Loss of clotting factors caused by bleeding and consumption in thrombosis, dilution of clotting factors for massive transfusion, and effects of acidosis and hypothermia on coagulation function are considered the main mechanism for coagulopathy in trauma patients in the early phase. This coagulation disorder is described as systemic acquired coagulopathy (SAC) [10]. Recent studies found that the exact mechanism may be not like that. Brohi and MacLeod et al. found that 25 % of patients with severe trauma developed acute traumatic coagulopathy before arriving at emergency room. These patients always did not present with acidosis and hypothermia. Acute coagulopathy could only be detected in trauma patients with tissue hypoperfusion and those with inadequate fluid resuscitation [6, 7]. This coagulopathy after trauma in early stages is also called endogenous acute coagulopathy (EAC) or ACoTS. Tissue damage and post-traumatic hypoperfusion are the necessary prerequisites for early ACoTS.

Further studies showed that low level of activated protein C led by tissue damage and systemic hypoperfusion in patients with traumatic shock was the main pathogenesis of early ACoTS [11]. Thrombin combined thrombomodulin (TM) on the endothelial cell surface activates protein C (APC) anticoagulation pathway. APC plays a role of anticoagulation by inactivating factor Va and VIIIa irreversibly. In vivo, endothelial protein C receptor (EPCR) could activate protein C by thrombin-TM complex, which amplified its anticoagulant effect tenfold [12].

Hyperfibrinolysis is very common after trauma due to tissue injury and shock. Protein C could develop its anticoagulant ability by activating and consumption of plasminogen activator inhibitor (PAI)-1. Which is leading to low levels of PAI-1 and the increased release of tPA from the vessel wall, and finally resulting in hyperfibrinolysis [13]. Brohi and his colleagues examined 208 trauma patients and found that coagulation was activated and thrombin generation was related to injury severity, but acidosis did not affect Factor VII or prothrombin fragments 1 + 2 levels [14].

The initial purpose of fibrinolysis may be to limit the infinite expansion of blood clots in damaged vessels. However, early clot in patients with traumatic shock always misses its physiological role. Instead, there happens the severe imbalance of coagulation and fibrinolysis.

Platelet dysfunction in the early stage after trauma remains obscure. Although the complete blood count with difference provides a platelet count, Swallow pointed that this quantitative test does not provide an assessment of platelet function [15]. Wohlauer and his colleagues reported in a study with 51 trauma patients that there were significant differences in the platelet response between trauma patients and healthy volunteers. In trauma patients, the median ADP inhibition of platelet function was 86.1 % compared with 4.2 % in healthy volunteers. The impairment of platelet function in response to arachidonic acid was 44.9 % compared with 0.5 % in volunteers [16].

Complement plays a central role in the innate immune system and is always activated in the early phase of trauma [17]. It has been reviewed that there is a significant amount of crosstalk between the complement and coagulation systems [18]. Katharina and his colleagues found that mannose-binding lectin-associated serine protease-1 (MASP-1) interacted with plasma clot formation on different levels and influenced fibrin structure. Although MASP-1-induced fibrin formation was thrombin-dependent, MASP-1 directly activated prothrombin, FXIII and TAFI. And they suggested that MASP-1, in concerted action with other complement and coagulation proteins, may play a role in fibrin clot formation [19]. On the other hand, coagulation proteases can activate the complement system. For example, thrombin, FXa, FIXa, and FXIa, can cleave the central complement components C3 and C5 into their bioactive fragments [20]. Expression of TM and activation of protein C seems to be complement-dependent in ischemia-reperfusion injury, which indicates that there may be a certain link between complement activation and ACoTS in the early stage of severe trauma.

In the late phase of trauma and traumatic shock , coagulopathy is caused by excessive consumption and dilution of coagulation factors due to bleeding and massive fluid resuscitation. Lack of clotting factors and platelets secondary to transfusion of blood and its components contributes to the development of ACoTS as well. Appropriate use of blood products in trauma patients can improve the coagulation function.

Fluid resuscitation for trauma shock based on blood products went through three stages: whole blood recovery before the 1970s, the strategy of blood component transfusion later, and currently the fluid resuscitation strategy based on plasma. The strategy of blood transfusion has been a controversial topic for a long time. The core problem is the ratio of FFP and RBC. Borgman and colleagues [21] found that the mortality of trauma patients who receiving massive transfusion with FFP: RBC = 1:1.4 was significantly lower than that with FFP: RBC = 1:2.5 or 1:8 group. Some scholars also believe that FFP: RBC = 1:2 can replenish clotting factors and improve the coagulation function in trauma shock [22].

Hypothermia worsens coagulopathy. The most significant effect is extending the coagulation cascade, which finally leads to bleeding. Hypothermia usually accompany with dissolved dysfunction of platelet and fibrin. Gregory and colleagues reported that 57 % of trauma patients got hypothermia after trauma, and body heat loss in emergency room is more severe. Large input of cryogenic liquids is the main cause of hypothermia [23]. Frank and colleagues [24] showed that body temperature less than 33 °C produced a significant coagulopathy that was functionally equivalent to factor deficiency states, which presented when clotting factor concentration was less than 50 %. Resuscitation with cold blood and fluids creates a vicious cycle of worsening haemodilution, acidosis, hypothermia and coagulopathy.