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Ann Thorac Surg 1998;66:1250-1253
© 1998 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Brain damage after aortic arch repair using selective cerebral perfusion

^a Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, Sendai, Japan
^b Department of Radiology, Tohoku University School of Medicine, Sendai, Japan

Accepted for publication April 26, 1998.

Address reprint requests to Dr Ohmi, Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai, 980-8574, Japan

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. Selective cerebral perfusion is one of the most popular methods for cerebral protection during aortic arch repair. However, causes of postoperative brain damage are not fully understood. We analyzed brain damage after aortic arch repair using selective cerebral perfusion for true aortic arch aneurysm in regard to preoperative cerebral infarction and intracranial and extracranial occlusive arterial disease.

Methods. Over a 9-year period, 60 patients with true aortic arch aneurysm underwent aortic arch repair using selective cerebral perfusion. Postoperative brain damage was evaluated in regard to preoperative cerebral infarction detected by computed tomography, magnetic resonance imaging, or both in 50 patients and intracranial and extracranial occlusive arterial disease detected by digital subtraction angiography, magnetic resonance angiography, or both in 35 patients.

Results. Seven (12%) of the 60 patients died within 30 days of operation. Postoperative brain damage occurred in 6 (10.5%) (3, coma, and 3, hemiplegia) of 57 patients; 3 patients who died without awakening were excluded. Preoperatively, old cerebral infarction was detected in 9 patients (18%), and silent cerebral infarction (lacunar infarction and leukoaraiosis) was diagnosed in 26 patients (52%). Postoperative brain damage occurred in 3 (33%) of the 9 patients with preoperative cerebral infarction and in 3 (23%) of 13 patients with negative preoperative brain findings; this excludes 2 patients who died without awakening. No patient with silent cerebral infarction had postoperative brain damage. Occlusive arterial disease was detected in 7 patients (20%). The incidence of brain damage in these patients was 71% (5/7), which was significantly greater than that of 4% (1/28) in patients without occlusive arterial disease (p < 0.001).

Conclusions. Silent cerebral infarction may not be a risk factor for postoperative brain damage. Preoperative evaluation of intracranial and extracranial occlusive arterial disease provides important information as to whether a patient might sustain brain damage after aortic arch repair using selective cerebral perfusion.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Cerebral protection is one of the most important concerns during aortic arch repair. Although various cerebral protection methods have been introduced, the incidence of postoperative brain damage ranges from 3.6% to 11% for deep hypothermia with circulatory arrest [1–3], 1.3% to 10.5% for selective cerebral perfusion (SCP) [4–6], and 0% to 11.8% for retrograde cerebral perfusion [7, 8]. We have preferentially been using SCP for aortic arch repair, and brain damage has occurred rarely in patients with true aneurysm but has not occurred in those with dissecting aneurysm. This complication was not related to duration of SCP, perfusion flow, or pressure and could be attributed to causes distinct from SCP [4]. In this study, we analyzed brain damage after aortic arch repair using SCP for true aortic arch aneurysm in regard to preoperative cerebral infarction and intracranial and extracranial occlusive arterial disease.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
We retrospectively evaluated the cases of 60 patients (53 men and 7 women) with true aortic arch aneurysm undergoing aortic arch repair using SCP between January 1988 and March 1997. The patients ranged in age from 55 to 79 years (mean age, 69 ± 5 years). Indications for aortic arch repair included saccular aneurysms and fusiform aneurysms measuring 50 mm in diameter. Preoperative cerebral infarction was evaluated by computed tomography (CT), magnetic resonance imaging (MRI), or both in 50 patients. Intracranial and extracranial arteries were evaluated for the existence of occlusive disease by digital subtraction angiography, magnetic resonance angiography, or both in 35 patients. At angiography, stenosis of 50% or more of the diameter was considered hemodynamically significant. Patients requiring emergency operation were excluded for lack of preoperative data. Types of operative procedures, number of hospital deaths, and number of patients with postoperative brain damage are shown in Table 1.

Selective cerebral perfusion
Early in this series, balloon cannulas for SCP were inserted through the opened aneurysm into the ostia of the brachiocephalic, left carotid, and left subclavian arteries. After April 1994, the cannulas were inserted through arteriotomies in the right subclavian, left carotid, and left subclavian arteries to perfuse the distal vascular bed in each of these regions. Both subclavian arteries were approached through infraclavicular skin incisions, and the perfusion cannula for the left carotid artery was inserted as distally as possible in the operative field of the upper mediastinum. Until April 1992, a single centrifugal pump was used for SCP. Thereafter, two roller pumps were used, one for the right subclavian artery and the other for the left carotid and subclavian arteries. The in-line cerebral perfusion pressure and flow rate were maintained higher than 40 mm Hg and around 10 mL · kg^-1 · min^-1, respectively. Twenty-two patients had one pump and 38, two pumps.

Statistical analysis
Values are expressed as the mean ± one standard deviation. For statistical analysis, unpaired t test and Fisher’s exact test were used, and significant differences were defined as a p value of less than 0.05.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
Seven (12%) of the 60 patients died within 30 days of operation. Of these 7 patients, 3 were excluded from postoperative neurologic analysis because 2 of them died in the operating room and 1 patient died on postoperative day 1 without awakening. The causes of death were low cardiac output (4 patients), coma (1 patient), bleeding (1), and rupture of the descending thoracic aneurysm (1). There were six late deaths (2 patients, coma; 2, multiple-organ failure, and 2, infection) more than 30 days after operations. The mean ages and the mean durations of SCP in patients with and without brain damage were 68 ± 2 years, and 140 ± 45 minutes and 69 ± 5 years and 135 ± 50 minutes, respectively. No significant differences were noted in age and duration of SCP between the two groups.

Twenty-two patients had one pump for SCP, and 3 (16%) of 19, excluding 3 patients who died without awakening, sustained postoperative brain damage (2, coma, and 1, hemiplegia). On the other hand, of the 38 patients with two pumps for SCP, brain damage occurred in 3 (8%) (1, coma, and 2, hemiplegia). There was no significant difference in the incidence of postoperative brain damage between the two groups.

Preoperative results from CT and MRI of the brain were analyzed in 50 patients. Old cerebral infarction was diagnosed in 9 patients (18%), and silent cerebral infarction including lacunar infarction and leukoaraiosis was found in 26 patients (52%); 15 patients (30%) had negative findings. Postoperative brain damage occurred in 3 (23%) of 13 patients with negative findings (excluding 2 patients who died without awakening) (1, hemiplegia, and 2, coma) and in 3 (33%) of 9 patients with preoperative cerebral infarction (2, hemiplegia, and 1, coma). However, no patient with silent cerebral infarction sustained postoperative brain damage. There were significant differences in the incidence of postoperative brain damage between patients with negative findings and those with silent cerebral infarction (p < 0.05) and between patients with silent cerebral infarction and those with preoperative cerebral infarction (p < 0.05).

Preoperative findings from digital subtraction angiography and magnetic resonance angiography of the intracranial and extracranial arteries were evaluated in 35 patients, and 7 (20%) proved to have intracranial or extracranial occlusive arterial disease or both. Postoperative brain damage occurred in 5 (71%) of these 7 patients and in 1 (4%) of the 28 patients without occlusive arterial disease. The difference between these two groups was significant (p < 0.001).

For the 3 patients who died in a coma, the causes of brain damage were thought to be ischemia resulting from unbalanced cerebral blood distribution (patient 1), thromboembolism from a coexisting abdominal aortic aneurysm (patient 5), and a hemorrhagic watershed type of cerebral infarction (patient 8). This last patient had undergone operation 2 months after a cerebral infarction of the right pons and basal ganglia region with left hemiplegia preoperatively without demonstrating positive findings of occlusive arterial disease. The types of intracranial and extracranial occlusive arterial disease, preoperative findings from brain CT and MRI, postoperative brain damage, and possible causes of brain damage are shown in Table 2.

	Comment

Top Abstract Introduction Patients and methods Results Comment References

Hayashi and colleagues [6] reported that neurologic deficits were observed in 15 (10.5%) of 143 patients who underwent aortic arch repair using SCP for nondissecting thoracic aneurysm. Two of them had a history of stroke, and the incidence of neurologic disabilities in patients aged 70 years or more and those aged 69 years or less was 16.7% and 6.7%, respectively. In the present study, postoperative brain damage occurred in 3 (33%) of 9 patients with preoperative cerebral infarction. However, 3 (23%) of 13 patients with negative preoperative findings from CT or MRI also sustained postoperative brain damage. Of these 3 patients, each had occlusive arterial disease in the right internal carotid artery (patient 1), the brachiocephalic artery (patient 2), and both the right internal carotid and vertebral arteries (patient 5) (see Table 2).

Recently, in association with increasing use of MRI, silent cerebral infarction has received a great deal of attention as a high-risk factor for stroke. Kase and colleagues [9] reported that 10% of initial stroke patients had silent cerebral infarction on CT in the Framingham study. In the Japanese population, the incidence of silent cerebral infarction is 15.2% in neurologically normal adults without a history of stroke, and the most important risk factor for silent cerebral infarction is hypertension [10]. The incidence of silent cerebral infarction significantly increases with age—5%, 11.4%, 25%, and 27.4%, in adults 40 to 49 years old, 50 to 59 years old, 60 to 69 years old, and older than 70 years, respectively [10]. In the present study, the mean age of the patients was 69 ± 5 years, and the incidence of silent cerebral infarction was 52%, which is much greater than the incidence of 25% in the Japanese population aged 60 to 69 years reported by Kobayashi and associates [10]. However, postoperative brain damage did not occur in the patients with silent cerebral infarction. Therefore, the existence of preoperative silent cerebral infarction does not appear to be a risk factor for postoperative brain damage in patients undergoing aortic arch repair using SCP.

McKhann and colleagues [11] examined the predictors of stroke risk in patients having coronary artery bypass grafting and found previous stroke, presence of carotid bruit, history of hypertension, increasing age, and history of diabetes mellitus to be significant preoperative factors and cardiopulmonary bypass time to be a significant intraoperative factor. Brener and associates [12] reported that 153 (3.8%) of 4,047 patients undergoing a cardiac operation had substantial carotid disease and that the incidence of transient ischemic attack or cerebrovascular accident after operation was 1.9% in patients with no carotid disease and 9.2% in patients with carotid lesions.

In aortic arch repair, a longer cardiopulmonary bypass time may be needed, special cerebral protection methods are mandatory, and patients generally are older and have a higher incidence of preoperative cerebral infarction and intracranial and extracranial occlusive arterial disease than patients undergoing general cardiac surgical procedures. As a result, postoperative brain damage could occur more frequently. Svensson and colleagues [2] found increased age, history of cerebrovascular disease, circulatory arrest time, previous aortic operation distal to the left subclavian artery, and cardiopulmonary bypass time to be predictors of transient or permanent stroke after aortic procedures using deep hypothermia with circulatory arrest. Judging from their report, we concluded brain damage could have occurred during cardiopulmonary bypass as well as circulatory arrest. The authors did not describe preoperative intracranial and extracranial occlusive arterial disease, but preoperative cerebrovascular disease appears to be one of the most important risk factors for brain damage after aortic arch repair.

In this study we examined postoperative brain damage in regard to preoperative findings from CT and MRI and intracranial and extracranial arterial disease in patients with true aortic aneurysm undergoing aortic arch repair. We found that 7 (20%) of 35 patients had the intracranial or extracranial occlusive arterial disease preoperatively, and postoperative brain damage occurred at a high incidence (5 [71%] of these 7 patients). Although further study will be needed to determine the causes of brain damage after aortic arch repair using SCP, we think that preoperative silent cerebral infarction may not be a risk factor for postoperative brain damage. Preoperative evaluation of intracranial and extracranial occlusive arterial disease provides important information on whether a patient may sustain brain damage after aortic arch repair using SCP for true aortic arch aneurysm.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

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