To the Editor:
In an observational study including 33,330 noncardiac surgeries performed in 27,381 patients with detailed intraoperative blood pressures, Walsh et al.1 showed that intraoperative mean arterial pressure less than 55 mmHg was associated with the development of postoperative acute kidney and myocardial injuries. This study makes an important contribution to the effort to define risk factors for acute vital organ injury after surgery. Strengths of this study include the large sample of patients and adjust for most of the known risk factors that can affect acute kidney and myocardial injuries after surgery. Furthermore, the authors openly discuss the limitations of their work. However, in our view, there are several aspects of this study design that should be discussed and clarified.
First, the body mass index and ethnicity were not included in the basic demographic data of patients for analysis and adjustment. It has been shown that in the noncardiac surgery patients, body mass index is independently associated with risk for postoperative acute kidney injury (AKI).2,3 Furthermore, obesity is an independent predictor of perioperative cardiac adverse events.4 In a retrospective study including 975,825 patients undergoing colorectal surgery, Masoomi et al.5 find that black race is associated with higher risk of postoperative AKI. Their trial design did also not include the detail about anesthesia techniques and intraoperative managements. Consequently, it is difficult to estimate the extent to which interventions by anesthesiologists might have influenced outcomes. A retrospective analysis including 9,171 patients undergoing joint-replacement operations shows that use of general anesthesia is independently associated with risk for postoperative AKI.2 Besides the transfusion volume adjusted by this study, other intraoperative managements, such as total vasopressor dose administered, use of a vasopressor infusion, and diuretic administration, have been shown to be independent predictors of postoperative AKI.3 In addition, intraoperative hypoxemia, tachycardia, and hypertension are associated independently with increased risk of myocardial injury after noncardiac surgery.6,7 Thus, we cannot exclude the possibility that the above confounding factors would have contributed to final analysis of their results.
Second, this study assessed occurrence of acute kidney and myocardial injuries within 7 days after surgery. However, the authors did not mention specific measurement times of serum creatinine, troponin T, and creatinine kinase-MB after surgery. In addition, the study design did not include the detail about postoperative recovery and managements of patients. Thus, this study cannot provide enough evidence to support that all kidney and myocardial injuries occurred within 7 days after surgery are attributed to intraoperative hypotension. Actually, serum troponin appears at 30 min to 6 h after myocardial injury.8 Although serum creatinine lags behind acute changes in renal function, but AKI (defined by a 50% or more increase in serum creatinine) by intraoperative causes can be often detected between 1 and 3 days after surgery.9 For early detection of the potential kidney and myocardial injuries by intraoperative factors, we would suggest that the related serum biomarkers be measured as soon as possible after surgery, especially for patients who are at high risk of kidney and myocardial injuries. To prevent new kidney and myocardial injuries or avoid aggravation of existing organ injury by postoperative low perfusion, we emphasize that perioperative hemodynamic optimization of noncardiac surgery patients should be continued to the postoperative period, modifying prognosis of patients.
Finally, 506 patients (1.5%) died within 30 days of surgery in this study. The authors should provide the detailed reasons of all death cases through analyzing death certificates, medical records, and autopsy reports, as described in previous studies.7,10 We would like to know how many of patients with postoperative AKI received kidney-replacement treatment, and how many of deaths are directly related to postoperative acute kidney and myocardial injuries. In addition, the authors should assess association between severity of postoperative acute vital organ and 30-day mortality. All these will help explore whether there is a causal relationship between postoperative acute vital organ injury and mortality or whether acute vital organ injury merely indicates a worse outcome.
The authors declare no competing interests.