IntroductionTraumatic injuries are amongst the leading causes of death worldwide, frequently as a result of uncontrolled hemorrhage. Critical deficiencies in clotting factors have been noted in trauma-induced coagulopathy. However, the exact underlying conditions that result in devastating coagulopathies remain unclear. The purpose of this study was to elucidate these underlying deficiencies.MethodsBlood samples were drawn from 45 severely injured trauma patients on their arrival at the resuscitation room, and the activities of all soluble clotting factors and routine coagulation tests were assessed. The Mann–Whitney-U-test was used to assess differences in coagulation activity between the patients and healthy controls. Furthermore, Spearman’s rank correlation was used to analyze the blood work.ResultsAfter severe trauma the levels of serum fibrinogen and calcium were significantly reduced. Furthermore, traumatized patients had a significantly increased International Normalized Ratio (INR) compared to healthy controls. The median activities of all clotting factors were reduced after severe multiple trauma, with the exception of factor VIII, which was increased. Statistically significant differences were observed for factors II (80 vs. 122 %, P < 0.0001), V (76 vs. 123 %, P < 0.0001), VII (90 vs. 114 %, P = 0.002), VIII (200 vs. 108 %, P < 0.0001), and X (86 vs. 122 %, P < 0.0001). Spearman’s correlation indicated a significant negative correlation between INR on arrival with fibrinogen and levels of factors II, V, and VII, whereas Partial Thromboplastin Time was significantly negatively correlated with factor VIII (all P < 0.0001).ConclusionsThese findings suggest a general but rather moderate impairment of clotting factor activities following severe multiple trauma. In the concept of a calculated coagulation therapy, this could demand for the use of factor concentrates with higher ratios of clotting factors. Finally, the physiological importance of strongly elevated factor VIII activity remains unclear, but a possible interference with ex vivo measurements of Partial Thromboplastin Time has to be considered.
Objective. The aim of this study was to identify routinely available clinical surrogate markers for potential clotting factor alterations following multiple trauma. Methods. In 68 patients admitted directly from the scene of the accident, all soluble clotting factors were analyzed and clinical data was collected prospectively. Ten healthy subjects served as control group. Results. Patients showed reduced activities of clotting factors II, V, VII, and X and calcium levels (all P < 0.0001 to 0.01). Levels of hemoglobin and base deficit correlated moderately to highly with the activities of a number of clotting factors. Nonsurvivors and patients who needed preclinical intubation or hemostatic therapy showed significantly reduced factor activities at admission. In contrast, factor VIII activity was markedly elevated after injury in general (P < 0.0001), but reduced in nonsurvivors (P < 0.05). Conclusions. Multiple trauma causes an early reduction of the activities of nearly all soluble clotting factors in general. Initial hemoglobin and, with certain qualifications, base deficit levels demonstrated a potential value in detecting those underlying clotting factor deficiencies. Nevertheless, their role as triggers of a hemostatic therapy as well as the observed response of factor VIII to multiple trauma and also its potential prognostic value needs further evaluation.
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