PHYSIOLOGICAL PREREQUISITES FOR HAEMOSTATIC RESUSCITATION IN CASE OF MASSIVE BLEEDING. PART 2

Abstract

Massive bleeding (MB) remains the major preventable cause of death both during elective and urgent surgical procedures, and both during the trauma in civilian settings and combat injuries. Modern MB treatment principles include rapid haemostatic resuscitation due to prompt transfusion of oxygen-carrying red blood cells (RBC), and coagulation factors, which diminish during the formation of blood clots. Haemostatic resuscitation of MB does not involve the transfusion of either colloid or crystalloid solutions, which have been part of the infusion-transfusion therapy algorithms for haemorrhagic shock for many decades. The habit of starting infusiontransfusion therapy with colloid and crystalloid solutions was based on the false idea that it is better to allow to flow out the diluted blood and then, after surgically stopping the bleeding, restore the deficiency of erythrocytes/haemoglobin, as well as coagulation factors. Over the past two decades, it has been established that such a notion is false primarily because the dilution of blood with both colloids and crystalloids leads to clinically significant coagulation disorders. One of the leading mechanisms of coagulation disorders during blood dilution is that when the haematocrit drops below 0.3, erythrocytes lose their ability to push platelets to the walls of small vessels and the loss of platelets increases significantly. In addition, early infusion of colloids and crystalloids can considerably increase blood pressure (BP), promoting the washout of primary thrombi from damaged vessels. Finally, most crystalloid solutions have a higher chlorine concentration and lower pH than blood plasma, which can further impair coagulation. As a result of these mechanisms, reliable haemostasis can be achieved later, the volume of blood loss increases significantly, and the volume of blood transfusions, which is required to compensate for the increased blood loss, also increases significantly. Therefore, in this work, we provide pathophysiological justifications for the potential harm from the early massive infusion of both colloid and crystalloid solutions, as well as the potential benefit from the early use of red blood cells (RBCs) as a key component of haemostatic resuscitation in MB. In particular, we present the physiological aspects of the oxygen transport function of blood and carbon dioxide transport, the participation of erythrocytes in the coagulation cascade and their volemic function. All these physiological justifications convincingly prove the need for transfusion of erythrocytes and fresh frozen plasma in the case of MB, and not a replacement of lost blood with solutions of colloids or crystalloids. In addition, we focus attention on the limited supply of coagulation factors and platelets in the human body, which should strengthen the reader's conviction about the need for transfusion in MB of fresh frozen plasma and other products that contain coagulation factors. Another pathophysiologically justified method of reducing the intensity of bleeding is permissive hypotension, which we have already mentioned in our previous publication. In it, we also outlined the principles of transfusion and infusion therapy for massive unexpected intraoperative blood loss. In a future publication, we plan to outline the role of coagulation factors and platelets as essential components of haemostatic resuscitation and consider the role of warm whole blood in conditions of deficiency or absence of these key components.