In this prospective study, we found that the morbidity of postoperative AKI was as high as 39.4% in critically ill patients undergoing emergency surgery, and the occurrence of postoperative AKI would further lead to adverse hospitalization results. Compared with previous studies, there was a little distinction for the morbidity of postoperative AKI, while the high risk of adverse hospitalization results was consistent [33–35]. On account of the heterogeneousness of the population in critically ill patients undergoing emergency surgery, and the numerous kinds of operations, so the incidence of postoperative AKI found in our study was higher than in previous studies. Furthermore, our study found that 93.4% of the patients reached postoperative AKI within 3 days after emergency operations, so physicians must take early surveillance and early intervention for those people who were at high risk of postoperative AKI. Therefore, with a large sample size, high population heterogeneity, and a wide range of surgeries, our research results have strong applicability and popularization in the clinic.
The independent risk factors of postoperative AKI occurrence included postoperative reoperation, postoperative APACHE II score, postoperative LAC, postoperative sCr. The risk factors for postoperative AKI varied in different clinical situations, and four of the above risk factors were identified in this emergency surgery cohort. Manifested by this study, postoperative reoperation was an independent risk factor for the occurrence of postoperative AKI, which was consistent with previous studies [23, 36]. Although the mechanism of postoperative AKI caused by reoperation had not been fully elucidated, a logical assumption was that reoperation involved in many factors related to the occurrence of postoperative AKI, such as hemodynamic damage and bleeding. In this condition, the body was overexcited by the sympathetic-adrenal medulla system, which promoted the increase of plasma catecholamine concentration and caused the dysfunction of neurohumoral regulation. Then, epithelial cells were degenerated and necrotic due to ischemia and hypoxia, and eventually, postoperative AKI occurred .
The APACHE II scoring system was usually used to assess the severity and prognosis of general diseases, which could more objectively reflect and comprehensively evaluate the current pathophysiology of patients . The higher APACHE II score indicated that the more severity of the patient's overall condition and the greater risk of death , which might make the patient susceptible to surgery and lead to a higher risk of postoperative AKI. As expected, the postoperative APACHE II score of the AKI group in this study was higher than that of the non-AKI group. Corrected by multivariate regression, the postoperative APACHE II score was still an independent risk factor for postoperative AKI, which was consistent with the previous study . We considered that a high postoperative APACHE II score indicated a serious condition. Under these circumstances, the body might be insufficiently perfused during emergency surgery, and the blood flow to the kidneys would be significantly reduced while ensuring the blood supply to important organs such as the heart and brain. Eventually, the kidneys were prone to develop postoperative AKI.
Similar to our study, some studies had also shown that the initial increase in LAC was related to the occurrence of AKI [40, 41]. Elevated LAC was often accompanied by hypoxia and hypoxia in tissues and organs, and insufficiency of systemic perfusion, so the patient's mortality rate increased significantly. The increase of serum LAC level after emergency surgery was generally related to the preoperative, intraoperative, and postoperative hypoxia and hypoperfusion , which caused the increase of catecholamines to accelerate glycolysis, the release of systemic inflammatory mediators and the reduction of liver and kidney clearance. In this study, the LAC level in the postoperative AKI group was significantly increased, suggesting that the ischemia and hypoxia in the postoperative AKI group were more serious, which represented a lower level of tissue perfusion. Above these were the predisposing factors for postoperative AKI.
It has been testified that high postoperative sCr would increase the incidence of postoperative AKI and the mortality of patients. A retrospective cohort study reported by Bihorac et al , which had involved 10,518 patients with AKI after major surgery, indicated that even small changes in sCr levels during hospitalization were associated with long-term mortality risk. What is more, according to a study of 19,982 AKI patients, an increase in sCr > or = 0.5 mg/dl was associated with a 6.5-fold increase in the odds of death, a 3.5-day increase in the length of stay, and nearly 7500 dollars in excess hospital costs . Increased postoperative sCr has become an independent risk factor for the morbidity of postoperative AKI and the poor prognosis, and our study got the same result.
More and more studies had shown that even relatively mild renal injury drugs were associated with increased risk of AKI morbidity and mortality . In our study, we also analyzed commonly prescribed medications that predispose to renal impairment, including NSAID, ACEI, ARB, immunosuppressants, aminoglycosides, vancomycin, acyclovir, and amphotericin. Even though nephrotoxic drugs were well known for their kidney damage, the use of them had little to do with the occurrence of AKI in this study. The one reason we were unable to obtain statistically significant conclusions might be due to the small number of patients using these drugs in our cohort. Simultaneously, physicians in ICU took more attention to carefully evaluate drugs in their potential injury to renal function and structure to avoid the damage in the kidney, which was consistent with the KDIGO standard.
Postoperative AKI was closely related to adverse hospital outcomes. To prevent the occurrence of complications, this study aimed to discuss the risk factors and morbidity of postoperative AKI in critically ill patients undergoing emergency surgery, which had important clinical significance. Despite the lack of effective treatment options, assessing the risk factors and morbidity of postoperative AKI might help formulate new strategies to prevent the occurrence of postoperative AKI. Therefore, we identified the risk factors and timeline that could induce postoperative AKI in advance. It was worth noting that all the above-identified risk factors and morbidity in our study were verifiable. Before translating our research into clinical applications, further intervention studies should be conducted to prove the effectiveness of these modifiable risk factors.
Compared with previous studies, this was the first prospective observational study on postoperative AKI in critically ill patients undergoing emergency surgery, which provided a basis for clarifying the epidemiological status of postoperative AKI in critically ill patients undergoing emergency surgery and improving clinical prevention strategies. However, our study still had some limitations and shortcomings. First, this was a single-center prospective study, and the number of cases was small. The influence of some confounding factors could not be completely ruled out, which might further lead to a certain deviation in the judgment of incidence, influencing factors, and prognosis. To reduce bias, it needed to be verified by a large sample, multi-center prospective study. Secondly, the data of this study were collected from the general ICU and did not fully represent all postoperative ICU patients, especially those patients who were undergoing cardiovascular surgery. Moreover, this study lacked long-term follow-up after discharge and fails to count kidney long-term prognosis.