The relationship between intraoperative oliguria and acute kidney injury
2019; Elsevier BV; Volume: 122; Issue: 6 Linguagem: Inglês
10.1016/j.bja.2019.03.008
ISSN1471-6771
Autores Tópico(s)Cardiac Arrest and Resuscitation
ResumoPostoperative acute kidney injury (AKI) is a significant contributor to postoperative mortality. In the International Surgical Outcomes Study, postoperative AKI was the second leading cause of death after cardiac arrest. It carried a 9.8% 30-day mortality risk, similar to that of pulmonary embolism and anastomotic leak.1International Surgical Outcomes Study GroupGlobal patient outcomes after elective surgery: prospective cohort study in 27 low-, middle-and high-income countries.Br J Anaesth. 2016; 117: 601-609Abstract Full Text Full Text PDF PubMed Scopus (297) Google Scholar In the African Surgical Outcomes Study (ASOS), postoperative AKI was the fifth leading cause of death after cardiac arrest, surgical site infections, bloodstream infections, and pneumonia, with a 30-day mortality risk of 35%.2Biccard B.M. Madiba T.E. Kluyts H.L. et al.Perioperative patient outcomes in the African Surgical Outcomes Study: a 7-day prospective observational cohort study.Lancet. 2018; 391: 1589-1598Abstract Full Text Full Text PDF PubMed Scopus (289) Google Scholar In a recent cohort study of intermediate-term outcomes, postoperative AKI was associated with an increased 1-yr mortality after major abdominal surgery.3Mizota T. Dong L. Takeda C. et al.Transient acute kidney injury after major abdominal surgery increases chronic kidney disease risk and 1-year mortality.J Crit Care. 2019; 50: 17-22Crossref PubMed Scopus (19) Google Scholar These observational studies defined AKI according to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines4Kidney Disease Outcomes Quality InitiativeKDIGO clinical practice guidelines for acute kidney injury.Kidney Int Suppl. 2012; 2: 19-22Google Scholar: a documented 1.5-fold increase in baseline serum creatinine concentration within 7 days, or a 30 μmol L−1 increase in serum creatinine within 48 h, or a urine output of <0.5 ml kg−1 h−1 for at least 6 h was necessary to make the diagnosis of AKI. These studies only documented routinely recorded data, likely underreporting the incidence of postoperative AKI because asymptomatic patients would not have had blood results to establish the diagnosis. For this reason, milder events of postoperative AKI are more likely to be missed than severe events, a scenario which overestimates the association between postoperative AKI and mortality. In contrast, the ranking of postoperative AKI as cause of death in these studies will be less affected by subclinical (or undetected disease), making ranking a reliable indicator of relative importance of AKI as a predictor of perioperative mortality. The Restrictive versus Liberal Fluid Therapy in Major Abdominal Surgery (RELIEF) trial5Myles P.S. Bellomo R. Corcoran T. et al.Restrictive versus liberal fluid therapy for major abdominal surgery.N Engl J Med. 2018; 378: 2263-2274Crossref PubMed Scopus (385) Google Scholar was an international pragmatic randomised controlled trial comparing restrictive zero-balance fluid management (5 ml kg−1 crystalloid loading dose during induction of anaesthesia, followed by a 5 ml kg−1 h−1 intraoperative infusion, and a 0.8 ml kg−1 h−1 postoperative infusion) with more liberal fluid management (10 ml kg−1 crystalloid loading dose during induction of anaesthesia, followed by a 8 ml kg−1 h−1 intraoperative infusion, and a 1.5 ml kg−1 h−1 postoperative infusion) for reducing postoperative complications and improving disability-free survival. The RELIEF trial showed no difference in disability-free survival at 1 yr. However, there was a significantly increased risk of postoperative AKI in the zero-balance (fluid restricted) group compared with the liberal fluid group. The findings challenge the zero-balance fluid management paradigm. The trial does not address the issue of excessive fluid administration. We suggest that it supports a Goldilocks scenario wherein too wet is known to be harmful, zero-balance is demonstrated to be too dry, and liberal (as described by the RELIEF trial) may be optimal. In this issue of the British Journal of Anaesthesia is a secondary data analysis of the RELIEF trial by Myles and colleagues.6Myles P.S. Bellomo R. Wallace S. Importance of intraoperative oliguria during major abdominal surgery: findings of the RELIEF trial.Br J Anaesth. 2019; Google Scholar The investigators explore the relationship between intraoperative oliguria (defined as urine output <0.5 ml kg−1 h−1 for at least 1 h) and postoperative AKI as diagnosed by an increase in serum creatinine concentration (KDIGO guidelines,4Kidney Disease Outcomes Quality InitiativeKDIGO clinical practice guidelines for acute kidney injury.Kidney Int Suppl. 2012; 2: 19-22Google Scholar excluding urine output criteria). They report a significant association between intraoperative oliguria and the development of postoperative AKI, risk ratio 1.38 (95% confidence interval, 1.14–1.44, P 6 h. The converse is also true; AKI can be diagnosed without the presence of oliguria on the basis of azotaemia alone. The presence of both oliguria and azotaemia in critically ill patients is associated with an increased need for renal replacement therapy and a reduction in survival.7Kellum J.A. Sileanu F.E. Murugan R. Lucko N. Shaw A.D. Clermont G. Classifying AKI by urine output versus serum creatinine level.J Am Soc Nephrol. 2015; 26: 2231-2238Crossref PubMed Scopus (314) Google Scholar It is possible that patients who develop perioperative AKI without oliguria have a milder form of the condition. This is supported by the finding by Myles and colleagues6Myles P.S. Bellomo R. Wallace S. Importance of intraoperative oliguria during major abdominal surgery: findings of the RELIEF trial.Br J Anaesth. 2019; Google Scholar that patients who developed postoperative AKI without intraoperative oliguria did not require renal replacement therapy. In adults, intraoperative oliguria has been defined as any urine output value <0.5 ml kg−1 h−1.8Shiba A. Uchino S. Fujii T. Takinami M. Uezono S. Association between intraoperative oliguria and acute kidney injury after major noncardiac surgery.Anesth Analg. 2018; 127: 1229-1235Crossref PubMed Scopus (30) Google Scholar The use of urine output to gauge intravascular volume status does not constitute evidence-based practice, as urine output is not simply a function of intravascular volume status. Urine output decreases appreciably and appropriately through the action of antidiuretic hormone in response to pain, nausea, and surgical intervention. Increases in aldosterone concentration also decrease urine output. Perioperative factors such as physiological stress, intra-abdominal pressure,9Nguyen N.T. Perez R.V. Fleming N. Rivers R. Wolfe B.M. Effect of prolonged pneumoperitoneum on intraoperative urine output during laparoscopic gastric bypass.J Am Coll Surg. 2002; 195: 476-483Abstract Full Text Full Text PDF PubMed Scopus (107) Google Scholar interstitial oedema, congestive heart failure, and medications can induce oliguria apart from volume depletion.10Zarbock A. Koyner J.L. Hoste E.A. Kellum J.A. Update on perioperative acute kidney injury.Anesth Analg. 2018; 127: 1236-1245Crossref PubMed Scopus (61) Google Scholar Although oliguria includes a continuum of decreasing urine output values, the degree of intraoperative oliguria is not necessarily associated with an increasing risk of postoperative AKI. For example, Myles and colleagues6Myles P.S. Bellomo R. Wallace S. Importance of intraoperative oliguria during major abdominal surgery: findings of the RELIEF trial.Br J Anaesth. 2019; Google Scholar did not find a difference in the risk of postoperative AKI at different degrees of intraoperative oliguria (<0.5 ml kg−1 h−1 vs <0.3 ml kg−1 h−1). This finding differs from a recent retrospective cohort study that only found an association with AKI at a urine output <0.3 ml kg−1 h−1.11Mizota T. Yamamoto Y. Hamada M. Matsukawa S. Shimizu S. Kai S. Intraoperative oliguria predicts acute kidney injury after major abdominal surgery.Br J Anaesth. 2017; 119: 1127-1134Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar Intravascular volume depletion is but one of many intra- and extrarenal pathways leading to postoperative AKI. Other important pathways include high venous pressure from right heart failure and increased intra-abdominal pressure that predisposes to AKI by reducing renal perfusion. In many cases of perioperative AKI, inflammation leading to endothelial and microvascular dysfunction with resulting tubular cell injury and tubular obstruction play a dominant role. Nephrotoxins and obstruction are other important risk factors for perioperative AKI.12Ostermann M. Liu K. Pathophysiology of AKI.Best Pract Res Clin Anaesthesiol. 2017; 31: 305-314Crossref PubMed Scopus (63) Google Scholar AKI is a heterogeneous condition, presenting as the final common pathway for a number of varying pathologies or renal insults.10Zarbock A. Koyner J.L. Hoste E.A. Kellum J.A. Update on perioperative acute kidney injury.Anesth Analg. 2018; 127: 1236-1245Crossref PubMed Scopus (61) Google Scholar This is illustrated by calculating the crude population attributable fraction for postoperative AKI associated with intraoperative oliguria in the RELIEF trial: Populationattributablefraction=Pc(1−1RR), where Pc is the prevalence of intraoperative oliguria in patients with postoperative AKI, and RR is the risk ratio calculated by multivariate logistic regression analysis.13Miettinen O.S. Proportion of disease caused or prevented by a given exposure, trait or intervention.Am J Epidemiol. 1974; 99: 325-332Crossref PubMed Scopus (813) Google Scholar We find that only 12% of postoperative AKI in this high-risk cohort was related to intraoperative oliguria. Acknowledging that the crude population attributable fraction is not a direct measure of aetiology, it still shows the relatively small contribution of intraoperative oliguria to the burden of postoperative AKI. The analysis by Myles and colleagues6Myles P.S. Bellomo R. Wallace S. Importance of intraoperative oliguria during major abdominal surgery: findings of the RELIEF trial.Br J Anaesth. 2019; Google Scholar confirms the poor predictive value of intraoperative oliguria for identifying patients at risk of postoperative AKI, and its limited clinical utility for detecting patients at risk of postoperative AKI is reflected in the likelihood ratios (Table 1). Based on the pre-test probability of AKI of 21% in the RELIEF substudy, oliguria would be associated with a post-test probability of AKI of 26%, while normal urine output would be associated with an 18% incidence of AKI. Using only intraoperative oliguria to assign risk in this population would miss the majority of postoperative AKI events. This points to the importance of including multiple pre- and intraoperative factors in AKI risk stratification. As oliguria is not a cause of AKI, but rather a renal response to various physiological and pathological processes, focusing only on oliguria is unlikely to reduce the burden or severity of postoperative AKI. Rather, the focus should be on identifying the patient that is at risk of postoperative AKI and on managing the cause of intraoperative oliguria. Unfortunately, no universally applicable AKI risk stratification tool is available for non-cardiac surgical patients.14Romagnoli S. Ricci Z. Ronco C. Perioperative acute kidney injury: prevention, early recognition, and supportive measures.Nephron. 2018; 140: 105-110Crossref PubMed Scopus (36) Google Scholar For now, providers should consider risk factors such as invasiveness of surgery, patient age, and the presence of comorbidities such as diabetes mellitus or anaemia to guide screening for postoperative AKI in the perioperative period, regardless of intraoperative urine output status. To reduce the burden of postoperative AKI, the KDIGO management guidelines recommend: i) avoiding nephrotoxic agents, ii) optimising renal perfusion, iii) appropriate use of haemodynamic monitoring, iv) monitoring serum creatinine and urine output, v) glycaemic control, and vi) avoiding radiocontrast studies.10Zarbock A. Koyner J.L. Hoste E.A. Kellum J.A. Update on perioperative acute kidney injury.Anesth Analg. 2018; 127: 1236-1245Crossref PubMed Scopus (61) Google Scholar In summary, various underlying physiological processes lead to the clinical sign of oliguria. Likewise, development of postoperative AKI is an endpoint for multiple pathophysiological pathways. Inflammation is probably a more important pathway than decreased global renal blood flow. This complexity explains the poor performance of intraoperative oliguria as a predictor of postoperative AKI. The work by Myles and colleagues6Myles P.S. Bellomo R. Wallace S. Importance of intraoperative oliguria during major abdominal surgery: findings of the RELIEF trial.Br J Anaesth. 2019; Google Scholar is important for three reasons. Firstly, they clearly show an important association between intraoperative oliguria and postoperative AKI. Secondly, their findings caution us against using intraoperative oliguria as an isolated predictor or screening tool for the development of postoperative AKI. Finally, their findings support the role of additional fluid administration to patients who are oliguric without signs of fluid overload. Both authors contributed to the planning, writing, and revising of this editorial. The authors declare that they have no conflicts of interest. This work was not supported by any funding.
Referência(s)