Ann Thorac Surg 2005;80:72-76
© 2005 The Society of Thoracic Surgeons
Original article: Cardiovascular
Surgical Results of Acute Aortic Dissection Complicated With Cerebral Malperfusion
Hiroshi Tanaka, MD*,
Kenji Okada, MD,
Teruo Yamashita, MD,
Yoshihisa Morimoto, MD,
Yujiro Kawanishi, MD,
Yutaka Okita, MD
Department of Cardiovascular, Thoracic, and Pediatric Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
Accepted for publication December 21, 2004.
* Address reprint requests to Dr Tanaka, Dept of Cardiovascular, Thoracic, and Pediatric Surgery, Kobe University Graduate School of Medicine, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe, Hyogo, Japan (Email: hirot{at}ams.odn.ne.jp).
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Abstract
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BACKGROUND: In patients with acute type A aortic dissection complicated by cerebral malperfusion, the surgical treatment remains challenging. This retrospective study reports the results of surgical interventions and the clinical features of these patients.
METHODS: From 1999 to 2004, 63 patients underwent surgical treatment for acute type A aortic dissection. Sixteen patients (25.3%) showed preoperative newly developed neurologic deficits (cerebral malperfusion). In patients with cerebral malperfusion, the characteristics, neurologic symptoms, computed tomography findings, interval from onset to operation, and operative details (procedure, arterial cannulation site, method of brain protection) were reviewed.
RESULTS: The hospital mortality rate was 43.7% (7 of 16 patients) for the cerebral malperfusion group and 17.0% (8 of 47 patients) for the noncerebral malperfusion group (all patients, 23.8%). Multivariate analysis showed preoperative cerebral malperfusion as the sole risk factor for hospital mortality. Six patients, including all patients in a preoperative coma, died of severe brain damage within 1 month after surgery. Most patients were diagnosed with right hemispheric cerebral infarction by postoperative brain computed tomography. The operative details and the time interval from onset to operation were not significant predictors of death. The cumulative survival rate at 4 years was 75.5% in patients without cerebral malperfusion and 50.1% with cerebral malperfusion (p = 0.091).
CONCLUSIONS: The results of surgical treatment for acute type A dissection complicated with cerebral malperfusion demonstrated high hospital mortality, but the long-term survival was similar to patients without cerebral malperfusion, with an acceptable neurologic outcome, excluding preoperative coma patients. Appropriate protection of ischemic brain tissue should be implemented to improve the surgical results in these patients.
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Introduction
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It is generally accepted that patients with acute type A aortic dissection require emergent surgical intervention. However, the optimal treatment of patients complicated with cerebral malperfusion remains controversial. Preoperative neurologic deficits resulting from cerebral malperfusion have been reported as a sign of poor prognosis [1]. These symptoms are not evaluated accurately because patients are often hemodynamically unstable and in shock owing to cardiac tamponade, coronary malperfusion, and aortic rupture. Recently, few reports have shown the treatment of acute type A aortic dissection complicated with cerebral malperfusion because of disappointing results, and some have shown that treatment is a relative contraindication even in emergent situations [2]. By establishing selective antegrade cerebral perfusion and retrograde cerebral perfusion techniques for brain protection during arch reconstruction or distal anastomosis, we have applied an aggressive surgical approach for patients with acute type A aortic dissection complicated with cerebral malperfusion since 1999. This report presents the results of surgical interventions and the clinical features of patients with preoperative neurologic deficits secondary to cerebral malperfusion, and discusses the treatment strategies for these patients.
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Patients and Methods
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From October 1999 to March 2004, in a series of 63 consecutive patients with acute type A aortic dissection, 16 patients showed preoperative newly developed neurologic deficits despite being in a hemodynamically stable condition (25.3%). These patients were defined as patients with aortic dissection complicated with cerebral malperfusion (CM group). The mean age was 67.5 ± 12.1 years, with a range of 36 to 83 years (CM group, 71.6 ± 7.7 years; non-CM group, 66.2 ± 12.4 years; p = 0.10). As they had neurologic deficits, patients with old cerebral infarction or in a hemodynamically unstable condition were excluded from the CM group. In the CM group, chest computed tomography and echocardiography were performed in all patients, ultrasonography of the neck vessels in 5 patients, and brain computed tomography in 2 patients as a preoperative evaluation of the aorta and its branches and of the brain. One patient referred to our hospital 2 days after the onset of loss of consciousness had right hemispheric cerebral infarction in brain computed tomography, and he underwent surgery 5 days later. Another patient was referred after 3 days of treatment for a cerebrovascular accident. The other 14 patients underwent emergent surgical intervention on the day of referral to our institution. No patients were refused surgery in this series. In the CM group, the operative details were reviewed, such as operative procedure, arterial cannulation site, method of cerebral protection, and interval from onset to operation. Postoperative brain computed tomography was performed in 13 patients regardless of their postoperative status.
Operative Procedures
All patients underwent median sternotomy with total cardiopulmonary bypass. The site of arterial cannulation was usually the femoral arteries; however, both femoral and right axillary arteries were used in 6 patients when brachiocephalic malperfusion was suspected. Using the right axillary artery for arterial inflow, an 8-mm polyethylene terephthalate fiber (Dacron) graft (Vascutek, Inchinnan, Renfrewshire, UK) was anastomosed to the artery. The site of the tear was resected whenever possible. Our brain protection methods were deep hypothermic circulatory arrest (DHCA) concomitant with retrograde cerebral perfusion or selective antegrade cerebral perfusion. Deep hypothermic circulatory arrest consists of core cooling during cardiopulmonary bypass to an average tympanic temperature 20°C. When aortic dissection extended to the aortic root and detachment of the aortic valve commissure occurred, the valvular resuspension technique was adopted.
Statistical Analysis
Comparisons between subgroups with and without CM were analyzed with the 
2 test and Student’s t test, and predictors for hospital death were analyzed with the logistic regression test. Long-term survival in each group was analyzed with the Kaplan-Meier method and log-rank test. Predictive operative factors of death as a result of severe brain injury were analyzed with the logistic regression test.
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Results
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Patient characteristics compared between the CM and non-CM groups are listed in Table 1. Preoperative factors were age, sex, pulmonary disease, old cerebral infarction, diabetes, hypertension, and renal dysfunction (serum creatinine level > 2.0 mg/dL). Factors associated with aortic dissection were shock, aortic insufficiency, acute myocardial infarction, tamponade, and entry location. The only significant difference was a history of old cerebral infarction (2 of 16, CM group; 0 of 47, non-CM group; p = 0.013). Table 2 shows the multivariate analysis of predictors of hospital death. Cerebral malperfusion was the only significant risk factor for hospital death (hazard ratio, 4.25; p = 0.033). Age, shock, and tamponade were significant predictors of univariate analysis; however, they were not significant in multivariate analysis. Tables 3–5 show the summaries of clinical presentation, surgical intervention, and surgical results of patients in the CM group. Patients who were not able to communicate, but were responsive to stimuli, were in a "drowsy" state. Preoperative chest computed tomography confirmed the presence of ascending aortic dissection involving the arch with extension into the brachiocephalic vessels in all patients, and ultrasonography demonstrated stenosis or occlusion of the carotid artery in patients 1, 4, 6, 9, and 14. Preoperative brain computed tomography of patient 3, who was referred to our hospital 2 days after the onset of neurologic symptoms, showed multiple cerebral infarctions. All patients in preoperative coma died of severe brain injury within 1 month after surgery. The causes of death were extensive right hemispheric cerebral infarction with or without hemorrhage in all cases, and most survivors also had right hemispheric cerebral infarction. Operative details such as the site of arterial cannulation, the method of cerebral protection, and the interval from onset to operation were not significant factors of death as a result of severe brain injury (p = 0.42, 0.09, and 0.50, respectively). Preoperative focal neurologic symptoms (hemiplegia) were not reversible, but survivors who recovered from consciousness impediment had acceptable quality of life. Long-term survival was similar in both groups (p = 0.09; Fig 1). The relationships between preoperative neurologic symptoms and postoperative outcomes and between the time interval from onset to surgery and postoperative neurologic outcome are shown in Figures 2 and 3 using the Glasgow Coma Scale Score [3]. The postoperative neurologic outcome tended to be better with a higher preoperative Glasgow Coma Scale Score.
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Table 2. Multivariate Analysis of Predictors of Hospital Death in Patients Undergoing Surgery for Acute Type A Aortic Dissection
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Fig 1. Cumulative survival of patients undergoing surgical intervention for acute type A aortic dissection. Patients without cerebral malperfusion are indicated by the solid line and filled circles, and those with cerebral malperfusion are indicated by the dotted line and open circles.
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Fig 2. Preoperative and postoperative Glasgow Coma Scale score of patients with cerebral malperfusion. Open circles indicate patients with transient ischemic attack, and filled circles indicate patients with stroke.
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Comment
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The results of surgical management of acute aortic dissection complicated by stroke are disappointing [4]. Borst [5] reported that 17 of 158 (10.7%) patients with acute proximal aortic dissection had symptomatic preoperative brain ischemia. A previous report in 1989 demonstrated that the surgical results of such patients showed a high mortality rate of 57% [1]. Their operative technique was as follows in all patients: the femoral artery was used for arterial pump inflow, and brain protection involved profound hypothermia and circulatory arrest. Recently, axillary artery cannulation and selective cerebral perfusion or retrograde cerebral perfusion for brain protection during circulatory arrest has been established, and our strategy for arch reconstruction or hemiarch replacement consists of these techniques [6]. In our cases, cerebral malperfusion significantly increased hospital mortality in patients with acute type A aortic dissection. Six patients died in the immediate postoperative period as a result of severe brain injury, 6 patients had persistent neurologic deficits, and 4 patients had no residual symptoms. All patients in a preoperative coma died. Some reports showed successful intentional delayed repair of acute proximal aortic dissection complicated by stroke with or without revascularization of impaired arch branches [7]. The effectiveness of revascularization of arch branches within 3 hours after onset of stroke was reported by the National Institute of Neurological Disorders and Stroke [8]. They showed successful outcome, demonstrating that symptoms were reversible within 3 hours after onset. We must consider early revascularization of the involved vessels when we encounter patients with acute aortic dissection complicated with cerebral malperfusion within 3 hours after onset. In this retrospective study, we could not revascularize the involved vessels within 3 hours in all cases. Postoperative brain computed tomography showed right hemispheric cerebral infarction to varying degrees in all patients, demonstrating that preoperative brain ischemia was irreversible. However, preoperative focal neurologic symptoms such as hemiplegia were reversible in some cases, and postoperative rehabilitation could achieve acceptable recovery. Recovery from consciousness impediment tended to be influenced on a preoperative level, but it was difficult to evaluate whether it was reversible because it was affected by factors such as age and the extent of infarction, even after stroke. Magnetic resonance imaging would be useful in emergent situations for the evaluation of ischemic brain tissue. In the application of selective antegrade cerebral perfusion or deep hypothermic circulatory arrest with retrograde cerebral perfusion in the distal anastomosis period, extracorporeal circulation would adversely affect brain ischemia.
The successful management of intraoperative brain malperfusion through retrograde cerebral perfusion has been reported [9]; however, in the unavoidable immediate application of cardiopulmonary bypass for aortic replacement, our experience showed no adequate method for brain protection in patients with preoperative brain malperfusion. It is unclear whether the mechanism of brain ischemia associated with aortic dissection is hemodynamic ischemia or thromboembolism. Benninger and colleagues [10] showed that thromboembolism is an essential mechanism in isolated cervical internal carotid artery dissection by evaluating computed tomography and magnetic resonance imaging. In 136 patients with isolated carotid artery dissection, 125 patients (91.9%) showed stenosis or occlusion of intracranial arteries. These patients were successfully treated with intravenous or intraarterial thrombolysis with a 70% to 80% excellent outcome [10–12]. Patients with aortic dissection complicated by severe neurologic symptoms could be treated successfully with revascularization of the involved vessels associated with aortic dissection before central aortic repair regardless of the risk of aortic rupture. However, thrombolysis therapy may increase the possibility of aortic rupture and difficulty of hemostasis in cases requiring emergent surgery; therefore, surgeons hesitate to apply this therapy and reluctantly operate immediately. Carotid stenting may be a good alternative to produce better results in this subset.
Finally, from our results, we have established some guidelines for the treatment of these patients:
- 1 Preoperative coma patients more than 3 hours after onset should be excluded as candidates for immediate central aortic repair surgery.
- 2 Patients within 3 hours after onset of stroke should undergo revascularization of the dissected vessels by carotid stenting or other methods.
- 3 Immediate surgery for patients with cerebral malperfusion, excluding preoperative coma patients, can achieve an acceptable neurologic outcome, although most preoperative neurologic symptoms are irreversible.
More sophisticated cardiopulmonary bypass methods of protection of ischemic brain tissue, consisting of selective cerebral perfusion, including the temperature and amount of cerebral flow, must be investigated for prevention against reperfusion and low perfusion injury.
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Fig 3. Postoperative Glasgow Coma Scale score of patients with cerebral malperfusion associated with the time interval from onset to surgery. Open circles indicate patients with transient ischemic attack, and filled circles indicate patients with stroke.
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References
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- Fann JI, Sarris GE, Miller DC, et al. Surgical management of acute aortic dissection complicated by stroke Circulation 1989;80:257-263.
- Cambria RP, Brewster DC, Gertler J, et al. Vascular complication associated with spontaneous aortic dissection J Vasc Surg 1988;7:199-209.[Medline]
- Teasdale G, Jannet B. Assessment of coma and impaired consciousnessa practical scale. Lancet 1974;2:81-82.[Medline]
- Lauterbach SR, Cambria RP, Brewster DC, et al. Contemporary management of aortic branch compromise resulting from acute aortic dissection J Vasc Surg 2001;33:1185-1192.[Medline]
- Borst HG. Organ ischemiaIn: Heinemann MK, Stone CD, editors. Surgical treatment of aortic dissection. 1st ed.. New York: Churchill Livingstone; 1996. pp. 249-271.
- Neri E, Massetti M, Capannini G, et al. Axillary artery cannulation in type A aortic dissection operations J Thorac Cadiovasc Surg 1999;118:324-329.[Abstract/Free Full Text]
- Piccione Jr W, Hamilton IN, Najafi H. Intentional delayed repair of acute dissection of the ascending aorta complicated by stroke J Thorac Cardiovasc Surg 1995;109:807-808.[Free Full Text]
- The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group Tissue plasminogen activator for acute ischemic stroke N Engl J Med 1995;24:1581-1587.
- De Paulis R, Collela DF, Bassano C, Ricci A, Chiariello L. Type A aortic dissectionmanagement of brain malperfusion through retrograde cerebral malperfusion. J Thorac Cardiovasc Surg 1994;108:788-789.[Free Full Text]
- Benninger DH, Georgiadis D, Kremer C, Studer A, Nedelchev K, Baumgartner RW. Mechanism of ischemic infarct in spontaneous carotid dissection Stroke 2004;35:482-485.[Abstract/Free Full Text]
- Arnold M, Nedeltchev K, Sturzenegger M, et al. Thrombolysis in patients with acute stroke caused by cervical artery dissection Arch Neurol 2002;59:549-553.[Abstract/Free Full Text]
- Dziewas R, Konrad C, Drager B, et al. Cervical artery dissection—clinical features, risk factors, therapy and outcome in 126 patients J Neurol 2003;250:1179-1184.[Medline]
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Abstract
Introduction
