No abstract

Background: Existing scoring systems to predict mortality in acute pancreatitis may not be directly applicable to the emergency department (ED). The objective of this study was to derive and validate the ED-SAS, a simple scoring score using variables readily available in the ED to predict mortality in patients with acute pancreatitis.Methods: This retrospective observational study was performed based on patient level data collected from electronic health records across 2 independent health systems, one used for the derivation cohort and one for the validation cohort. Adult patients who were eligible presented to the ED, required hospital admission, and had a confirmed diagnosis of acute pancreatitis. Patients with chronic or recurrent episodes of pancreatitis were excluded. The primary outcome was 30-day mortality. Analyses tested and derived candidate variables to establish a prediction score and that was subsequently applied to the validation cohort to assess odds ratio for the primary and secondary outcomes. Results: The derivation cohort included 599 patients, and the validation cohort 2011 patients. Thirty-day mortality was 4.2% and 3.9% respectively. From the derivation cohort, 3 variables were established for use in the predictive scoring score: ≥2 systemic inflammatory response syndrome (SIRS) criteria, age >60 years, and SpO2 <96%. Summing the presence or absence of each variable yielded an ED-SAS score ranging from 0 to 3. In the validation cohort, the odds of 30-day mortality increased with each subsequent ED-SAS point: 4.4 (95% CI 1.8 – 10.8) for 1 point, 12.0 (95% CI 4.9 – 29.4) for 2 points, and 41.7 (95% CI 15.8 – 110.1) for 3 points (c-statistic = 0.77).Conclusion: An ED-SAS score that incorporates SpO2, age, and SIRS measurements provides a rapid method for predicting 30-day mortality in acute pancreatitis.

No abstract

Background Existing scoring systems to predict mortality in acute pancreatitis may not be directly applicable to the emergency department (ED). The objective of this study was to derive and validate the ED-SAS, a simple scoring score using variables readily available in the ED to predict mortality in patients with acute pancreatitis. Methods This retrospective observational study was performed based on patient data collected from electronic health records across 2 independent health systems; 1 was used for the derivation cohort and the other for the validation cohort. Adult patients who were eligible presented to the ED, required hospital admission, and had a confirmed diagnosis of acute pancreatitis. Patients with chronic or recurrent episodes of pancreatitis were excluded. The primary outcome was 30-day mortality. Analyses tested and derived candidate variables to establish a prediction score, which was subsequently applied to the validation cohort to assess odds ratios for the primary and secondary outcomes. Results The derivation cohort included 599 patients, and the validation cohort 2011 patients. Thirty-day mortality was 4.2 and 3.9%, respectively. From the derivation cohort, 3 variables were established for use in the predictive scoring score: ≥2 systemic inflammatory response syndrome (SIRS) criteria, age > 60 years, and SpO2 < 96%. Summing the presence or absence of each variable yielded an ED-SAS score ranging from 0 to 3. In the validation cohort, the odds of 30-day mortality increased with each subsequent ED-SAS point: 4.4 (95% CI 1.8–10.8) for 1 point, 12.0 (95% CI 4.9–29.4) for 2 points, and 41.7 (95% CI 15.8–110.1) for 3 points (c-statistic = 0.77). Conclusion An ED-SAS score that incorporates SpO2, age, and SIRS measurements, all of which are available in the ED, provides a rapid method for predicting 30-day mortality in acute pancreatitis.

Introduction: Recent progress has been focused on severe aortic stenosis (AS), while its antecedent, moderate AS, still poses a clinical challenge. Notably, in moderate AS, depressed LV performance, like symptomatic status, may be due to non-valvular causes, e.g. CAD, primary myocardial dysfunction, hypertension or noncardiac diseases, all of which require different management. LV hypertrophy (LVH), traditionally perceived as an adaptive mechanism to preserve LV systolic function, frequently develops already in moderate AS. However, inappropriately high LV mass, i.e. disproportionate to LV afterload, predicts adverse outcome in AS and hypertension. Additionally, in concentric LVH, indices based on LV midwall mechanics reflect LV systolic function more accurately than EF which overestimates LV performance. Aim: To assess whether renal function is related to LV systolic performance and the appropriateness of LVH in real-world patients with moderate AS. Methods:We reviewed hospital records of 150 subjects with moderate degenerative AS, out of whom 70 with pure AS in sinus rhythm, with EF>40% and stable in-hospital creatinine entered the final analysis. The patients were compared according to GFR [ml/ min per 1.73 m 2 ] estimated by the CKD-EPI equation from averaged serum creatinine: group A (GFR>85), B (GFR = 60¡85) and C (GFR = 15¡59). From routine echocardiographic records and blood pressure, we calculated valvulo-arterial impedance (Zva), an index of global LV afterload, and excess of LV mass (ELVM). ELVM is the deviation from the LVM predicted individually from hemodynamic load, expressed as a proportion of the predicted LVM. LV midwall fractional shortening (mwFS) was also derived from standard records, assuming a constant LV wall volume during the cardiac cycle. Results: The 3 groups did not differ in aortic valve area, EF, Zva, LV mass, prevalence of symptoms, CAD or diabetes. ELVM increased gradually across decreasing GFR categories (p = 0.01 for trend). Compared to group A, group B subjects had lower mwFS (p < 0.05), higher relative LV wall thickness (p < 0.05) and LV mass/volume ratio (p < 0.05), all of which were yet similar in groups B and C. GFR correlated to ELVM (r = ¡0.46, p < 0.001) and mwFS (r = 0.31, p < 0.01). ELVM and mwFS were closely interrelated (r = ¡0.57, p < 0.001), which was maintained upon adjustment for GFR and Zva. Conclusions: Progressive GFR deterioration seems associated with excessive LVH and LV dysfunction at the midwall level in moderate AS, irrespective of global LV afterload and EF. Excessive LVH can be triggered by slightly reduced LV contractility already in mild renal impairment as a compensatory, yet ineffective, mechanism aimed at restoring LV performance by lowering LV wall stress. Whether prevention of early GFR decline may attenuate LVH and improve prognosis in AS, remains to be studied.Background: Percent predicted peak oxygen uptake (%ppVO2) is a useful tool to help stratify risk in patients with heart failure with reduced ejection fraction (HFrEF). However, insuffic...