Trauma-Induced Coagulopathy and Massive Bleeding: Current Hemostatic Concepts and Treatment Strategies

Abstract

Hemorrhage after trauma remains a significant cause of preventable death. Trauma-induced coagulopathy (TIC) at the time of hospital admission is associated with an impaired outcome. Rather than a universal phenotype, TIC represents a complex hemostatic disorder, and standard coagulation tests are not designed to adequately reflect the complexity of TIC. Viscoelastic testing (VET) has gained increasing interest for the characterization of TIC because it provides a more comprehensive depiction of the coagulation process. Thus, VET has been established as a point-of-care-available hemostatic monitoring tool in many trauma centers. Damage-control resuscitation and early administration of tranexamic acid provide the basis for treating TIC. To improve survival, ratio-driven massive transfusion protocols favoring early and high-dose plasma transfusion have been implemented in many trauma centers around the world. Although plasma contains all coagulation factors and inhibitors, only high-volume plasma transfusion allows for adequate substitution of lacking coagulation proteins. However, high-volume plasma transfusion has been associated with several relevant risks. In some European trauma facilities, a more individualized hemostatic therapy concept has been implemented. The hemostatic profile of the bleeding patient is evaluated by VET. Subsequently, goal-directed hemostatic therapy is primarily based on coagulation factor concentrates such as fibrinogen concentrate or prothrombin complex concentrate. However, a clear difference in survival benefit between these two treatment strategies has not yet been shown. This concise review aims to summarize current evidence for different diagnostic and therapeutic strategies in patients with TIC.

Evolving concepts and strategies in the management of polytrauma patients

“…Viscoelastic testing (VET) such as ROTEM and TEG, a monitoring tool in many trauma centers helps in the comprehensive depiction of the coagulation process. 49 The aim of DCR should minimize any resuscitation-induced coagulopathy and correction of any existing coagulopathy. The key elements of DCR include control of hemorrhage, permissive hypotension, hemostatic resuscitation, prevention/correction of acidosis, hypothermia, and correction of hypocalcemia.…”

“…48,50 In some European trauma facilities, the use of various agents like fibrinogen concentrate or prothrombin complex concentrate as part of hemostatic management has been advocated. 49…”

Effect of Goal-Directed Crystalloid versus Colloid Administration on Perioperative Hemostasis in Partial Hepatectomy: A Randomized, Controlled Trial

“…Impaired fibrin polymerization has been identified as the most prominent contributor to hemostatic derangement following the use of HES [ 16 ]. Among a number of other disadvantages when used in the perioperative setting, conventional coagulation tests, such as prothrombin time (PT), activated partial thromboplastin time (aPTT), and fibrinogen levels fail to sufficiently detect impaired fibrin polymerization [ 17 ]. In contrast, viscoelastic coagulation test methods, such as rotational thromboelastometry (ROTEM), allow the detection of impaired fibrin polymerization.…”

Hemostatic Balance in Severe Trauma

“…Hypoperfusion and hypoxia promote platelet and endothelial dysfunction that further trigger activation of protein C and impaired thrombin generation, as well as major changes in the fibrinolytic pathway (6). In addition, defects in collagen deposition related to endothelial dysfunction, downregulated platelet glycoprotein receptors, and complement activation are all thought to be contributors to Trauma Induced Coagulopathy (TIC) (7). In a prospective trial in pediatric trauma patients with an age of >15 years, the probability of life-threatening coagulopathy was low with minor to moderate injury, but coagulopathy was present in almost all patients with an injury severity score >25, hypotension, hypothermia, and acidosis (8).…”