The main findings of this study were a high incidence of AKI (15.8%) with high mortality in noncardiac surgery patients admitted to the ICU and the association of AKI with infection, reoperation, circulatory shock, preoperative anemia, and positive fluid balance.
Major surgeries account can reach 40% of cases of hospital-acquired AKI [13]. Patients with AKI admitted to the ICU during the postoperative period in cardiovascular surgery accounted for 7.7–40% of cases [14], and gastrointestinal tract surgery patients accounted for almost 22% [15].
The presence of AKI during the perioperative period in this subgroup of patients undergoing major surgery was associated with unfavorable outcomes, with a hospital mortality rate of 27.6%. In addition, the length of hospital stay of patients with AKI was higher than that of patients without AKI; patients with AKI spent approximately one extra week in the hospital. Similarly, a large multicenter observational study in European countries reported that mortality among patients with AKI was more than twice that observed in other patients [16]. In a recent study, the occurrence and severity of AKI were strongly associated with risk of death after surgery. However, the relationship between preoperative renal function, as assessed by serum creatinine-based estimated GFR, and the risk of death depended on patient age and whether AKI developed postoperatively [17]. In our study, we identified a high mean age (over 60 years), but we did not analyze small existing changes in renal function that could indicate a low physiological reserve and thus predispose the patient to a higher risk of AKI.
In our study, patients who developed AKI were more severe (higher SAPS 3), had a greater need for advanced support with catecholamines and frequently had infections. The systemic inflammatory response that occurs in patients with infection is correlated with the induction of AKI. Although the pathophysiology of sepsis-induced renal disorders is still poorly understood, experimental models suggest that, at least in the initial phase of the disease, functional changes associated with microvascular shunting and tubular cell injury are part of the picture [18]. In addition, the intensity of the inflammatory response to surgical trauma determines both tissue hypoperfusion and the ischemia-reperfusion response, which intensifies the inflammatory response. Furthermore, mechanical ventilation, intra-abdominal hypertension, pain and surgical stress are factors that increase the release of antidiuretic hormones and contribute to the development of AKI. Prospective studies have reported a relationship between AKI and sepsis and the need for mechanical ventilation [6, 19, 20].
There is a close correlation between hypotension and the development of AKI. A recent meta-analysis showed that goal-directed hemodynamic adjustments reduce the likelihood of AKI in orthopedic and abdominal surgery patients [21]. We observed the most frequent use of vasopressors in this group of patients. The duration of intraoperative hypotension (particularly relative to the patient’s normal arterial blood pressure), including brief episodes of mean arterial pressure lower than 55 mmHg, has been associated with kidney injury [5]. Careful maintenance of cardiovascular stability, including fluid infusion, throughout this period is vital for protecting renal perfusion while avoiding volume overload. A study of high-risk surgical patients showed that the customized maintenance of blood pressure according to the patient's previous levels during surgery was able to reduce organ dysfunction [22]. Moreover, the association between the use of vasoactive drugs and mortality is consistent with the results of other studies [23–25].
Interestingly, a correlation was noted between preoperative anemia (such as hemoglobin concentration less than 10 g/dl) and impaired renal function. This pathophysiology is multifactorial, but mainly involves a decrease in the oxygen transport capacity and subsequent tissue hypoxia [26].
Besides, patients who developed AKI had a more positive mean daily fluid balance. In fact, reduced ultrafiltration is rarely the only cause of AKI; inflammation, direct vascular injury or tubular obstruction usually accompany kidney injury during the perioperative period. The subsequent rupture of intercellular junctions leads to the release of cells into the tubular lumen and to polarity loss of the transmembrane ion channel. It is expected that, in many cases, simply restoring the circulating volume does not improve the results and may be counterproductive [4, 5]. Elevated intratubular pressure decreases glomerular filtration and activation of tubuloglomerular feedback, with consequent preglomerular vasoconstriction, which leads to an additional reduction in glomerular filtration. Studies have shown that excess fluid is an independent factor for the development of AKI and that in patients with AKI, a more positive fluid balance was correlated with higher mortality [27]. In general, a positive fluid balance, if necessary, can be applied with caution within the first 36 hours. After this, a more conservative approach to volume is the most appropriate and safe method. Regarding the type of solution used, epidemiologic data suggest that 0.9% saline solution, when compared with balanced salt solutions such as balanced solutions, may increase the risk of AKI, the need for renal replacement therapy and mortality in ICU patients. In addition, there is evidence of harm (increased rates of AKI) with the use of hetastarch solutions, which should generally be avoided [28]. In our study, we did not detect a negative influence of any type of colloid on the development of AKI.
Major advances associated with a decrease in postoperative mortality have been observed worldwide in recent years, but the complication rates remain high [29]. AKI is associated with significant morbidity and mortality after major surgery. Patients should be stratified according to their risk of developing AKI based on their exposure and susceptibility, including such factors as severity, the presence of sepsis, mechanical ventilation use and vasoactive drug use, among others [30, 31], and preemptive measures should be taken [5]. We must remember that there are well-established interventions in the KDIGO guidelines that, when used, can reduce the impact of AKI in high-risk surgical patients [32].
Study limitations
The main strengths of our study are associated with its multicenter nature, as it included ICUs located in several regions of Brazil. However, there was a reasonable rate of refusal to participate in the study that affected external validity to some degree. In addition, the adjusted regression model could be performed with a priori defined AKI prediction variables, and no based on statistically important findings from the unadjusted analysis.
There were failures in capturing some relevant data that could have been included in the analyses. Additionally, the need to obtain informed consent in epidemiological studies such as this tends to skew the sample due to the nonconsent of more critical patients, whose families may be psychologically fragile. Another aspect to be considered is the lack of standardization among the centers regarding indications for postoperative intensive care. In addition, this study was not able to assess long-term complications and mortality, and some complications may have occurred after the study period.