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Objective: 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., Design: 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., Setting: Emergency Department of a 310-bed teaching hospital., Patients: Patients between 18 and 85 years old presenting with fever to the Emergency Department., Interventions: None., Measurements and Main Results: 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., Conclusions: 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.

Objective: Bacterial sepsis causes widespread vascular inflammation that frequently leads to disseminated intravascular coagulation (DIC). Although intravascular coagulation contributes to organ failure, it is often debated whether anticoagulant therapy produces any beneficial effects in patients with DIC. The aim of this study was to document potential beneficial effects of low molecular weight heparin (LMWH) in a lipopolysaccharide-induced DIC model., Design: Controlled animal experiment combined with an in vitro laboratory study., Setting: Academic research laboratory., Subjects: C57BL/6 mice subjected to two injections of Serratia Marcescens lipopolysaccharide (LPS) resulting in the generalized Shwartzman's reaction as a model for DIC., Interventions: LMWH (5 IU of anti-Xa activity) or saline was administered before both LPS injections and 10 hrs after the first exposure to LPS. To test the effect of LMWH on LPS-driven monocyte inflammatory responses, a human monocyte-human umbilical vein endothelial cell co-culture was used to determine E-selectin expression as a marker of monocyte adherence., Measurements and Main Results: In our murine DIC model, LMWH had no effect on markers of inflammation. In addition, no effect of LMWH was detected on monocyte adherence in the human monocyte-human umbilical vein endothelial cell co-culture. Organ damage, contrarily, was significantly reduced as determined by hepatic necrosis (p < .05), lung epithelial protein leakage (p < .05), and creatinine release from kidneys into plasma (p < .01). LMWH protection from organ failure resulted in an increase in survival (p = .06) in this model for DIC., Conclusions: These results demonstrate the significance of blood coagulation in the progression of DIC and hint at a beneficial role for LMWH anticoagulation in the management of DIC.

Objective: To review the dual characteristics of disseminated intravascular coagulation (DIC), as both a contributor to multiple organ failure as well as a symptom of severe underlying disease associated with systemic vascular changes., Data Sources: Published literature data and unpublished results from the authors., Data Summary: Clinical and experimental studies strongly suggest that DIC contributes to multiple organ failure and death in patients with severe systemic disorders such as sepsis. DIC is evoked by systemic cytokine activity, and the inflammatory response aggravates vascular permeability, inflammation, and cell damage in tissues. In addition to intravascular fibrin formation, thrombin and fibrin generation in tissues is also an important aspect of DIC. An example of DIC at the organ level is adult respiratory distress syndrome, where fibrin in the lung is a characteristic feature. Intravascular fibrin formation and occlusion may elicit a hypoxic response with induction of hypoxia related transcription factors. The resulting ischemic preconditioning may offer protective effects to the involved organ(s)., Conclusions: Overall, the beneficial or harmful effects of activated coagulation and fibrin formation for organ pathology and recovery from DIC remain to be explored. This may be a critical element in the assessment of ischemia-reperfusion effects of specific anticoagulant therapy.