First, to determine whether procalcitonin (PCT) significantly adds diagnostic value in terms of sensitivity and specificity to a common set of markers of infection, including C-reactive protein (CRP), at the Emergency Department. Second, to create a simple scoring rule implementing PCT values. Third, to determine and compare associations of CRP and PCT with clinical outcomes.
The additional diagnostic value of PCT was determined using multiple logistic regression analysis. A score was developed to help distinguish patients with a culture-proven bacterial infection from patients not needing antibiotic treatment using 16 potential clinical and laboratory variables. The prognostic value of CRP and PCT was determined using Spearman's correlation and logistic regression.
Emergency Department of a 310-bed teaching hospital.
Patients between 18 and 85 years old presenting with fever to the Emergency Department.
A total of 211 patients were studied (infection confirmed, n = 73; infection likely, n = 58; infection not excluded, n = 46; no infection, n = 34). CRP and chills were the strongest predictors for the diagnosis of bacterial infection. After addition of PCT to these parameters, model fit significantly improved (p = .003). The resulting scoring rule (score = 0.01 * CRP + 2 * chills + 1 * PCT) was characterized by an AUC value of 0.83 (sensitivity 79%; specificity of 71%), which was more accurate than physician judgment or SIRS (systemic inflammatory response syndrome). PCT levels were significantly associated with admission to a special care unit, duration of intravenous antibiotic use, total duration of antibiotic treatment, and length of hospital stay, whereas CRP was related only to the latter two variables.
These data suggest that PCT may be a valuable addition to currently used markers of infection for diagnosis of infection and prognosis in patients with fever at the Emergency Department.
From the Department of Internal Medicine (MDdK, ML, HG, DPMB, ECMvG), Slotervaart Hospital, Amsterdam; Center for Experimental and Molecular Medicine (MDdK, ML, CAS) and Department of Clinical Epidemiology and Biostatistics (PMB), Academic Medical Center, University of Amsterdam, Amsterdam; Laboratory for Clinical Thrombosis and Hemostasis (HtC), Department of Internal Medicine, Cardiovascular Research Institute Maastricht, University Maastricht, Maastricht; Department of Hematology (PHR), University of Leiden, Leiden, The Netherlands.
This study was designed and performed at the Department of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands. Data analysis was performed at the Center for Experimental and Molecular Medicine Academic Medical Center, University of Amsterdam. Measurements of PCT were performed in a blinded fashion by B·R·A·H·M·S Aktiengesellschaft, Hennigsdorf, Germany.
The authors have not disclosed any potential conflicts of interest.
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