Background The pathogenic role of disseminated intravascular coagulation (DIC) during septic shock is incompletely understood.
Aim To 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.
Methods 14 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.
Results Eight 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.
Conclusions The 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.
- Inflammatory mediators
- tissue hypoxygenation
- septic shock
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Competing interests None.
Patient consent Obtained.
Ethics approval This study was conducted with the approval of the institutional review board and the hospital committee on ethics.
Provenance and peer review Not commissioned; externally peer reviewed.
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