Semin Thromb Hemost 2020; 46(02): 155-166
DOI: 10.1055/s-0040-1702178
Review Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Changes in Coagulation following Brain Injury

Marc Maegele
1  Department of Trauma and Orthopaedic Surgery, Cologne-Merheim Medical Center, University of Witten/Herdecke, Cologne-Merheim Campus, Cologne, Germany
2  Institute for Research in Operative Medicine, University of Witten/Herdecke, Cologne-Merheim Campus, Cologne, Germany
,
John Aversa
3  Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana
,
Mathew K. Marsee
4  Indiana University School of Medicine, South Bend Campus, Notre Dame, Indiana
,
Ross McCauley
4  Indiana University School of Medicine, South Bend Campus, Notre Dame, Indiana
,
Swetha Hanuma Chitta
5  Beacon Health Trauma Center, South Bend, Indiana
,
Sudhir Vyakaranam
6  Saint Joseph Regional Medical Center, Mishawaka, Indiana
,
Mark Walsh
4  Indiana University School of Medicine, South Bend Campus, Notre Dame, Indiana
5  Beacon Health Trauma Center, South Bend, Indiana
6  Saint Joseph Regional Medical Center, Mishawaka, Indiana
› Author Affiliations
Further Information

Publication History

Publication Date:
11 March 2020 (online)

Abstract

Traumatic brain injury (TBI) is a worldwide public health concern due to increasing mortality, affecting around 10 million patients per year. A wide variety of clinical presentations are a function of the magnitude of injury and the anatomical perturbation of the brain parenchyma, supporting structures, and cerebral vasculature, with subsequent alteration of the blood–brain barrier. These disturbances correspond with the evolution of intracerebral hemorrhage and clinical outcomes. The associated hemostatic alterations associated with TBI are caused by the disruption of the delicate balance between bleeding and thrombosis formation, which can exacerbate initial injury. TBI-associated coagulopathy is a function of a cross-talk between coagulation and inflammation, with varying influences on the immunomodulation and regulation of coagulation that occur on platelets and the endothelium of injured TBI patients. In addition to the severity of initial injury, the following factors modulate the hemocoagulative response to TBI: time from the onset of injury to treatment, age, gender, catecholamine secretion, platelet dysfunction, endotheliopathy, premorbid anticoagulation, fibrinolysis, tissue factor, and activated protein C contribution. All these entities are intertwined and influence the pathologic evolution of TBI. These factors have implications for therapeutic options such as the choice of blood components for transfusion and hemostatic agents such as tranexamic acid. Monitoring hemostatic changes of TBI patients requires an understanding of these interactions between immunology and coagulation, which can be discerned by point-of-care viscoelastic testing with specific limitations. This review considers the implications of these interrelated influences on the evaluation of coagulopathy in TBI.