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Changes of the hemostatic network in critically ill patients--is there a difference between sepsis, trauma, and
1Department of Anesthesiology and Intensive Care Medicine Klinikum der Stadt Ludwigshafen, Germany.
Objective:
To study the time course of coagulation data in intensive care patients.
Design:
Prospective, descriptive study.
Setting:
Clinical investigation on a surgical and neurosurgical intensive care unit of a university hospital.
Patients:
Fifteen patients with severe trauma (injury severity score, 15 to 25), 15 sepsis patients secondary to major surgery, and 15 neurosurgery patients (cancer surgery) were studied.
Interventions:
Standardized intensive care therapy.
Measurements And Main Results:
Standard coagulation data and molecular markers of coagulation activation and fibrinolytic activity (soluble thrombomodulin, protein C, free protein S, thrombin/antithrombin III complex, plasmin-alpha 2-antiplasmin complex, tissue plasminogen activator, platelet factor 4, beta-thromboglobulin were measured from arterial blood samples on the day of admission to the intensive care unit (trauma/neurosurgery patients) or on the day of diagnosis of sepsis (baseline value) and serially during the next 5 days. Antithrombin III, fibrinogen, and platelet counts were highest in neurosurgery patients but without significant differences between sepsis and trauma patients. Thrombin/antithrombin III complex increased in the sepsis patients (from 22.6+/-4.2 microg/L to 39.9+/-6.8 microg/L), but decreased in trauma (from 40.2+/-5.1 microg/L to 17.6+/-4.0 microg/L) and neurosurgery patients (from 28.2+/-4.2 microg/L to 16.2+/-3.8 microg/L). Tissue plasminogen activator increased in the sepsis patients (from 14.4+/-3.9 microg/L to 20.7+/-3.8 microg/mL) and remained almost unchanged in the other two groups. Soluble thrombomodulin plasma concentration increased significantly in the sepsis group (max, 131.8+/-22.5 ng/mL), while it remained elevated in the trauma (max, 75.5+/-5.9 ng/mL) and was almost normal in the neurosurgery patients. Protein C and free protein S remained decreased only in the sepsis group.
Conclusions:
Alterations of the hemostatic network were seen in all three groups of critically ill patients. Hemostasis normalized in the neurosurgery patients and posttraumatic hypercoagulability recovered within the study period. By contrast, monitoring of molecular markers of the coagulation process demonstrated abnormal hemostasis in the sepsis patients during the entire study period indicating ongoing coagulation disorders and abnormalities in fibrinolysis in these patients.