Exposure to traumatic events among youth is relatively common. Almost all youth experience initial distress as a reaction to such events, but for most, natural resilience causes the distress to gradually subside. However, a substantial minority continue to experience distress in the months after trauma exposure. The Cognitive Behavioral Intervention for Trauma in Schools (CBITS) program is designed for use with groups of students who have experienced significant traumatic experiences and are suffering from related emotional or behavioral problems, particularly symptoms of post-traumatic stress disorder. Delivered by school-based clinicians and taking into account cultural context, it uses a variety of proven cognitive behavioral techniques in an early intervention approach, including psychoeducation about trauma and its consequences, relaxation training, learning to monitor stress or anxiety levels, recognizing maladaptive thinking, challenging unhelpful thoughts, social problem-solving, creating a trauma narrative and processing the traumatic event, and facing trauma-related anxieties rather than avoiding them. CBITS focuses primarily on three goals: decreasing current symptoms related to trauma exposure, building skills for handling stress and anxiety, and building peer and caregiver support.
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These standards detail the principles regarding resources, performance improvement patient safety processes, data collection, protocols, research, and education for a trauma center. The VRC program evaluates the care, aligned to the standards and expected scope of practice at each institution.
Hemorrhage is the most important contributing factor of acute-phase mortality in trauma patients. Previously, traumatologists and investigators identified iatrogenic and resuscitation-associated causes of coagulopathic bleeding after traumatic injury, including hypothermia, metabolic acidosis, and dilutional coagulopathy that were recognized as primary drivers of bleeding after trauma. However, the last 10 years has seen a widespread paradigm shift in the resuscitation of critically injured patients, and there has been a dramatic evolution in our understanding of trauma-induced coagulopathy. Although there is no consensus regarding a definition or an approach to the classification and naming of trauma-associated coagulation impairment, trauma itself and/or traumatic shock-induced endogenous coagulopathy are both referred to as acute traumatic coagulopathy (ATC), and multifactorial trauma-associated coagulation impairment, including ATC and resuscitation-associated coagulopathy is recognized as trauma-induced coagulopathy. Understanding the pathophysiology of trauma-induced coagulopathy is vitally important, especially with respect to the critical issue of establishing therapeutic strategies for the management of patients with severe trauma.
Regarding the management of patients requiring massive transfusion, it has been repeatedly suggested that patients are more likely to die from intraoperative metabolic failure than from the failure to complete organ repairs [7, 8]. Coagulopathy is one of the most preventable causes of death in trauma and has been implicated as the cause of almost half of hemorrhagic deaths in trauma patients [8, 9].
Coagulopathy in the acute phase of trauma patients consists of two core components: (1) trauma itself and/or traumatic shock-induced endogenous ATC and (2) resuscitation-associated coagulopathy [20] (Fig. 1).
Time phase of two components of trauma-induced coagulopathy following injury: acute traumatic coagulopathy (ATC) and resuscitation-associated coagulopathy. Endogenous ATC caused by trauma itself and traumatic shock presents immediately after injury and continue during resuscitation phase. Resuscitation-associated coagulopathy, involving hypothermia, metabolic acidosis, and dilutional coagulopathy, aggravates the ATC accompanied with therapeutic resuscitation and continue to post-resuscitation phase
Although no consensus has been reached regarding a definition and there are different approaches to the classification and naming of trauma-associated coagulation impairment, in this manuscript, we define ATC as trauma itself (directly trauma-induced) and/or traumatic shock-induced endogenous ATC and trauma-induced coagulopathy as multifactorial trauma-associated coagulation impairment, including ATC and resuscitation-associated coagulopathy associated with hypothermia, metabolic acidosis, and dilutional coagulopathy [11, 18]. Gando and Hayakawa summarized the important components of trauma-induced coagulopathy, consisting of endogenously (trauma- and traumatic shock-induced) primary pathologies and exogenous secondary pathologies (Table 1) [21].
Cap and Hunt classified trauma-associated coagulopathies into three phases [11]. The first phase is immediate activation of multiple hemostatic pathways, with increased fibrinolysis, in association with tissue injury and/or tissue hypoperfusion. The second phase involves therapy-related factors during resuscitation. The third, post-resuscitation, phase is an acute-phase response leading to a prothrombotic state predisposing to venous thromboembolism.
Of these three phases, the first phase corresponds to ATC, and the clinical features of the first phase along with the pathophysiologic factors of the second phase provide the characteristics of trauma-induced coagulopathy (Fig. 2) [22]. Recently, the clinical features and pathophysiology of trauma-induced coagulopathy have been recognized as the comprehensive condition of ATC involving resuscitation-associated coagulopathy, a systemic inflammatory response to tissue injury, and predisposing factors [23]. Currently recommended management lists for the first and second phases based on The European guideline on management of major bleeding and coagulopathy are summarized as Table 2 [24]. It is also recommended that early mechanical thromboprophylaxis with intermittent pneumatic compression or anti-embolic stockings followed by pharmacological thromboprophylaxis within 24 h after bleeding has been controlled [24].
Trauma-induced coagulopathy and acute traumatic coagulopathy (ATC). Trauma itself and/or traumatic shock-induced endogenous ATC are referred to as ATC, and multifactorial trauma-associated coagulation impairment, including ATC and resuscitation-associated coagulopathy involving hypothermia, metabolic acidosis, and dilutional coagulopathy, is termed trauma-induced coagulopathy
Although the pathophysiology of coagulation impairment in the acute phase of trauma has not yet been elucidated, ATC plays a pivotal role. It has been repeatedly demonstrated that ATC is a frequent complication in patients with severe trauma [9, 10, 13, 25].
Coagulopathy in trauma patients is associated with higher transfusion requirements, longer intensive care unit and hospital stays, prolonged mechanical ventilation support, and a greater incidence of multiple organ dysfunction. Compared with patients without coagulopathy, those with coagulopathy have a three- to fourfold greater mortality and up to eight times higher mortality within the initial 24 h of injury [9, 10, 31, 32].
It has been argued that activated protein C plays a central role in the mechanism of ATC. In initial observations in trauma patients with systemic hypoperfusion, defined by an elevated base deficit, a correlation was found between ATC and increased levels of activated protein C, reduced levels of protein C, and elevated soluble thrombomodulin [31]. The activation of the thrombomodulin-protein C system has been suggested as a principle pathway mediating ATC, characterized as hyperfibrinolysis and a hypocoagulable state, and this proposed mechanism is distinct from clotting factor consumption or dysfunction [31, 33].
Sustained tissue hypoperfusion is associated with elevated levels of soluble thrombomodulin secondary to endothelial damage, which can increase the availability of thrombomodulin to bound thrombin [31]. As a result of complex formation with thrombomodulin, the role of thrombin can be diverted from procoagulant to anticoagulant by excess activation of protein C [31, 38]. This hypothetical condition has been named acute coagulopathy of trauma-shock (ACOTS) [39, 40]. Although the precise pathophysiology remains to be elucidated, these mechanisms may lead to the hyperfibrinolytic state in patients with ATC, which is reflected in increased tissue plasminogen activator (t-PA), decreased PAI, and increased d-dimer levels [31, 33].
The Scientific and Standardization Committee on DIC of ISTH commented on two concepts regarding the hemostatic changes occurring early after trauma: DIC with the fibrinolytic phenotype and coagulopathy of trauma (COT) and ACOTS. Although there are differences between these two conditions and more information is needed to elucidate the pathogenesis of these entities, it has been suggested that COT/ACOTS is not a new concept but a disease entity similar to or the same as DIC with the fibrinolytic phenotype [49].
DIC is defined as a clinicopathologic syndrome characterized by widespread activation of coagulation resulting in intravascular formation of fibrin and thrombotic occlusion of vessels [50, 51]. Almost all severely traumatized patients, especially those with ATC, are diagnosed as having DIC according to the scoring systems of the ISTH and Japanese Association for Acute Medicine [48, 52, 53]. However, no anatomopathologic evidence, e.g., intravascular formation of fibrin and thrombotic occlusion of vessels, has been demonstrated, and consumption coagulopathy leading to platelet and coagulation factor deficiency is not a common finding in patients with ATC [27].
Thrombin is a central molecule in hemostasis. Thrombin generation converts fibrinogen to fibrin, resulting in fibrin strand formation, and activates platelets, leukocytes, and endothelium. However, thrombin also stimulates the production of t-PA from the endothelium, an effect previously known as secondary fibrinolysis. Stimulation of t-PA release from the endothelium by other factors such as hypoxia, adrenaline, and vasopressin is known as primary fibrinolysis [11]. Traumatic shock-induced tissue hypoperfusion has also been demonstrated to promote the production of t-PA from the endothelium, and increased t-PA levels have been reported in coagulopathic trauma patients [42, 56]. 2ff7e9595c
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