الفهرس 
Normal haemostasisOnly 14 pages are availabe for public view
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Abstract
Trauma remains a leading cause of death and permanent disability in adults despite advances in systematic approaches including prevention, resuscitation, surgical management, and critical care.
Bleeding accounts for 30–40% of all trauma-related deaths and typically occurs within hours after injury. Although the mortality of trauma patients requiring massive transfusion exceeds 50%, at least 10% of deaths after traumatic injury are potentially preventable, and 15% of those are due to hemorrhage; many of these deaths occur within the first few hours of definitive care, with coagulopathy playing a crucial role.
Previous landmark studies identified iatrogenic and resuscitation-associated causes of coagulopathic bleeding after traumatic injury, of which hypothermia, metabolic acidosis, and dilutional coagulopathy were recognized as primary drivers of bleeding after trauma. However, endogenous acute coagulopathy, which occurs within minutes following injury, before and independent of iatrogenic factors, is clearly recognized and accepted as the primary cause of perturbed coagulation after injury.
Hemorrhage is the most common preventable cause of death after trauma. Many of these deaths occur within the first few hours of definitive care, with coagulopathy playing a major role. A widespread paradigm shift in the resuscitation of critically injured patients with hemorrhagic shock has changed the management of severe trauma from a definitive surgical approach to damage control surgery during the past two decades. Rewarming efforts, early correction of acidosis, and aggressive crystalloid resuscitation in patients requiring damage control surgery have been the prime tenets of a trauma resuscitation strategy. This focus on early correction of physiologic abnormalities has prompted the era of damage control surgery. However, improvement of clinical outcomes in patients requiring damage control surgery, even accompanied by aggressive correction of physiologic derangements, is still insufficient.
Cap and Hunt classified trauma-associated coagulopathies into three phases. 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.
Routine coagulation tests (RCoT), namely, PT and PTT have been traditionally used to assess coagulation. A value of international normalized ratio (INR) > 1.2 is regarded as the clinically significant threshold for defining ATC. Plasma based assays, like PT and PTT, have many limitations as they have limited utility in monitoring coagulopathy or in guiding transfusion therapy in trauma.
Viscoelastic hemostatic assays (VHA) assess the whole blood components of coagulation including platelet function. The common VHAs in practice are thromboelastography, thromboelastometry and platelet function analysis.
There are two main lacunae identified with respect to the use of VHAs in clinical practice. Firstly, there is no universally accepted definition of clinical coagulopathy defined by thromboelastography or thromboelastometry (TEM) and there is a need to standardize the methods. Secondly, their value in predicting coagulopathy in the patients who are on antiplatelet therapy is not known.
Recognizing a patient in extremis may seem straightforward; however, with the use of specific triggers for Damage Control Resuscitation (DCR), the art of early identification becomes more scientific.
The two strongest predictors for MT in the first 6 hours were INR >1.5 and Base Deficit ≤ 6 of note, viscoelastic coagulation tests were not used in this analysis yielding limitations. Notably, thromboelastometry parameters have similar predictability.
Other strong predictors included systolic arterial pressure < 90 mm Hg, haemoglobin < 11 g dL -1, and positive Focused Assessment with Sonography in Trauma exam (FAST). The weaker predictors included heart rate > 120 bpm and penetrating injury. When combined into a massive transfusion score (MTS), a linear relationship is seen for massive transfusion. This method of identification is both sensitive (MTS > 2, 85% sensitivity of MT in 24 h) and has a high negative prediction value (MTS < 2, NPV 89% not receiving MT).
Another, more recent concept being used in damage control situations and massive transfusion protocols is goal-directed resuscitation using viscoelastic measurements to guide component therapy. These protocols take advantage of the rapidly available data to modify component therapy for individual clotting abnormalities. Massive transfusion often begins with predefined ratios of blood components, whereas goal-directed component therapy replaces predefined ratios as soon as possible. No standardized treatment algorithm exists, but many institutions have developed their own. Alternative products, such as lyophilized plasma, TXA, PCC, FC, and possibly recombinant activated factor VIIa (rFVIIa), should also be considered to avoid delays in product availability and complications associated with increasing plasma and platelet fractions.