Abstract
IntroductionThe inflammatory response to an invading pathogen in sepsis leads to complex alterations in hemostasis by dysregulation of procoagulant and anticoagulant factors. Recent treatment options to correct these abnormalities in patients with sepsis and organ dysfunction have yielded conflicting results. Using thromboelastometry (ROTEM®), we assessed the course of hemostatic alterations in patients with sepsis and related these alterations to the severity of organ dysfunction.MethodsThis prospective cohort study included 30 consecutive critically ill patients with sepsis admitted to a 30-bed multidisciplinary intensive care unit (ICU). Hemostasis was analyzed with routine clotting tests as well as thromboelastometry every 12 hours for the first 48 hours, and at discharge from the ICU. Organ dysfunction was quantified using the Sequential Organ Failure Assessment (SOFA) score.ResultsSimplified Acute Physiology Score II and SOFA scores at ICU admission were 52 ± 15 and 9 ± 4, respectively. During the ICU stay the clotting time decreased from 65 ± 8 seconds to 57 ± 5 seconds (P = 0.021) and clot formation time (CFT) from 97 ± 63 seconds to 63 ± 31 seconds (P = 0.017), whereas maximal clot firmness (MCF) increased from 62 ± 11 mm to 67 ± 9 mm (P = 0.035). Classification by SOFA score revealed that CFT was slower (P = 0.017) and MCF weaker (P = 0.005) in patients with more severe organ failure (SOFA ≥ 10, CFT 125 ± 76 seconds, and MCF 57 ± 11 mm) as compared with patients who had lower SOFA scores (SOFA <10, CFT 69 ± 27, and MCF 68 ± 8). Along with increasing coagulation factor activity, the initially increased International Normalized Ratio (INR) and prolonged activated partial thromboplastin time (aPTT) corrected over time.ConclusionsKey variables of ROTEM® remained within the reference ranges during the phase of critical illness in this cohort of patients with severe sepsis and septic shock without bleeding complications. Improved organ dysfunction upon discharge from the ICU was associated with shortened coagulation time, accelerated clot formation, and increased firmness of the formed blood clot when compared with values on admission. With increased severity of illness, changes of ROTEM® variables were more pronounced.
Highlights
The inflammatory response to an invading pathogen in sepsis leads to complex alterations in hemostasis by dysregulation of procoagulant and anticoagulant factors
During the intensive care unit (ICU) stay the clotting time decreased from 65 ± 8 seconds to 57 ± 5 seconds (P = 0.021) and clot formation time (CFT)
Classification by Sequential Organ Failure Assessment (SOFA) score revealed that CFT was slower (P = 0.017) and maximal clot firmness (MCF) weaker (P = 0.005) in patients with more severe organ failure (SOFA ≥ 10, CFT 125 ± 76 seconds, and MCF 57 ± 11 mm) as compared with patients who had lower SOFA scores (SOFA
Summary
The inflammatory response to an invading pathogen in sepsis leads to complex alterations in hemostasis by dysregulation of procoagulant and anticoagulant factors. Recent treatment options to correct these abnormalities in patients with sepsis and organ dysfunction have yielded conflicting results. Using thromboelastometry (ROTEM®), we assessed the course of hemostatic alterations in patients with sepsis and related these alterations to the severity of organ dysfunction. Organ failure contributes cumulatively to mortality in patients with sepsis [1]. One of the mechanisms that is believed to contribute to the pathogenesis of organ failure in sepsis is microvascular thrombosis [2,3,4,5]. Pathways involved in the prothrombotic state of critically ill patients include tissue factor-mediated thrombin generation and impaired anticoagulant and fibrinolytic mechanisms [6]. The effect of anticoagulant therapies on outcome is controversial [10,11,12,13]
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