title: Combined activation of coagulation and inflammation has an important role in multiple organ dysfunction and poor outcome after severe trauma.
abstract: We tested the hypothesis that activated neutrophil-endothelial cell interaction in DIC can cause endothelial injury contributing to multiple organ dysfunction syndrome (MODS) and a poor outcome after trauma. Fifty-eight severe trauma patients, 29 with DIC and 29 without DIC were studied. Serial levels of soluble L-, P-, and E-selectins, ICAM-1, VCAM-1, thrombomodulin, and neutrophil elastase were measured on days 0-4 after trauma. The numbers of systemic inflammatory response syndrome (SIRS) criteria that patients met were determined, simultaneously. In the DIC patients, higher DIC scores, lower platelet counts, and a longer duration of SIRS were found compared with the non-DIC patients. The incidence of ARDS and MODS were higher in patients with DIC than in those patients without DIC, and the DIC patients had poor outcome. Soluble L-selectin (sL-selectin) level on Day 1 in the DIC patients who died was markedly lower than those in the non-DIC patients. The levels of sP- and sE-selectins, sICAM-1, and sVCAM-1 were more elevated in the patients with DIC than in those without DIC on days 2 to 4. Neutrophil elastase and sThrombomodulin levels in the DIC patients persistently increased during the study period compared to those in the non-DIC patients. Maximum DIC scores in the DIC group showed good correlations with peak levels of sICAM-1, sVCAM-1, neutrophil elastase, sThrombomodulin, and the number of dysfunctioning organs. Highly activated and sustained inflammation caused by neutrophil-endothelium interaction in DIC gives rise to MODS and poor outcome in patients with severe trauma. These results suggest a close relationship between inflammation and thrombosis in posttrauma DIC.
authors.affiliation: Division of Acute and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan. sgando@med.hokudai.ac.jp
authors.forename: Satoshi
authors.initials: S
authors.lastname: Gando
authors.forename: Takashi
authors.initials: T
authors.lastname: Kameue
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Matsuda
authors.forename: Mineji
authors.initials: M
authors.lastname: Hayakawa
authors.forename: Toshiteru
authors.initials: T
authors.lastname: Ishitani
authors.forename: Yuji
authors.initials: Y
authors.lastname: Morimoto
authors.forename: Osamu
authors.initials: O
authors.lastname: Kemmotsu
mesh_terms: D000328:Adult; D001777:Blood Coagulation; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000097:blood; D004211:Disseminated Intravascular Coagulation / Q000097:blood / Q000209:etiology; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000209:etiology*; D019272:Leukocyte Elastase / Q000097:blood; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D009102:Multiple Organ Failure / Q000097:blood* / Q000209:etiology*; D011379:Prognosis; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000209:etiology; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood / Q000209:etiology; D018180:Thrombomodulin / Q000097:blood; D014947:Wounds and Injuries / Q000097:blood* / Q000150:complications*
chemical_list: D015815:Cell Adhesion Molecules; D018180:Thrombomodulin; D019272:Leukocyte Elastase