Introduction Patients with head trauma resulting in brain tissue injury display various degrees of disordered haemo- stasis including overt disseminated intravascular coagulation (DIC). 1–13 Postmortem examinations after fatal head injury have revealed microthrombi in the brain, kidneys, liver and lungs. 1,5–7 The severity of such post-traumatic coagulopathy is considered to be a major detrimental factor that could decide the outcome in head injury patients. 12–14 A general feature of these earlier studies is the wide variation in the haemostatic assays, as well as the timing of blood samples after injury, predominantly within the rst 24 h postinjury and this could account, in part, for the wide variation in the reported haemostatic changes after head injury. Recently more precise assays of the molecular markers of the activation of the haemostatic sys- tem, both clotting, (prothrombin fraction 1 + 2 and thrombin-antithrombin complex) and brinolysis (the complex brin degradation product D-dimer), have become available and can give an accurate reection of haemostatic activation in vivo. Scherer & Spangenberger 15 were able to show a rise in thrombin-antithrombin complex (TAT), F1 + 2 and D-dimer, soon after admission to the ICU and three hours later. Also the levels of TAT and F1 + 2, but not D-dimer were higher in jugular than central venous blood in the few hours following head injury. Another, more recent, study of ve patients 16 also conrmed the very elevated levels of these markers in arterial blood in the rst day after injury and drop- ping sharply in the three days thereafter. Earlier British Journal of Neurosurgery 2002; 16(4): 362–369 ORIGINAL ARTICLE The coagulopathy in acute head injury: comparison of cerebral versus peripheral measurements of haemostatic activation markers W. R. MURSHID 2 & A. G. M. A. GADER 1 Division of Neurosurgery and 1 The Coagulation Laboratory, Department of Physiology, College of Medicine & King Khalid University Hospital, Riyadh, Saudi Arabia Abstract 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 reection 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 signicantly higher than in both peripheral venous and arterial blood on admission and 24 h later. Thereafter, the levels in the three locations dropped signicantly, 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 signicantly prolonged in the three locations in the rst two days. Plasma brinogen levels dropped very signicantly in the jugular vein, and increased to above reference values later. Protein S and factor VII showed a signicant drop in the rst 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. Key words: Coagulopathy, D-dimer , F1 + 2, haemostatic markers, head injury, TAT, trauma. Correspondence: Professor A. M. A. Gader, The Coagulation Laboratory, Department of Physiology, Director of the Blood Bank, King Khalid University Hospital, Riyadh 11461, Saudi Arabia. Tel: 966 1 4671042. Fax: 966 1 467 2549. E-mail: amagader@ksu.edu.sa Received for publication 19 June 2000. Accepted 25 April 2002. ISSN 0268–8697 print/ISSN 1360–046X online/02/040362–08 © The Neurosurgical Foundation DOI: 10.1080/0268869021000007597