Background Prior studies show that lactate is a useful prognostic marker in sepsis. Objective To study the feasibility and accuracy of a point-of-care (POC) analyzer capable of performing bedside serum lactate measurements; and to determine if other measurements (pH, base excess) are predictive of mortality. Methods: Design: prospective cohort study of adult (age 18 years or older) Emergency Department (ED) patients with suspected infection during the study period of May 2006 through March 2007. Setting A 55,000-annual-visit urban tertiary care ED. Intervention A point-of-care device (i-STAT, Abbott Point of Care Inc., Princeton, NJ) was deployed using a standardized training and quality assurance process. Using POC testing, we measured serum lactate, pH, and base excess, as well as concomitant lactate measurement via a central laboratory. Statistics Area under the curve (AUC) for receiver operator characteristic curve, Bland-Altman statistics along with a correlation coefficient, and relative risk with 95% confidence intervals reported. Results There were 699 patients enrolled, of whom 34 (4.9%) died. The AUCs for mortality prediction were: POC lactate 0.72, laboratory lactate 0.70, pH measurement 0.60, and base excess 0.60. Bland-Altman showed that POC lactate was, on average, 0.32 (95% confidence interval −0.35– 0.98) lower than laboratory lactate, with agreement kappa = 0.97. Conclusions A point-of-care testing device provides a reliable and feasible way to measure serum lactate at the bedside. The pH and base excess were less helpful.

Objectives: The objective was to investigate the association between statin therapy and mortality in emergency department (ED) patients with suspected infection. Results: Of 2,132 patients with suspected infection, 2,036 (95%) had interpretable pharmacy data and were analyzed. The cohort had a median age of 61 years (interquartile range [IQR] = 46-78 years) and a mortality of 3.9% (95% confidence interval [CI] = 3.1% to 4.8%). Patients who received statins (n = 474) had a lower unadjusted crude mortality (1.9%; 95% CI = 0.6% to 3.3%) compared to those who did not (4.5%; 95% CI = 3.4% to 5.4%; p £ 0.01). When adjusting for gender, MEDS score, Charlson Comorbidity Index, and duration of statin therapy, the odds of death for statin patients was 0.27 (95% CI = 0.1 to 0.72; p £ 0.01). Conclusions:Patients who were admitted to the hospital with infection and received statin therapy while hospitalized had a significantly lower in-hospital mortality compared to patients who did not receive a statin.

Objectives: Radiocontrast nephropathy (RCN) is a known complication of procedures in which intravascular iodinated contrast material is used. The authors sought to determine the risk factors for RCN after emergency department (ED) contrast-enhanced computerized tomography (CECT).Methods: This was a retrospective case-control study of patients presenting to a tertiary care ED between January 1, 2004, and December 31, 2006. Inclusion criteria were CECT performed in the ED, serum creatinine measured prior to CECT, and serum creatinine measured 48 to 96 hours after CECT. Exclusion criterion was dialysis-dependent renal failure prior to CECT. The outcome of RCN was defined as an absolute creatinine increase of greater than or equal to 0.5 mg/dL, or a 25% increase above baseline. The charts of all RCN patients and a random sample of non-RCN patients were reviewed to document the presence or absence of potential risk factors. Univariate analysis was performed using chisquare and multiple logistic regression applying a weighted technique to account for sampling of non-RCN patients.Results: Among the 5,006 patients meeting inclusion criteria, 349 (7%) developed RCN. Multiple regression analysis demonstrated that serum creatinine > 2 mg/dL, liver disease, heart failure, hematocrit < 30%, hypertension, and diabetes were risk factors for RCN, whereas age > 75 years, vascular disease, and serum creatinine > 1.5 mg/dL were not. The area under the curve (AUC) for the model was 0.65. Although the risk of RCN increased with the number of risk factors present, we could not develop a model with sufficient diagnostic accuracy to guide clinical decision-making. Conclusions:The authors report risk factors for RCN in a large case-control study, but could not develop an accurate decision tool to identify patients at increased risk for RCN after ED CECT.ACADEMIC EMERGENCY MEDICINE 2013; 20:40-45 © 2013 by the Society for Academic Emergency Medicine R adiocontrast nephropathy (RCN) is a known complication of procedures that use intravascular radiocontrast media. Although most of the medical literature regarding RCN describes patients undergoing coronary procedures, RCN may occur after emergency department (ED) contrast-enhanced computerized tomography (CECT) as well. RCN is usually defined as an absolute increase in serum creatinine of 0.5 mg/dL or a relative increase of 25% above baseline value several days after contrast administration. [1][2][3][4] RCN is a leading cause of hospital-acquired renal insufficiency 5 and is associated with increased mortality both during hospitalization and after discharge. 1,4,[6][7][8] The rate of RCN after ED CECT varies greatly by study and has been reported as 2% to 3% in patients undergoing computed tomography (CT) angiography for stroke, 9-11 2% to 5% in trauma patients undergoing various studies, [12][13][14][15] 4.5% in patients undergoing

The development of organ dysfunction is a key contributor to morbidity and mortality in sepsis. End-tidal carbon dioxide levels measured by non-invasive end-tidal capnography (ETCO2) may provide a rapid assessment of a patient's underlying metabolic status. The objective of this study was to explore the association between ETCO2 and (1) organ dysfunction [sequential organ failure assessment (SOFA) score], and (2) serum lactate levels in febrile emergency department (ED) patients. Prospective, observational cohort study of a convenience sample of 97 adult (age 18 years or older) patients presented to an academic urban ED with a fever and suspected infection. The outcomes were ED SOFA score and serum lactate level. Based on prior studies, we categorized an ETCO2 <35 mmHg, a priori, as abnormal for the exposure. We defined clinically significant organ failure as a SOFA score of >2, and an abnormal lactate as >4 mmol/L. The correlation of ETCO2 with SOFA and lactate level was analyzed using Pearson correlation coefficient. Operating characteristics were calculated with 95% confidence intervals, along with the area under the curve (AUC). Among 97 patients enrolled, 5 (5%) had an abnormal lactate and 34 (35%) had a SOFA score >2. A significant correlation was found between ETCO2 and SOFA score (r = -0.35, p < 0.01), and ETCO2 and lactate level (r = -0.35, p < 0.01). A receiver operator curve for ETCO2 and SOFA >2 had an AUC of 0.69. ETCO2 of <35 has a sensitivity of 0.73 (95% CI 0.56-0.85) and specificity 0.50 (0.38-0.62) in predicting SOFA scores >2. ETCO2 <35 has a sensitivity of 0.60 (0.22-0.88) and specificity 0.42 (0.32-0.52) in predicting lactate >4 with an AUC of 0.62. We found a small, but statistically significant correlation, between ETCO2 and SOFA scores; however, based on questionable operating characteristics, the test seems to have limited ability to meaningfully impact clinical decision making. Larger confirmatory studies are required before final assessment.