S. E. Dekker1, H. M. De Vries1, A. Duvekot1, L. M. Geeraedts2, S. M. Peerdeman3, M. C. De Waard4, P. Schober1, C. Boer1 1VU University Medical Center,Anesthesiology,Amsterdam, NH, Netherlands 2VU University Medical Center,Surgery,Amsterdam, NH, Netherlands 3VU University Medical Center,Neurosurgery,Amsterdam, NH, Netherlands 4VU University Medical Center,Intensive Care,Amsterdam, NH, Netherlands
Introduction: A severe, frequently overlooked complication of traumatic brain injury (TBI) is the development of coagulopathy, which may contribute to poor outcome. It has been suggested that cerebral hypoperfusion might be one of the causes of coagulopathy. This study investigated the relationship between cerebral and somatic tissue oxygenation and hemostatic derangements in TBI patients.
Methods: Rotational thromboelastometry (ROTEM) and tissue oxygenation were simultaneously measured in 92 trauma patients with suspicion of TBI at ED admission. Overall, 52 patients were diagnosed with TBI (head AIS ≥ 3). The level of hypoperfusion was characterized by tissue hemoglobin oxygenation index (TOI) using noninvasive near infrared spectroscopy (NIRS) located at the forehead (cerebral) or arm (somatic), base excess, and lactate. Coagulopathy was defined as an INR >1.2 and/or activated partial thromboplastin time (aPTT) >40 seconds and/or thrombocytopenia (<120*10-9/L). Patients who used anticoagulant medication (vitamin K antagonists, clopidogrel and dabigatran) were excluded from the study.
Results: Trauma patients with acute coagulopathy had a higher head-AIS level compared to trauma patients without coagulopathy [5 (4 to 5) vs. 4 (4 to 5); P=0.038]. TBI-patients with coagulopathy (42%) had significantly lower levels of fibrinogen [1.8 (1.1 to 2.3) vs. 2.8 (2.4 to 3.2) g/L; P<0.001], and higher D-dimers [17.6 (9.0 to 67.1) vs. 6.4 (2.7 to 13.2) mg/L; P=0.032] compared to TBI-patients without coagulopathy. TBI patients with coagulopathy had more signs of tissue hypoperfusion as indicated by increased lactate levels [1.9 (1.1 to 3.2) vs. 1.2 (1.0 to 1.7) mmol/L; P=0.026] and base excess [-3.1 (-4.6 to -2.0) vs. -0.1 (-2.5 to 1.8) mmol/L; P<0.001] than patients without coagulopathy. There was no difference in NIRS cerebral or somatic TOI between TBI patients with or without coagulopathy. However, we found an inverse relationship between NIRS cerebral TOI and fibrinolysis as measured by D-dimers (P=0.038), fibrinogen (P=0.041), and maximum lysis in the aptem ROTEM test (P=0.016). The presence of coagulopathy was associated with both an increased in-hospital mortality (47.6 vs. 6.9%; P=0.002) and one-year mortality (65 vs. 16%; P=0.002) compared to patients without coagulopathy.
Conclusion: This is the first study to investigate the relationship between hemostatic derangements and cerebral and somatic tissue oxygenation using NIRS in TBI patients. This study showed that TBI-related coagulopathy is more profound in patients with metabolic acidosis and increased lactate levels. While there was no difference in NIRS cerebral or somatic tissue oxygenation between patients with or without coagulopathy, we found an inverse relationship between NIRS tissue oxygenation levels and fibrinolysis.