Selective visceral perfusion improves renal flow and hepatic function in neonatal aortic arch repair

Selective visceral perfusion improves renal flow and hepatic function in neonatal aortic arch repair Abstract OBJECTIVES The aortic arch repair in the neonatal period is a complex procedure with significant morbidity. We define a useful double-perfusion technique and its effect on the function of abdominal organs in the postoperative course. METHODS Nine patients with double perfusion (Group 1) were compared with 14 patients with antegrade cerebral perfusion (Group 2). The objective was to discern the incidence of postoperative acute kidney injury and impaired hepatic function, as well as tissue perfusion and myocardial function parameters. Mechanical ventilation time, postoperative length of stay and 30-day mortality were measured. We excluded patients with extracorporeal membrane oxygenation, early mortality (<72 h) and preoperative renal or hepatic insufficiency. RESULTS Nine (39%) patients developed postoperative acute kidney injury, with 22% (n = 2) in Group 1 and 50% (n = 7) in Group 2 (P = 0.183). A higher urine output was observed during the first 24 h for Group 1 (P = 0.032). Eleven patients developed impaired hepatic function in the immediate postoperative period: 2 (18.2%) in Group 1 and 9 (81.8%) in Group 2 (P = 0.04). The international normalized ratio (P = 0.006–0.031) and prothrombin time (P = 0.007–P = 0.016) were significantly lower in the double-perfusion group during the first 72 h. Significant difference was observed in lactate levels in the first 72 h (P = 0.001–0.009). There was no postoperative mortality in either group. CONCLUSIONS Selective visceral perfusion is a safe procedure that provides a better urine output, hepatic function and tissue perfusion. This technique allows for the repair of complex aortic arch anomalies in neonates without deep hypothermic circulatory arrest. Neonates, Aortic arch repair, Visceral perfusion, Acute kidney injury, Hepatic function INTRODUCTION Even though improvements in medical management, surgical technique and postoperative care have resulted in reduced neonatal hospital mortality in complex aortic arch surgery, it is still a procedure associated with high morbidity [1]. Such repair can be performed under various perfusion techniques for the protection of different organs: deep hypothermic circulatory arrest (DHCA) or a combination of cerebral and visceral protection [2]. With the use of antegrade cerebral perfusion (ACP) techniques, several studies have shown an improvement in neurological outcomes in these patients when compared with the DHCA strategy, although other studies have demonstrated otherwise [3–9]. At the same time, there is a similar debate regarding the degree of visceral protection provided by double perfusion, cerebral and abdominal, with respect to isolated ACP. It provides better renal protection, but the effects on liver function remain unclear. [10]. For these reasons, there is no consensus on whether a selective visceral perfusion (SVP) should be added as a perfusion strategy due to the scarcity of scientific evidence to demonstrate the grade of visceral protection. We propose that double perfusion is an adequate strategy to reduce renal and hepatic insufficiency in the postoperative period of a complex neonatal aortic arch procedure. We describe the double-perfusion technique in complex neonatal aortic arch repair by studying the potential protective effect at renal, hepatic and tissue perfusion level when compared with an isolated ACP strategy. MATERIALS AND METHODS From April 2015 to October 2016, data on 10 consecutive neonates (Group 1) with complex aortic arch pathology with the double-perfusion technique were prospectively collected. This group was compared with a retrospective cohort (Group 2) of 17 neonates treated with ACP strategy during the period between March 2013 and April 2015. Patients with less than 72-h survival, preoperative renal and/or hepatic failure and those who required extracorporeal membrane oxygenation (ECMO) in the postoperative period were excluded from the analysis, as these clinical situations could influence the study parameters or cause missing data. From Group 1, 1 patient who required ECMO was excluded. From Group 2, 3 patients were excluded: 2 required postoperative ECMO and 1 had <72-h survival after surgery. A total of 9 patients in Group 1 were included in the study and compared with the historical cohort of 14 patients in Group 2. The preoperative characteristics of both groups are shown in Table 1. Concomitant procedures included ventricular septal defect closure, atrial septal defect closure, aortopulmonary window repair and subaortic stenosis release. Table 1: Preoperative characteristics of Group 1 (double perfusion) and Group 2 (antegrade cerebral perfusion)   Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum    Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum  Prematurity was defined by a gestational age of less than 37 weeks at the time of delivery. AAH: aortic arch hypoplasia; AVSD: atrioventricular septal defect; AP: aortopulmonary; CoA: coarctation of the aorta; DORV: double-outlet right ventricle; IAA: •••; LV: left ventricle; MAA: mitral-aortic atresia; TA: tricuspid atresia; TGA: transposition of the great arteries; VSD: ventricular septal defect. Table 1: Preoperative characteristics of Group 1 (double perfusion) and Group 2 (antegrade cerebral perfusion)   Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum    Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum  Prematurity was defined by a gestational age of less than 37 weeks at the time of delivery. AAH: aortic arch hypoplasia; AVSD: atrioventricular septal defect; AP: aortopulmonary; CoA: coarctation of the aorta; DORV: double-outlet right ventricle; IAA: •••; LV: left ventricle; MAA: mitral-aortic atresia; TA: tricuspid atresia; TGA: transposition of the great arteries; VSD: ventricular septal defect. The objective of the study was to determine the incidence of postoperative acute kidney injury (AKI), impaired hepatic function and changes in tissue perfusion and in myocardial function parameters. We noted the duration of mechanical ventilation, postoperative length of stay (PLOS) and 30-day mortality. AKI was defined as an increase in the baseline creatinine (the lowest creatinine within 3 days before arch repair in mg/dl) according to the AKI network criteria and/or a decrease in the estimated glomerular filtration rate (eGFR) (ml/min/1.73 m2) according to the Paediatric Risk, Injury, Failure, Loss, End Stage Renal Disease (p-RIFLE) score during the first 24, 48 and 72 h postoperatively [11]. eGFR was calculated by using the Schwartz formula [12]. The urine output (ml/kg/h) was also collected during the cardiopulmonary bypass (CPB) and in the immediate postoperative period (0–6 h, 6–12 h and 12–24 h). Impaired hepatic function was defined as a 2-fold increase of the baseline alanine transaminase level (IU/l), an increase greater than 3 s in the baseline prothrombin time or an increase of the international normalized ratio above 1.5 measured during the first 72 h postoperatively [13]. The clotting time values in the immediate postoperative period were not included, as transfusion of blood products or use of procoagulant drugs could have affected them. The lactate levels, as a parameter of tissue perfusion, were recorded according to the following criteria: a peak value intraoperatively, every 6 h for the first 24 h, and a single determination between 48 and 72 h after CPB. Similarly, the mixed venous saturation intraoperative nadir value was also recorded at 24, 48 and 72 h postoperatively. The cardiac function was estimated by using the inotropic score defined as the maximum dose of dopamine (μg/kg/min) + dobutamine (μg/kg/min) + 100 × adrenaline (μg/kg/min) [14]. All patients were operated by the same surgeon. The surgical complexity was measured using the basic Aristotle score. Surgical double-perfusion technique An arterial catheter Seldicath 2F (Prodimed, Neulliy en Thelle, France) is placed in the right radial artery and a Seldicath 3F in femoral artery. Bilateral cerebral and visceral oximetries are monitored using near-infrared spectroscopy INVOS™ (Covidien, Mansfield, MA, USA) with a Paediatric SomaSensor® (Covidien) placed in the posterior and left lumbar area throughout the intervention. Body temperature is measured by the introduction of a nasopharyngeal and rectal probe (9 Fr, GE Healthcare, Helsinki, Finland). Bladder catheterization is performed to control diuresis. The priming of the CPB circuit does not differ between groups. Initially, the patient is placed in the right lateral decubitus position. A left posterolateral minithoracotomy (<5 cm) is performed at the 4th intercostal space. The following vascular structures are dissected: descending thoracic aorta, ductus and aortic arch, providing mobility to facilitate the anastomosis. Nerve structures are identified as the left vagus, recurrent and phrenic nerves. The first 2 intercostal arteries and the left subclavian artery are ligated, if necessary. The descending aorta is partially clamped, and a 4 mm-diameter Gore-Tex® conduit (Gore Inc., Flagstaff, AZ, USA) is sutured 3 cm below the patent ductus arteriosus (PDA) (Fig. 1A). The conduit is heparinized to prevent thrombosis. The distal end is closed by vascular clips Ligaclip® (Ethicon Endo-Surgery LLC., Guaynabo, PR, USA). After verifying haemostasis, the thoracotomy is closed according to the usual technique. Then, the patient is placed in the supine position for a median sternotomy. After total heparinization, the first brachiocephalic trunk is cannulated with a 4-mm Gore-Tex conduit. The left pleura is opened to retrieve the conduit from the descending aorta taking it under the left phrenic nerve. After checking appropriate levels of activated coagulation time (>400 s), a Biomedicus™ 10-Fr cannula (Medtronic Inc., Minneapolis, MN, USA) is inserted into the Gore-Tex conduit located in the brachiocephalic trunk that will serve for cerebral perfusion. A Biomedicus 8-Fr cannula is then inserted through the Gore-Tex conduit on the descending thoracic aorta for visceral perfusion. Both cannulae are connected to the arterial line (Fig. 1B). A bicaval cannulation is made using the Stöcker venous cannula (Sorin Group, Mirandola, Italy) according to the appropriate patient size, and the CPB is started. The PDA is ligated. The procedure is performed under moderate hypothermia, 26–28°C, with a blood flow calculated per body surface and temperature. The median arterial blood pressure is 25–30 mmHg registered in both arterial extremities. Figure 1: View largeDownload slide Surgical perfusion technique. (A) Left thoracotomy placing the Gore-Tex® conduit in the descending aorta. (B) Arterial perfusion Y-connection between the brachiocephalic trunk and the descending aorta cannula. Figure 1: View largeDownload slide Surgical perfusion technique. (A) Left thoracotomy placing the Gore-Tex® conduit in the descending aorta. (B) Arterial perfusion Y-connection between the brachiocephalic trunk and the descending aorta cannula. After the ascending aorta is clamped, a perfusion of Custodiol® (Dr Frank Köhler Chemie GmbH, Bensheim, Germany) cardioplegia is administered in the aortic root. We proceed to the occlusion of the supra-aortic trunks maintaining ACP through the brachiocephalic trunk cannula. In a similar way, the descending thoracic aorta is clamped 2 cm below the PDA, maintaining visceral perfusion through the cannula located in the descending thoracic aorta. Then, the correction of the aortic arch is completed. The technique of repair did not differ between groups without circulatory arrest in any case. The Norwood procedure was performed with a modified Blalock–Taussig shunt in both groups. When the surgical correction is finished, all vascular clamps are removed, and the patient is rewarmed. When the patient’s rectal temperature reaches 34°C, the visceral perfusion is stopped, maintaining the arterial blood flow only through the cannula located in the brachiocephalic trunk. The Gore-Tex conduit connected to the descending thoracic aorta is clipped and sutured at its distal end. All patients underwent modified ultrafiltration after discontinuation of CPB. Statistical analysis We performed a Kolmogorov–Smirnov’s test to study normality. Qualitative variables are reported as frequency and percentage and compared using the χ2 or Fisher’s exact test. Quantitative variables are expressed as mean ± standard deviation or as median with 25th and 75th percentile values and compared with the Student’s t-test or the Mann–Whitney U-test according to normal distribution. The statistical software used was SPSS version 24.0 (SPSS Inc., Chicago, IL, USA). RESULTS Demographics and intraoperative variables In total, 56.5% of the patients were boys and 43.5% were girls. The mean age of patients at the time of operation was 13.6 ± 9.8 days, the average weight was 3.2 ± 0.52 kg and average height was 50.3 ± 2.89 cm. The mean Aristotle score was 11.7 ± 3.1, CPB time was 164.5 ± 58.4 min, aortic cross-clamp time was 77.5 ± 32 min and biventricular repair was 60.9%. The average length of intubation was 6.09 ± 3.7 days, the average length of stay in the intensive care unit was 17.5 ± 12.3 days, PLOS was 39.3 ± 18 days and 30-day mortality was 0%. Groups 1 and 2 were not significantly different in terms of sex (P = 0.998), age (P = 0.135), weight (P = 0.770), height (P = 0.686), Aristotle score (P = 0.154), CPB time (P = 0.734), aortic cross-clamp time (P = 0.551), biventricular repair (P = 0.675), length of intubation (P = 0.592), length intensive care unit (P = 0.369) and PLOS (P = 0.850). Renal parameters The statistical analysis showed that the patients undergoing SVP were not significantly different in terms of creatinine serum and eGFR evolution (Fig. 2A). Only 9 (39%) patients developed postoperative AKI: Group 1, 2 (22%) patients and Group 2, 7 (50%) patients, with no statistical significance between both groups (P = 0.183). A higher urine output during the first 24 h was observed in Group 1 (P = 0.007–0.032) (Fig. 2B), with the exception of the 6–12 h period (P = 0.961). Figure 2: View largeDownload slide (A) Perioperative eGFR (ml/min/1.73 m2) calculated using the Schwartz formula. Patients undergoing double perfusion did not have significant differences in eGFR preoperatively (P = 0.206), intraoperatively (GFR0, P = 0.652) and in the first 3 days (GFR1, P = 0.612; GFR2, P = 0.395 and GFR3, P = 0.661) after surgery. (B) Perioperative urine output. Patients undergoing double perfusion had significantly higher urine output intraoperatively (P = 0.007), 0–6 h postoperatively (P = 0.018) and 12–24 h postoperatively (P = 0.032) but not in the 6–12-h interval postoperatively (P = 0.961). ACP: anterograde cerebral perfusion; eGFR: estimated glomerular filtration rate; Intraop: intraoperative; Postop: postoperative; preop: preoperative. Figure 2: View largeDownload slide (A) Perioperative eGFR (ml/min/1.73 m2) calculated using the Schwartz formula. Patients undergoing double perfusion did not have significant differences in eGFR preoperatively (P = 0.206), intraoperatively (GFR0, P = 0.652) and in the first 3 days (GFR1, P = 0.612; GFR2, P = 0.395 and GFR3, P = 0.661) after surgery. (B) Perioperative urine output. Patients undergoing double perfusion had significantly higher urine output intraoperatively (P = 0.007), 0–6 h postoperatively (P = 0.018) and 12–24 h postoperatively (P = 0.032) but not in the 6–12-h interval postoperatively (P = 0.961). ACP: anterograde cerebral perfusion; eGFR: estimated glomerular filtration rate; Intraop: intraoperative; Postop: postoperative; preop: preoperative. Hepatic parameters Eleven patients developed impaired hepatic function in the immediate postoperative period: Group 1, 2 (18.2%) cases and Group 2, 9 (81.8%) cases (P = 0.04). Furthermore, patients undergoing SVP showed faster recovery of international normalized ratio (P = 0.006–0.031) and prothrombin time (P = 0.007–0.016) during the first 72 h (Fig. 3). Figure 3: View largeDownload slide (A) Postoperative PT. Patients undergoing double perfusion had lower PT postoperatively (PT 24 h, P = 0.007; PT 48 h, P = 0.016; PT 72 h, P = 0.011). (B) Postoperative INR. Patients undergoing double perfusion had lower INR postoperatively (INR 24 h, P = 0.006; INR 48 h, P = 0.031; INR 72 h, P = 0.020). ACP: anterograde cerebral perfusion; INR: international normalized ratio; PT: prothrombin time. Figure 3: View largeDownload slide (A) Postoperative PT. Patients undergoing double perfusion had lower PT postoperatively (PT 24 h, P = 0.007; PT 48 h, P = 0.016; PT 72 h, P = 0.011). (B) Postoperative INR. Patients undergoing double perfusion had lower INR postoperatively (INR 24 h, P = 0.006; INR 48 h, P = 0.031; INR 72 h, P = 0.020). ACP: anterograde cerebral perfusion; INR: international normalized ratio; PT: prothrombin time. Perfusion and cardiac parameters Group 1 had lower lactate levels in the first 72 h (P = 0.001–0.028; Fig. 4). In contrast, mixed venous saturation and inotropic score did not show statistically significant differences. Figure 4: View largeDownload slide Perioperative lactate levels. Patients undergoing double perfusion had lower lactate levels intraoperatively (P = 0.006), in the first 24 h peak (P = 0.001), 48 h (P = 0.014) and 72 h (P = 0.028) after surgery. ACP: anterograde cerebral perfusion; Interop: intraoperative; Postop: immediate postoperative. Figure 4: View largeDownload slide Perioperative lactate levels. Patients undergoing double perfusion had lower lactate levels intraoperatively (P = 0.006), in the first 24 h peak (P = 0.001), 48 h (P = 0.014) and 72 h (P = 0.028) after surgery. ACP: anterograde cerebral perfusion; Interop: intraoperative; Postop: immediate postoperative. Table 2 illustrates a more accurately statistical comparison of renal, hepatic and tissue perfusion parameters. Table 2: Comparison of renal, hepatic and tissue perfusion parameters Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  All data are distributed normally except lactate levels. Continuous variables are presented as mean ± standard deviation except lactate levels (median and 25th–75th percentile). The intra- and postoperative evolution of renal, hepatic and tissue perfusion parameters is shown. INR: international normalized ratio; POD: postoperative day; SvO2: mixed venous oxygen saturation. Table 2: Comparison of renal, hepatic and tissue perfusion parameters Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  All data are distributed normally except lactate levels. Continuous variables are presented as mean ± standard deviation except lactate levels (median and 25th–75th percentile). The intra- and postoperative evolution of renal, hepatic and tissue perfusion parameters is shown. INR: international normalized ratio; POD: postoperative day; SvO2: mixed venous oxygen saturation. In addition, we selected a subgroup of single-ventricle physiology patients and we compared all the parameters studied before according to the perfusion techniques used but we did not demonstrate statistical significance. DISCUSSION DHCA has been the perfusion technique of choice used for most surgical corrections when beginning congenital heart surgery, allowing the presence of a bloodless field [10]. It has been widely used for the complex repair of the neonatal aortic arch, and it is a much debated topic if it is associated with greater neurological alterations when compared with ACP [3–9]. However, DHCA morbidity should not be focused exclusively on neurological damage. It also produces a significant increase in inflammatory response, causing tissue oedema, neutrophil activation and increased oxidative stress [15]. In addition, the lack of systemic perfusion causes a higher incidence of postoperative AKI which conditions an increase in mechanical ventilation time, PLOS, morbidity, mortality and the associated costs of care [16]. The incidence of AKI after aortic arch repair varies from 11% to 52% according to some series, being higher in the neonatal group due to a greater susceptibility to ischaemia secondary to the immaturity of their organs [17]. When compared with DHCA, it has been proposed that ACP would provide a visceral flow that could act as a protector factor against visceral organ damage. Algra et al. [18] demonstrate that abdominal near-infrared spectroscopy levels vary in patients with ACP because the different patterns of collateral arteries do not guarantee a correct abdominal perfusion. Therefore, different groups have added abdominal perfusion to their procedures to improve AKI. These groups report lower incidence compared with the isolated ACP without technique-related complications and with a shorter CPB time when it is performed without hypothermia due to a shorter rewarming period [10, 19]. In our study, we demonstrate an improvement in the urine output in the group with SVP during the first postoperative hours reflecting a greater renal flow but that has not been enough to prove a decrease in the occurrence of postoperative AKI, eGFR or creatinine levels. These results are not consistent with data published by other authors [10, 19] who were able to demonstrate, in a larger sample size, a reduction in the postoperative AKI when SVP was added. We believe these observed differences may be due to the smaller sample size since the perfusion techniques are similar. In addition, the DHCA effect has also been reported on other abdominal organs. It is known that there is an increase in intestinal permeability reflecting a relative intestinal deficit perfusion following the Norwood surgery with DHCA [20]. An increase in lactates and intestinal mucosa lesion biomarkers has also been reported in patients with DHCA when compared with ACP [18]. In this sense, the presence of circulating free radicals due to a prolonged tissue ischaemia produces an increase in left ventricular pressures, affecting myocardial function [21]. We have not demonstrated significant differences regarding mixed venous oxygen saturation and inotropic score as parameters of cardiac dysfunction. This is probably due to the pH and mixed venous oxygen saturation in both groups being maintained at optimal levels during CPB and the modified ultrafiltration effect releasing the proinflammatory molecules. As we know, there are no published studies about the effect of SVP on liver function and its relevance in the postoperative period of these patients. We know that postoperative impaired hepatic function significantly increases mechanical ventilation time, PLOS and mortality, probably related to the occurrence of postoperative cardiogenic shock [22]. In these cases, the use of a ‘hepatic score’ has been described to measure the grade of hepatic impairment. This score has not been validated in paediatric patients and relies inconveniently on bilirubin levels as a parameter. The presence of hyperbilirubinemia is a physiological fact in neonates, so it is not useful as a dynamic parameter of postoperative liver dysfunction in this age group as this value alters the results. In contrast, we can use the usual parameters to define hepatic dysfunction such as altered coagulation tests and increased transaminase levels within 72 h after surgery. We have not used green indocyanine as a liver function test as its results may be affected by the cardiac output and CPB [23]. In this study, we were able to demonstrate differences regarding the incidence of hepatic dysfunction. ACP patients showed more hepatic impairment than those operated using SVP, particularly as a result of a significant increase in international normalized ratio and prothrombin time but not in hepatic enzymes. In addition, patients with SVP corrected their coagulation alterations faster. We have also shown an improvement in lactate levels during and after the first 3 postoperative days as a reflection of a conserved aerobic metabolism. Both facts confirm that SVP improves blood flow throughout the visceral territory. In this study, we have demonstrated physiological advantages but not clinical benefits. This may be due to the small sample size or the heterogeneity of the group. As we have commented, we did an analysis of single-ventricle physiology patients with no statistical differences, probably for the same reason. These patients have a longer cross-clamp time and a higher risk of renal and hepatic insufficiency when compared with biventricular physiology patients. We believe that a future study comparing the 2 perfusion techniques in the single-ventricle subgroup would be appropriate. Regarding the visceral perfusion technique, Yasui et al. [24] described the initial technique of a thoracotomy through the 4th intercostal space and interposing a Gore-Tex conduit as we did. In this sense, Imoto et al. [25] published a technique modification, where they approached the thoracic aorta through the sternotomy itself, with an opening in the posterior pericardium, because they considered thoracotomy a very invasive procedure. We also believe that minithoracotomy (<5 cm) is invasive when compared with the median approach, but it allows complex neonatal aortic arch repair without circulatory arrest and mild/moderate hypothermia. Furthermore, we perform the entire thoracic aortic dissection, left bronchus separation, entire ductal tissue section and a better recurrent nerve identification. The aortic arch anastomoses can now be performed tension-free and in any position due to the aortic mobility achieved by this easy technique. We have not studied the possible benefit of this extended dissection and the total PDA release as a way to decrease the incidence of aortic arch coarctation. We believe this could be another positive advantage of this approach and the subject of future studies. Other groups have introduced less invasive techniques for visceral perfusion like femoral or umbilical cannulation [26]. These procedures provide a questionable visceral flow, because they use a smaller catheter and offer no benefits to thoracic aortic dissection. Limitations This study has several limitations, the first of which are inherent to its retrospective design; however, it should be emphasized that all patients were operated on and managed by the same group. Second, it has a relatively small number of patients and this can bias the results. Third, we have not studied gastric or intestinal injury biomarkers as a method to more accurately determine the potential benefits of adding an antegrade visceral perfusion line. Finally, we have not compared blood loss and the need for transfusion of blood components as a parameter of liver dysfunction and the possible clinical benefit of the SVP. 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Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Interactive CardioVascular and Thoracic Surgery Oxford University Press

Selective visceral perfusion improves renal flow and hepatic function in neonatal aortic arch repair

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Oxford University Press
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© The Author(s) 2018. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
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1569-9293
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1569-9285
D.O.I.
10.1093/icvts/ivy091
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Abstract

Abstract OBJECTIVES The aortic arch repair in the neonatal period is a complex procedure with significant morbidity. We define a useful double-perfusion technique and its effect on the function of abdominal organs in the postoperative course. METHODS Nine patients with double perfusion (Group 1) were compared with 14 patients with antegrade cerebral perfusion (Group 2). The objective was to discern the incidence of postoperative acute kidney injury and impaired hepatic function, as well as tissue perfusion and myocardial function parameters. Mechanical ventilation time, postoperative length of stay and 30-day mortality were measured. We excluded patients with extracorporeal membrane oxygenation, early mortality (<72 h) and preoperative renal or hepatic insufficiency. RESULTS Nine (39%) patients developed postoperative acute kidney injury, with 22% (n = 2) in Group 1 and 50% (n = 7) in Group 2 (P = 0.183). A higher urine output was observed during the first 24 h for Group 1 (P = 0.032). Eleven patients developed impaired hepatic function in the immediate postoperative period: 2 (18.2%) in Group 1 and 9 (81.8%) in Group 2 (P = 0.04). The international normalized ratio (P = 0.006–0.031) and prothrombin time (P = 0.007–P = 0.016) were significantly lower in the double-perfusion group during the first 72 h. Significant difference was observed in lactate levels in the first 72 h (P = 0.001–0.009). There was no postoperative mortality in either group. CONCLUSIONS Selective visceral perfusion is a safe procedure that provides a better urine output, hepatic function and tissue perfusion. This technique allows for the repair of complex aortic arch anomalies in neonates without deep hypothermic circulatory arrest. Neonates, Aortic arch repair, Visceral perfusion, Acute kidney injury, Hepatic function INTRODUCTION Even though improvements in medical management, surgical technique and postoperative care have resulted in reduced neonatal hospital mortality in complex aortic arch surgery, it is still a procedure associated with high morbidity [1]. Such repair can be performed under various perfusion techniques for the protection of different organs: deep hypothermic circulatory arrest (DHCA) or a combination of cerebral and visceral protection [2]. With the use of antegrade cerebral perfusion (ACP) techniques, several studies have shown an improvement in neurological outcomes in these patients when compared with the DHCA strategy, although other studies have demonstrated otherwise [3–9]. At the same time, there is a similar debate regarding the degree of visceral protection provided by double perfusion, cerebral and abdominal, with respect to isolated ACP. It provides better renal protection, but the effects on liver function remain unclear. [10]. For these reasons, there is no consensus on whether a selective visceral perfusion (SVP) should be added as a perfusion strategy due to the scarcity of scientific evidence to demonstrate the grade of visceral protection. We propose that double perfusion is an adequate strategy to reduce renal and hepatic insufficiency in the postoperative period of a complex neonatal aortic arch procedure. We describe the double-perfusion technique in complex neonatal aortic arch repair by studying the potential protective effect at renal, hepatic and tissue perfusion level when compared with an isolated ACP strategy. MATERIALS AND METHODS From April 2015 to October 2016, data on 10 consecutive neonates (Group 1) with complex aortic arch pathology with the double-perfusion technique were prospectively collected. This group was compared with a retrospective cohort (Group 2) of 17 neonates treated with ACP strategy during the period between March 2013 and April 2015. Patients with less than 72-h survival, preoperative renal and/or hepatic failure and those who required extracorporeal membrane oxygenation (ECMO) in the postoperative period were excluded from the analysis, as these clinical situations could influence the study parameters or cause missing data. From Group 1, 1 patient who required ECMO was excluded. From Group 2, 3 patients were excluded: 2 required postoperative ECMO and 1 had <72-h survival after surgery. A total of 9 patients in Group 1 were included in the study and compared with the historical cohort of 14 patients in Group 2. The preoperative characteristics of both groups are shown in Table 1. Concomitant procedures included ventricular septal defect closure, atrial septal defect closure, aortopulmonary window repair and subaortic stenosis release. Table 1: Preoperative characteristics of Group 1 (double perfusion) and Group 2 (antegrade cerebral perfusion)   Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum    Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum  Prematurity was defined by a gestational age of less than 37 weeks at the time of delivery. AAH: aortic arch hypoplasia; AVSD: atrioventricular septal defect; AP: aortopulmonary; CoA: coarctation of the aorta; DORV: double-outlet right ventricle; IAA: •••; LV: left ventricle; MAA: mitral-aortic atresia; TA: tricuspid atresia; TGA: transposition of the great arteries; VSD: ventricular septal defect. Table 1: Preoperative characteristics of Group 1 (double perfusion) and Group 2 (antegrade cerebral perfusion)   Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum    Age (days)  Weight (kg)  Sex  Prematurity  Diagnosis  Surgery  Group 1   1  10  3.5  Female  No  DORV + VSD + AAH and LV hypoplasia  Norwood   2  4  3.1  Male  No  MAA  Norwood   3  35  3.8  Male  No  MAA  Norwood   4  8  2.9  Female  No  IAA + VSD  Repair of IAA + VSD   5  39  2.3  Male  No  IAA + AP window  Repair of IAA + AP window   6  11  3.5  Male  No  AAH + borderline ventricle  Biventricular repair of hypoplastic LV   7  9  3.8  Female  No  Left isomerism + AVSD + mitral atresia + AAH  Norwood   8  10  2.7  Female  No  AP window + IAA  Repair of IAA + AP window   9  15  4.1  Male  No  IAA + VSD  Repair of IAA + VSD  Group 2   1  36  2.04  Female  No  AAH + VSD  Repair of aortic arch + VSD   2  10  3.4  Female  No  TGA + AAH and right ventricle hypoplasia  Norwood   3  5  3.5  Male  No  MAA  Norwwod   4  4  2.9  Male  No  MAA  Norwood   5  13  4  Male  No  DORV + VSD + AAH + LV hypoplasia+ CoA  Norwood   6  13  3.4  Male  No  AAH + CoA  Repair of aortic arch   7  10  2.7  Female  No  AAH  Repair of aortic arch   8  7  3.2  Female  No  IAA + VSD  Repair of aortic arch + VSD   9  8  3.7  Female  No  IAA + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   10  17  2.9  Female  No  AAH + subaortic stenosis + VSD  Repair of aortic arch + VSD + resection of conal septum   11  18  2.9  Male  No  IAA + VSD  Repair of aortic arch + VSD   12  9  3.5  Male  No  TA + TGA + AAH + VSD  Norwood   13  9  3.3  Male  No  AAH  Repair of aortic arch   14  13  3.9  Male  No  AAH + VSD + subaortic stenosis  Repair of aortic arch + VSD + resection of conal septum  Prematurity was defined by a gestational age of less than 37 weeks at the time of delivery. AAH: aortic arch hypoplasia; AVSD: atrioventricular septal defect; AP: aortopulmonary; CoA: coarctation of the aorta; DORV: double-outlet right ventricle; IAA: •••; LV: left ventricle; MAA: mitral-aortic atresia; TA: tricuspid atresia; TGA: transposition of the great arteries; VSD: ventricular septal defect. The objective of the study was to determine the incidence of postoperative acute kidney injury (AKI), impaired hepatic function and changes in tissue perfusion and in myocardial function parameters. We noted the duration of mechanical ventilation, postoperative length of stay (PLOS) and 30-day mortality. AKI was defined as an increase in the baseline creatinine (the lowest creatinine within 3 days before arch repair in mg/dl) according to the AKI network criteria and/or a decrease in the estimated glomerular filtration rate (eGFR) (ml/min/1.73 m2) according to the Paediatric Risk, Injury, Failure, Loss, End Stage Renal Disease (p-RIFLE) score during the first 24, 48 and 72 h postoperatively [11]. eGFR was calculated by using the Schwartz formula [12]. The urine output (ml/kg/h) was also collected during the cardiopulmonary bypass (CPB) and in the immediate postoperative period (0–6 h, 6–12 h and 12–24 h). Impaired hepatic function was defined as a 2-fold increase of the baseline alanine transaminase level (IU/l), an increase greater than 3 s in the baseline prothrombin time or an increase of the international normalized ratio above 1.5 measured during the first 72 h postoperatively [13]. The clotting time values in the immediate postoperative period were not included, as transfusion of blood products or use of procoagulant drugs could have affected them. The lactate levels, as a parameter of tissue perfusion, were recorded according to the following criteria: a peak value intraoperatively, every 6 h for the first 24 h, and a single determination between 48 and 72 h after CPB. Similarly, the mixed venous saturation intraoperative nadir value was also recorded at 24, 48 and 72 h postoperatively. The cardiac function was estimated by using the inotropic score defined as the maximum dose of dopamine (μg/kg/min) + dobutamine (μg/kg/min) + 100 × adrenaline (μg/kg/min) [14]. All patients were operated by the same surgeon. The surgical complexity was measured using the basic Aristotle score. Surgical double-perfusion technique An arterial catheter Seldicath 2F (Prodimed, Neulliy en Thelle, France) is placed in the right radial artery and a Seldicath 3F in femoral artery. Bilateral cerebral and visceral oximetries are monitored using near-infrared spectroscopy INVOS™ (Covidien, Mansfield, MA, USA) with a Paediatric SomaSensor® (Covidien) placed in the posterior and left lumbar area throughout the intervention. Body temperature is measured by the introduction of a nasopharyngeal and rectal probe (9 Fr, GE Healthcare, Helsinki, Finland). Bladder catheterization is performed to control diuresis. The priming of the CPB circuit does not differ between groups. Initially, the patient is placed in the right lateral decubitus position. A left posterolateral minithoracotomy (<5 cm) is performed at the 4th intercostal space. The following vascular structures are dissected: descending thoracic aorta, ductus and aortic arch, providing mobility to facilitate the anastomosis. Nerve structures are identified as the left vagus, recurrent and phrenic nerves. The first 2 intercostal arteries and the left subclavian artery are ligated, if necessary. The descending aorta is partially clamped, and a 4 mm-diameter Gore-Tex® conduit (Gore Inc., Flagstaff, AZ, USA) is sutured 3 cm below the patent ductus arteriosus (PDA) (Fig. 1A). The conduit is heparinized to prevent thrombosis. The distal end is closed by vascular clips Ligaclip® (Ethicon Endo-Surgery LLC., Guaynabo, PR, USA). After verifying haemostasis, the thoracotomy is closed according to the usual technique. Then, the patient is placed in the supine position for a median sternotomy. After total heparinization, the first brachiocephalic trunk is cannulated with a 4-mm Gore-Tex conduit. The left pleura is opened to retrieve the conduit from the descending aorta taking it under the left phrenic nerve. After checking appropriate levels of activated coagulation time (>400 s), a Biomedicus™ 10-Fr cannula (Medtronic Inc., Minneapolis, MN, USA) is inserted into the Gore-Tex conduit located in the brachiocephalic trunk that will serve for cerebral perfusion. A Biomedicus 8-Fr cannula is then inserted through the Gore-Tex conduit on the descending thoracic aorta for visceral perfusion. Both cannulae are connected to the arterial line (Fig. 1B). A bicaval cannulation is made using the Stöcker venous cannula (Sorin Group, Mirandola, Italy) according to the appropriate patient size, and the CPB is started. The PDA is ligated. The procedure is performed under moderate hypothermia, 26–28°C, with a blood flow calculated per body surface and temperature. The median arterial blood pressure is 25–30 mmHg registered in both arterial extremities. Figure 1: View largeDownload slide Surgical perfusion technique. (A) Left thoracotomy placing the Gore-Tex® conduit in the descending aorta. (B) Arterial perfusion Y-connection between the brachiocephalic trunk and the descending aorta cannula. Figure 1: View largeDownload slide Surgical perfusion technique. (A) Left thoracotomy placing the Gore-Tex® conduit in the descending aorta. (B) Arterial perfusion Y-connection between the brachiocephalic trunk and the descending aorta cannula. After the ascending aorta is clamped, a perfusion of Custodiol® (Dr Frank Köhler Chemie GmbH, Bensheim, Germany) cardioplegia is administered in the aortic root. We proceed to the occlusion of the supra-aortic trunks maintaining ACP through the brachiocephalic trunk cannula. In a similar way, the descending thoracic aorta is clamped 2 cm below the PDA, maintaining visceral perfusion through the cannula located in the descending thoracic aorta. Then, the correction of the aortic arch is completed. The technique of repair did not differ between groups without circulatory arrest in any case. The Norwood procedure was performed with a modified Blalock–Taussig shunt in both groups. When the surgical correction is finished, all vascular clamps are removed, and the patient is rewarmed. When the patient’s rectal temperature reaches 34°C, the visceral perfusion is stopped, maintaining the arterial blood flow only through the cannula located in the brachiocephalic trunk. The Gore-Tex conduit connected to the descending thoracic aorta is clipped and sutured at its distal end. All patients underwent modified ultrafiltration after discontinuation of CPB. Statistical analysis We performed a Kolmogorov–Smirnov’s test to study normality. Qualitative variables are reported as frequency and percentage and compared using the χ2 or Fisher’s exact test. Quantitative variables are expressed as mean ± standard deviation or as median with 25th and 75th percentile values and compared with the Student’s t-test or the Mann–Whitney U-test according to normal distribution. The statistical software used was SPSS version 24.0 (SPSS Inc., Chicago, IL, USA). RESULTS Demographics and intraoperative variables In total, 56.5% of the patients were boys and 43.5% were girls. The mean age of patients at the time of operation was 13.6 ± 9.8 days, the average weight was 3.2 ± 0.52 kg and average height was 50.3 ± 2.89 cm. The mean Aristotle score was 11.7 ± 3.1, CPB time was 164.5 ± 58.4 min, aortic cross-clamp time was 77.5 ± 32 min and biventricular repair was 60.9%. The average length of intubation was 6.09 ± 3.7 days, the average length of stay in the intensive care unit was 17.5 ± 12.3 days, PLOS was 39.3 ± 18 days and 30-day mortality was 0%. Groups 1 and 2 were not significantly different in terms of sex (P = 0.998), age (P = 0.135), weight (P = 0.770), height (P = 0.686), Aristotle score (P = 0.154), CPB time (P = 0.734), aortic cross-clamp time (P = 0.551), biventricular repair (P = 0.675), length of intubation (P = 0.592), length intensive care unit (P = 0.369) and PLOS (P = 0.850). Renal parameters The statistical analysis showed that the patients undergoing SVP were not significantly different in terms of creatinine serum and eGFR evolution (Fig. 2A). Only 9 (39%) patients developed postoperative AKI: Group 1, 2 (22%) patients and Group 2, 7 (50%) patients, with no statistical significance between both groups (P = 0.183). A higher urine output during the first 24 h was observed in Group 1 (P = 0.007–0.032) (Fig. 2B), with the exception of the 6–12 h period (P = 0.961). Figure 2: View largeDownload slide (A) Perioperative eGFR (ml/min/1.73 m2) calculated using the Schwartz formula. Patients undergoing double perfusion did not have significant differences in eGFR preoperatively (P = 0.206), intraoperatively (GFR0, P = 0.652) and in the first 3 days (GFR1, P = 0.612; GFR2, P = 0.395 and GFR3, P = 0.661) after surgery. (B) Perioperative urine output. Patients undergoing double perfusion had significantly higher urine output intraoperatively (P = 0.007), 0–6 h postoperatively (P = 0.018) and 12–24 h postoperatively (P = 0.032) but not in the 6–12-h interval postoperatively (P = 0.961). ACP: anterograde cerebral perfusion; eGFR: estimated glomerular filtration rate; Intraop: intraoperative; Postop: postoperative; preop: preoperative. Figure 2: View largeDownload slide (A) Perioperative eGFR (ml/min/1.73 m2) calculated using the Schwartz formula. Patients undergoing double perfusion did not have significant differences in eGFR preoperatively (P = 0.206), intraoperatively (GFR0, P = 0.652) and in the first 3 days (GFR1, P = 0.612; GFR2, P = 0.395 and GFR3, P = 0.661) after surgery. (B) Perioperative urine output. Patients undergoing double perfusion had significantly higher urine output intraoperatively (P = 0.007), 0–6 h postoperatively (P = 0.018) and 12–24 h postoperatively (P = 0.032) but not in the 6–12-h interval postoperatively (P = 0.961). ACP: anterograde cerebral perfusion; eGFR: estimated glomerular filtration rate; Intraop: intraoperative; Postop: postoperative; preop: preoperative. Hepatic parameters Eleven patients developed impaired hepatic function in the immediate postoperative period: Group 1, 2 (18.2%) cases and Group 2, 9 (81.8%) cases (P = 0.04). Furthermore, patients undergoing SVP showed faster recovery of international normalized ratio (P = 0.006–0.031) and prothrombin time (P = 0.007–0.016) during the first 72 h (Fig. 3). Figure 3: View largeDownload slide (A) Postoperative PT. Patients undergoing double perfusion had lower PT postoperatively (PT 24 h, P = 0.007; PT 48 h, P = 0.016; PT 72 h, P = 0.011). (B) Postoperative INR. Patients undergoing double perfusion had lower INR postoperatively (INR 24 h, P = 0.006; INR 48 h, P = 0.031; INR 72 h, P = 0.020). ACP: anterograde cerebral perfusion; INR: international normalized ratio; PT: prothrombin time. Figure 3: View largeDownload slide (A) Postoperative PT. Patients undergoing double perfusion had lower PT postoperatively (PT 24 h, P = 0.007; PT 48 h, P = 0.016; PT 72 h, P = 0.011). (B) Postoperative INR. Patients undergoing double perfusion had lower INR postoperatively (INR 24 h, P = 0.006; INR 48 h, P = 0.031; INR 72 h, P = 0.020). ACP: anterograde cerebral perfusion; INR: international normalized ratio; PT: prothrombin time. Perfusion and cardiac parameters Group 1 had lower lactate levels in the first 72 h (P = 0.001–0.028; Fig. 4). In contrast, mixed venous saturation and inotropic score did not show statistically significant differences. Figure 4: View largeDownload slide Perioperative lactate levels. Patients undergoing double perfusion had lower lactate levels intraoperatively (P = 0.006), in the first 24 h peak (P = 0.001), 48 h (P = 0.014) and 72 h (P = 0.028) after surgery. ACP: anterograde cerebral perfusion; Interop: intraoperative; Postop: immediate postoperative. Figure 4: View largeDownload slide Perioperative lactate levels. Patients undergoing double perfusion had lower lactate levels intraoperatively (P = 0.006), in the first 24 h peak (P = 0.001), 48 h (P = 0.014) and 72 h (P = 0.028) after surgery. ACP: anterograde cerebral perfusion; Interop: intraoperative; Postop: immediate postoperative. Table 2 illustrates a more accurately statistical comparison of renal, hepatic and tissue perfusion parameters. Table 2: Comparison of renal, hepatic and tissue perfusion parameters Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  All data are distributed normally except lactate levels. Continuous variables are presented as mean ± standard deviation except lactate levels (median and 25th–75th percentile). The intra- and postoperative evolution of renal, hepatic and tissue perfusion parameters is shown. INR: international normalized ratio; POD: postoperative day; SvO2: mixed venous oxygen saturation. Table 2: Comparison of renal, hepatic and tissue perfusion parameters Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  Variables  Group 1 (n = 9)  Group 2 (n = 14)  P-value  Creatinine (mg/dl)         Preoperative  0.42 ± 0.15  0.49 ± 0.19  0.752   POD 0  0.52 ± 0.12  0.56 ± 0.18  0.209   POD 1  0.62 ± 0.11  0.59 ± 0.18  0.389   POD 2  0.56 ± 0.11  0.62 ± 0.16  0.503   POD 3  0.44 ± 0.10  0.48 ± 0.16  0.134  eGFR (ml/min/1.73 m2)         Preoperative  60.8 ± 19.6  50.7 ± 16.9  0.206   POD 0  45.54 ± 8.1  43.26 ± 13.3  0.652   POD 1  38.16 ± 6.4  40.04 ± 9.6  0.612   POD 2  42.09 ± 0.1  38.27 ± 10.9  0.395   POD 3  54.38 ± 13.7  51.31 ± 17.4  0.661  Urine output (ml/kg/h)         Intraoperative  6 ± 2.3  3.2 ± 2.1  0.007   0–6 h  4.8 ± 2.3  2.7 ± 0.7  0.018   6–12 h  3.97 ± 0.7  4.04 ± 3.6  0.961   12–24 h  5.13 ± 1.1  3.74 ± 1.6  0.032  INR         Preoperative  1.14 ± 0.1  1.21 ± 0.1  0.129   POD 1  1.35 ± 0.1  1.65 ± 0.2  0.006   POD 2  1.36 ± 0.1  1.52 ± 0.3  0.031   POD 3  1.2 ± 0.1  1.34 ± 0.2  0.020  Prothrombin time (s)         Preoperative  13.45 ± 1.2  14.56 ± 2.9  0.297   POD 1  15.71 ± 1.7  19.39 ± 3.5  0.007   POD 2  15.66 ± 1.9  18.09 ± 4.5  0.016   POD 3  14.32 ± 1.5  16.73 ± 3.9  0.011  Lactate levels (mmol/l)         Intraoperative peak  5.6 (5.1–6)  6 (6–6.9)  0.006   24 h peak  4.3 (3.8–5.1)  7.5 (6.2–9.3)  0.001   48 h  1.3 (1–2.3)  2.8 (2.5–4.3)  0.014   72 h  0.9 (0.8–1.1)  1.8 (1.3–2.3)  0.028  SvO2 (%)         Intraoperative  68.66 ± 5.6  68.92 ± 9.9  0.165   POD 1  64.44 ± 4.7  67.57 ± 6.1  0.337   POD 2  67.33 ± 3.8  66.92 ± 4.9  0.330   POD 3  65.33 ± 5.4  68.57 ± 2.1  0.237  All data are distributed normally except lactate levels. Continuous variables are presented as mean ± standard deviation except lactate levels (median and 25th–75th percentile). The intra- and postoperative evolution of renal, hepatic and tissue perfusion parameters is shown. INR: international normalized ratio; POD: postoperative day; SvO2: mixed venous oxygen saturation. In addition, we selected a subgroup of single-ventricle physiology patients and we compared all the parameters studied before according to the perfusion techniques used but we did not demonstrate statistical significance. DISCUSSION DHCA has been the perfusion technique of choice used for most surgical corrections when beginning congenital heart surgery, allowing the presence of a bloodless field [10]. It has been widely used for the complex repair of the neonatal aortic arch, and it is a much debated topic if it is associated with greater neurological alterations when compared with ACP [3–9]. However, DHCA morbidity should not be focused exclusively on neurological damage. It also produces a significant increase in inflammatory response, causing tissue oedema, neutrophil activation and increased oxidative stress [15]. In addition, the lack of systemic perfusion causes a higher incidence of postoperative AKI which conditions an increase in mechanical ventilation time, PLOS, morbidity, mortality and the associated costs of care [16]. The incidence of AKI after aortic arch repair varies from 11% to 52% according to some series, being higher in the neonatal group due to a greater susceptibility to ischaemia secondary to the immaturity of their organs [17]. When compared with DHCA, it has been proposed that ACP would provide a visceral flow that could act as a protector factor against visceral organ damage. Algra et al. [18] demonstrate that abdominal near-infrared spectroscopy levels vary in patients with ACP because the different patterns of collateral arteries do not guarantee a correct abdominal perfusion. Therefore, different groups have added abdominal perfusion to their procedures to improve AKI. These groups report lower incidence compared with the isolated ACP without technique-related complications and with a shorter CPB time when it is performed without hypothermia due to a shorter rewarming period [10, 19]. In our study, we demonstrate an improvement in the urine output in the group with SVP during the first postoperative hours reflecting a greater renal flow but that has not been enough to prove a decrease in the occurrence of postoperative AKI, eGFR or creatinine levels. These results are not consistent with data published by other authors [10, 19] who were able to demonstrate, in a larger sample size, a reduction in the postoperative AKI when SVP was added. We believe these observed differences may be due to the smaller sample size since the perfusion techniques are similar. In addition, the DHCA effect has also been reported on other abdominal organs. It is known that there is an increase in intestinal permeability reflecting a relative intestinal deficit perfusion following the Norwood surgery with DHCA [20]. An increase in lactates and intestinal mucosa lesion biomarkers has also been reported in patients with DHCA when compared with ACP [18]. In this sense, the presence of circulating free radicals due to a prolonged tissue ischaemia produces an increase in left ventricular pressures, affecting myocardial function [21]. We have not demonstrated significant differences regarding mixed venous oxygen saturation and inotropic score as parameters of cardiac dysfunction. This is probably due to the pH and mixed venous oxygen saturation in both groups being maintained at optimal levels during CPB and the modified ultrafiltration effect releasing the proinflammatory molecules. As we know, there are no published studies about the effect of SVP on liver function and its relevance in the postoperative period of these patients. We know that postoperative impaired hepatic function significantly increases mechanical ventilation time, PLOS and mortality, probably related to the occurrence of postoperative cardiogenic shock [22]. In these cases, the use of a ‘hepatic score’ has been described to measure the grade of hepatic impairment. This score has not been validated in paediatric patients and relies inconveniently on bilirubin levels as a parameter. The presence of hyperbilirubinemia is a physiological fact in neonates, so it is not useful as a dynamic parameter of postoperative liver dysfunction in this age group as this value alters the results. In contrast, we can use the usual parameters to define hepatic dysfunction such as altered coagulation tests and increased transaminase levels within 72 h after surgery. We have not used green indocyanine as a liver function test as its results may be affected by the cardiac output and CPB [23]. In this study, we were able to demonstrate differences regarding the incidence of hepatic dysfunction. ACP patients showed more hepatic impairment than those operated using SVP, particularly as a result of a significant increase in international normalized ratio and prothrombin time but not in hepatic enzymes. In addition, patients with SVP corrected their coagulation alterations faster. We have also shown an improvement in lactate levels during and after the first 3 postoperative days as a reflection of a conserved aerobic metabolism. Both facts confirm that SVP improves blood flow throughout the visceral territory. In this study, we have demonstrated physiological advantages but not clinical benefits. This may be due to the small sample size or the heterogeneity of the group. As we have commented, we did an analysis of single-ventricle physiology patients with no statistical differences, probably for the same reason. These patients have a longer cross-clamp time and a higher risk of renal and hepatic insufficiency when compared with biventricular physiology patients. We believe that a future study comparing the 2 perfusion techniques in the single-ventricle subgroup would be appropriate. Regarding the visceral perfusion technique, Yasui et al. [24] described the initial technique of a thoracotomy through the 4th intercostal space and interposing a Gore-Tex conduit as we did. In this sense, Imoto et al. [25] published a technique modification, where they approached the thoracic aorta through the sternotomy itself, with an opening in the posterior pericardium, because they considered thoracotomy a very invasive procedure. We also believe that minithoracotomy (<5 cm) is invasive when compared with the median approach, but it allows complex neonatal aortic arch repair without circulatory arrest and mild/moderate hypothermia. Furthermore, we perform the entire thoracic aortic dissection, left bronchus separation, entire ductal tissue section and a better recurrent nerve identification. The aortic arch anastomoses can now be performed tension-free and in any position due to the aortic mobility achieved by this easy technique. We have not studied the possible benefit of this extended dissection and the total PDA release as a way to decrease the incidence of aortic arch coarctation. We believe this could be another positive advantage of this approach and the subject of future studies. Other groups have introduced less invasive techniques for visceral perfusion like femoral or umbilical cannulation [26]. These procedures provide a questionable visceral flow, because they use a smaller catheter and offer no benefits to thoracic aortic dissection. Limitations This study has several limitations, the first of which are inherent to its retrospective design; however, it should be emphasized that all patients were operated on and managed by the same group. Second, it has a relatively small number of patients and this can bias the results. Third, we have not studied gastric or intestinal injury biomarkers as a method to more accurately determine the potential benefits of adding an antegrade visceral perfusion line. Finally, we have not compared blood loss and the need for transfusion of blood components as a parameter of liver dysfunction and the possible clinical benefit of the SVP. 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Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

Interactive CardioVascular and Thoracic SurgeryOxford University Press

Published: Mar 26, 2018

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