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Background The precise incidence of perioperative myocardial infarction (MI) after noncardiac surgery remains unclear. We determined the incidence and risk factors for perioperative MI after noncardiac surgery and the risk of MI and mortality compared with matched non-surgical patients. Methods Patients >18 yr undergoing noncardiac surgery in 23 Swedish hospitals from 2007 to 2014 were included in this national observational retrospective cohort study. We combined national surgical and outcome databases with Swedeheart, a national quality registry capturing data from patients with acute MI. The primary outcome was incidence of MI within 30 days of surgery. Multivariable logistic regression identified preoperative risk factors associated with MI, including ASA grade, diabetes mellitus, and cardiovascular pathology including previous MI. Standardised incidence rate ratios were calculated. Mortality rates were estimated using Cox proportional hazards. Results A total of 1605/400 742 (0.41%) patients (median age: 64 [49–75] yr) had an MI after surgery, which was independently associated with increasing age, comorbidities and higher risk (vascular, thoracic), emergency surgery, or all. The incidence of perioperative MI (per 1000 surgeries) varied from 0.064 (95% confidence interval [CI], 0.02–012) in low-risk patients (ASA physical status 1) to 15.8 (95% CI, 14.9–16.8) among higher risk patients (ASA physical status ≥3, age ≥80 yr, high-risk surgery). Perioperative MI was associated with higher 30-day mortality (adjusted odds ratio: 5.49 [95% 4.76–6.32]). Compared with the non-surgical Swedish population, the perioperative standardised incidence rate ratio was five-fold higher (odds ratio: 5.35 [95% CI: 5.09–5.61]). Conclusions In a large Swedish surgical cohort, the incidence of MI within 30 days of noncardiac surgery was 0.41%, chiefly occurring in a small subset of higher risk patients.

Acute kidney injury (AKI) has a number of triggers, including ischaemia, nephrotoxins, radiocontrast, and bacterial endotoxins. It occurs in around one-third of patients treated in intensive care unit (ICU) and is even more prevalent in cardiac surgery patients. There is a higher mortality in patients with AKI compared with non-AKI counterparts, and in severe AKI requiring renal support, the 6 month mortality is >50%. Unlike the progressive development of biomarkers in cardiology, there have been few changes in kidney diagnostic markers. Creatinine is still used as an indicator of kidney function but not of the parenchymal kidney injury. Serum creatinine (sCr) concentration does not change until around 50% of kidney function is lost, and varies with muscle mass, age, sex, medications, and hydration status. The lag time between injury and loss of function, risks missing a therapeutic opportunity, and may explain the high associated mortality. Novel biomarkers of AKI- and failure include neutrophil gelatinase-associated lipocalin, N-acetyl-β-d-glucosaminidase, kidney injury molecule-1, interleukin-18, and cystatin C. The pathophysiology associated with accumulation of these markers in plasma and urine is not clear, but a common denominator is inflammation. Some of these new AKI biomarkers may have clinical applicability in anaesthesia and intensive care in the future. It is possible that a 'kidney biomarker panel' will become standard before and after major surgery. If elevated or positive, the anaesthetist must take special care to optimize the patients after operation on the surgical wards or ICU to avoid further nephrotoxic insults and initiate supplementary care.