventricular tachycardia or atrial fibrillation, and any cardiac events that resulted in death. Respiratory complications included prolonged postoperative ventilation and a variety of events such as pneumothorax, hemothorax, pleural effusions requiring drainage, chylothorax, empyema, prolonged chest tube drainage for fluid or air leak, atelectasis requiring bronchoscopy, pneumonia, adult respiratory distress syndrome, and need for tracheostomy. To determine the independent predictors of early 30-day deaths, two sets of analyses were performed; the first set was performed with preoperative and operative variables and the second set entered the postoperative variables into the first stepwise logistic regression model. The reason for doing two stepwise logistic regression analyses was, first, so that if a surgeon wanted to assess the risks of operation, knowing the independent preoperative and operative variables (Table IV) predictive of 30-day risk of death, then a better estimate could be made.
The second analysis was done, because once the operation has been performed and complications occur, the surgeon may want to know how the complications will influence survival. Thus Table V shows the independent predictors of 30-day death, including the influence of postoperative variables.
It should be noted, however, that there is a covariance between some preoperative or operative variables and the postoperative variables. Because stepwise logistic regression selects out the best independent predictive variables, one variable usually is displaced from the model and is no longer significant when there is covariance between two variables. For example, because there is a close correlation between preoperative and postoperative creatinine levels and because a postoperative level greater than 3 mg/dl was defined as a renal complication, the variable of postoperative kidney failure displaces preoperative creatinine level from the stepwise logistic regression model when all the variables are included (Table V). Although the variable of postoperative renal complication is the better predictor of death, this does not mean that the preoperative creatinine level is not important; it only means it is less important as a predictor of death when compared with the other predictors included in the model when all are considered together, including postoperative renal complications. | | |  | Variable | Comparison | Adjusted odds ratio (95% CI) | p Value | |
|---|
| Age | 1 yr ↑ | 1.03 (1.00, 1.06) | 0.06 | |
| Preoperative creatinine | 1 mg/dl ↑ | 1.01 (0.78, 1.31) | 0.96 | |
| Concurrent proximal aortic aneurysm | Yes/no | 2.20 (1.10, 4.37) | 0.032 | |
| History of CAD | Yes/no | 1.06 (0.64, 1.76) | 0.82 | |
| Aortic clamp time | 1 min ↑ | 1.00 (0.99, 1.01) | 0.92 | |
| Chronic lung disease | Yes/no | 1.52 (0.94, 2.48) | 0.088 | |
| Cardiac complication | Yes/no | 5.34 (3.20, 8.92) | <0.0001 | |
| Stroke complication | Yes/no | 6.17 (2.57, 14.8) | 0.0001 | |
| Renal complication | Yes/no | 5.13 (2.97, 8.89) | <0.0001 | |
| Gastrointestinal bleeding | Yes/no | 2.91 (1.23, 6.85) | 0.018 | |
| | | | | |
For the determination of the independent predictors of paraplegia or paraparesis or of kidney failure, only the preoperative and operative variables were used. In Table I, Table III continuous variables were grouped by quartiles for easier interpretation. For the multivariate analysis, however, these variables were treated as continuous variables. Nonparametric plots of variables against events were done by locally weighted smoothing of the data with the method of distant weighted least squares. This method smoothes the data so that the risk of an event changes as a function of the variable without making any assumptions about the function other than that the function is smooth.8 Results The 30-day survival rate over the 30-year period of study was 92% (1386/1509), with an in-hospital survival rate of 90% (1354/1509). Postoperative complications included the in-hospital occurrence of paraplegia or paraparesis in 16% of patients (45% [105/234] had paraplegia and 55% [129/234] had paraparesis); neurogenic bladder dysfunction in 0.5% (9); kidney failure that required dialysis in 9% (136); postoperative stroke in 3% (39); pulmonary complications in 33% (502); pulmonary embolism in 1% (19); cardiac complications in 12% (178); postoperative bleeding requiring repeat operation in 7% (108); postoperative sepsis in 8% (116); gastrointestinal complications in 7% (101); and postoperative coagulopathy in 4% of patients (58). The postoperative complications and their univariate association with paraplegia or paraparesis and kidney failure are shown in Table III. There was little difference in the incidence of postoperative complications with respect to the presence of aortic dissection except for the incidence of paraplegia or paraparesis, which was higher for all extents in patients with aortic dissection (no aortic dissection vs aortic dissection: Crawford type I, 13% vs 21%; type II, 31% vs 33%; type III, 6% vs 13%; and type IV, 4% vs 11%, respectively). Furthermore, type II patients (n = 442) had the highest rate of mortality (9.7%), dialysis (10.4%), paraplegia or paraparesis (31.5%), stroke (5%), pulmonary complications (45%), cardiac complications (12%), postoperative bleeding requiring repeat operation (9.5%), postoperative sepsis (12%), and coagulopathy (6.5%). The variables significantly associated with 30-day deaths, paraplegia or paraparesis, and kidney failure are shown in Table I, Table III. On multivariate analysis the preoperative and operative factors predictive of 30-day deaths in 1446 patients in whom complete data were available were (p < 0.05, Table IV) increasing age, serum creatinine level, concurrent aneurysms proximal to left subclavian artery, history of coronary artery disease, evidence of chronic lung disease, and total aortic cross-clamp time. When the postoperative variables are also included in the stepwise logistic regression analysis, then the independent predictors included (p < 0.05, Table V) increasing age, proximal aneurysm, chronic lung disease, cardiac complications, stroke, renal complications, and gastrointestinal bleeding. The independent predictors of paraplegia of paraparesis in 1494 patients in whom complete data were available included (p < 0.05, Table VI) extent of aneurysm resection, aortic cross-clamp time, presence of aortic rupture, increasing age, concurrent proximal aortic aneurysmal disease (aneurysm or aortic dissection of the ascending or aortic arch not repaired at the time of surgery), and preoperative renal dysfunction.
Fig. 1, A, shows the relationship between total aortic cross-clamp time and the risk of paraplegia or paraparesis.
Similarly, Fig. 1, B, shows the relationship with the visceral ischemia time. Fig. 1, C, shows the effect of extent of aneurysm repair according to clamp time as calculated with nonparametric analysis, and Fig. 1, D, shows the effect as calculated with multiple logistic regression analysis. The independent predictors of kidney failure in 1396 patients were (p < 0.05, Table VII) increasing age, male sex, renal occlusive disease, preoperative renal dysfunction, history of cerebrovascular disease, preoperative serum creatinine level, and visceral ischemic time.
Fig. 2 shows the Kaplan-Meier curves of cumulative survival according to atherosclerotic heart disease, aortic dissection, paraplegia or paraparesis, and postoperative kidney failure.
The early and late causes of death are shown in Table VIII.
Discussion Great strides have been made in reducing the operative mortality rate for thoracoabdominal aortic operations; a 97% 30-day survival rate has been reported in a recent prospective study of 210 patients.7, 8 In this study the independent factors identified on multivariate analysis as determinants of 30-day deaths (8%) over a 30-year period clearly show the importance of patient variables, such as concomitant medical problems, in determining survival. Few of the preoperative variables can be significantly altered to reduce the risk of surgery and the resultant mortality rate. Of the preoperative variables, detecting and treating coronary artery disease has the greatest potential success for reducing the risk of thoracoabdominal operations and also prolonging long-term survival as shown in the Kaplan-Meier curves. Maximizing respiratory function and cessation of smoking are important in patients with chronic lung disease.8 Total aortic cross-clamp time should also be kept to a minimum, because a prolonged aortic clamp time was associated with a higher mortality rate. Despite the better recent operative survival rate,7, 8 however, the incidence of serious complications has changed little in comparison to the previous report.6 Therefore further research is needed to reduce the most serious complications, particularly neurologic deficits and kidney failure. Furthermore, the application of newly discovered techniques needs to be evaluated in large, prospective randomized studies. Paraplegia or paraparesis This complication is the most serious, because if the patient does not recover, it is a major cause of morbidity in the patient7 and may shorten the life of the patient as seen in the Kaplan-Meier curve of long-term survival. The cause of postoperative paraplegia or paraparesis, both at the cellular level3, 15 and at a more gross pathophysiologic level3, 15, 16 is better understood as a result of extensive animal research, which has been reviewed previously.3, 13, 15, 16, 17, 18 Our understanding of the physiologic changes with aortic cross-clamping in humans has increased considerably with the following findings: (1) Cerebrospinal fluid pressure increases progressively with anesthetic maneuvers during aortic surgery19 and with aortic cross-clamping, and this correlates with the central venous pressure.7, 19 (2) Oxygenation of the spinal cord falls rapidly with aortic cross-clamping, even with deep hypothermia and circulatory arrest.20 (3) Failure to reattach patent segmental arteries T11, T12, and L1 is associated with an increased risk of paraplegia or paraparesis.13 (4) Mere inspection of segmental arteries cannot identify those supplying the spinal cord as shown by hydrogen testing.13 (5) Perfusion of the vessels that supply the spinal cord by atriofemoral bypass does result in hydrogen reaching the spinal cord.13 (6) Identification of segmental arteries that supply the spinal cord, either by highly selective preoperative angiography21, 22 or by intraoperative hydrogen testing13 and successfully reattachment of identified arteries that supply the spinal cord result in reestablishment of spinal cord blood flow. (7) Reattachment of segmental intercostal or lumbar arteries needs to be successful, because we have documented that a high proportion of the reattached arteries are not patent on postoperative highly selective angiographic examination.13 From this study and the above research we conclude that the occurrence of immediate postoperative paraplegia or paraparesis is largely dependent on the degree and duration of spinal cord ischemia during aortic cross-clamping (the degree of ischemia is dependent on the diameter of available collateral arteries, including the anterior and posteriolateral spinal arteries, and on the extent of the aneurysm) and on the continuation of spinal cord ischemia caused by failure to successfully reattach critical segmental arteries.13, 18 Delayed paraplegia or paraparesis, which accounted for approximately one third of cases in the prospective study,7 seems to be due to several factors, the most important of these being decreased spinal cord oxygenation.20 This loss of spinal cord oxygenation occurs either because of hypotension with decreased blood supply through collateral vessels or because of respiratory failure.13, 20 In porcine experiments we have shown that hypotension in animals that are dependent on the collateral blood supply to oxygenate the spinal cord resulted in paraplegia or paraparesis and that this could be reversed by immediately raising the blood pressure.13 We have had similar experiences in this series of patients by using dopamine and phenylephrine to raise the blood pressure and reverse delayed paraparesis. Other factors associated with delayed paraplegia or paraparesis probably include occlusion of critical segmental arteries, including reattached arteries, either by emboli or thrombosis13; spinal cord edema; secondary spinal cord injury, which we have noted in porcine experiments20 and which has also been reported by Moore and Hollier23 in rabbit experiments; and a reperfusion injury,15 most likely related to white blood cells rather than to the de novo generation of oxygen radicals from mitochondria.3 Although some of the origins of the multifactorial causes of paraplegia or paraparesis have been established as a result of this and other studies,*the means of fully preventing this dreaded complication in humans are still lacking. In a prospective randomized study of cerebrospinal fluid drainage, we7 were unable to show that drainage of 20 ml before aortic cross-clamping and up to 50 ml during aortic cross-clamping (a median of 52.5 ml was withdrawn) reduced the risk of paraplegia or paraparesis, or that cerebrospinal fluid drainage significantly altered the severity of the neuromuscular deficits.7 In nonhuman primate studies we reported that vasodilation of the anterior spinal artery with intrathecal papaverine increased spinal cord blood flow and prevented paraplegia after 60 minutes of normothermic aortic cross-clamping.15 A subsequent prospective study in humans without reattachment of segmental intercostal or lumbar arteries was encouraging.19, 25 In a prospective randomized study, which included the preoperative localization of the spinal cord blood supply, reattachment of critical identified segmental arteries, and femorofemoral cardiopulmonary bypass, Kieffer26 has shown (p < 0.05) that no permanent deficits and no paraplegia occurred in 29 patients randomized to treatment with intrathecal papaverine, whereas seven permanent deficits and three cases of paraplegia occurred in the control group of 33 patients. Four cases of reversible neurogenic bladder dysfunction or paraparesis occurred in the papaverine group. Furthermore, in Kieffer's continued use of intrathecal papaverine, paraplegia per se has occurred only in those patients whose spinal cord blood supply could not be identified or in those whose segmental arteries could not be successfully reattached.22, 26 Other preventive measures that may be important, as determined by animal studies or retrospective studies, are the use of steroids27; membrane stabilizers, such as lidocaine20; prostaglandin E1, as used by Grabetz et al.28; thiopental, which has been shown to be effective in animal studies29; and the usual method of atriofemoral bypass.24 The latter method has been examined previously by Crawford et al.24 and was not found to be effective, which agrees with our findings. Nonetheless, if atriofemoral bypass is used in conjunction with sequential and segmental repairs of the aorta, we have shown, by hydrogen testing13, 20 that blood supply to the spinal cord can be maintained while the proximal anastomosis is being performed. Previous animal studies by us15 have shown that distal aortic perfusion of only the arteria radicularis magna (artery of Adamkiewicz) results specifically in an increased blood flow to the lumbar spinal cord below the level of the arteria radicularis magna but not to the thoracic spinal cord. Prevention of hyperglycemia seems to be important.30 Moderate hypothermia, as initially reported by DeBakey et al.,31 seems to be protective, because we observed in this study that if we kept the patients normothermic during aortic cross-clamping with the atriofemoral bypass pump, the incidence of neuromuscular dysfunction increased significantly. Deep hypothermia is also clearly protective to the spinal cord both in animal studies32 and in our experience with deep hypothermia and circulatory arrest. Kouchoukos et al.33 have reported that this technique for repair of thoracoabdominal aneurysms prevents paraplegia or paraparesis. In a previous report of 25 patients who underwent deep hypothermia with circulatory arrest for descending thoracic or thoracoabdominal aortic aneurysms, mostly for technical indications, Crawford et al.34 reported that four patients died and in two patients paraplegia or paraparesis developed after operation. Similarly, in our recent report on the identification of the spinal cord blood supply with use of hydrogen,13, 20 one patient who did not need to have any segmental arteries reattached underwent deep hypothermia and circulatory arrest for technical indications but had reversible paraparesis after operation. Thus although the use of this technique may reduce the incidence of neuromuscular deficits, complications still arise. More ominously, application of this method may sometimes be at the expense of a considerably increased rate of mortality, blood usage, and pulmonary complications.34 In an attempt to cool the spinal cord locally, various means, such as epidural cooling,28, 35 continuous perfusion of the aneurysm,36 perfusion of the intrathecal space with cold saline solution,37 and use of a single dosage of cold “spinoplegia,”20 have been tried in animals, often with considerable success in preventing postoperative paraplegia or paraparesis. If such a technique can be developed for safe use in humans, it will undoubtedly be a useful adjunct. Of particular value would be the increased operative “window of safety” period18 that would enable sufficient time for the successful reattachment of those identified segmental arteries that supply the spinal cord. Kidney failure Until now, prevention of kidney failure that requires dialysis has not been much researched by investigators. In our retrospective clinical study11 of 1525 patients who underwent descending thoracic or thoracoabdominal repairs, the need for dialysis was not significantly reduced by cold perfusion of the kidneys with Ringer's lactate or by atriofemoral bypass. In a more recent evaluation of patients who had visceral artery occlusive disease and who also had thoracoabdominal aortic repairs,9 however, this subgroup of patients seemed to benefit from cold perfusion of the renal arteries because of the high incidence of preoperative renal dysfunction. From this we conclude that cold perfusion is not required for most patients who have no preoperative renal dysfunction and no renal artery occlusive disease or for whom a clamp time of less than approximately 30 to 45 minutes is expected. If these variables are present, then cold perfusion of the kidneys should be undertaken. The addition of other medications to the solution, such as heparin, lidocaine, calcium channel blockers, and prostaglandins (prostaglandin E1, 20 μg/L), may also be useful. We advocate the use of a gentle diuresis with dopamine after the operation. We avoid the use of diuretics such as furosamide (Lasix) because of the risk that a precipitously reduced cardiac preload may result in hypotension and the development of delayed paraplegia or paraparesis, which we have reported to occur with overly vigorous diuresis.3, 7 Although a higher preload may delay extubation of the patient, we deem that this is preferable to the risks of neuromuscular deficits and kidney failure caused by a reduced cardiac and renal preload. Respiratory failure and gastrointestinal complications In a previous prospective study,8 we found that development of postoperative respiratory failure was determined by a history of smoking and the presence of chronic lung disease. Because this was a retrospective study, respiratory failure was not evaluated. Nevertheless, the marked effect of chronic lung disease on early mortality rates was clearly documented in the present study. The low incidence of gastrointestinal complications in both this study and previous reports by us8, 9 suggests that with short aortic cross-clamp times and the liberal use of medications to prevent postoperative stress ulceration, gastrointestinal complications in patients should not be a frequent problem. Note should be taken, however, of the deaths of the 13 patients in whom aortointestinal fistulas, usually aortoesophageal, developed. Preoperative aortoesophageal fistulas can be treated by primary repair of the esophagus, graft replacement of the aorta, and rotation of an omental pedicle between the esophageal repair and the aorta.38 In this study the mortality rate was high when gastrointestinal complications did occur and there was a high association between this complication and kidney failure or neuromuscular deficits. In conclusion, in this study of the senior author's experience with repair of thoracoabdominal aortic aneurysms, a remarkably good survival rate has been achieved over the 30-year period. Postoperative complications, however, remain a problem, but ongoing research may reduce the incidence. Acknowledgements Claudia Alley assisted with preparation of the manuscript, and Marion Robinson, PhD, assisted with the editing.
Discussion Dr. Peter Gloviczki (Rochester, Minn.). Dr. Svensson has presented a landmark paper on the experience of Dr. Crawford, a pioneer in vascular surgery. The results of this series of 1509 patients who underwent 1679 thoracoabdominal aortic reconstructions by the senior author cannot be compared with any other series, because there is no comparable series. A 30-day survival rate of 92% and a mean aortic cross-clamp time of 45 minutes for the entire 30 years are the amazing achievements of a master surgeon. The data are invaluable in defining the risks of thoracoabdominal reconstruction. The best preoperative predictors of death were advanced age, kidney failure, coronary artery disease, and chronic obstructive lung disease. The best intraoperative predictor was the length of aortic cross-clamp time. With improved survival rates two major complications of thoracoabdominal reconstruction, that is, paraplegia and kidney failure, have become apparent. Dr. Svensson has presented the best predictors of these complications and discussed methods of prevention. My first comment concerns protection of the spinal cord, specifically the use of atriofemoral bypass. In experiments from our laboratory the benefit of bypass has been consistently demonstrated. Unfortunately our experience in patients was different. In our modest clinical material, which with 181 patients amounts to only 11% of Dr. Crawford's experience and which included only 30% of type I and type II aneurysms and 9% of the patients who had dissections, bypass was not protective. We had a paraplegia rate of 19% with bypass or shunt and 6% without. These results are similar to your data, wherein the group that underwent aortic bypass had an 8% higher paraplegia rate than those who did not undergo bypass. Still, Dr. Crawford used bypass in 258 patients. Based on this experience do you recommend atriofemoral bypass and, if yes, for what indication? In our patients kidney failure that required dialysis did not occur in those 67 patients who had cold perfusion during surgery. In contrast, 11 of 114 patients without cold perfusion needed dialysis. Most of us do not have the dexterity of Dr. Crawford, and we needed an average of 55 minutes for renal revascularization, in contrast to 36 minutes, as you have reported. Under these circumstances would you recommend cold perfusion as a low-risk and effective technique for renal protection, even if there were no evidence of preoperative renal dysfunction or renal artery occlusive disease? Your article sets the highest standards for repair of thoracoabdominal aortic aneurysms. In addition, you provide ample encouragement for future generations of vascular surgeons to continue much needed research in this field. As a surgeon of the next generation, I would like to assure you, Dr. Crawford, that nothing in vascular surgery has been more inspiring than your tremendous work for the past 30 years. Dr. Lars G. Svensson. Thank you for your kind words, and I will convey them to Dr. Crawford. He certainly has set a very high standard in thoracoabdominal aortic surgery that will be difficult to emulate. Your first question is whether atriofemoral bypass is protective and what are the indications. Dr. Crawford tended to clamp the aorta beyond the aneurysm, and in type II patients he would clamp just above the celiac artery where possible but generally beyond the aneurysm. The risk of paraplegia or paraparesis was increased in this group of patients with the use of atriofemoral bypass. However, this can be partly attributed to a period when we kept the patients normothermic during the period of aortic cross-clamping with atriofemoral bypass and subsequently showed statistically that the patients with atriofemoral bypass who were kept normothermic had a significantly higher rate of paraplegia/paraparesis. The indirect suggestion would therefore be that patients should be kept moderately hypothermic at a temperature of about 30° to 34° C during aortic clamping and atriofemoral bypass. As you pointed out, the animal experiments do show that atriofemoral bypass or shunts are protective, and in our own experiments in baboons, we did find that lumbar spinal cord blood flow below the artery of Adamkiewicz was increased and that a shunt was protective. However, the thoracic part of the spinal cord was not protected because of the anatomy of the artery of Adamkiewicz. It appears, therefore, to be important to supply the thoracic part of the spinal cord with blood. To do this, one has to perfuse the thoracic radicular arteries, which can supply blood both up and down the length of the spinal cord, whereas the artery of Adamkiewicz can only supply blood downward. I believe atriofemoral bypass is protective if one modifies the technique somewhat. For types I and II, I personally like to clamp between the carotid artery and the left subclavian and then clamp a segment of the aneurysmal aorta just sufficient to do the proximal anastomosis so that the rest of the aneurysm is perfused with the pump. With hydrogen testing we have been able to show that segmental clamping allows for perfusion of the spinal cord while the proximal anastomosis is performed. The distal clamp is then moved to just above the celiac artery, the intercostal vessels on a Carrell patch are reattached, and then the proximal clamp is taken off to reperfuse the intercostal vessels. The visceral repair is completed while the pump is used as much as possible. Some recent evidence suggests that this may be protective. Perhaps segmental repairs with atrifemoral bypass will prove to be worthwhile for spinal cord protection. In this study the patients who underwent atriofemoral bypass had a significantly lower incidence of renal dysfunction and kidney failure, and thus there is evidence from this study that the kidneys are protected by atriofemoral bypass. The presumptive indications for atriofemoral bypass would therefore appear to be renal dysfunction, aortic dissection, segmental repairs, complex aneurysms, and types I and II aneurysms. Concerning renal protection and cold perfusion, in this study it seemed that the critical time interval for increased incidence of kidney failure was 33 minutes of ischemia. We have shown that patients who had renal dysfunction or renal occlusive disease benefitted from cold perfusion. Thus if the visceral ischemia time is expected to be more than about 30 to 40 minutes, or preoperative renal dysfunction is present, then renal protection by cold perfusion is probably worthwhile, particularly since there is little risk involved. Dr. Sandmann's group has suggested the use of prostaglandin El at a concentration of 20 μg/L in the cold solution has an additional protective effect. Dr. Larry H. Hollier (New Orleans, La.). Many surgeons remain concerned and somewhat confused regarding the relatively high incidence of paraplegia and paraparesis that they report. Is it possible to reduce this risk of paraplegia? I believe Dr. Svensson has given us some very strong suggestions that it might be. In my own experience now with repair of 180 thoracoabdominal aneurysms, more than 96% of patients have survived long enough to determine postoperative neurologic status. The overall incidence of neurologic injury has been 4.4%. Since 1989 I have operated on 72 patients under our expanded protocol for cord protection, which includes routine intercostal reimplantation, barbiturate coma, mild hypothermia, and routine attempts at prolonged cerebrospinal fluid (CSF) drainage. These patients have sustained an overall incidence of neurologic injury of 2.7%, and in patients with type I and type II thoracoabdominal aneurysms, the neurologic deficit rate is 2.8%. Do you still attempt to maintain normothermia, or have you shifted over toward mild hypothermia during aneurysm repair? Also, please comment on the extent to which you attempt intercostal reimplantation. Recently you said you had done some segmental reimplantation. In those patients in whom paraplegia has developed, what percentage had no intercostal reimplantation at all, and in those undergoing reimplantation of intercostal vessels, have they been primarily isolated or extensive intercostal reimplantations? I believe the difference in our results may lie primarily in these variables of the completeness of intercostal reimplantation and the relative degree of use of hypothermia. Dr. Svensson. I believe it is critical in these groups of patients to define very clearly what we are dealing with. We have always defined paraplegia or paraparesis as all lower limb neurologic events that occur in the hospital, and we have been very careful in referring to all unilateral lower limb deficits as paraparesis or paraplegia unless there is significant evidence of a stroke. Patient mix also is very important. In your own study you have not had many patients with aortic dissection, and I noted in one of your articles that your stroke incidence was 15% compared with 3% in this study. Our patients are generally older, and this might also be a factor. Your results, however, are very encouraging. Concerning the hypothermia question, the considerably higher incidence of paraplegia or paraparesis in the patients with normothermia would appear to confirm that moderate hypothermia is protective. Therefore we now generally let our patients, particularly those on atriofemoral bypass, drift down to a temperature of about 30° to 32° C, and I personally make no attempt to rewarm the patients with atriofemoral bypass. It is critical for the prevention of paraplegia that the most important intercostal vessels are identified. As you know, Dr. Kieffer and Dr. Williams have used preoperative angiography with variable success. We have used hydrogen as a marker to identify the vessels. This is something that still needs to be evaluated more fully. In the patients for whom we do not have hydrogen testing available, we routinely reanastomose the vessels from T8 to L1. In the prospective randomized study that we performed with CSF drainage, that showed no protective effect of CSF drainage, we did a subanalysis to determine whether the presence or absence of the intercostal arteries at various levels and whether or not they were reattached had an effect on the development of postoperative deficits. In the patients with intercostal arteries from T3 down to T5, it made no difference whether they were reattached or whether they were present. At the level of T11, T12, and L1, the incidence of paraplegia or paraparesis was 67% if the vessels were present but were not reattached to the new graft. If they were reattached, it was 20%, which was significantly lower. Obviously the critical vessels need to be reattached, and the problem is how to identify these vessels and make sure that the reattachment is successful. In our postoperative angiograms in patients who have had reattachment of intercostal arteries, we have found that many of these arteries no longer are perfused and they have clotted off or occluded for various reasons. This is another problem that needs to be addressed. In response to your question of whether the risk of paraplegia can be reduced, my own experience in a considerably smaller series of patients in comparison to Dr. Crawford's outstanding results would suggest new techniques can reduce the incidence of paraplegia. Continuing research efforts, including your own, we hope will identify the best methods. References 1.
1
Etheredge SN, Yee J, Smith JV, Schonberger S, Goldman MJ.
Successful resection of a large aneurysm of the upper abdominal aorta and replacement with homograft.
Surgery. 1955;38:1071–1075. MEDLINE 2.
2
DeBakcy ME, Creech O, Morris GC.
Aneurysm of thoracoabdominal aorta involving the celiac, superior mesenteric, and renal arteries: report of four cases treated by resection and homograft replacement.
An Surg. 1956;144:549–573. 3.
3Svensson LG, Crawford ES. Aortic dissection and aortic aneurysm surgery: clinical observations, experimental investigations and statistical analyses. Curr Probl Surg (in press). 4.
4
Crawford ES, Palamara AE, Saleh SA, Roehm JOF.
Aortic aneurysm: current status of surgical treatment.
Surg Clin North Am. 1979;59:597–636. MEDLINE 5.
5
Crawford ES, Crawford JL.
Diseases of the aorta including an atlas of angiographic pathology and surgical technique.
Baltimore: Williams and Wilkins; 1984;. 6.
6
Crawford ES, Crawford JL, Safi HJ, et al.
Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operation in 605 patients.
J Vasc Surg. 1986;3:389–404. Abstract |
Full-Text PDF (5992 KB)
7.
7
Crawford ES, Svensson LG, Hess KR, et al.
A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta.
J Vasc Surg. 1991;13:36–46. Abstract | Full Text |
Full-Text PDF (880 KB)
8.
8
Svensson LG, Hess KR, Coselli JS, Safi HJ, Crawford ES.
A prospective study of respiratory failure after high-risk surgery on the thoracoabdominal aorta.
J Vasc Surg. 1991;14:271–282. Abstract | Full Text |
Full-Text PDF (1066 KB)
9.
9
Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ.
Thoracoabdominal aortic aneurysms associated with celiac, superior mesenteric, and renal artery occlusive disease: methods and analysis of results in 271 patients.
J Vasc Surg. 1992;16:378–390. Abstract | Full Text |
Full-Text PDF (3919 KB)
10.
10
Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ.
Dissection of the aorta and dissecting aortic aneurysms: improving early and long-term surgical results.
Circulation. 1990;82(Suppl V):IV–24–IV–38. 11.
11
Svensson LG, Coselli JS, Safi HJ, Hess KR, Crawford ES.
Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta.
J Vasc Surg. 1989;10:230–239. Abstract | Full Text |
Full-Text PDF (893 KB)
12.
12
Svensson LG, Crawford ES.
Aneurysms involving the descending and upper abdominal aorta.
Chest Surg Clin North Am. 1992;2:311–328. 13.
13
Svensson LG, Patel V, Robinson MF, Ueda T, Roehm JOJ, Crawford ES.
Influence of preservation or perfusion of intraoperatively identified spinal cord blood supply on spinal motor evoked potentials and paraplegia after aortic surgery.
J Vasc Surg. 1991;13:355–365. Abstract | Full Text |
Full-Text PDF (1230 KB)
14.
14
Crawford ES, Coselli JS, Svensson LG, Safi HJ, Hess KR.
Diffuse aneurysmal disease (chronic aortic dissection, Marfan, and mega aorta syndromes) and multiple aneurysm: treatment by subtotal and total aortic replacement emphasizing the elephant trunk operation.
Ann Surg. 1990;211:521–537. MEDLINE 15.
15
Svensson LG, Von Ritter CM, Groenveld HT, et al.
Cross-clamping of the thoracic aorta: influence of aortic shunts, laminectomy, papaverine, calcium channel blockers, allopurinol, and superoxide dismutase on spinal cord blood flow and paraplegia in baboons.
Ann Surg. 1986;204:38–47. MEDLINE 16.
16Shenaq SA, Svensson LG. Paraplegia following aortic surgery J Cardiothorac Vasc Anes (in press). 17.
17
Laschinger JC, Izumoto H, Kouchoukos NT.
Evolving concepts in prevention of spinal cord injury during operations on the descending thoracic and thoracoabdominal aorta.
Ann Thorac Surg. 1987;44:667–674. MEDLINE 18.
18
Svensson LG, Loop FD.
Prevention of spinal cord ischemia in aortic surgery.
In:
Bergan JJ, Yao JST editor.
Arterial surgery: new diagnostic and operative techniques. New York: Grune & Stratton; 1988;p. 273–285. 19.
19
Svensson LG, Grum DF, Bednarski M, Cosgrove DM, Loop FD.
Appraisal of cerebrospinal fluid alterations during aortic surgery with intrathecal papaverine administration and cerebrospinal fluid drainage.
J Vasc Surg. 1990;11:423–429. Abstract | Full Text |
Full-Text PDF (684 KB)
20.
20
Svensson LG, Crawford ES, Patel V, Jones JW, DeBakey ME.
Spinal cord oxygenation, intraoperative blood supply localization, cooling and function with aortic clamping.
Ann Thorac Surg. 1992;54:74–79. MEDLINE 21.
21
Williams GM, Perler BA, Burdick JF, et al.
Angiographic localization of spinal cord blood supply and its relationship to postoperative paraplegia.
J Vasc Surg. 1991;13:23–33. Abstract | Full Text |
Full-Text PDF (4030 KB)
22.
22
Kieffer E, Richard T, Chiras J, Godet G, Cormier E.
Preoperative spinal cord arteriography in aneurysmal disease of the descending thoracic and thoracoabdominal aorta: preliminary results in 45 patients.
Ann Vasc Surg. 1989;3:34–46. Abstract |
Full-Text PDF (1354 KB)
23.
23
Moore WMJ, Hollier LH.
The influence of severity of spinal cord ischemia in the etiology of delayed-onset paraplegia.
Ann Surg. 1991;213:427–431. MEDLINE 24.
24
Crawford ES, Mizrahi EM, Hess KR, Coselli JS, Safi HJ, Patel VM.
The impact of distal aortic perfusion and somatosensory evoked potential monitoring on prevention of paraplegia after aortic aneurysm operation.
J Thorac Cardiovasc Surg. 1988;95:357–367. MEDLINE 25.
25
Svensson LG, Stewart RW, Cosgrove DM, et al.
Preliminary results and rationale for the use of intrathecal papaverine for the prevention of paraplegia after aortic surgery.
S Afr J Surg. 1988;26:153–160. MEDLINE 26.
26Kieffer E. Commentary: Lund University Conference on Thoracoabdominal Aorta Operations. Eur J Vasc Surg (in press). 27.
27
Woloszyn TT, Marini CP, Coons MS, et al.
Cerebrospinal fluid drainage and steroids provide better spinal cord protection during aortic cross-clamping than does either treatment alone.
Ann Thorac Surg. 1990;49:78–82. MEDLINE 28.
28
Grabitz K, Freye E, Prior R, Schror K, Sandmann W.
Does prostaglandin El and superoxide dismutase prevent ischaemic spinal cord injury after thoracic aortic cross-clamping?.
Eur J Vasc Surg. 1990;4:19–24. 29.
29
Nylander WA, Plunkett RJ, Hammon JW, Oldfield EH, Meacham WF.
Thiopental modification of ischemic spinal cord injury in the dog.
Ann Thorac Surg. 1982;33:64–68. MEDLINE 30.
30
LcMay DR, Neal S, Neal S, Zelenock GB, D'Alecy LG.
Paraplegia in the rat induced by aortic cross-clamping: model characterization and glucose exacerbation of neurologic deficit.
J Vasc Surg. 1987;6:383–390. Abstract | Full Text |
Full-Text PDF (701 KB)
31.
31
DeBakey ME, Cooley DA, Creech OJ.
Resection of the aorta for aneurysms and occlusive disease with particular reference to the use of hypothermia: analysis of 240 cases.
J Am Coll Cardiol. 1955;5:153–157. 32.
32
Rokkas CK, Sundaresan S, Shuman TA, et al.
A primate model of spinal cord ischemia: evaluation of spinal cord blood flow and the protective effect of hypothermia.
Surg Forum. 1991;42:265–267. 33.
33
Kouchoukos NT, Wareing TH, Izumoto H, Klausing W, Abboud N.
Elective hypothermic cardiopulmonary bypass and circulatory arrest for spinal cord protection during operations on the thoracoabdominal aorta.
J Thorac Cardiovasc Surg. 1990;99:659–664. MEDLINE 34.
34
Crawford ES, Coselli JS, Safi HJ.
Partial cardiopulmonary bypass, hypothermic circulatory arrest, and posterolateral exposure for thoracic aortic aneurysm operation.
J Thorac Cardiovasc Surg. 1987;94:824–827. MEDLINE 35.
35
Kaschner AG, Sandmann W, Kniemeyer HW, Schier R, Larkamp H.
Evaluation of epidural perfusion cooling to protect the spinal cord during thoracic aortic cross-clamping: monitoring of spinal evoked electrogram.
J Cardiovasc Surg. 1985;26:97–98. 36.
36
Colon R, Frazier OH, Cooley DA, McAllister HA.
Hypothermic regional perfusion for protection of the spinal cord during periods of ischemia.
Ann Thorac Surg. 1987;43:639–643. MEDLINE 37.
37
Berguer R, Porto J, Fedoronko B, Dragovic L.
Selective deep hypothermia of the spinal cord prevents paraplegia after aortic cross-clamping in the dog model.
J Vasc Surg. 1992;15:62–72. Abstract | Full Text 38.
38
Coselli JS, Crawford ES.
Primary aortoesophageal fistula from aortic aneurysm: successful surgical treatment by use of omental pedicle graft.
J Vasc Surg. 1990;12:269–277. Abstract | Full Text |
Full-Text PDF (3714 KB)
Department of Surgery, Baylor College of Medicine, Houston. Houston, Texas ☆ Reprint requests: Lars G. Svensson, MD, Department of Surgery, Division of Cardiovascular Surgery, Lahey Clinic, 41 Mall Rd., Burlington, MA 01805. PII: 0741-5214(93)90421-H doi:10.1067/mva.1993.42297 © 1993 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter. Published by Elsevier Inc. All rights reserved. | |
|
FULL TEXT
