Optimizing transfusion strategies in damage control resuscitation: current insights

Abstract

From clinical and laboratory studies of specific coagulation defects induced by injury, damage control resuscitation (DCR) emerged as the most effective management strategy for hemorrhagic shock. DCR of the trauma patient who has sustained massive blood loss consists of 1) hemorrhage control; 2) permissive hypotension; and 3) the prevention and correction of trauma-induced coagulopathies, referred to collectively here as acute coagulopathy of trauma (ACOT). Trauma patients with ACOT have higher transfusion requirements, may eventually require massive transfusion, and are at higher risk of exsanguinating. Distinct impairments in the hemostatic system associated with trauma include acquired quantitative and qualitative platelet defects, hypocoagulable and hypercoagulable states, and dysregulation of the fibrinolytic system giving rise to hyperfibrinolysis or a phenomenon referred to as fibrinolytic shutdown. Furthermore, ACOT is a component of a systemic host defense dysregulation syndrome that bears several phenotypic features comparable with other acute systemic physiological insults such as sepsis, myocardial infarction, and postcardiac arrest syndrome. Progress in the science of resuscitation has been continuing at an accelerated rate, and clinicians who manage catastrophic blood loss may be incompletely informed of important advances that pertain to DCR. Therefore, we review recent findings that further characterize the pathophysiology of ACOT and describe the application of this new information to optimization of resuscitation strategies for the patient in hemorrhagic shock.

Damage control resuscitation in children

“…However, such strengths of whole blood are offset by the short storage period of 21 days, leading to frequent use of fractionated blood products 25) . ACOT, also known as trauma-induced coagulopathy, is a collective term encompassing a wide range of systemic host defense dysregulation syndromes, manifesting various defects in hemostatic process 28) . This entity is aggravated by hypothermia, acidosis, dilution of coagulation factors, and fibrinolysis 29) .…”

“…This entity is aggravated by hypothermia, acidosis, dilution of coagulation factors, and fibrinolysis 29) . ACOT occurs in up to 25% at presentation, and increases mortality 4-fold 28) . A recent rat study using thromboelastography shows that induced hemorrhage was associated with significant increases in the time intervals to thrombin generation, without changes in the other time intervals to clot formation, fibrin cross-link, PLT aggregation, and fibrinolysis 30) .…”

Surgery in Traumatic Injury and Perioperative Considerations

“…Damage control resuscitation is a term used to describe the overarching management strategy used by trauma teams to treat life-threatening hemorrhage after injury. 18 There are two main parts: (1) DCS, which involves the direct localization (and control) of sites of bleeding with surgical or radiological techniques, and (2) hemostatic resuscitation, in which RBC and blood components are administered immediately in high ratio (i.e., a "balanced transfusion" given initially as an empiric ratio and subsequently given according to clotting tests) with the avoidance of crystalloid 19,20 while maintaining a lower than normal blood pressure (permissive hypotension). 21,22 (Notably, permissive hypotension should not be used for patients with traumatic brain injury.)…”

Transfusion strategies for major haemorrhage in trauma

“…Damage control resuscitation is a key management strategy employed by trauma teams to manage significant haemorrhage after injury. It is defined by rapid surgical or radiological haemorrhage control with an empiric and balanced resuscitation of blood and blood components in high ratios and avoidance of crystalloids (Naumann et al , ; Pohlman et al , ). The premise of this haemostatic strategy is to prevent the coagulopathy caused by resuscitation, although it may have a limited effect on reversal of traumatic coagulopathy during active bleeding (Khan et al , ).…”