Computed tomography (CT) has become the predominant test for diagnosing acute appendicitis in adults. In children and young adults, exposure to CT radiation is of particular concern. We evaluated the rate of negative (unnecessary) appendectomy after low-dose versus standard-dose abdominal CT in young adults with suspected appendicitis.

Background: Studies have shown that long‐term exposure to air pollution such as fine particulate matter (≤2.5 μm in aerodynamic diameter [ PM _2.5 ]) increases the risk of all‐cause and cardiovascular mortality. To date, however, there are limited data on the impact of air pollution on specific cardiovascular diseases. This study aimed to evaluate cardiovascular effects of long‐term exposure to air pollution among residents of Seoul, Korea. Methods and Results: Healthy participants with no previous history of cardiovascular disease were evaluated between 2007 and 2013. Exposure to air pollutants was estimated by linking the location of outdoor monitors to the ZIP code of each participant's residence. Crude and adjusted analyses were performed using Cox regression models to evaluate the risk for composite cardiovascular events including cardiovascular mortality, acute myocardial infarction, congestive heart failure, and stroke. A total of 136 094 participants were followed for a median of 7.0 years (900 845 person‐years). The risk of major cardiovascular events increased with higher mean concentrations of PM _2.5 in a linear relationship, with a hazard ratio of 1.36 (95% confidence interval, 1.29–1.43) per 1 μg/m ³ PM _2.5 . Other pollutants including PM _2.5–10 of CO , SO ₂ , and NO ₂ , but not O ₃ , were significantly associated with increased risk of cardiovascular events. The burden from air pollution was comparable to that from hypertension and diabetes mellitus. Conclusions: This large‐scale population‐based study demonstrated that long‐term exposure to air pollution including PM _2.5 increases the risk of major cardiovascular disease and mortality. Air pollution should be considered an important modifiable environmental cardiovascular risk factor.

Aim: The aim of this study was to evaluate the clinical utility of the lactate/albumin (L/A) ratio as a predictive factor of 28-day mortality in critically ill sepsis patients. Methods: This is a retrospective observational study from a prospectively collected multicenter registry of 10 emergency departments (EDs) in teaching hospitals that participated in the Korean Shock Society. It enrolled patients who were 19 years of age or older who had a suspected or confirmed infection and evidence of refractory hypotension or hypoperfusion. The prognostic performance of the L/A ratio and lactate level for predicting 28-day mortality was assessed. Lactate and albumin levels were measured immediately after ED arrival. Results: A total of 946 patients were included, with 22.5% overall 28-day mortality. The area under the receiver operating characteristic curve (AUROC) value of the L/A ratio (0.69, 95% confidence interval [CI] 0.64–0.73, P < 0.01) was higher than that of lactate (0.65, 95% CI 0.61–0.70, P < 0.01) for predicting 28-day mortality. The optimal cutoff of the L/A ratio was 1.32. The AUROC value of the L/A ratio was better than that of lactate regardless of lactate level (normal [<2.0 mmol/L]: 0.68 vs. 0.55; intermediate [≥2.0, < 4.0 mmol/L]: 0.65 vs. 0.50; high [≥4.0 mmol/L]: 0.66 vs. 0.62). In the subgroup with decreased lactate elimination, the AUROC value of the L/A ratio was also significantly higher than that of lactate (hepatic dysfunction: 0.70 vs. 0.66; renal dysfunction: 0.71 vs. 0.67). The L/A ratio cut-off and hypoalbminemia showed further discriminative value for 28-day mortality even in patients with normal or intermediate lactate levels. Conclusions: The prognostic performance of the L/A ratio was superior to that of a single lactate measurement for predicting 28-day mortality of critically ill sepsis patients. L/A ratio can be a useful prognostic factor regardless of initial lactate level and the presence of hepatic or renal dysfunction.