The coagulopathy in acute head injury: comparison of cerebral versus peripheral measurements of haemostatic activation markers.
Brain injury is known to result in various degrees of disordered haemostasis. Moreover, the recently developed assays of molecular markers of haemostasis can give an accurate reflection of its activation in vivo. The aim of this study was to monitor the levels of prothrombin fraction 1 + 2 (F1 + 2), thrombin antithrombin complexes (TAT) and D-dimer on the admission of patients to the ICU and up to the fourth day postinjury. Seventeen patients with head injury (Glasgow Coma scale 12 or less) were studied at King Khalid University Hospital, Riyadh. Their ages ranged from 10 to 40 years (mean 26). Blood samples were collected from the internal jugular vein, peripheral vein and artery. The mean levels of TAT and F1 + 2 in the internal jugular vein was significantly higher than in both peripheral venous and arterial blood on admission and 24 h later. Thereafter, the levels in the three locations dropped significantly, but remained elevated above controls. D-dimer levels were very markedly elevated to a similar extent in the three locations throughout the study period. The prothrombin time was significantly prolonged in the three locations in the first two days. Plasma fibrinogen levels dropped very significantly in the jugular vein, and increased to above reference values later. Protein S and factor VII showed a significant drop in the first two days and increased to normal range thereafter. Outcome was evaluated using the Glasgow Outcome Scale at 6 months postinjury. Haemostatic measurements could not predict good outcome (12 patients) or bad outcome (four deaths). It was concluded that haemostatic activation is a transient, but common phenomenon after head injury and is more prominent in cerebrovascular than in peripheral blood. The number of patients studied is too small to allow reliable association to be drawn between haemostatic changes on admission and prediction of outcome.
Murshid
W R
WR
Division of Neurosurgery, College of Medicine & King Khalid University Hospital, Riyadh, Saudi Arabia.
Gader
A G M A
AG
D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D000933:Antifibrinolytic Agents / Q000097:blood; D000990:Antithrombin III; D015415:Biomarkers / Q000097:blood; D001778:Blood Coagulation Disorders / Q000097:blood* / Q000209:etiology; D001780:Blood Coagulation Tests; D002648:Child; D006259:Craniocerebral Trauma / Q000097:blood* / Q000150:complications; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D008297:Male; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D011486:Protein C / Q000032:analysis; D017293:Protein S / Q000032:analysis; D011516:Prothrombin; D016896:Treatment Outcome
D000933:Antifibrinolytic Agents; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D010446:Peptide Fragments; D011486:Protein C; D017293:Protein S; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases