Practical Understanding of Hemostasis and Approach to the Bleeding Patient in the Operating Room

Coagulation and inflammation are biologic damage response systems activated and amplified following tissue injury. Although they were once thought to be separate and distinct processes, we now know that they are intrinsically linked and interactive systems.[1] Bleeding, thrombosis and maladaptive inflammatory responses are major causes of perioperative morbidity and mortality for trauma and “non-trauma” patients.[2-4] Thus, coagulation and inflammation warrant serious consideration by all who care for surgical patients. New information regarding care of the bleeding trauma patient have led us to revisit our core concepts of caring for other patients with massive bleeding as well. In this article we will briefly review the different models of coagulation, discuss management of the acute coagulopathy associated with severe trauma and relate that to the care of other bleeding patients. Classical coagulation cascade Observation leading to discovery Astute physicians, noting unusual bleeding tendencies in their patients, in collaboration with brilliant scientists deduced the proteolytic activation of zymogens in plasma leading to fibrin formation. This “Waterfall/Cascade” described more than fifty years ago, has been the basis for testing and monitoring anticoagulant effects of various medications for decades.[5] (Figure 1) Figure 1 Waterfall cascade, the classical description of coagulation Beyond the “Waterfall/Cascade” Although the intrinsic and extrinsic pathways seem somewhat complex, they were never thought to be the full explanation of human hemostasis. This classical model addresses plasma and the factors within it. It does not include considerations of the dynamic cellular processes that are now known to play major roles in procoagulant and anticoagulant physiology. The newer “cellular model” takes some of these into consideration. Thrombus formation within this model is typically divided into three overlapping phases: initiation, amplification and propagation. (Figure 2) Figure 2 Cellular model of coagulation Regulation In its normal state, blood within the circulatory system remains in a liquid state, freely flowing throughout the body. Excessive and uninhibited procoagulant and inflammatory processes with concomitant lack of tissue perfusion lead to multi-organ failure (MOF) and death. Thrombosis and inflammation must be localized to the site of injury, thus the processes are regulated in several ways. Localization occurs primarily by endothelial processes, flow dilution of factors and active fibrinolysis. Inhibitory processes within the coagulation system play major roles in regulation of thrombosis. (Table 1)[6] Table 1 Effects of the main natural anticoagulant proteins on the coagulation cascade Endothelial roles in regulation The endothelium has been found to be intrinsically involved in regulation of coagulation in many ways. The endothelium first comes into play with vasoconstriction as an initial defense against blood loss. Endothelium is known to express antithrombin, thrombomodulin, tissue factor pathway inhibitor (TFPI), and tissue factor among other roles. (List 1)[7, 8] List 1 Examples of endothelial interactions with coagulation Importance of the endothelial glycocalyx The endothelial glycocalyx is now known to be extremely important in both localizing thrombosis and preventing inappropriate thrombosis, in preventing tissue edema, and in modulating immune activation. If this luminal anticoagulant covering is damaged, endothelial activation of coagulation and inflammation occur. This is considered one of the important mechanisms of MOF from trauma at distant sites.[9-11]