Coagulation and complement system in critically ill patients

Issue title: Selected Presentations held at the 34th Conference of the German Society for Clinical Microcirculation and Hemorheology, Regensburg, Germany, 27–28 November, 2015

Guest editors: L. Prantl, E.M. Jung and F. Jung

Article type: Research Article

Authors: Helling, H.^a | Stephan, B.^b | Pindur, G.^{b; *}

Affiliations: [a] University Hospital of North Norway, Tromsoe, Norway | [b] Saarland University Hospital, Homburg, Germany

Correspondence: [*] Corresponding author: Gerhard Pindur, Institute of Clinical Haemosatseology and Transfusion Medicine, Saarland University Hospital, DE-66421 Homburg, Germany. E-mail: gerhard.pindur@uniklinikum-saarland.eu

Abstract: Activation of coagulation and inflammatory response including the complement system play a major role in the pathogenesis of critical illness. However, only limited data are available addressing the relationship of both pathways and its assessment of a predictive value for the clinical outcome in intense care medicine. Therefore, parameters of the coagulation and complement system were studied in patients with septicaemia and multiple trauma regarded as being exemplary for critical illness. 34 patients (mean age: 51.38 years (±16.57), 15 females, 19 males) were investigated at day 1 of admittance to the intensive care unit (ICU). Leukocytes, complement factors C3a and C5a were significantly (p <  0.0500) higher in sepsis than in trauma, whereas platelet count and plasma fibrinogen were significantly lower in multiple trauma. Activation markers of coagulation were elevated in both groups, however, thrombin-antithrombin-complex was significantly higher in multiple trauma. DIC scores of 5 were not exceeded in any of the two groups. Analysing the influences on mortality (11/34; 32.35% ), which was not different in both groups, non-survivors were significantly older, had significantly higher multiple organ failure (MOF) scores, lactate, abnormal prothrombin times and lower C1-inhibitor activities, even more pronounced in early deaths, than survivors. In septic non-survivors protein C was significantly lower than in trauma. We conclude from these data that activation of the complement system as part of the inflammatory response is a significant mechanism in septicaemia, whereas loss and consumption of blood components including parts of the coagulation and complement system is more characteristic for multiple trauma. Protein C in case of severe reduction might be of special concern for surviving in sepsis. Activation of haemostasis was occurring in both diseases, however, overt DIC was not confirmed in this study to be a leading mechanism in critically ill patients. MOF score, lactate, C1-inhibitor and prothrombin time have been the only statistically significant predictors for lethal outcome suggesting that organ function, microcirculation, haemostasis and inflammatory response are essential elements of the pathomechanism and clinical course of diseases among critically ill patients.

Keywords: Septicemia, multiple trauma, coagulation, complement, critical illness

DOI: 10.3233/CH-151993

Journal: Clinical Hemorheology and Microcirculation, vol. 61, no. 2, pp. 185-193, 2015