EVALUATION STUDIES
JOURNAL ARTICLE
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Evaluation of risk factors for transient neurological dysfunction and adverse outcome after repair of acute type A aortic dissection in 122 consecutive patients.

OBJECTIVES: The aim of this retrospective study was to assess pre- and intraoperative factors leading to neurological complications and early death following repair of acute type A aortic dissection (ATAAD).

METHODS: There were 122 patients (85 male, age: 58.6 ± 12.5 years) with ATAAD, treated consecutively from August 2003 to August 2010. Pre- and intraoperative variables were analysed using a logistic regression model in order to identify risk factors for temporary neurological dysfunction (TND) and adverse outcome (AO), defined as stroke and 30-day mortality.

RESULTS: The 30-day mortality rate was 16.4%. Forty-one patients (33.6%) suffered transient neurological dysfunction and 20 (16.4%) had a postoperative stroke. Mean hypothermic circulatory arrest (HCA) temperature was 24 ± 4 °C. Selective cerebral perfusion (SCP) was performed in 99 (82%) patients, with a mean SCP flow rate of 10.3 ml/kg/min. The duration of lower body ischaemia (LBI) was 36 ± 27 min, of HCA 8.7 ± 15.5 min and of SCP 34 ± 28 min, respectively. Male gender [odds ratio (OR): 3.30, 95% confidence interval (CI): 1.15-9.47], diabetes (OR: 3.95, 95% CI: 1.18-13.24), compromised consciousness (OR: 6.65, 95% CI: 1.41-31.48) and manifest arterial atherosclerosis (OR: 6.68, 95% CI: 1.31-34.09) were detected as risk factors for TND, whereas a high body mass index (OR: 1.14, 95% CI: 1.01-1.3), a preoperative malperfusion syndrome (OR: 2.28, 95% CI: 0.84-6.18) and left ventricular ejection fraction <50% (OR: 3.84, 95% CI: 1.41-10.43) were detected as independent predictors for an AO. A dissection entry localized in the aortic arch or the descending aorta independently increased the risk for a postoperative stroke. A prolonged LBI increased the risk for AO (OR: 1.02, 95% CI: 1.00-1.04), whereas femoral cannulation showed a trend to an increased stroke incidence (OR: 4.2, 95% CI: 0.8-21.3).

CONCLUSIONS: Regardless of standardized neuroprotective techniques, treatment of ATAAD remains a high-risk operation. Preoperatively, the presence of a reduced ejection fraction, a malperfusion syndrome or a high body mass index may increase the perioperative risk for an adverse outcome. A dissection 'entry' localized in the aortic arch or the descending aorta may increase the risk for postoperative stroke. Intraoperatively, cannulation of the femoral artery and extension of the LBI time over 45 min should be avoided. Especially in patients with manifest preoperative cerebral and/or end-organ malperfusion, the cannulation modality as well as the entire neuroprotective management should be chosen individually, respecting its limitations.

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