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Coagulopathy After Traumatic Brain Injury: Incidence, Pathogenesis, and Treatment Options

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Coagulopathy After Traumatic Brain Injury: Incidence, Pathogenesis, and Treatment Options ORIGINAL ARTICLE Coagulopathy after traumatic brain injury: incidence, pathogenesis, and treatment options Marc Maegele raumatic brain injury (TBI) is often associated Coagulopathy after traumatic brain injury (TBI) is frequent with hemocoagulative disorders but incidence and represents a powerful predictor related to outcome rates vary considerably between studies (10%- and prognosis. The complex pathophysiological mecha- 90%) due to differences in study design, incon- nisms of the coagulopathy of TBI are multifactorial and Tsistency in the definition for coagulopathy, diversity in the remain still undefined. The nature of the coagulation magnitude of injury, and the mix between early and abnormalities differs between severe TBI and non-TBI delayed disturbances.1 According to a recent meta- with somatic injuries. The current hypothesis for the analysis of 34 studies reporting the frequencies of coagu- development of coagulopathy after TBI includes combi- lopathy after civilian TBI, one out of three patients nations of both hypo- and hypercoagulable states pro- suffering from TBI displays signs of coagulopathy.1 While moted by the magnitude and the extent of the injury hemocoagulative disorders may occur in >60% of patients resulting in a variable degree of secondary injury via with severe TBI,2 in mild head injury coagulopathy is subsequent ischemic and hemorrhagic lesioning. The uncommon (<1%).3 Wafaisade and coworkers have proposed underlying mechanisms may comprise the recently assessed retrospectively the TR-DGU (Trauma- release of tissue factor (TF), hyperfibrinolysis, shock, and Registry of the German Society for Trauma Surgery) data- hypoperfusion thus triggering the protein C pathway, dis- base for frequency, outcome, and risk factors of acute seminated intravascular coagulation, and platelet dys- coagulopathy in isolated TBI.4 Out of 3114 patients, 706 function. Hemocoagulative disorders after TBI may be (22.7%) were coagulopathic upon emergency room (ER) amenable to treatment, and adequate and timely man- arrival and stepwise logistic regression analysis identified agement may protect from secondary injury and poor the following independent risk factors for the develop- outcomes. Functional assays such as viscoelastic tests ment of acute coagulopathy after TBI: 1) severity of head may be supportive in early detection, diagnosis, and guid- trauma as reflected by Abbreviated Injury Scale for head ance of treatment. This review summarizes the current (AIShead); 2) Glasgow Coma Scale (GCS) at scene Յ8 points; understanding with regard to frequency, pathogenesis, 3) hypotension Յ90 mmHg at scene or upon ER arrival; 4) diagnosis, and treatment of the coagulopathy after TBI. prehospital intravenous fluid administration Ն2000 mL; and 5) age Ն75 years. It has been observed that the number of patients with isolated TBI and coagulopathy may double within the first 24 hours after trauma, and that hemostatic abnormalities reflected by impaired global coagulation parameters may continue until the third day after injury or even longer.5 Lustenberger and coworkers have reported on 127 From the Department of Trauma and Orthopedic Surgery, and patients with isolated severe TBI in which coagulopathy Institute for Research in Operative Medicine (IFOM), University defined as thrombocytopenia and/or elevated interna- of Witten/Herdecke, Cologne-Merheim Medical Center tional normalized ratio (INR) and/or prolonged activated (CMMC), Cologne, Germany. partial thromboplastin time (aPTT) occurred at mean Address reprint requests to: Marc Maegele, MD, PhD, 23 Ϯ 2 hours (range 0.1-108 hr [0-4.5 days]) after ER Department of Trauma and Orthopedic Surgery, University of admission with a mean duration of 68 Ϯ 7.4 hours (range Witten/Herdecke, Cologne-Merheim Medical Center (CMMC), 2.6-531 hr [0.1-22.1 days]).6 In this study, the time interval Ostmerheimerstr. 200, D-51109 Cologne, Germany; e-Mail: to the onset of coagulopathy decreased substantially with [email protected]. increasing magnitude of injury. Early hemocoagulative doi: 10.1111/trf.12033 abnormalities occurring within 12 hours after admission TRANSFUSION 2013;53:28S-37S. along with markers of devastating head injury (AIShead 5), 28S TRANSFUSION Volume 53, January 2013 Supplement COAGULOPATHY AFTER TBI better predictor for outcome and mortality than midline shift or pupillary reactivity,7 and a variety of parameters have been suggested, e.g., fibrinogen degradation products (FDPs), aPTT, plasmin-a2-plasmin inhibitor complex, and/or decreased fibrinogen levels. Recently, the International Mission for Progression and Clinical Trial (IMPACT) proposed the prothrombin time (PT) as a powerful independent prognostic factor after TBI.8 Abnor- malities in mean PT, aPTT, and platelet counts upon ER arrival have been associated with the development of TBI- related but delayed injury defined by new intracranial lesions or lesion progression. Von Willebrand factor and thrombomodulin (TM) have been suggested as indicators of cerebral endothelial injury and increased TM levels to predict delayed brain lesioning.9 In general, alterations in almost every single coagulation parameter after TBI have been associated with prognosis, but the interpretation of the predictive value of these parameters and outcome of different studies is complex as the result of heterogeneity in study design and/or size, populations assessed, and definitions of coagulopathy.1 Moreover, peripheral hema- tologic studies may not entirely reflect persistent coagul- opathy in the cerebral circulation.10 However, the strong Fig. 1. Cranial computed tomography of a 70-year-old male prognostic value of coagulopathy during the first 24 to 72 with significant TBI showing bilateral subdural hematoma, hours after TBI and the association between clotting subarachnoid hemorrhage, midline shift to the right, and abnormalities and delayed intracerebral hemorrhage war- brain edema. Upon arrival in the trauma bay global labora- rants early and repetitive coagulation monitoring as well tory testings indicated severe coagulopathy with an INR 2.04, as adequate control of it. aPTT 81.1 seconds, and d-dimer >35 mg/L. PATHOGENESIS OF COAGULOPATHY penetrating mechanism, subdural hematoma (SDH), and IN TBI low GCS were independent risk factors for mortality. Those patients developing coagulopathy within 24 hours The complex pathophysiological mechanisms behind the of injury had a mortality rate of 55% versus 23% in those coagulopathy of TBI are multifactorial and remain poorly developing abnormalities at a later stage after 24 hours.6 defined. In healthy individuals, coagulation and lysis are Figure 1 shows a computed tomography (CT) scan of well balanced to control hemorrhage and thrombosis. TBI the head of a 70-year-old male with significant traumatic patients are at risk of developing abnormalities in both injury to the brain after a 3-meter fall from a garage roof coagulation and lysis, and the loss of this tightly regulated resulting in combined bilateral SDH, subarachnoid hem- equilibrium can either result in hypercoagulation with orrhage, midline shift to the right, and massive brain microthrombosis and ischemia or in hypocoagulation edema with beginning entrapment. The global coagula- with substantial bleeding and progression of hemorrhagic tion profile upon ER arrival showed an INR of 2.04, an lesions.11 To date, there is no precise definition of what aPTT of 81.1 seconds, and d-dimer of >35 mg/L. constitutes a coagulopathy after TBI. The likely mecha- nisms discussed at the moment have been summarized by 11 COAGULOPATHY IN TBI IS A PREDICTOR Laroche and coworkers in a systematic review. FOR PROGNOSIS Figure 2 provides an overview of laboratory tests cur- rently available to assess coagulopathic states. Diagnostic Coagulopathy upon ER arrival in TBI represents a power- tests and criteria for the coagulopathy of TBI are still ful predictor related to outcome and prognosis.1,4,5 The not commonly defined but usually include a clinical con- risk of dying in patients with coagulopathy after TBI is dition consistent with coagulopathy, e.g., severe injury, about 10 times higher than in patients without coagulopa- together with thrombocytopenia, i.e., platelet counts thy, and the risk of unfavorable outcome in surviving <100.000 mm3, and abnormal global coagulation tests, i.e., patients is even more than 30 times higher if coagulopathy elevated INR and/or prolonged aPTT.1,4,6-8,12 Real-time is present upon ER arrival.1 Several authors have claimed viscoelastic tests, e.g., thrombelastometry (ROTEM) or that laboratory parameters for coagulation may be a thrombelastography (TEG), allow the assessment of both Volume 53, January 2013 Supplement TRANSFUSION 29S MAEGELE physiological initiator of coagulation, is ENZYMATIC FIBRINOLYSIS expressed, to a high degree, as a trans- COAGULATION membrane protein in different cell types of the central nervous system INR/PT D-Dimer and thus at the injury site but may also aPTT Fibrinogen degradation Fibrinogen products (FDP) occur blood-borne contributing to the Thrombin Time Plasminogen activator ongoing amplification of coagulation Thrombin-AT III complex inhibitor-1 (PAI-1) after initial injury.16 The quantity and Prothrombin cleavage Viscoelastic tests the temporo-spatial pattern of TF fragments 1 and 2 Viscoelastic tests release has been associated to alter- ations in the blood-brain-barrier after traumatic impact, and it is suggested PLATELETS that this activation depends upon the Platelet count amount of TF released from
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