Posttrauma coagulation and fibrinolysis.
OBJECTIVE
To determine the effects of disseminated intravascular coagulation (DIC) and head injury on posttrauma coagulation and fibrinolysis.


METHODS
Case-control study.


METHODS
General ICU (tertiary care center) in a city hospital serving a population of 150 million people.


METHODS
Forty trauma victims: 15 with DIC; 25 without DIC.


METHODS
Measurement of six types of coagulation and fibrinolytic molecular markers (fibrinopeptide A, fibrinopeptide B beta 15-42, plasmin antiplasmin complex, D-dimer, tissue plasminogen activator antigen concentration, tissue plasminogen activator activity) immediately after trauma, 3 days later, and 6 days later. Anticoagulant treatment with gabexate mesilate at 1.45 +/- 0.06 mg/kg/hr.


RESULTS
Fibrinopeptide A, fibrinopeptide B beta 15-42, plasmin antiplasmin complex, and D-dimer showed high values immediately after trauma and exceeded normal activity for the first 6 days. When trauma was complicated with DIC, the molecular markers showed significantly higher values than those for non-DIC patients on all days. In the head-injured patients, such effect was not noted. Tissue plasminogen activator antigen concentration and tissue plasminogen activator activity were within a normal physiologic range of variation. By contrast, tissue plasminogen activator antigen concentration increased significantly after trauma in patients with DIC. When anticoagulant treatment was found effective, it caused a reduction in fibrinopeptide A.


CONCLUSIONS
a) Fibrinolytic shut-down and its reactivation cannot be confirmed after trauma. b) Head injury does not lead to an increase in posttrauma coagulation or fibrinolytic activity. c) DIC enhances posttrauma coagulation and fibrinolytic activity and plasminogen activator inhibitor activity can be inferred in DIC patients. d) Increase in tissue plasminogen activator antigen concentration without tissue plasminogen activator activation may be a prognostic factor indicative of DIC and its chances of improvement, and fibrinopeptide A as an assessment criterion for the effectiveness of anticoagulant treatment.
Gando
S
S
Department of Emergency and Critical Care Medicine, Sapporo City General Hospital, Japan.
Tedo
I
I
Kubota
M
M
D000328:Adult; D000933:Antifibrinolytic Agents / Q000032:analysis; D000936:Antigen-Antibody Complex / Q000032:analysis; D000941:Antigens / Q000097:blood; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D001778:Blood Coagulation Disorders / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D016022:Case-Control Studies; D006259:Craniocerebral Trauma / Q000150:complications*; D004211:Disseminated Intravascular Coagulation / Q000097:blood / Q000150:complications* / Q000453:epidemiology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005341:Fibrinolysin / Q000276:immunology; D005342:Fibrinolysis; D005344:Fibrinopeptide A / Q000032:analysis; D005345:Fibrinopeptide B / Q000032:analysis; D015600:Glasgow Coma Scale; D006769:Hospitals, General; D006801:Humans; D015601:Injury Severity Score; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D009104:Multiple Trauma / Q000150:complications*; D010314:Partial Thromboplastin Time; D010976:Platelet Count; D011237:Predictive Value of Tests; D011517:Prothrombin Time; D010959:Tissue Plasminogen Activator / Q000276:immunology
D000933:Antifibrinolytic Agents; D000936:Antigen-Antibody Complex; D000941:Antigens; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D005344:Fibrinopeptide A; D005345:Fibrinopeptide B; D000990:Antithrombin III; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin