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This article is part of the supplement: Sepsis 2009

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Disseminated intravascular coagulation during human septic shock: relation with lactate levels

KJ Hartemink12*, CE Hack3 and ABJ Groeneveld1

  • * Corresponding author: KJ Hartemink

Author Affiliations

1 Department of Intensive Care and the Institute for Cardiovascular Research, Amsterdam, the Netherlands

2 Department of Surgery, Amsterdam, the Netherlands

3 Department of Clinical Chemistry, VU University Medical Center, Amsterdam, the Netherlands

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Critical Care 2009, 13(Suppl 4):P35  doi:10.1186/cc8091

The electronic version of this article is the complete one and can be found online at:

Published:11 November 2009

© 2009 BioMed Central Ltd.


The exact pathogenic role of disseminated intra-vascular coagulation (DIC) during septic shock is incompletely understood.


We studied the relation between sensitive and specific markers for DIC and lactate levels in the course of time, to evaluate whether DIC could contribute to microvascular obstruction and tissue hypoxygenation.


We prospectively studied 14 consecutive septic shock patients with a pulmonary artery catheter in place. For 3 days after admission, hemodynamic variables, and plasma levels of lactate, thrombin-antithrombin complexes (TAT), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI) and plasmin-α2-antiplasmin complexes and TNFα, IL-6 and complement activation product C3a were measured 6-hourly.


Of the 14 patients, eight died in the ICU. Patients had a hyperdynamic circulation with tachycardia, mild hypotension and increased cardiac index. The course of TAT, tPA and particularly of PAI predicted the course of lactate levels, independently of hemodynamic and inflammatory factors. Lactate and PAI elevations persisted in nonsurvivors versus survivors.


Our observations show that, in the course of human septic shock, activation of coagulation and, particularly, inhibition of activated fibrinolysis are independently associated with hyperlactatemia. This suggests a contribution of DIC resulting from a coagulation/fibrinolysis imbalance to microvascular obstruction, tissue hypoxygenation and thereby to ultimate demise.