Abstract： Objective To determine the risk factors for acute kidney injury (AKI) after thoracic aortic arch replacement surgery under deep hypothermic circulatory arrest (DHCA). Methods We retrospectively analyzed the clinical data of 139 patients who underwent thoracic aortic arch replacement surgery under DHCA between January 2004 and December 2008 in Beijing Anzhen Hospital Affiliated to Capital University of Medical Sciences. The patients were divided into two gro-ups according to whether AKI occurred after thoracic aortic arch replacement surgery. In the AKI gro-up (n=48), there were 39 males and 9 females with an age of 57.67±9.56 years. In the normal renal function gro-up (n=91), there were 69 males and 22 females with an age of 41.30±13.37 years. We observed the clinical data of the patients in both gro-ups, including left ventricular ejecting fraction (LVEF) before operation, diameter of the left ventricle, diameter of the ascending aorta, renal function, cardiopulmonary bypass time, aortic crossclamp time, and DHCA time. The risk factors for AKI and death after operation were evaluated by univariate analysis and stepwise logistic regression analysis. Results Among all the patients, AKI occurred in 48 (34.53%), 17 (12.23%) of whom underwent continuous renal replacement therapy (CRRT). Respiratory failure occurred in 27 patients (19.42%). Twentynine patients (20.86%) had cerebral complications, including temporary cerebral dysfunction in 26 patients and permanent cerebral dysfunction in 3 patients. In all the patients, 14 (10.07%) died, including 4 patients of heart failure, 9 patients of multiple organ failure, and 1 patient of cerebral infarction. There were 3 (3.30%)deaths in the normal renal function gro-up and 11 (22.92%) deaths in the AKI gro-up with a significant difference of mortality rate between the two gro-ups (P=0.011). A total of 118 patients were followed -up and 7 were lost. The follow-up time was from 5 to 56 months with an average time of 42 months. During the follow-up period, 7 patients died, including 3 patients of heart failure, 2 patients of cerebral apoplexy, and 2 patients of unknown reasons. The logistic regression analysis revealed that creatinine level was greater than 13260 μmol/L before operation (OR=1.042, P=0.021) and respiratory failure (OR=2.057, P=0.002) were independent determinants for AKI after the operation. Conclusion AKI is the most common complication of thoracic aortic arch replacement surgery under DHCA, and is the risk factor of mortality after the surgery. It is important to enhance perioperative protection of the renal function.
Objective To investigate different gases and hematocrits on cerebral injury during deep hypothermic circulatory arrest (DHCA) in a piglet model including monitoring by near-infrared spectroscopy (NIRS). Methods Twenty-four piglets were assigned to 4 groups with respect to different blood gas and hematocrit during DHCA. Group A: hematocrit was maintained between 0.25 to 0.30, pH-stat strategy during cooling phases and alpha stat strategy in other phases; group B: hematocrit was maintained between 0.25 to 0.30 and alpha stat strategy; group C: hematocrit was maintained between 0.20 to 0.25, pH-stat strategy during cooling phases and alpha stat strategy in other phases; group D: hematocrit was maintained between 0.20 to 0.25 and alpha stat strategy. Cerebral oxygenations of piglets were monitored continuously by NIRS. The brain was fixed in situ at 6 hours after operation and a histological score for neurological injury was assessed. Results Oxygenated hemoglobin (HbO2) and total hemoglobin (HbT) signals detected by NIRS were significantly lower in group D than those in group A and group B during cooling (Plt;0.05). Oxygenated hemoglobin nadir time was significantly shorter in group A(Plt;0.05). All piglets with oxygenated hemoglobin signal nadir time less than 25 minutes were free from histological evidence of brain injury. Conclusion Combination of pH-stat strategy and higher hematocrit reduces neurological injury after DHCA.
Abstract： Objective To evaluate the clinical safety and neurological outcomes of right axillary artery cannulation with a side graft compared with a direct approachin aortic arch replacement for patients with acute Stanford type A aortic dissection. Methods Between July 2008 and July 2010， 280 consecutive patients with acute Stanford type A aortic dissection underwent right axillary artery cannulation for cardiopulmonary bypass （CPB） in total arch replacement and stented “elephant trunk” implantation in our hospital.These 280 patients were divided into two groups according to the method of axillary artery cannulation in operation:direct arterial cannulation was used in 215 patients（direct arterial cannulationgroup， DG group， mean age of 43.1±9.5 years）， while cannulation with a side graft was used in 65 patients（ indirect cannulation group， IG group， mean age of 44.7±8.3 years）. Clinical characteristics of both groups were similar except their axillary artery cannulation method. Patient outcomes were compared as to the prevalence of clinical complications， especially neurological deficits and postoperative morbidity. Results The overall hospital mortality was 3.6% （10/280）， 3.3% （7/215） in DG group and 4.6% （3/65） in IG group respectively.Right axillary artery cannulation was successfully performed in all cases without any occurrence of malperfusion. Postoperatively， 25 patients（8.9%）developed temporaryneurological deficits， 19 cases in DG group（8.8%）， and 6 cases in IG group （9.2%）， and all these patients were cured after treatment. The incidence of postoperative complications directly related to axillary artery cannulation was significantly lower in IG group than that in DG group（1 case vs. 19 cases， P=0.045）. There were no statistical differences in arterial perfusion peak flow， peak pressure，antegrade cerebral perfusion time， deep hypothermic circulatory arrest time， and CPB time between the two groups（P ＞ 0.05）. Conclusion Right axillary artery cannulation with a side graftcan significantly reduce the postoperative complications of axillary artery cannulation. It is a safe and effective method for patients undergoing surgery for acute Stanford type A aortic dissection.
Objective Through establishment of brain slice model in rats with perfusion and oxygen glucose deprivation (OGD), we investigated whether this model can replicate the pathophysiology of brain injury in cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) or not and whether perfusion and OGD can induce preoligodendrocytes (preOL) injury or not, to provide cytological evidence for white matter injury after cardiopulmonary bypass. Methods Three to five living brain slices were randomly obtained from each of forty seven-day-old (P7) Sprague-Dawley (SD) rats with a mean weight of 14.7±1.5 g. Brain slices were randomly divided into five groups with 24 slices in each group: control group with normothermic artificial cerebralspinal fluid (aCSF) perfusion (36℃) and DHCA groups: OGD at 15℃, 25℃, 32℃ and 36℃. The perfusion system was established, and the whole process of CPB and DHCA in cardiac surgery was simulated. The degree of oligodendrocyte injury was evaluated by MBP and O4 antibody via application of immunohistochemistry. Results In the OGD group, the mature oligodendrocytes (MBP-positive) cells were significantly damaged, their morphology was greatly changed and fluorescence expression was significantly reduced. The higher the OGD temperature was, the more serious the damage was; preOL (O4-positive) cells showed different levels of fluorescence expression reduce in 36℃, 32℃ and 25℃ groups, and the higher the OGD temperature was, the more obvious decrease in fluorescence expression was. There was no statistically significant difference in the O4-positive cells between the control group and the 15℃ OGD group. Conclusion The perfused brain slice model is effective to replicate the pathophysiology of brain injury in CPB/DHCA which can induce preOL damage that is in critical development stages of oligodendrocyte cell line, and reduce differentiation of oligodendrocyte cells and eventually leads to hypomyelination as well as cerebral white matter injury.
ObjectiveTo establish a novel animal model of deep hypothermic circulatory arrest (DHCT) in rabbits without thoracotomy, and investigate acute kidney injury (AKI) induced by DHCT and early novel biomarkers of AKI. MethodsForty-two New Zealand big ear rabbits (3.5-4.0 kg, male or female) were randomly divided into 2 groups with 21 rabbits in each group. Cardiopulmonary bypass (CPB) was established via the right carotid artery and jugular vein in both groups. In Group A, CPB continued when the rectal temperature was maintained at 28℃. In group B, DHCT started when the rectal temperature reached 16℃ to 18℃ and lasted for 60 minutes before CPB was resumed and rewarming was started. The rectal temperature was restored to 35℃ within 30 minutes, then CPB was maintained for 30 minutes. CPB time was same in both groups. Preoperatively and 6 hours, 24 hours and 48 hours after the operation, venous blood samples were taken to examine serum creatinine (Cr) and β-trace protein (β-TP), and urine samples were taken to examine neutrophil gelatinase-associated lipocalin (NGAL). Four rabbits were sacrificed at respective above time points to measure renal malondialdehyde (MDA) content. Hematoxylin-Eosin (HE) staining, TUNEL assay and transmission electron microscopy were used to examine morphological changes of renal tubular epithelial cells (TECs). ResultsFour rabbits died in group A and five rabbits died in Group B during the experiment.(1)Blood Cr:There was no statistical difference between different time points in Group A (P > 0.05). In Group B, serum Cr at 24 hours after the operation was significantly higher than other time points, and also significantly higher than that of group A (P < 0.05).(2)Blood β-TP and urinary NGAL:There was no statistical difference between different time points in Group A (P > 0.05). In Group B, blood β-TP and urinary NGAL at the time of 6 hours, 24 hours and 48 hours postoperatively were significantly higher than preoperative levels (P < 0.05). Blood β-TP and urinary NGAL at the time of 24 hours postoperatively were significantly higher than other time points (P < 0.05). Blood β-TP and urinary NGAL at the time of 6 hours, 24 hours and 48 hours postoperatively were significantly higher than those of group A (P < 0.05).(3)Renal MDA content of Group B at the time of 24 hours postoperatively was significantly higher than other time points as well as that of Group A (P < 0.05).(4) HE staining showed serious pathological injuries of renal TECs at the time of 24 hours postoperatively in Group B. There was no significant pathological injury of renal TECs at the time of 24 hours postoperatively in Group A. (5)TUNEL-positive rate of group B at the time of 24 hours postoperatively was significantly higher than other time points as well as that of group A (P < 0.05).(6)Transmission electron microscope showed serious pathological injuries of renal TECs organelles at the time of 24 hours postoperatively in Group B. There was no significant pathological injury of renal TECs organelles in Group A. ConclusionsThis DHCT rabbit model without thoracotomy is a simple, convenient, and economical animal model with long-term animal survival for the study of DHCT-induced organ injury. AKI is most serious at the time of 24 hours after DHCA. Blood β-TP and urinary NGAL can be used as early biomarkers of DHCT-induced AKI.