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Soluble triggering receptor expressed on myeloid cells 1 (sTREM-1) and procalcitonin (PCT) are often considered to be specific markers for infection. We evaluated plasma levels of sTREM-1 and PCT in patients with systemic inflammatory response syndrome but no sepsis. Noninfected patients undergoing elective heart surgery with cardiopulmonary bypass (n = 76) and patients admitted after out-of-hospital cardiac arrest (n = 54) were followed up for 3 days. Patients with severe sepsis (n = 55) and healthy volunteers (n = 31) were included as positive and negative controls, respectively. Plasma levels of PCT were higher in sepsis patients than in patients who survived after cardiac arrest or after heart surgery. In contrast, peak plasma levels of sTREM-1 in heart surgery and in cardiac arrest patients overlapped with those measured in patients with sepsis. Both sTREM-1 and PCT were significantly higher in cardiac arrest patients who died of refractory shock than in those who died of neurological failure or survived without major neurological damage. In the cardiac arrest patients with refractory shock, sTREM-1 and PCT levels were similar to those in the patients with severe sepsis. In conclusion, sTREM-1 and PCT are not specific for infection and can increase markedly in acute inflammation without infection.

Aims: Out-of-hospital cardiac arrest (OHCA) is common and carries a bleak prognosis. Early prediction of unfavourable outcomes is difficult but crucial to improve resource allocation. The aim of this study was to develop a simple tool for predicting survival with good neurological function in the overall population of patients with successfully resuscitated cardiac arrest., Methods and Results: We used logistic regression analysis to identify clinical and laboratory variables that were both readily available at admission and predictive of poor outcomes (death or severe neurological impairment) in a development cohort of 130 consecutive OHCA patients admitted to a French intensive care unit (ICU) between 1999 and 2003. To test the prediction score built from these variables, we used a validation cohort of 210 patients recruited in four French ICUs between 2003 and 2005. Initial rhythm, estimated no-flow and low-flow intervals, blood lactate, and creatinine levels determined using whole blood analyzers were independently associated with poor outcomes and were used to build a continuous severity score. Goodness-of-fit tests indicated good performance (P=0.79 in the development cohort and P=0.13 in the validation cohort). The area under the receiver-operating characteristics curve was 0.82 in the development cohort and 0.88 in the validation cohort., Conclusion: The outcome can be accurately predicted after OHCA using variables that are readily available at ICU admission.

Objectives: We investigated coagulation abnormalities in out-of-hospital cardiac arrest (OHCA) patients, with special attention to the protein C anticoagulant pathway., Background: Successfully resuscitated cardiac arrest is followed by a systemic inflammatory response and by activation of coagulation, both of which may contribute to organ failure and neurological dysfunction., Methods: Coagulation parameters were measured in all patients admitted after successfully resuscitated OHCA., Results: At admission, 67 patients had a systemic inflammatory response with increased interleukin-6 and coagulation activity (thrombin-antithrombin complex), reduced anticoagulation (antithrombin, protein C, and protein S), activated fibrinolysis (plasmin-antiplasmin complex), and, in some cases, inhibited fibrinolysis (increased plasminogen activator inhibitor-1 with a peak on day 1). These abnormalities were more severe in patients who died within two days (50 of 67, 75%) and were most severe in patients dying from early refractory shock. Protein C and S levels were low compared to healthy volunteers and discriminated OHCA survivors from nonsurvivors. Furthermore, a subgroup of patients had a transient increase in plasma-activated protein C at admission followed by undetectable levels. This, along with an increase in soluble thrombomodulin over time, suggests secondary endothelial injury and dysfunction of the protein C anticoagulant pathway similar to that observed in severe sepsis., Conclusions: Major coagulation abnormalities were found after successful resuscitation of cardiac arrest. These abnormalities are consistent with secondary down-regulation of the thrombomodulin-endothelial protein C receptor pathway.

The postresuscitation phase after out-of-hospital circulatory arrest shares similarities with severe sepsis. Corticosteroid replacement is beneficial in patients with septic shock and adrenal dysfunction. The goal of this study was to assess baseline cortisol and adrenal reserve of out-of-hospital circulatory arrest patients after recovery of spontaneous circulation. Thirty-three consecutive patients successfully resuscitated after cardiac arrest were prospectively included between March 2002 and June 2003. A serum cortisol assay and a corticotropin test (250 microg i.v.) were done 6 to 36 h after circulatory arrest. A cortisol increase smaller than 9 microg/dL after corticotropin (nonresponders) defined adrenal reserve insufficiency. Response status was compared in the three outcome groups: survival with full neurologic recovery (n = 4), early death from refractory shock (n = 10), or later death from neurologic dysfunction (n = 19). Patients who died of early refractory shock had lower baseline cortisol levels than patients who died of neurologic dysfunction (27 microg/dL [15-47] vs. 52 microg/dL [28-73], respectively; P < 0.01), suggesting an inadequate adrenal response to severe systemic inflammation. Corticotropin response status was not associated with standard severity markers and seemed uninfluenced by therapeutic hypothermia. In conclusion, patients who die of early refractory shock after cardiopulmonary resuscitation may have an inadequate adrenal response to the stress associated with this condition. Thresholds for cortisol levels at baseline and after corticotropin need to be determined in this clinical setting.