Purpose The Acute Disease Quality Initiative (ADQI) Workgroup recently released a consensus definition of sepsis-associated acute kidney injury (SA-AKI), combining Sepsis-3 and Kidney Disease Improving Global Outcomes (KDIGO) AKI criteria. This study aims to describe the epidemiology of SA-AKI. Methods This is a retrospective cohort study carried out in 12 intensive care units (ICUs) from 2015 to 2021. We studied the incidence, patient characteristics, timing, trajectory, treatment, and associated outcomes of SA-AKI based on the ADQI definition. Results Out of 84,528 admissions, 13,451 met the SA-AKI criteria with its incidence peaking at 18% in 2021. SA-AKI patients were typically admitted from home via the emergency department (ED) with a median time to SA-AKI diagnosis of 1 day (interquartile range (IQR) 1–1) from ICU admission. At diagnosis, most SA-AKI patients (54%) had a stage 1 AKI, mostly due to the low urinary output (UO) criterion only (65%). Compared to diagnosis by creatinine alone, or by both UO and creatinine criteria, patients diagnosed by UO alone had lower renal replacement therapy (RRT) requirements (2.8% vs 18% vs 50%; p < 0.001), which was consistent across all stages of AKI. SA-AKI hospital mortality was 18% and SA-AKI was independently associated with increased mortality. In SA-AKI, diagnosis by low UO only, compared to creatinine alone or to both UO and creatinine criteria, carried an odds ratio of 0.34 (95% confidence interval (CI) 0.32–0.36) for mortality. Conclusion SA-AKI occurs in 1 in 6 ICU patients, is diagnosed on day 1 and carries significant morbidity and mortality risk with patients mostly admitted from home via the ED. However, most SA-AKI is stage 1 and mostly due to low UO, which carries much lower risk than diagnosis by other criteria.

In septic shock, the optimal timing of adjunctive vasopressin initiation shock is unknown. We aimed to assess the effect of its early initiation for patients with septic shock. We conducted a multicenter target trial emulation to estimate the intensive care unit (ICU) mortality effect of early (≤ 6 h) adjunctive vasopressin compared with usual care. Eligible patients had septic shock diagnosed within 6 h of ICU admission. The primary outcome of this study was 30-day ICU mortality. Subgroup analyses were conducted to test the interaction of early vasopressin start with peak norepinephrine-equivalent dose (NED) at 6 h, APACHE score, peak lactate at 6 h and invasive mechanical ventilation. Secondary outcomes were the impact of delayed vasopressin introduction on 30-day ICU mortality and effect of NED at vasopressin start on 30-day ICU mortality. We used the parametric g-formula to emulate a target trial. Overall, 3,105 patients fulfilled the inclusion criteria. Mean age was 62 years and mean APACHE III score was 83. In the first six hours of vasopressor therapy, 1,864 (60%) patients were invasively ventilated. Estimated 30-day ICU mortality was 19.34% (95%CI, 17.0 to 21.68) in the no vasopressin group and 18.45% (95%CI, 16.26 to 20.63) in the early vasopressin group; relative risk 0.95 (95%CI, 0.93 to 0.98). The estimated 30-day ICU mortality effect of starting vasopressin was particularly strong at lower norepinephrine doses (< 0.25 µg.kg−1.min−1) and significant at lower norepinephrine doses than recommended by the Surviving Sepsis Campaign Guidelines. Vasopressin administration progressively increased over the study period, from 35.2% (95%CI, 30.0 to 40.5) in 2015 to 45.1% (95%CI, 40.7 to 49.6) in 2021 (ß = + 1.3% per year; 95%CI, + 0.46 to + 2.16, p = 0.011). Patients had progressively lower norepinephrine equivalent dose (ß = − 0.05 µg.kg−1.min−1 per year; 95%CI, − 0.09 to − 0.002, p = 0.038) and lower total SOFA score (ß = − 0.1 point per year; 95%CI, − 0.18 to − 0.07, p < 0.001) at vasopressin start. In this emulation of a hypothetical target trial, patients with septic shock benefited from early vasopressin administration. These findings can help design prospective randomised-control trials of early adjunctive vasopressin use in septic shock.

Importance Distinguishing type 2 (T2MI) from type 1 myocardial infarction (T1MI) in clinical practice can be difficult, and the management and prognosis for T2MI remain uncertain. Objective To compare precipitating factors, risk factors, investigations, management and outcomes for T2MI and T1MI. Data sources Medline and Embase databases as well as reference list of recent articles were searched January 2009 to December 2020 for term ‘type 2 myocardial infarction’. Study selection Studies were included if they used a universal definition of MI and reported quantitative data on at least one variable of interest. Data extraction and synthesis Data were pooled using random-effect meta-analysis. Risk of bias was assessed using Newcastle-Ottawa quality assessment tool. Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines were followed. All review stages were conducted by two reviewers. Main outcomes and measures Risk factors, presenting symptoms, cardiac investigations such as troponin and angiogram, management and outcomes such as mortality. Results 40 cohort studies comprising 98 930 patients with T1MI and 13 803 patients with T2MI were included. Compared with T1MI, patients with T2MI were: more likely to have pre-existing chronic kidney disease (OR 1.87; 95% CI 1.53 to 2.28) and chronic heart failure (OR 2.35; 95% CI 1.82 to 3.03), less likely to present with typical cardiac symptoms of chest pain (OR 0.19; 95% CI 0.13 to 0.26) and more likely to present with dyspnoea (OR 2.64; 95% CI 1.86 to 3.74); more likely to demonstrate non-specific ST-T wave changes on ECG (OR 2.62; 95% CI 1.81 to 3.79) and less likely to show ST elevation (OR 0.22; 95% CI 0.17 to 0.28); less likely to undergo coronary angiography (OR 0.09; 95% CI 0.06 to 0.12) and percutaneous coronary intervention (OR 0.06; 95% CI 0.04 to 0.10) or receive cardioprotective medications, such as statins (OR 0.25; 95% CI 0.16 to 0.38) and beta-blockers (OR 0.45; 95% CI 0.33 to 0.63). T2MI had greater risk of all cause 1-year mortality (OR 3.11; 95% CI 1.91 to 5.08), with no differences in short-term mortality (OR 1.34; 95% CI 0.63 to 2.85). Conclusion and relevance This review has identified clinical, management and survival differences between T2MI and T1MI with greater precision and scope than previously reported. Differential use of coronary revascularisation and cardioprotective medications highlight ongoing uncertainty of their utility in T2MI compared with T1MI.