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Ann Thorac Surg 1997;64:1669-1675
© 1997 The Society of Thoracic Surgeons
Section of Thoracic Surgery, The University of Michigan Hospitals, Ann Arbor, Michigan
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentReferences |
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Methods. The surgical delay approach was adopted for malperfused patients, and treatment in these patients included percutaneous reperfusion, with aortic fenestration and branch stenting where appropriate. Twenty patients had a type A dissection and malperfusion shown by pulsed-wave Doppler echocardiography, transesophageal echocardiography, or spiral computed tomographic scanning. Malperfusion was documented by angiography. After reperfusion, all patients' conditions were stabilized in the intensive care unit; intravenous beta-blockers were administered to decrease the maximum rate of increase of left ventricular pressure. Once patients completely recovered from the consequences of malperfusion, surgical repair was performed. Statistical comparison of the non-delay and delay groups was performed using Fisher's exact test and Student's t test. Multiple logistic regression analysis was used to establish independent predictors for mortality.
Results. The mean delay to repair was 20 days (2 to 67 days). Four (31%) patients were discharged home and readmitted for operation. Three patients (15%) died preoperatively, 1 of retrograde dissection and rupture and 2 of reperfusion injury. Seventeen underwent surgical repair, with two deaths (12%); 15 (75%) were discharged, with an average follow-up of 16.8 months (p < 0.003). Delay was the only independent predictor of outcome.
Conclusions. Patients with an acute type A dissection and malperfusion should undergo percutaneous reperfusion, and surgical repair should be delayed until the reperfusion injury resolves.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Malperfusion is a devastating complication of type A acute aortic dissection, with a reported incidence of 16% to 33% [1–3]. Review of our population of patients with a type A dissection seen from January 1992 through May 1994 showed that preoperative malperfusion was associated with the highest risk for death of all variables analyzed. Malperfusion is defined as a complication in an organ system secondary to ischemia and resulting in organ dysfunction and systemic metabolic abnormalities. Clinical presentations of malperfusion included myocardial, visceral, neurologic, and limb ischemia. Despite corrective procedures and an intact surgical repair, these patients died of metabolic abnormalities and end-organ failure.
Because of previous poor results in malperfused patients, in June 1994 we began using another approach that included surgical delay, nonoperative reperfusion where appropriate accomplished using percutaneous fenestration and stenting, and intensive medical management of the systemic blood pressure. By correcting all the metabolic abnormalities and allowing for end-organ failure to resolve before surgically repairing the aortic dissection, we hoped to improve both the short-term and long-term outcome.
In this article we describe the delayed approach to a type A dissection with malperfusion and compare the results in a retrospective manner with those in our earlier malperfused patients with an acute type A dissection who were treated with emergent surgical repair.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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From May 1994 through December 1996, 52 patients with a type A acute dissection without malperfusion underwent emergent surgical repair of the dissection. However, the condition in an additional 20 patients with malperfusion was stabilized medically; they were reperfused using percutaneous fenestration and stenting, where appropriate, with the intent to perform surgical repair at a later date once all metabolic and medical abnormalities had resolved.
Malperfusion in each of the various organ systems is defined as follows: myocardial: acute infarct diagnosed on the basis of electrocardiographic changes or myocardial specific enzyme elevations associated with new-onset ventricular dysfunction, or both findings; neurologic: new-onset severe neurologic deficit lasting more than 48 hours, either localized or a generalized nonresponsiveness; visceral: pain associated with physical findings compatible with an acute abdomen and associated abnormal laboratory findings; limb: new-onset loss of pulse for more than 4 hours, associated with pain, neurologic findings, and physical findings compatible with threatened limb function.
Ten patients with a type A dissection diagnosed on the basis of an emergent transesophageal echocardiogram and physical findings compatible with the malperfusion syndrome were admitted to the University of Michigan Hospital during January 1992 through May 1994. Three patients had visceral ischemia, 3 had myocardial ischemia, 1 had limb ischemia, 1 had limb and visceral ischemia, and 2 had a neurologic deficit (Table 1
). Nine underwent emergent repair of their acute type A dissection, and the tenth patient, who presented with an acute rigid abdomen and evidence of dead bowel, underwent emergent resection of the dead bowel followed by percutaneous fenestration of his abdominal aortic dissection flap. Two of the 9 patients who underwent emergent repair underwent ascending aortic replacement with open distal anastomosis using hypothermic circulatory arrest (HCA). One other patient underwent root replacement, and another patient underwent root replacement with a hemiarch; both procedures were performed using HCA. Five other patients underwent repair using HCA with retrograde cerebral perfusion. Of these 5, 1 underwent root replacement; 3, root replacement with a hemiarch; and 1, root replacement with a complete arch together with replacement of the left common carotid vessel. Five of the patients underwent simultaneous coronary artery bypass grafting. The tenth patient underwent root replacement with a complete arch using HCA with retrograde cerebral perfusion 67 days after his initial bowel resection and percutaneous aortic fenestration for the management of the acute dissection. This patient is included in the delay group for statistical analysis.
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). All 19 patients underwent angiography to confirm the diagnosis, and flow was reestablished to ischemic areas using fenestration of the aortic dissection flap to equalize pressure between the true and false lumens and thus reestablish flow into the vital organs, accompanied by the stenting of compromised branch vessels, where appropriate. After reperfusion all patients were admitted to the thoracic intensive care unit, where hemodynamics were monitored by invasive techniques and ß-blockers and calcium-channel blockers were administered intravenously to decrease the change in pressure in relationship to the change in time of the left ventricle. Target goals for treatment were a heart rate of less than 80 beats/min, a systemic systolic blood pressure of less than 120 mm Hg, a diastolic pressure of less than 80 mm Hg, and a cardiac index of more than 2.5 L • min-1 • m-2. In patients who suffered from myocardial ischemia with the low-output syndrome, appropriate inotropic agents were administered to maintain an index of more than 2.0 L • min-1 • m-2. Simultaneously all metabolic disturbances were corrected medically. Once hemodynamic stability was established, patients were converted to receiving medications orally, monitors were discontinued, and the patients were transferred to a general care unit. Once patients had completely recovered from the sequelae of malperfusion, a corrective aortic surgical procedure was performed. Four patients were discharged home and readmitted at a later date for operation.
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). Two patients underwent repair using a closed distal technique; one had a root replacement and the other an ascending aorta replacement. The remaining 15 patients underwent repair using HCA and retrograde cerebral perfusion. Procedures consisted of five root-hemiarch, four root–complete arch, three ascending aorta–complete arch, two ascending aorta–hemiarch, and one ascending aorta repair. Seven of the 17 patients had simultaneous coronary artery bypass grafting. Three patients died before operation, 2 of sudden cardiac arrest and 1 as the result of the elective termination of support.
Patients were categorized in two ways for univariate analysis. First they were separated into delay versus non-delay groupings and then into outcome groupings (alive versus dead). The variables analyzed for both groupings were age, sex, HCA times, the location of the procedure, the type of procedure, redo operation, associated coronary artery bypass grafting, the pump time, and the cross-clamp time. In addition, the outcome variable was studied in the delay versus non-delay grouping and the delay variable was studied in the alive versus dead grouping. Categorical variables were compared using two-sided Fisher's exact test, and continuous variables were compared using Student's t test after log transformation for those not normally distributed. All results for the continuous variables are reported as the mean ± standard deviation. The significance for all analysis was set at p less than 0.05 (Tables 3 to 6). To establish which variables were independent predictors of mortality, we used multiple logistic regression modeling with patient outcome as the dependent variable.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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). Of the 20 patients in whom operation was delayed, 3 (15%) died before operation. One patient with neurologic, visceral, and limb malperfusion never regained consciousness, and after 16 days of medical treatment, her life support systems were withdrawn. Another patient who had visceral and limb malperfusion died on day 2 of medical treatment secondary to hypoxia resulting from reperfusion lung injury with subsequent arrhythmias and cardiac arrest. Autopsy confirmed no rupture, tamponade, or retrograde dissection into the coronary arteries. The last patient died of retrograde dissection with sudden rupture of the ascending aortic dissection into the pericardium, resulting in tamponade, confirmed at autopsy, on day 12 of medical treatment. Seventeen (85%) of the patients successfully survived medical therapy and underwent surgical repair an average of 21 days (range, 2 to 67 days) after the diagnosis of an acute type A aortic dissection. Fifteen (88%) of the 17 patients undergoing surgical repair survived, were discharged from the hospital, and are fully functional at an average of 16.8 months after operation. The overall survival rate with discharge in the delay group was 75% (15/20), with only 1 patient (5%) dying of tamponade secondary to retrograde dissection and rupture. Only 1 patient (11%) in the non-delay group survived and was discharged from the hospital.
Comparison of the variables given in the Methods section between the delay and non-delay groups showed that the only significant difference was in outcome (p = 0.003) (see Table 3). Comparison of the outcomes groups (alive versus dead) for the variables mentioned showed that delay versus non-delay was significant (p = 0.003) and also that the type of procedure performed was significant (p = 0.005), with more complete arch procedures performed in the alive group (see Table 5). Although both the type of procedure and delay were univariately associated with mortality, multiple logistic regression analysis showed that only delay was an independent predictor of mortality (odds ratio, 0.03; 95% confidence interval, 0.02–0.343) and that the type of procedure was no longer predictive of patient death.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Review of this patient population showed that these patients died of pulmonary failure as a consequence of the reperfusion injury, which may have been magnified by cardiopulmonary bypass, HCA, and the blood product transfusions required in patients who undergo surgical repair. The strong clinical evidence that the reperfusion of ischemic tissue is associated with pulmonary dysfunction characterized by increased lung vascular permeability and pulmonary hypertension independent of cardiac function supports the fact that reperfusion injury plays a significant role in the death of patients with an acute type A dissection associated with malperfusion who undergo immediate surgical correction [11–14]. In previous experimental studies, increased lung vascular permeability was documented and quantitated by the leakage of iodine 125–labeled albumen and extravasation of chromium 51–labeled red blood cells. The degree of lung vascular injury was proportional to the time of limb ischemia and was associated with the accumulation of myeloperoxidase (used to indirectly quantitate polymorphonuclear neutrophils [PMNs]) and complement consumption [15]. Investigations have shown that PMN-derived oxygen free radicals and proteinases play an important role in the development of limb ischemia-reperfusion injury. The PMNs are activated by the serum of ischemic tissue [16], and the resultant release of oxygen radicals and elastase damages endothelial cells directly [17]. Limb ischemia-reperfusion is associated with significantly increased serum levels of tumor necrosis factor 
and interleukin-1, which reach maximum levels at 2 hours. These cytokines cause the accumulation of PMNs by up-regulating adhesion molecules on both PMNs and endothelial cells. The neutrophil ß2 integrins (CD11a/CD18 and CD11b/CD18) are required for PMNs to adhere to endothelial cells. Endothelial adhesion molecules, intercellular adhesion molecule–1, and E-selectin are required for PMN-mediated lung injury to occur [18]. Complement (C5a) has a chemotactic activity that draws PMNs into the lung; it also up-regulates P-selectin on the endothelial cells. Thus the combination of cytokines and complement attracts PMNs into the lung, up-regulates adhesion molecules, and causes oxidant production and direct endothelial cell damage, with a subsequently increased permeability [19]. Ischemia-reperfusion of visceral (hepatic) and intestinal organs elicits the same inflammatory response as the limb, resulting in lung damage [20, 21].
Cardiopulmonary bypass activates the complement system and increases serum levels of C3a and C5a [22]. In addition, it causes an increase in thromboxane and cytokine levels, all of which significantly contribute to the inflammatory process. In a patient with malperfusion injury, reperfusion in association with prolonged cardiopulmonary bypass and the administration of large volumes of blood products leads to the development of a severe pulmonary capillary leak with end-organ damage resulting in patient death. Clearly our patients with limb, visceral, and intestinal malperfusion who underwent immediate surgical repair suffered from a severe reperfusion injury that was aggravated by cardiopulmonary bypass, causing end-organ failure. In addition, surgical repair of the tear with replacement of the ascending aorta, root, and arch does not guarantee reperfusion, because multiple reentry tears can cause unknown avenues of blood flow after repair and continued malperfusion.
Patients suffering severe myocardial injury and subsequent ventricular dysfunction as a result of malperfusion do not respond well to the prolonged cross-clamp times necessary for dissection repair and coronary artery revascularization and are unable to withstand the increased pulmonary vascular resistance resulting from combined reperfusion and cardiopulmonary bypass–induced lung injury. Patients with neurologic injury secondary to malperfusion should be assessed and their conditions fully stabilized before being subjected to lengthy cardiopulmonary bypass with HCA, which further insults the brain and causes permanent damage.
We propose medical support to allow recovery from reperfusion injury accompanied by reperfusion with percutaneous aortic fenestration and stenting of compromised branch vessels before surgical repair be the management approach used in patients with acute type A dissection complicated by malperfusion resulting in end-organ dysfunction. Treatment with intravenous ß-blockade can decrease the change in pressure in relationship to the change in time and help decrease the probability of rupture during the delay. Our experience shows there is a 5% risk of rupture and death over an average 20-day delay period, versus an 89% risk of death in such patients who undergo immediate repair. The other 10% of the patients in the delay group who died before operation died secondary to their malperfusion-reperfusion sequence, therefore the delay protocol avoided an unnecessary operation in these patients and a wasteful use of precious medical resources. Our proposal is supported by the fact that delay alone was the only independent variable predictive of outcome, demonstrating that the likelihood of death in patients with an acute type A dissection complicated by malperfusion is 33 times greater if they undergo immediate surgical repair as opposed to the delay sequence. We therefore will continue to follow our policy of percutaneous reperfusion and medical treatment of malperfusion injury before surgical repair of the dissected aorta.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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Address reprint requests to Dr Deeb, Section of Thoracic Surgery, The University of Michigan Hospitals, 1500 E. Medical Center Dr, 2124 Taubman Center, Box 0344, Ann Arbor, MI 48109-0344 (e-mail: mdeeb{at}umich.edu).
This article has been selected for the open discussion forum on the STS Web site: http://www.sts.org/annals
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References |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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and interleukin-1 in limb ischemia/reperfusion injury and associated lung injury. Am J Pathol 1993;143:453–63.[Abstract]
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