• Koen J Hartemink, C Erik Hack, and A B Johan Groeneveld.
• Department of Intensive Care and the Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands. kjhartemink@hetnet.nl
• J. Clin. Pathol. 2010 Nov 1;63(11):1021-6.

BackgroundThe pathogenic role of disseminated intravascular coagulation (DIC) during septic shock is incompletely understood.AimTo study the relation between indicators of DIC and lactate concentrations over time to evaluate whether a coagulation/fibrinolysis imbalance could directly contribute to tissue hypoxygenation.Methods14 consecutive septic shock patients with a pulmonary artery catheter in place were prospectively studied. For 3 days after admission, haemodynamic variables and plasma concentrations of lactate, thrombin-antithrombin complexes, tissue plasminogen activator, plasminogen activator inhibitor (PAI), plasmin-α2-antiplasmin complexes, fibrinogen, and the inflammatory mediators tumour necrosis factor-α and interleukin-6, as well as activated partial thromboplastin time (aPTT), prothrombin time (PT) and platelet counts were serially measured.ResultsEight of the 14 patients died in the intensive care unit. All patients had a hyperdynamic circulation with an increased cardiac index and mild hyperlactataemia. They had prolonged PT, thrombocytopenia and raised inflammatory, coagulation and fibrinolysis variables. The time course of PAI best predicted the time course of lactate, independently of haemodynamics, inflammatory mediators, PT, fibrinogen and platelet counts. High lactate, PAI and PT concentrations persisted in non-survivors compared with survivors.ConclusionsThe course of human septic shock, particularly inhibition of activated fibrinolysis during DIC, may be independently associated with hyperlactataemia; therefore a coagulation/fibrinolysis imbalance may contribute to tissue hypoxygenation and ultimately thereby to demise.

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