ICU Panel Session 1 – October 28, 2021 CO:12| Volume 35, SUPPLEMENT 1, S11, October 2021



      The rate of acute kidney injury (AKI) after open heart surgery is between 3.1% and 42%. Nephrotoxins, ischemia and reperfusion, venous congestion, inflammation, oxidative stress and genetics have been implicated in the development of AKI. ¹
      The primary aim of this study was to investigate the effect of goal-directed fluid therapy in the perioperative period on the development of AKI in the early period in patients undergoing cardiac surgery. The secondary aim was to determine the independent risk factors for the development of AKI.


      Coronary artery by-pass greft (CABG) and valvuler heart disease patients undergoing open heart surgery were randomly divided into two groups according to their perioperative fluid management: Group Control (Group C, n=30): Fluid management was performed with the traditional monitoring method. Group Study (Group S, n=30): Applied with transesophageal doppler and transthoracic doppler fluid management. It was aimed to keep the hemodynamics of the patients at normal values.²
      Clinical and haemodynamic data were recorded at preoperative baseline (t1), postoperative 4th hour (t2), 24th hour (t3) and 48th hour (t4). Serum creatinine, GFR, Cystatin-C and KIM-1 values obtained at the same time intervals as indicators of AKI. Akut kidney injury was defined by KDIGO clasifications.
      Two independent groups were compared statistically with appropriate parametric and non-parametric tests. The development of postoperative AKI was investigated by “Forward Stepwise Binary Logistic Regression” analysis.


      Postoperative fluid requirement was significantly lower in the study group (p=0.002). Postoperative total balance was significantly more negative in the study group than in the control group (p<0.0001). ERT requirement was significantly lower in the study group compared to the control group (intraoperative, p=0.02; postoperative, p=0.002). Cystatin-C was significantly lower in the study group at the postoperative 24th and 48th hours. (respectively, p<0.04, p<0.02) (Fig.1). AKI development rates were similar between the groups (p>0.05). In the study group, only age (r=0.60, p=0.02) and only intraoperative urine output in the control group (r=1.1;p=0.02) were determined as independent risk factors for the development of AKI. When all cases were evaluated, the Cystatin-C level at the postoperative 4th hour (r=0.03; p=0.02), intraoperative noradrenalin requirement (r=0.74; p=0.04) and Euroscore (r=0.61, p=0.04) parameters were independent risk factors.


      The incidence of AKI development after cardiac surgery was not different between groups. Cystatin-C in Group S patients were significantly lower at the postoperative 24th and 48th hours. Cystatin-C clearence was affected more earlier than creatinine clearence in patients with AKI. Fluid and ERT requirements were less in Group S than Group C and the hospital stay was significantly shorter than the control group.
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