Abstract
IntroductionInflammation and coagulation are closely linked, and both can be triggered by endotoxin. Thrombelastometry and impedance aggregometry are of diagnostic and predictive value in critically ill patients. In this observational study we investigated the correlation of endotoxin activity with thrombelasometric and aggregometric variables in patients with systemic inflammation.MethodsBased on a daily screening on a tertiary academic surgical ICU, patients, as soon as they fulfilled two or more criteria for systemic inflammatory response syndrome (SIRS), were included. In whole blood we performed endotoxin activity (EA) assay, thrombelastometry (ROTEM®) and impendance aggregometry (Multiplate®).ResultsIn total, 49 patients were included with a broad spread of EA levels of (median (minimum to maximum)) 0.27 (0.01 to 0.72), allowing expedient correlative analysis. Clot formation time (CFT) (263 s (60 to 1,438 s)) and clotting time (CT) (1,008 s (53 to 1,481 s)) showed a significant negative correlation with EA level (r = -0.38 (P < 0.005) and r = -0.29 (P < 0.05)). Positive correlations were found for alpha-angle (50° (17 to 78°), r = 0.40 (P < 0.005)) and maximum clot firmness (MCF) (55 mm (5/76), r = 0.27 (P < 0.05)). No significant correlations were found between Lysis Index at 60 minutes (LI60) and EA levels. There was no correlation between EA level and aggregometric values, or classical coagulation parameters.ConclusionsIn patients with systemic inflammation, increasing endotoxin concentrations correlate with increased clot formation.
Highlights
Inflammation and coagulation are closely linked, and both can be triggered by endotoxin
LPS is released into sterile compartments of the organism and in turn is detected by pattern recognition receptors (PRRs), like toll-like receptor (TLR)4, resulting in initiation of inflammation and coagulation [2,3]
Thrombosis prophylaxis was provided with heparin-infusion in 29 (59.2%) or low molecular weight heparin (LMWH) in 13 (26.5%) patients
Summary
Inflammation and coagulation are closely linked, and both can be triggered by endotoxin. Thrombelastometry and impedance aggregometry are of diagnostic and predictive value in critically ill patients. In this observational study we investigated the correlation of endotoxin activity with thrombelasometric and aggregometric variables in patients with systemic inflammation. Endotoxin (lipopolysaccharide (LPS)), can originate from invading Gram-negative bacteria and/or translocation of endogenous Gramnegative wall fragments. In vitro and in vivo models demonstrate the potential of LPS to initiate clotting. LPS reduces clotting time (CT) as measured with (rotational) thrombelastometry (TEM) [7,8]. Both postoperative patients and patients with sepsis demonstrate shorter CTs and clot formation times (CFTs) [9]. CFT seems to correlate well with clinical condition and outcome [10]
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