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Chinese expert consensus on diagnosis and treatment of trauma-induced hypercoagulopathy


Trauma-induced coagulopathy (TIC) is caused by post-traumatic tissue injury and manifests as hypercoagulability that leads to thromboembolism or hypocoagulability that leads to uncontrollable massive hemorrhage. Previous studies on TIC have mainly focused on hemorrhagic coagulopathy caused by the hypocoagulable phenotype of TIC, while recent studies have found that trauma-induced hypercoagulopathy can occur in as many as 22.2–85.1% of trauma patients, in whom it can increase the risk of thrombotic events and mortality by 2- to 4-fold. Therefore, the Chinese People’s Liberation Army Professional Committee of Critical Care Medicine and the Chinese Society of Thrombosis, Hemostasis and Critical Care, Chinese Medicine Education Association jointly formulated this Chinese Expert Consensus comprising 15 recommendations for the definition, pathophysiological mechanism, assessment, prevention, and treatment of trauma-induced hypercoagulopathy.


Trauma causes at least 5.8 million deaths every year in the whole world, which account for 9% of annual deaths [1]. Trauma-induced coagulopathy (TIC) is an independent risk factor for poor prognosis of trauma patients [2, 3]. According to the recommendation of the International Society on Thrombosis and Hemostasis, TIC is defined as coagulation dysfunction caused by post-traumatic tissue injury, and manifests as hypercoagulability that leads to thromboembolism or hypocoagulability that leads to uncontrollable massive hemorrhage [4]. Previous studies have mainly focused on hemorrhagic coagulopathy and uncontrolled bleeding caused by the hypocoagulable phenotype of TIC [5], while it has recently been shown that the incidence of trauma-induced hypercoagulopathy can reach 22.2–85.1% in trauma patients, increasing thrombotic events and mortality by 2–4 times [3, 6, 7]. Therefore, the People’s Liberation Army Professional Committee of Critical Care Medicine and the Chinese Society of Thrombosis, Hemostasis and Critical Care formed a committee of experts, who met initially in November 2020 and eventually reached a consensus concerning the definition, pathophysiological mechanism, assessment, prevention, and treatment of trauma-induced hypercoagulopathy. The consensus includes 15 recommendations, which may help guide relevant clinical research and practice.


Recommendation 1: trauma-induced hypercoagulopathy is a coagulation disorder caused by post-traumatic tissue injury, and it manifests as pathological hypercoagulability causing a prothrombotic condition or thromboembolism

Rapid blood coagulation was first described in 1772, while the association of blood loss with hypercoagulability was first reported in 1955. In 1964, Innes et al. [8] monitored serial changes in coagulation and fibrinolysis among 42 trauma patients after admission, and found that the clotting time was significantly shortened in the early stage of trauma. During trauma, blood enters a moderate hypercoagulable state to achieve rapid hemostasis. However, excessive blood clotting and post-traumatic imbalance of coagulation system may promote trauma-induced hypercoagulopathy [4, 9], a TIC hypercoagulable phenotype characterized by endothelial injury, excessive thrombin generation, hyperfibrinogenemia, platelet hyperactivity, anticoagulant pathways impairment and fibrinolysis shutdown [10].

Thrombotic complications such as venous thrombosis, arterial thrombosis, and microthrombosis may occur in patients with trauma-induced hypercoagulopathy, but the location of thrombus deposition depends on the blood flow turbulence, hypercoagulable state, vascular injury site, and original pathological changes such as atherosclerosis and angionoma [11]. Venous thrombosis is more common in the femoral, internal iliac, and intermuscular veins, than in the subclavian, intracranial, portal, and splenic veins [12, 13]. Particularly, venous thromboembolism (VTE) has been defined as a disease that encompasses two primary entities, deep venous thrombosis (DVT) and pulmonary embolism. In contrast, arterial thrombosis often occurs in pulmonary, intracranial, and coronary arteries, while it can sometimes be found in the aorta as well as peripheral, carotid, splenic, and mesenteric arteries [14].

Recommendation 2: the incidence of trauma-induced hypercoagulopathy depends on the patient’s sex, age, and weight, as well as the type and severity of injury

Thromboelastography (TEG) of 464 patients (23% female) with injury severity scores (ISS) > 15 showed that α angle, an index of the dynamics of clot formation, was an average of 3° larger in women than men, while maximum amplitude (MA), a measure of clot strength, was an average of 3 mm larger in women [15]. This may help explain why after trauma, women show a significantly more hypercoagulable state and lower mortality rate than men. Another study on 7194 trauma patients showed that the VTE incidence in patients younger than 13 years remained below 1.5%, but gradually increased with age: it was 2.3% for patients older than 13 years, 5.1% for patients older than 15 years, 5.5% for patients 31–35 years, and 7.6% for patients 46–50 years. However, VTE risk was lower among patients older than 50 years than among younger patients [16]. In a prospective study of 687 trauma patients to examine the relationship between obesity [body mass index (BMI) ≥ 30 kg/m2] and post-injury hypercoagulability, obese patients showed higher MA values, lower fibrinolysis [clot lysis achieved 30 min after MA (LY30%)], and higher incidence of VTE than non-obese patients [17]. A study of 72 morbidly obese patients undergoing bariatric surgery showed that the average BMI of obese patients decreased from 44.6 kg/m2 to 31.4 kg/m2 by 6 months after surgery. After surgery, patients also showed longer time to clot initiation (TEG R-time; 1.3 s on average), lower MA (2.4 mm on average), and significantly greater sensitivity to tissue-type plasminogen activator (t-PA) than before surgery [18].

Serial TEG on 95 blunt trauma patients without surgery indicated that all patients were hypercoagulable, 58% were in a state of fibrinolysis shutdown, and 50% showed resistance to t-PA [19]. Another study showed that VTE incidence among 603 patients with severe traumatic brain injury was 19.7%, and it usually occurred within 6 days after admission [20]. Serial TEG of 118 trauma patients also revealed an association between injury severity and trauma-induced hypercoagulability [6]. The number of hypercoagulable patients in that study gradually increased with increasing ISS, and the highest hypercoagulopathy incidence (38.7%) was observed among patients with ISS 6–15. However, the number of hypercoagulable patients gradually decreased with further increase of the ISS. In addition, a competing risks analysis of 2370 trauma patients showed that 11.2% developed DVT and that 38% of DVT cases occurred within 48 h after admission, implying that severe injury (ISS ≥ 15) is an independent risk factor for DVT [21].

Pathophysiological mechanism

Recommendation 3: tissue damage, inflammation and stress are the main pathophysiological mechanisms of trauma-induced hypercoagulopathy

During tissue injury, the transmembrane glycoprotein tissue factor is released in large amounts, activating extrinsic coagulation factors and platelets, in turn triggering and expanding massive thrombin generation and promoting thrombosis [22,23,24] (Fig. 1). High circulating actin and myosin released due to cell death can also promote clot propagation and fibrinolysis shutdown, reflected in low TEG LY30%, high α angle, and elevated levels of plasminogen activator inhibitor type-1 (PAI-1) [25, 26]. Moreover, uncontrolled systemic release of endogenous damage-associated molecular patterns (DAMPs) after trauma triggers inflammasomes to activate caspases, which leads in turn to the release of interleukin-1β and interleukin-18 as well as promotes pyroptosis [27]. Simultaneously, numerous inflammatory mediators activate the coagulation system and amplify coagulation disorders through the crosstalk between inflammation and coagulation [28]. At the same time, numerous inflammatory mediators activate the coagulation system and enhance coagulation disorders through crosstalk between inflammation and coagulation [28]. Trauma-induced inflammation may also stimulate a continuous increase in plasma fibrinogen levels and promote heparin resistance, contributing to clot formation [29]. Further studies have shown that sympathetic hyperactivity and catecholamine release induced by traumatic stress promote endotheliopathy [30]. TF released after endothelial damage can activate the coagulation pathway, increase the activity of factor VII, and enhance thrombin-induced platelet aggregation, leading to hypercoagulability [31].

Fig. 1

Pathophysiological mechanism of TIC. The blue box represents hypercoagulable mechanism, and the red box represents hypocoagulable mechanism. TIC, trauma-induced coagulopathy

Recommendation 4: TIC is characterized by a phenotypic transformation between hypercoagulability and hypocoagulability

An early study showed that prothrombin time (PT) and activated partial prothrombin time (APTT) are shortened in hemorrhagic shock patients but prolonged in refractory shock patients [32]. A study of 42 injury patients based on serial coagulation and fibrinolysis assays [8] showed that clot lysis and clotting time accelerated in the first hours after trauma, after which fibrinolysis and clotting time prolonged. Although the platelet count and plasma fibrinogen levels decreased for about 3 days, they subsequently increased and remained at unusually high levels for 1 week. Further studies have confirmed that increased levels of endogenous thrombopoietin promote thrombocytosis after trauma [33, 34].

Trauma patients with low ISS may develop hypercoagulability to facilitate hemostasis and rehabilitation. However, if venous, arterial, or microvascular thrombosis develops at the same time, the patient is considered to have trauma-induced hypercoagulopathy [3, 4]. With increasing ISS and blood loss, the proportion of hypercoagulability in trauma patients gradually decreased and the proportion of hypocoagulability increased accordingly. Hypercoagulable phenotype may transform into hypocoagulable phenotype in the patients with continuous bleeding. These patients may return to a hypercoagulable or normocoagulable state within 48 h if bleeding stops [35]. However, in the event of uncontrollable bleeding, the hypocoagulable phenotype will develop into disseminated intravascular coagulation (DIC) (Fig. 2).

Fig. 2

TIC phenotypes transformation between hypercoagulability and hypocoagulability

The pathophysiological mechanism of the hypercoagulable-to-hypocoagulable phenotype transformation is shown in Fig. 1. Tissue hypoperfusion induced by traumatic hemorrhagic shock can cause endothelial injury and glycocalyx shedding as well as activate the protein C pathway, while secondary endogenous heparinization can inhibit the activity of coagulation factors [36, 37]. Injury and swelling of vascular endothelial cells lead to the enlargement of the endothelial cell gap and the development of capillary leakage syndrome, thus exacerbating tissue hypoperfusion and coagulation disorders [30, 38]. Moreover, activated protein C released by endothelial cells can inhibit PAI-1, leading to hyperfibrinolysis; and it can inhibit factors V and VIII, leading to hypocoagulability [39]. The massive blood loss and fluid resuscitation can then induce hemodilution, acidosis, and hypothermia, which in turn lead to secondary coagulopathy [40]. The inflammatory responses induced by tissue injury and hypoperfusion lead to platelet exhaustion after the adenosine diphosphate (ADP)-induced release of massive granules [41], while hyperfibrinolysis and the consumption of coagulation factors promote hypofibrinogenemia, thus contributing to coagulation dysfunction and increasing risk of mortality in trauma patients [42].


Recommendation 5: routine coagulation tests are recommended for screening patients for trauma-induced hypercoagulopathy

Routine coagulation tests include: 1) assessment of the exogenous coagulation system based on measurement of PT or the International Standardized Ratio (INR); 2) assessment of the endogenous coagulation system based on measurement of APTT; 3) assessment of the common coagulation pathways based on measurement of thrombin time (TT) and fibrinogen levels; 4) assessment of the fibrinolytic system based on assays of D-dimers (DD) and fibrinogen (or fibrin) degradation products (FDPs); and 5) estimation of the platelet count. Previous studies have recommended that patients whose PT > 18 s, INR > 1.5, APTT >60s, or TT > 15 s can be diagnosed as hypocoagulable phenotype of TIC without the influence of anticoagulant drugs or abnormal blood specimens [43]. In contrast, no diagnostic criteria have yet been reported for the hypercoagulable phenotype of TIC based on routine coagulation tests; this reflects the insensitivity of the conventional coagulation indexes to hypercoagulability [44, 45]. However, these tests can still indicate trauma-induced hypercoagulopathy. In particular, shortened APTT and PT are indicators of the coagulation factor hyperfunction, suggesting the occurrence of hypercoagulability [46]. In addition, hyperfibrinogenemia contributes to post-traumatic hypercoagulability, which is defined by a plasma fibrinogen concentration > 4.0 g/L [29, 47], while thrombocytosis contributes to post-injury hypercoagulability defined by a platelet count >400 × 109/L [48, 49]. Nevertheless, DD and FDPs levels are not efficient indicators of trauma-induced hypercoagulopathy, as they are commonly elevated during secondary fibrinolysis after post-injury thrombosis [50]. In contrast, the thrombin–antithrombin complex is a sensitive marker of thrombin formation and, combined with other indicators, it can reliably predict blood hypercoagulability [51].

Recommendation 6: viscoelasticity coagulation tests are recommended for the diagnosis of trauma-induced hypercoagulopathy

Point of care assays of viscoelastic coagulation can comprehensively and accurately evaluate the coagulation state by taking whole blood as test sample [52,53,54]. Therefore, it is recommended that viscoelastic tests are used to evaluate the coagulation function of severe trauma patients and guide replacement therapy [5, 55]. Viscoelastic coagulation tests involve TEG@, rotation thromboelastometry (ROTEM@), and coagulation and platelet function analysis (Sonoclot@ or Centuryclot@). The main indices of TEG@ include R-time for coagulation factor activity, α angle and K-time for fibrinogen function, MA for platelet function and LY30% for fibrinolytic function. The hypercoagulability may be implied by shortened R-time for coagulation factors hyperfunction, increased α - angle and shortened K-time for fibrinogen hyperfunction, increased MA for platelet hyperfunction and LY30% < 0.8% for fibrinolysis shutdown. The main indicators of Sonoclot@ or Centuryclot@ include activated clotting time (ACT) for coagulation factor function, clot rate (CR) for fibrinogen function and PF for platelet function. The hypercoagulability may be identified by shortened ACT for coagulation factors hyperfunction, increased CR for fibrinogen hyperfunction and increased PF for platelet hyperfunction [56].

Although 35 TEG-based criteria have been reported for the diagnosis of hypercoagulopathy, the diagnostic criteria for trauma-induced hypercoagulopathy have yet not been certified. A meta-analysis of 1893 studies on the relationship between TEG and post-injury hypercoagulability and thrombosis suggested that MA > 66.7 mm could be used as a diagnostic criterion for trauma-induced hypercoagulopathy [57]. In addition, a retrospective study of 983 trauma patients found that 582 (85.1%) patients developed hypercoagulοpathy at admission, while 99 (14.5%) of them were diagnosed with DVT by ultrasound scan. The incidence of DVT was significantly higher in trauma patients with hypercoagulopathy based on TEG than in patients without hypercoagulopathy [odds ratio (OR) 2.41, 95% confidence interval (CI) 1.11–5.24, P = 0.026] [7].

Recommendation 7: Doppler ultrasound is recommended as a routine method for detecting thrombotic complications associated with trauma-induced hypercoagulopathy

The thrombotic risk assessment scale need not be used with patients who have trauma-induced hypercoagulopathy, because the scale always classifies such patients as being at high risk [58]. Instead, thrombus examination can be performed using radiology or Doppler ultrasonography, a non-invasive and reproducible method that does not require contrast agents or patient handling [59]. Doppler ultrasonography can accurately diagnose thrombosis in deep blood vessels of the lower extremities, as well as in neck, abdominal organ, and cardiopulmonary blood vessels, making it suitable for detecting thrombotic complications in patients with trauma-induced hypercoagulopathy. If necessary, computed radiography, magnetic resonance, and digital subtraction angiography can be further used to accurately diagnose thrombosis in brain, lung, and other organs [59]. However, risks of these imaging modalities due to patient transport, injection of contrast agent, and invasive procedures should be considered in light of the patient’s condition.

Recommendation 8: thrombophilia testing is recommended for patients with recurrent post-traumatic thromboembolism

Thrombophilia is a pathological state with high thromboembolic tendency due to genetic deficiency, acquired defects or risk factors. Hereditary thrombophilia is induced by 1) deficiencies of antithrombin, protein C, or protein S; 2) deficiencies of coagulation factors manifesting as prothrombin G20210A mutation, abnormal fibrinogenemia, or activated protein C resistance; 3) fibrinolysin deficiency manifesting as hypoplasminogenemia, t-PA deficiency, and increased PAI-1 levels; 4) hyperhomocysteinemia, a defect associated with homocysteine metabolism; and 5) increased levels of coagulation factors [60]. In contrast, acquired thrombophilia can develop due to myeloproliferative tumor, antiphospholipid syndrome, paroxysmal nocturnal hemoglobinuria, nephrotic syndrome, or inflammatory bowel disease. Acquired risk factors of thrombophilia include pregnancy,surgery, long-term bed rest, oral contraceptives, hormone replacement therapy, and trauma-induced hypercoagulopathy. Trauma patients with thrombosis need not be routinely examined for hereditary thrombophilia [61]. In contrast, thrombotic events are 2–20 times more likely to occur in trauma patients with other types of thrombophilia [62], so thrombophilia testing is recommended for patients with recurrent post-traumatic thromboembolism or family history of thrombotic disease [63] (Table 1).

Table 1 Thrombophilia testing


Recommendation 9: iatrogenic factors causing thrombosis should be avoided in patients with trauma-induced hypercoagulopathy

Hemostatic drugs can reduce bleeding in trauma patients, but excessive dosage or extended drug administration may lead to acquired thrombosis. Tranexamic acid (trans-4-aminomethylcyclohexane-1-carboxylic acid; TXA) is a synthetic lysine analogue that can competitively bind to the lysine binding site of plasminogen and prevent its interaction with fibrin. In the CRASH-2 (clinical randomization of an antifibrinolytic in significant hemorrhage) trial, 20,211 trauma patients were randomly treated with TXA or placebo [64]. Specifically, patients in the TXA group (n = 10,096) received a loading dose of 1 g TXA intravenously over 10 min, followed by 1 g TXA over 8 h. Risk of all-cause death was significantly lower in the TXA group than in the placebo group (14.5% vs. 16.0%), as was death due to bleeding (4.9% vs. 5.7%), but there was no difference in the incidence of thrombotic events (1.7% vs. 2.0%). The retrospective MATTERs (military application of tranexamic acid in trauma emergency resuscitation) study demonstrated that the rate of all-cause mortality among patients who underwent emergency resuscitation in military combat was significantly lower among those who received TXA than those who did not (17.4% vs. 23.9%), but VTE incidence in the TXA group was about 10 times that in the untreated group [65]. A retrospective cohort study of 549 combat casualties admitted to US military hospitals from October 2010 to November 2012 also indicated that TXA was an independent risk factor for the development of VTE [66]. According to a retrospective analysis of 3773 military casualties, the use of TXA was not associated with mortality but did increase the risk of VTE [67]. TXA overuse can be defined as the administration of TXA to a hemodynamically stable trauma patient, while TXA underuse can be defined as failing to administer TXA, or delaying its administration, to a trauma patient who receives a massive blood transfusion. Both TXA overuse and underuse were observed in US military combat support hospitals in Afghanistan [68]. Therefore, hemostatic drugs should be used rationally in order to prevent iatrogenic thrombosis in patients with trauma-induced hypercoagulopathy.

Repeated vascular puncture and catheter implantation during trauma treatment are also independent risk factors for thrombosis, especially in pediatric trauma patients [69, 70]. However, both can cause vascular endothelial injury, activate the coagulation system, and promote thrombosis at sites of injury in blood vessels. In severe cases, pseudoaneurysm, arteriovenous fistula, intimal denudation, and even vascular rupture may occur [71]. Therefore, to reduce vascular injury, ultrasound-guided vascular puncture may be performed during invasive surgery in trauma patients [72,73,74].

Recommendation 10: mechanical prevention alone or combined with pharmacologic prophylaxis is recommended for preventing thrombosis in patients with trauma-induced hypercoagulopathy

In order to prevent deep vein thrombosis, patients with trauma -induced hypercoagulopathy should receive early rehabilitation when traumatic condition permits [75]. However, the risk of bleeding should first be assessed based on the patient’s characteristics [76], including 1) Patient factors: age ≥ 85 years old, taking oral antiplatelet drugs or anticoagulants. 2) Basic diseases: uncontrolled active bleeding, previous history of intracranial hemorrhage, peptic ulcer, recent stroke, liver and kidney dysfunction. 3) Treatment: planned surgical operation or within 12 h after operation.

For patients at high bleeding risk, mechanical prevention is recommended; for patients at low bleeding risk, mechanical prevention combined with pharmacologic prophylaxis is recommended [77]. One study on the anticoagulation timing of patients with traumatic hypercoagulability suggested that patients who had blunt solid organ injury but had not undergone surgery could initiate VTE chemoprophylaxis if TEG indicated fibrinolytic shutdown (LY30% < 0.5% at 12 h after trauma) or hypercoagulation (MA > 65.8 mm at 24 h after trauma) [19]. One study on the anticoagulation timing of patients with traumatic hypercoagulability suggested that patients who had blunt solid organ injury but had not undergone surgery could initiate VTE chemoprophylaxis if TEG indicated fibrinolytic shutdown (LY30% < 0.5% at 12 h after trauma) or hypercoagulation (MA > 65.8 mm at 24 h after trauma) [19].

Mechanical prevention, including intermittent pneumatic compression and wearing of graded static compression stockings, should be performed in patients at high risk of thrombosis, until the risk factors are eliminated [78]. Proper pressure adjustment and rigorous monitoring are required to avoid complications. Absolute contraindications to mechanical prevention of DVT include lower extremity trauma, lower extremity tissue transplantation, or major limb surgery. Incidence of DVT among trauma patients is significantly lower among those receiving pharmacologic prophylaxis (15–20%) than those not receiving it (20–50%), but craniocerebral injury and fracture are considered independent risk factors for delayed pharmacologic prophylaxis [21]. Moreover, VTE risk is 2–4 times higher in patients with intracranial hemorrhage than in patients with acute ischemic stroke [79]. In contrast, the risk of pulmonary embolism was significantly lower in patients with intracranial hemorrhage receiving low-molecular-weight heparin (LMWH) or unfractionated heparin (UFH) than in patients without pharmacologic prophylaxis in one study [4.2% vs 3.3%; Risk ratio (RR) 0.37; 95% CI 0.17–0.80; P = 0.01), but no significant effects were observed on the incidence of DVT, hematoma enlargement, or mortality [80, 81]. Moreover, anticoagulants did not aggravate the hematoma and had no significant effects on mortality or the incidence of DVT in those studies. Therefore, intermittent pneumatic compression along with pharmacologic prophylaxis should be applied to patients with intracranial hemorrhage 1) at 48 h after admission if there is no hematoma enlargement or hypocoagulability, 2) at 24 h after craniotomy, or 3) at 72 h after spinal cord injury [82].

In order to reduce the risk of bleeding, subcutaneous injection of LMWH is recommended for patients with normal renal function. The dose of LMWH can be adjusted by monitoring the anti-Xa activity in a target range of (0.2–0.5) IU/mL. In contrast, subcutaneous injection of UFH is recommended for trauma patients with renal dysfunction [83, 84]. Adjustment of the LMWH dose in trauma patients based on the differences in the TEG R-time did not affect the incidence of VTE in the intervention or control groups of one study [85], probably due to the mild condition of the selected patients. This suggests that TEG is insensitive to LMWH treatment. Moreover, among patients who underwent hip and knee arthroplasty, the incidence of DVT among those treated with fondaparinux sodium, a chemically synthesized inhibitor of the Xa factor that does not cause heparin-induced thrombocytopenia (HIT), was 50% lower than the incidence among those receiving enoxaparin, an LMWH anticoagulant (6.8% vs. 13.7%, P < 0.001) [86]. For patients at high risk of postoperative thromboembolism and bleeding, the European consensus recommends the administration of low-dose novel anticoagulants (NOACs) at 24 h after surgery [87].

Antiplatelet drugs can also prevent DVT. Weekly follow-up of 74 patients with severe trauma using ROTEM showed that 81% of the patients developed hypercoagulability at admission for 7 days due to platelet hyperfunction [88]. A retrospective analysis of 110 trauma patients showed that the incidence of DVT was significantly lower among patients who took aspirin prior to trauma than among those who did not [89]. The Pulmonary Embolism Prevention study, which enrolled 13,356 hip fracture patients randomly selected from 148 hospitals in Australia, New Zealand, South Africa, Sweden, and the United Kingdom, as well as 4088 hip replacement patients randomly selected from 22 hospitals in New Zealand, also demonstrated that the incidence of VTE in patients receiving aspirin 160 mg /day (n = 6679) was 36% lower than that in patients receiving placebo (n = 6677) [90].


Thrombosis complicated by trauma-induced hypercoagulopathy can be addressed by treating the primary disease as well as by applying anticoagulant, antiplatelet, interventional, and thrombolytic therapies. However, the site, time, and severity of thrombus formation need to be considered when planning treatment (Table 2).

Table 2 Antithrombotic treatment for different thrombotic complications of trauma -induced hypercoagulopathy

Recommendation 11: reducing stress and tissue damage are prerequisites for improving trauma-induced hypercoagulopathy

Animal experiments showed that epinephrine can accelerate blood clotting, which was confirmed in a study showing that a small epinephrine dose can shorten clotting time to 50–70% of the normal value, whereas a large dose can prolong clotting time [91]. A study of plasma epinephrine and norepinephrine levels in 34 patients undergoing cardiac surgery indicated that stressed patients (given 5 μg/kg fentanyl) had significantly higher levels of both hormones and higher activities of factor VIII and von Willebrand factor than non-stressed patients (given 50 μg/kg fentanyl) [92]. In addition, stress-induced elevated catecholamine concentrations in plasma can damage endothelial cells, activate platelets, inhibit the activity of antithrombin, aggravate inflammation, and promote hypercoagulability [26, 34]. Therefore, reducing stress is recommended to reduce vascular endothelial damage and oxygen consumption, and improve organ perfusion to alleviate hypercoagulability [93].

Recommendation 12: bleeding risk needs to be assessed before initiating anticoagulant therapy in patients with trauma-induced hypercoagulopathy

In order to prevent thrombus formation and propagation, anticoagulant therapy is required in patients with trauma-induced hypercoagulopathy. In the GARFIELD-VTE (Global Anticoagulant Registry in the Field of VTE) study between 2014 and 2017, 90.9% of 10,685 patients with VTE received anticoagulant therapy, while thrombolysis, intervention, or surgical treatment was applied to only 5.1% of patients, indicating that anticoagulants are the main treatment for thrombosis [94]. However, before trauma patients receive anticoagulant therapy, their risk of post-traumatic thrombosis and post-therapeutic bleeding should be assessed. Since active bleeding is a contraindication to anticoagulant therapy, patients with potentially life-threatening thrombosis but withoutactive hemorrhage should be treated with anticoagulants as soon as possible after trauma [95].

UFH, LMWH, fondaparinux, argatroban, and bivalirudin are well-known parenteral anticoagulants that act at different steps within the coagulation cascade. UFH is recommended as a first-line treatment due to its short half-life, easy monitoring, and neutralization by protamine. In the treatment of pulmonary embolism, the recommended initial dose of UFH for intravenous administration is 80 U/kg, followed by a maintenance dose of 18 U/ (kg·h) adjusted every 4–6 h based according to the APTT [76]. In the treatment of coronary artery embolism, a loading dose of 60 μg/kg UFH is injected intravenously (≤ 4000 U) along with antiplatelet and thrombolytic therapy, followed by a maintenance dose of 12 U/(kg·h) (≤ 1000 U/h) that is adjusted until the APTT reaches 1.5–2.5 times the control value [96]. After administration of UFH, HIT can be diagnosed based on the 4T's score or anti-HIT antibody if a significant reduction in platelet count combined with thrombosis is observed. Non-heparin anticoagulant drugs should be used instead of UFH in patients with strongly suspected or confirmed HIT. In contrast to UFH, LMWH can be injected subcutaneously at a dose in the target range of 0.6–1.0 IU/mL, adjusted based on the anti-Xa activity [97]. Monitoring the anti-Xa activity is crucial to prevent bleeding in patients with renal insufficiency or thrombocytopenia [86].

Fondaparinux is a synthetic anticoagulant that acts via antithrombin III to selectively inhibit the activity of factor Xa. Doses of 5, 7.5, and 10 mg for respective body weights of < 50, 50–100, and > 100 kg have been approved for the prophylaxis or treatment of VTE and acute coronary syndrome (ACS) [76]. However, fondaparinux cannot be used in patients with severe renal insufficiency (creatinine clearance rate < 30 mL/min), while the dose should be halved in patients with moderate renal insufficiency (creatinine clearance rate = 30–50 mL/min) [98]. Argatroban, a direct thrombin inhibitor, is metabolized in the liver and can significantly prolong thrombin time. The recommended infusion rate is 2 μg/ (kg·min), which can be adjusted until the APTT reaches 1.5–3 times the initial baseline value. However, an initial dose of 0.5–1.2 μg/(kg·min) is recommended for patients with moderate liver dysfunction or heart failure, while even lower initial doses 0.2–0.5 μg/(kg·min) are recommended for patients with multiple organ dysfunction [76, 82]. Bivalirudin is another direct thrombin inhibitor with short half-life (25–30 min) that can be administered to patients with HIT or ACS undergoing percutaneous coronary intervention. The recommended starting dose is 0.05 mg/ (kg·h) and should be adjusted depending on the APTT [98].

Oral anticoagulants include warfarin, rivaroxaban, apixaban, dabigatran, and edoxaban. Warfarin is a classic oral anticoagulation drug and a vitamin K antagonist that can completely inhibit the synthesis of coagulation factors II, VII, IX, and X after continuous administration for 4–5 days. In case of concomitant treatment of patients with parenteral anticoagulation and warfarin, the two therapies should overlap for at least 5 days to achieve a therapeutic INR for 24 h, at which time parenteral anticoagulant should be discontinued [72]. Dabigatran, rivaroxaban, apixaban, and edoxaban are also known as NOACs that have a short half life and can be rapidly absorbed. Dabigatran is a thrombin inhibitor, while rivaroxaban, apixaban, and edoxaban inhibit the activity of factor Xa. Patients treated with dabigatran or edoxaban should be pretreated with parenteral anticoagulant for up to 5–10 days. A higher dose is administered during the first 3 weeks of therapy for patients receiving rivaroxaban, but only during the first week for patients receiving apixaban [99].

Recommendation 13: the risk of bleeding needs to be assessed before initiating antiplatelet therapy in patients with trauma-induced hypercoagulopathy complicated by arterial thrombosis

Antiplatelet drugs inhibit cyclooxygenase (COX)-1, P2Y12 receptor, phosphodiesterase (PDE), or GPIIb/IIIa. This class of drugs is the first-line treatment for arterial thrombosis, but it can also increase bleeding risk in trauma patients [100]. Therefore, any antiplatelet therapy should only be planned after careful assessment of the bleeding risk in patients with trauma-induced hypercoagulopathy complicated by arterial thrombosis.

Aspirin can irreversibly inhibit the COX-1 enzyme, block the production of thromboxane, prolong the platelet production cycle, and ultimately reduce platelet aggregation. Aspirin also affects coagulation via the non-TXA2 pathway by inhibiting thrombin generation and platelet function in a dose-dependent manner and accelerating fibrinolysis [101, 102]. The plasma concentration of enteric-coated aspirin is maximal at 3–4 h after ingestion or at 30 min after chewing, and it significantly inhibits platelets within 1 h [103].

Clopidogrel and ticagrelor are the most commonly used P2Y12 receptor inhibitors. Clopidogrel, which is oxidized by the cytochrome P450 in liver enzymes, can irreversibly block the P2Y12 receptor of ADP on the platelet surface, thereby preventing activation of the ADP-mediated glycoprotein GPIIb/IIIa complex and reducing platelet aggregation. The plasma concentration of clopidogrel is maximal at 24 h with a routine dose of 75 mg, or at 4–6 h with a loading dose of 300–600 mg. Clopidogrel can also reduce platelet aggregation by 50–60%, which can return to normal within 7 days of drug withdrawal. Ticagrelor can reversibly and non-competitively bind the ADP P2Y12 receptor to reduce platelet aggregation. The platelet inhibition rate reaches 41% in 30 min and 88% in 2 h after loading of 180 mg ticagrelor, and platelet aggregation returned to normal 3–5 days after drug withdrawal. Large randomized trials support the use of ticagrelor in ACS, ischemic stroke, and peripheral vascular diseases [104]. Dual antiplatelet therapy can reduce the risk of thrombosis in patients with ACS or percutaneous coronary intervention, while aspirin is preferably combined with ticagrelor in ACS patients. In addition, clopidogrel may be used when the bleeding risk is high or the patient does not tolerate ticagrelor [105].

The most common PDE inhibitors are dipyridamole and cilostazol. Dipyridamole can inhibit the phosphodiesterase enzymes PDE-3 and PDE-5, reduce the levels of cyclic adenosine monophosphate and cyclic guanosine monophosphate, ultimately inhibiting platelet aggregation. Dipyridamole can also inhibit fibrin formation, increase extracellular adenosine levels, and cause vasodilation. The extended-release formulation of dipyridamole (200 mg) and aspirin (25 mg) is commonly used in the secondary prevention of cerebrovascular diseases [106]. Cilostazol also inhibits PDE-3 as well as platelet aggregation by reducing the expression of P-selectin. Therefore, cilostazol is mainly used to treat lower extremity arteriosclerosis and prevent stent thrombosis and stroke, while it serves as an antiplatelet therapy in case of resistance to clopidogrel [107].

The platelet–fibrinogen interaction via the GPIIb/IIIa complex is the final step in the platelet aggregation pathway. The GP IIb/IIIa inhibitors abciximab, eptifibatide and tirofiban can inhibit platelet aggregation by preventing the binding of fibrinogen to the GPIIb/IIIa complex. However, hemoglobin level and platelet count should be monitored in real time during treatment with GP IIb/IIIa inhibitors in order to closely monitor clinical bleeding.

Recommendation 14: interventional therapy is recommended for traumatic patients complicated by thrombosis who are at high risk of bleeding

Interventional therapy is recommended for patients with trauma-induced hypercoagulopathy complicated by thrombosis, especially when anticoagulation or thrombolysis is not effective, or the risk of bleeding is high. This type of treatment includes catheter-directed thrombolysis, percutaneous mechanical thrombectomy, venoplasty, stent implantation, and inferior vena cava filter placement. In general, interventional therapy requires lower thrombolytic drug dosages and treatment time than other therapeutic methods, while bleeding complications may also be reduced. Better thrombus clearance can also be achieved, as transcatheter administration can prevent drugs from bypassing the occluded venous segment through collateral branches, thus achieving a high drug concentration in the thrombus, while mechanical thrombectomy can improve the effectiveness of thrombolysis.

Primary percutaneous coronary intervention is recommended for patients with trauma-induced hypercoagulopathy complicated by myocardial infarction exhibiting ischemia symptoms for ≤12 h and persistent ST-segment elevation or progressive ischemia symptoms for > 12 h suggestive of hemodynamic instability or life-threatening arrhythmias [108]. Intravascular thrombectomy is recommended for patients with trauma-induced hypercoagulopathy complicated by ischemic stroke who have a middle cerebral artery occlusion within 6 h of onset and are not eligible for thrombolysis, who have a posterior circulation occlusion within 24 h of onset, or who exhibit contraindications to thrombolysis [109]. Inferior vena cava filter placement is preferred in patients with acute pulmonary embolism and anticoagulant contraindications to prevent DVT in lower extremities [76]. Catheter-directed thrombolysis is recommended for patients with intracranial venous thrombosis who have no intracranial hemorrhage and who do not respond to anticoagulant therapy, as well as for DVT patients whose acute iliofemoral venous thrombosis symptoms last fewer than 14 days and who are at high risk of recurrence [110, 111]. Mechanical thrombectomy is recommended for patients with intracranial venous thrombosis complicated by progressive symptoms after anticoagulation therapy, new bleeding after thrombolytic therapy, or severe intracranial hemorrhage at admission. Both catheter-directed thrombolysis and mechanical thrombectomy are also recommended for patients with severe acute pulmonary embolism who have thrombolytic contraindication or are at high risk of bleeding [110].

Recommendation 15: routine systemic thrombolysis is not recommended for patients with trauma-induced hypercoagulopathy complicated by thrombosis

Systemic thrombolysis refers to intravenous injection of thrombolytic drugs away from the target vessel and its absolute contraindications include active hemorrhage, recent skull fracture, recent brain or spinal cord surgery, ischemic stroke within 3 months of onset, intracranial structural lesions, and aortic dissection [112]. Although successful systemic thrombolysis can rapidly dissolve the thrombus and restore blood supply to tissues, it can also increase the bleeding risk. Therefore, trauma-induced hypercoagulopathy is considered another contraindication to systemic thrombolytic therapy, which can be performed without interventional therapy only in patients with trauma-induced hypercoagulopathy complicated by acute life-threatening thrombosis [96]. However, cautious risk-benefit analysis is required prior to treatment, including the risk of thrombosis-related mortality and the risk of bleeding associated with thrombolytic therapy.


Trauma-induced hypercoagulopathy is a TIC hypercoagulable phenotype induced by tissue injury, inflammation and stress, which may transform into hypocoagulable phenotype with increasing blood loss. If trauma patients are diagnosed as hypercoagulable state by viscoelastic coagulation tests, mechanical prevention alone or combined with pharmacologic prophylaxis should be planned for preventing thrombosis. If patients with trauma-induced hypercoagulopathy are complicated by thrombosis, the risk of bleeding needs to be assessed before initiating individualized antithrombotic or interventional therapy.

Availability of data and materials

Not applicable.



Acute coronary syndrome


Adenosine diphosphate


Activated protein C


Antiphospholipid antibody syndrome


Activated partial prothrombin time






Complete blood count






Disseminated intravascular coagulation


Deep venous thrombosis


Fibrinogen degradation products


Heparin-induced thrombocytopenia


International standardized ratio


Injury severity score


Janus kinase


Lupus anticoagulant


Lactate dehydrogenase


Low molecular weight heparin


Maximum amplitude


New oral anticoagulants


Plasminogen activator inhibitor type-1




Paroxysmal nocturnal hemoglobinuria


Systemic lupus erythematosus




Trauma-induced coagulopathy


Tissue-type plasminogen activator


Prothrombin time


Thrombin time


Tranexamic acid


Unfractionated heparin


Vitamin K antagonist


Venous thromboembolism


  1. 1.

    GBD 2016 Causes of Death Collaborators. Global, regional, and national age-sex specific mortality for 264 causes of death, 1980–2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. 2017;390(10100):1151–210.

    Article  Google Scholar 

  2. 2.

    Xu SX, Wang L, Zhou GJ, Zhang M, Gan JX. Risk factors and clinical significance of trauma-induced coagulopathy in ICU patients with severe trauma. Eur J Emerg Med. 2013;20(4):286–90.

    Article  PubMed  Google Scholar 

  3. 3.

    Moore HB, Moore EE, Liras IN, Wade C, Huebner BR, Burlew CC, et al. Targeting resuscitation to normalization of coagulating status: hyper and hypocoagulability after severe injury are both associated with increased mortality. Am J Surg. 2017;214(6):1041–5.

    Article  PubMed  PubMed Central  Google Scholar 

  4. 4.

    Moore HB, Gando S, Iba T, Kim PY, Yeh CH, Brohi K, et al. Subcommittees on fibrinolysis, disseminated intravascular coagulation, and perioperative and critical care thrombosis and hemostasis. Defining trauma-induced coagulopathy with respect to future implications for patient management: communication from the ssc of the ISTH. J Thromb Haemost. 2020;18(3):740–7.

    Article  PubMed  Google Scholar 

  5. 5.

    Spahn DR, Bouillon B, Cerny V, Duranteau J, Filipescu D, Hunt BJ, et al. The European guideline on management of major bleeding and coagulopathy following trauma: fifth edition. Crit Care. 2019;23(1):98.

    Article  PubMed  PubMed Central  Google Scholar 

  6. 6.

    Branco BC, Inaba K, Ives C, Okoye O, Shulman I, David JS, et al. Thromboelastogram evaluation of the impact of hypercoagulability in trauma patients. Shock. 2014;41(3):200–7.

    Article  PubMed  Google Scholar 

  7. 7.

    Brill JB, Badiee J, Zander AL, Wallace JD, Lewis PR, Sise MJ, et al. The rate of deep vein thrombosis doubles in trauma patients with hypercoagulable thromboelastography. J Trauma Acute Care Surg. 2017;83(3):413–9.

    Article  PubMed  Google Scholar 

  8. 8.

    Innes D, Sevitt S. Coagulation and fibrinolysis in injured patients. J Clin Pathol. 1964;17(1):1–13.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  9. 9.

    Coe NP, Salzman EW. Thrombosis and intravascular coagulation. Surg Clin North Am. 1976;56(4):875–90.

    CAS  Article  PubMed  Google Scholar 

  10. 10.

    Petros S. Trauma-induced coagulopathy. Hamostaseologie. 2019;39(1):20–7.

    Article  PubMed  Google Scholar 

  11. 11.

    Dahl OE, Harenberg J, Wexels F, Preissner KT. Arterial and venous thrombosis following trauma and major orthopedic surgery: molecular mechanisms and strategies for intervention. Semin Thromb Hemost. 2015;41(2):141–5.

    Article  PubMed  Google Scholar 

  12. 12.

    Rich NM. Management of venous trauma. Surg Clin North Am. 1988;68(4):809–21.

    CAS  Article  PubMed  Google Scholar 

  13. 13.

    Krings T, Geibprasert S, Lasjaunias PL. Cerebrovascular trauma. Eur Radiol. 2008;18(8):1531–45.

    Article  PubMed  Google Scholar 

  14. 14.

    Wilson RF. Pre-existing peripheral arterial disease in trauma. Crit Care Clin. 1994;10(3):567–93.

    CAS  Article  PubMed  Google Scholar 

  15. 15.

    Coleman JR, Moore EE, Samuels JM, Cohen MJ, Sauaia A, Sumislawski JJ, et al. Trauma resuscitation consideration: Sex matters. J Am Coll Surg. 2019;228(5):760–8.

    Article  PubMed  PubMed Central  Google Scholar 

  16. 16.

    Liras IN, Rahbar E, Harting MT, Holcomb JB, Cotton BA. When children become adults and adults become most hypercoagulable after trauma: an assessment of admission hypercoagulability by rapid thrombelastography and venous thromboembolic risk. J Trauma Acute Care Surg. 2016;80(5):778–82.

    Article  PubMed  Google Scholar 

  17. 17.

    Samuels JM, Moore EE, Coleman JR, Sumislawski JJ, Cohen MJ, Silliman CC, et al. Obesity is associated with postinjury hypercoagulability. J Trauma Acute Care Surg. 2019;87(4):876–82.

    Article  PubMed  PubMed Central  Google Scholar 

  18. 18.

    Samuels J, Lawson PJ, Morton AP, Moore HB, Hansen KC, Sauaia A, et al. Prospective assessment of fibrinolysis in morbid obesity: tissue plasminogen activator resistance improves after bariatric surgery. Surg Obes Relat Dis. 2019;15(7):1153–9.

    Article  PubMed  PubMed Central  Google Scholar 

  19. 19.

    Coleman JR, Kay AB, Moore EE, Moore HB, Gonzalez E, Majercik S, et al. It's sooner than you think: blunt solid organ injury patients are already hypercoagulable upon hospital admission - results of a bi-institutional, prospective study. Am J Surg. 2019;218(6):1065–73.

    Article  PubMed  PubMed Central  Google Scholar 

  20. 20.

    Skrifvars MB, Bailey M, Presneill J, French C, Nichol A, Little L, et al. Venous thromboembolic events in critically ill traumatic brain injury patients. Intensive Care Med. 2017;43(3):419–28.

    Article  PubMed  Google Scholar 

  21. 21.

    Van Gent JM, Calvo RY, Zander AL, Olson EJ, Sise CB, Sise MJ, et al. Risk factors for deep vein thrombosis and pulmonary embolism after traumatic injury: a competing risks analysis. J Trauma Acute Care Surg. 2017;83(6):1154–60.

    Article  PubMed  Google Scholar 

  22. 22.

    Kornblith LZ, Moore HB, Cohen MJ. Trauma-induced coagulopathy: the past, present, and future. J Thromb Haemost. 2019;17(6):852–62.

    Article  PubMed  PubMed Central  Google Scholar 

  23. 23.

    Seyfer AE, Seaber AV, Dombrose FA, Urbaniak JR. Coagulation changes in elective surgery and trauma. Ann Surg. 1981;193(2):210–3.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  24. 24.

    Ehrhardt JD Jr, Boneva D, McKenney M, Elkbuli A. Antithrombin deficiency in trauma and surgical critical care. J Surg Res. 2020;256:536–42.

    CAS  Article  PubMed  Google Scholar 

  25. 25.

    Carter KT, Palei AC, Spradley FT, Witcher BM, Martin L, Hester RL, et al. A rat model of orthopedic injury-induced hypercoagulability and fibrinolytic shutdown. J Trauma Acute Care Surg. 2020;89(5):926–31.

    CAS  Article  PubMed  Google Scholar 

  26. 26.

    Coleman JR, Moore EE, Freeman K, Grubinger ND, Hennig GW, Cohen MJ, et al. Actin is associated with tissue injury in trauma patients and produces a hypercoagulable profile in vitro. J Trauma Acute Care Surg. 2020;89(1):87–95.

    CAS  Article  PubMed  Google Scholar 

  27. 27.

    Bortolotti P, Faure E, Kipnis E. Inflammasomes in tissue damages and immune disorders after trauma. Front Immunol. 2018;9:1900.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  28. 28.

    Gando S, Otomo Y. Local hemostasis, immunothrombosis, and systemic disseminated intravascular coagulation in trauma and traumatic shock. Crit Care. 2015;19(1):72.

    Article  PubMed  PubMed Central  Google Scholar 

  29. 29.

    Harr JN, Moore EE, Chin TL, Ghasabyan A, Gonzalez E, Wohlauer MV, et al. Postinjury hyperfibrinogenemia compromises efficacy of heparin-based venous thromboembolism prophylaxis. Shock. 2014;41(1):33–9.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  30. 30.

    Johansson PI, Stensballe J, Ostrowski SR. Shock induced endotheliopathy (SHINE) in acute critical illness - a unifying pathophysiologic mechanism. Crit Care. 2017;21(1):25.

    Article  PubMed  PubMed Central  Google Scholar 

  31. 31.

    Brozović M. Physiological mechanisms in coagulation and fibrinolysis. Br Med Bull. 1977;33(3):231–8.

    Article  PubMed  Google Scholar 

  32. 32.

    Hardaway RM. The significance of coagulative and thrombotic changes after haemorrhage and injury. J Clin Pathol Suppl (R Coll Pathol). 1970;4:110–20.

    CAS  Article  Google Scholar 

  33. 33.

    Kaushansky K. Determinants of platelet number and regulation of thrombopoiesis. Hematol Am Soc Hematol Educ Program. 2009;2009(1):147–52.

    Article  Google Scholar 

  34. 34.

    Stansbury LG, Hess AS, Thompson K, Kramer B, Scalea TM, Hess JR. The clinical significance of platelet counts in the first 24 hours after severe injury. Transfusion. 2013;53(4):783–9.

    Article  PubMed  Google Scholar 

  35. 35.

    Sumislawski JJ, Kornblith LZ, Conroy AS, Callcut RA, Cohen MJ. Dynamic coagulability after injury: is delaying venous thromboembolism chemoprophylaxis worth the wait? J Trauma Acute Care Surg. 2018;85(5):907–14.

    Article  PubMed  PubMed Central  Google Scholar 

  36. 36.

    Rahbar E, Cardenas JC, Baimukanova G, Usadi B, Bruhn R, Pati S, et al. Endothelial glycocalyx shedding and vascular permeability in severely injured trauma patients. J Transl Med. 2015;13(1):117.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  37. 37.

    Ostrowski SR, Johansson PI. Endothelial glycocalyx degradation induces endogenous heparinization in patients with severe injury and early traumatic coagulopathy. J Trauma Acute Care Surg. 2012;73(1):60–6.

    CAS  Article  PubMed  Google Scholar 

  38. 38.

    Thomas DP. Effect of catecholamines on platelet aggregation caused by thrombin. Nature. 1967;215(5098):298–9.

    CAS  Article  PubMed  Google Scholar 

  39. 39.

    Brohi K, Cohen MJ, Ganter MT, Schultz MJ, Levi M, Mackersie RC, et al. Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis. J Trauma. 2008;64(5):1211–7.

    Article  PubMed  Google Scholar 

  40. 40.

    Noel P, Cashen S, Patel B. Trauma-induced coagulopathy: from biology to therapy. Semin Hematol. 2013;50(3):259–69.

    Article  PubMed  Google Scholar 

  41. 41.

    Fields AT, Matthay ZA, Nunez-Garcia B, Matthay EC, Bainton RJ, Callcut RA, et al. Good platelets gone bad: the effects of trauma patient plasma on healthy platelet aggregation. Shock. 2021;55(2):189–97.

    Article  PubMed  Google Scholar 

  42. 42.

    Hagemo JS, Stanworth S, Juffermans NP, Brohi K, Cohen M, Johansson PI, et al. Prevalence, predictors and outcome of hypofibrinogenaemia in trauma: a multicentre observational study. Crit Care. 2014;18(2):R52.

    Article  PubMed  PubMed Central  Google Scholar 

  43. 43.

    Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma. 2003;54(6):1127–30.

    Article  PubMed  Google Scholar 

  44. 44.

    Tur Martínez J, Petrone P, Axelrad A, Marini CP. Comparison between thromboelastography and conventional coagulation test: should we abandon conventional coagulation tests in polytrauma patients? Cir Esp. 2018;96(7):443–9.

    Article  PubMed  Google Scholar 

  45. 45.

    Sumislawski JJ, Christie SA, Kornblith LZ, Stettler GR, Nunns GR, Moore HB, et al. Discrepancies between conventional and viscoelastic assays in identifying trauma-induced coagulopathy. Am J Surg. 2019;217(6):1037–41.

    Article  PubMed  PubMed Central  Google Scholar 

  46. 46.

    Song J, Drobatz KJ, Silverstein DC. Retrospective evaluation of shortened prothrombin time or activated partial thromboplastin time for the diagnosis of hypercoagulability in dogs: 25 cases (2006-2011). J Vet Emerg Crit Care (San Antonio). 2016;26(3):398–405.

    Article  Google Scholar 

  47. 47.

    Kvasnicka J, Bríza J, Krska Z, Kudrna K, Pesková M, Pecen L. Increase of soluble cytoadhesive molecules sE-selectin and sICAM-1 and hyperfibrinogenaemia in patients with polytrauma without septicaemia. Sb Lek. 1998;99(2):93–6.

    CAS  PubMed  Google Scholar 

  48. 48.

    Valade N, Decailliot F, Rébufat Y, Heurtematte Y, Duvaldestin P, Stéphan F. Thrombocytosis after trauma: incidence, aetiology, and clinical significance. Br J Anaesth. 2005;94(1):18–23.

    CAS  Article  PubMed  Google Scholar 

  49. 49.

    Salim A, Hadjizacharia P, DuBose J, Kobayashi L, Inaba K, Chan LS, et al. What is the significance of thrombocytosis in patients with trauma? J Trauma. 2009;66(5):1349–54.

    Article  PubMed  Google Scholar 

  50. 50.

    Siragusa S. D-dimer testing: advantages and limitations in emergency medicine for managing acute venous thromboembolism. Intern Emerg Med. 2006;1(1):59–66.

    Article  PubMed  Google Scholar 

  51. 51.

    Rimpo K, Tanaka A, Ukai M, Ishikawa Y, Hirabayashi M, Shoyama T. Thrombin-antithrombin complex measurement using a point-of-care testing device for diagnosis of disseminated intravascular coagulation in dogs. Plos One. 2018;13(10):e0205511.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  52. 52.

    Long B, Long DA, Koyfman A. Emergency medicine misconceptions: utility of routine coagulation panels in the emergency department setting. Am J Emerg Med. 2020;38(6):1226–32.

    Article  PubMed  Google Scholar 

  53. 53.

    Holli Halset J, Hanssen SW, Espinosa A, Klepstad P. Thromboelastography: variability and relation to conventional coagulation test in non-bleeding intensive care unit patients. BMC Anesthesiol. 2015;15(1):28.

    Article  PubMed  PubMed Central  Google Scholar 

  54. 54.

    Van Haren RM, Valle EJ, Thorson CM, Jouria JM, Busko AM, Guarch GA, et al. Hypercoagulability and other risk factors in trauma intensive care unit patients with venous thromboembolism. J Trauma Acute Care Surg. 2014;76(2):443–9.

    CAS  Article  PubMed  Google Scholar 

  55. 55.

    Inaba K, Rizoli S, Veigas PV, Callum J, Davenport R, Hess J, et al. 2014 consensus conference on viscoelastic test-based transfusion guidelines for early trauma resuscitation: report of the panel. J Trauma Acute Care Surg. 2015;78(6):1220–9.

    Article  PubMed  Google Scholar 

  56. 56.

    Pivalizza EG, Abramson DC, Harvey A. Perioperative hypercoagulability in uremic patients: a viscoelastic study. J Clin Anesth. 1997;9(6):442–5.

    CAS  Article  PubMed  Google Scholar 

  57. 57.

    Brown W, Lunati M, Maceroli M, Ernst A, Staley C, Johnson R, et al. Ability of thromboelastography to detect hypercoagulability: a systematic review and meta-analysis. J Orthop Trauma. 2020;34(6):278–86.

    Article  PubMed  Google Scholar 

  58. 58.

    Rogers FB, Shackford SR, Horst MA, Miller JA, Wu D, Bradburn E, et al. Determining venous thromboembolic risk assessment for patients with trauma: the trauma embolic scoring system. J Trauma Acute Care Surg. 2012;73(2):511–5.

    Article  PubMed  Google Scholar 

  59. 59.

    Critical Care Branch of Chinese Medical Association. Guidelines for prevention of deep venous thrombosis in ICU patients (2009). Zhonghua Nei Ke Za Zhi. 2009;48(09):788–92 [in Chinese].

    Google Scholar 

  60. 60.

    Thrombosis and hemostasis group, hematology branch, Chinese Medical Association. Chinese expert consensus on diagnosis of thrombophilia (2012 Edition). Chin J Hematol. 2012;33(11):982 [in Chinese].

    Google Scholar 

  61. 61.

    Cannon KA, Badiee J, Brill JB, Olson EJ, Sise MJ, Bansal V, et al. Hereditary thrombophilia in trauma patients with venous thromboembolism: is routine screening necessary? J Trauma Acute Care Surg. 2018;84(2):330–3.

    Article  PubMed  Google Scholar 

  62. 62.

    Rybstein MD, DeSancho MT. Hypercoagulable states and thrombophilias: risks relating to recurrent venous thromboembolism. Semin Intervent Radiol. 2018;35(2):99–104.

    Article  PubMed  PubMed Central  Google Scholar 

  63. 63.

    Moran J, Bauer KA. Managing thromboembolic risk in patients with hereditary and acquired thrombophilias. Blood. 2020;135(5):344–50.

    Article  PubMed  Google Scholar 

  64. 64.

    CRASH-2 trial collaborators, Shakur H, Roberts I, Bautista R, Caballero J, Coats T, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376(9734):23–32.

    Article  Google Scholar 

  65. 65.

    Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military application of tranexamic acid in trauma emergency resuscitation (MATTERs) study. Arch Surg. 2012;147(2):113–9.

    CAS  Article  PubMed  Google Scholar 

  66. 66.

    Walker PF, Schobel S, Caruso JD, Rodriguez CJ, Bradley MJ, Elster EA, et al. Trauma embolic scoring system in military trauma: a sensitive predictor of venous thromboembolism. Trauma Surg Acute Care Open. 2019;4(1):e000367.

    Article  PubMed  PubMed Central  Google Scholar 

  67. 67.

    Howard JT, Stockinger ZT, Cap AP, Bailey JA, Gross KR. Military use of tranexamic acid in combat trauma: does it matter? J Trauma Acute Care Surg. 2017;83(4):579–88.

    CAS  Article  PubMed  Google Scholar 

  68. 68.

    Johnston LR, Rodriguez CJ, Elster EA, Bradley MJ. Evaluation of military use of tranexamic acid and associated thromboembolic events. JAMA Surg. 2018;153(2):169–75.

    Article  PubMed  Google Scholar 

  69. 69.

    Nehler MR, Taylor LM Jr, Porter JM. Iatrogenic vascular trauma. Semin Vasc Surg. 1998;11(4):283–93.

    CAS  PubMed  Google Scholar 

  70. 70.

    Galyfos G, Kerasidis S, Stefanidis G, Stamatatos I, Kastrisios G, Giannakakis S, et al. Iatrogenic and non-iatrogenic arterial injuries in an urban level I trauma center in Greece. Int Angiol. 2016;35(5):526–30.

    PubMed  Google Scholar 

  71. 71.

    Giswold ME, Landry GJ, Taylor LM, Moneta GL. Iatrogenic arterial injury is an increasingly important cause of arterial trauma. Am J Surg. 2004;187(5):590–2.

    Article  PubMed  Google Scholar 

  72. 72.

    Thorn S, Gopalasingam N, Bendtsen TF, Knudsen L, Sloth E. A technique for ultrasound-guided blood sampling from a dry and gel-free puncture area. J Vasc Access. 2016;17(3):265–8.

    Article  PubMed  Google Scholar 

  73. 73.

    Slattery MM, Goh GS, Power S, Given MF, McGrath FP, Lee MJ. Comparison of ultrasound-guided and fluoroscopy-assisted antegrade common femoral artery puncture techniques. Cardiovasc Intervent Radiol. 2015;38(3):579–82.

    Article  PubMed  Google Scholar 

  74. 74.

    Riaz A, Shan Khan RA, Salim F. Ultrasound guided internal jugular venous cannulation: comparison with land-mark technique. J Coll Physicians Surg Pak. 2015;25(5):315–9.

    PubMed  Google Scholar 

  75. 75.

    Liew NC, Alemany GV, Angchaisuksiri P, Bang SM, Choi G, DE Silva DA, et al. Asian venous thromboembolism guidelines: updated recommendations for the prevention of venous thromboembolism. Int Angiol. 2017;36(1):1–20.

    Article  PubMed  Google Scholar 

  76. 76.

    Pulmonary Embolism and Pulmonary Vascular Disease Group, Respiratory Branch of Chinese Medical Association, Pulmonary Embolism and Pulmonary Vascular Disease Working Committee, Respiratory Branch of Chinese Medical Association, National Pulmonary Embolism and Pulmonary Vascular Disease Prevention and Treatment Cooperation Group. Guidelines for diagnosis, treatment and prevention of pulmonary thromboembolism. Natl Med J China. 2018;98(14):1060–87 [in Chinese].

    Google Scholar 

  77. 77.

    Iyama K, Ikeda S, Inokuma T, Sato S, Yamano S, Tajima G, et al. How to safely prevent venous thromboembolism in severe trauma patients. Int Heart J. 2020;61(5):993–8.

    Article  PubMed  Google Scholar 

  78. 78.

    Lacut K, Bressollette L, Le Gal G, Etienne E, De Tinteniac A, Renault A, et al. Prevention of venous thrombosis in patients with acute intracerebral hemorrhage. Neurology. 2005;65(6):865–9.

    CAS  Article  PubMed  Google Scholar 

  79. 79.

    Gregory PC, Kuhlemeier KV. Prevalence of venous thromboembolism in acute hemorrhagic and thromboembolic stroke. Am J Phys Med Rehabil. 2003;82(5):364–9.

    Article  PubMed  Google Scholar 

  80. 80.

    Paciaroni M, Agnelli G, Venti M, Alberti A, Acciarresi M, Caso V. Efficacy and safety of anticoagulants in the prevention of venous thromboembolism in patients with acute cerebral hemorrhage: a meta-analysis of controlled studies. J Thromb Haemost. 2011;9(5):893–8.

    CAS  Article  PubMed  Google Scholar 

  81. 81.

    Rodier SG, Kim M, Moore S, Frangos SG, Tandon M, Klein MJ, et al. Early anti-xa assay-guided low molecular weight heparin chemoprophylaxis is safe in adult patients with acute traumatic brain injury. Am Surg. 2020;86(4):369–76.

    Article  PubMed  Google Scholar 

  82. 82.

    Nyquist P, Bautista C, Jichici D, Burns J, Chhangani S, DeFilippis M, et al. Prophylaxis of venous thrombosis in neurocritical care patients: an evidence-based guideline: a statement for healthcare professionals from the Neurocritical care society. Neurocrit Care. 2016;24(1):47–60.

    CAS  Article  PubMed  Google Scholar 

  83. 83.

    Guyatt GH, Eikelboom JW, Gould MK, Garcia DA, Crowther M, Murad MH, et al. Approach to outcome measurement in the prevention of thrombosis in surgical and medical patients: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e185S–94S.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  84. 84.

    Rakhra S, Martin EL, Fitzgerald M, Udy A. The ATLANTIC study: anti-Xa level assessment in trauma intensive care. Injury. 2020;51(1):10–4.

    Article  PubMed  Google Scholar 

  85. 85.

    Connelly CR, Van PY, Hart KD, Louis SG, Fair KA, Erickson AS, et al. Thrombelastography-based dosing of enoxaparin for thromboprophylaxis in trauma and surgical patients: a randomized clinical trial. JAMA Surg. 2016;151(10):e162069.

    Article  PubMed  Google Scholar 

  86. 86.

    Turpie AG, Bauer KA, Eriksson BI, Lassen MR. Fondaparinux vs enoxaparin for the prevention of venous thromboembolism in major orthopedic surgery: a meta-analysis of 4 randomized double-blind studies. Arch Intern Med. 2002;162(16):1833–40.

    CAS  Article  PubMed  Google Scholar 

  87. 87.

    Ahmed A, Kozek-Langenecker S, Mullier F, Pavord S, Hermans C. ESA VTE guidelines task force. European guidelines on perioperative venous thromboembolism prophylaxis: patients with preexisting coagulation disorders and after severe perioperative bleeding. Eur J Anaesthesiol. 2018;35(2):96–107.

    Article  PubMed  Google Scholar 

  88. 88.

    Allen CJ, Murray CR, Meizoso JP, Ray JJ, Teisch LF, Ruiz XD, et al. Coagulation profile changes due to Thromboprophylaxis and platelets in trauma patients at high-risk for venous thromboembolism. Am Surg. 2015;81(7):663–8.

    Article  PubMed  Google Scholar 

  89. 89.

    Brill JB, Calvo RY, Wallace JD, Lewis PR, Bansal V, Sise MJ, et al. Aspirin as added prophylaxis for deep vein thrombosis in trauma: a retrospective case-control study. J Trauma Acute Care Surg. 2016;80(4):625–30.

    CAS  Article  PubMed  Google Scholar 

  90. 90.

    Pulmonary Embolism Prevention (PEP) trial Collaborative Group. Prevention of pulmonary embolism and deep vein thrombosis with low dose aspirin: pulmonary Embolism prevention (PEP) trial. Lancet. 2000;355(9212):1295–302.

    Article  Google Scholar 

  91. 91.

    Forwell GD, Ingram GI. The effect of adrenaline infusion on human blood coagulation. J Physiol. 1957;135(2):371–83.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  92. 92.

    Kuitunen A, Hynynen M, Salmenperä M, Rasi V, Järvinen A, Scheinin M, et al. Anaesthesia affects plasma concentrations of vasopressin, von Willebrand factor and coagulation factor VIII in cardiac surgical patients. Br J Anaesth. 1993;70(2):173–80.

    CAS  Article  PubMed  Google Scholar 

  93. 93.

    Astapenko D, Benes J, Pouska J, Lehmann C, Islam S, Cerny V. Endothelial glycocalyx in acute care surgery - what anaesthesiologists need to know for clinical practice. BMC Anesthesiol. 2019;19(1):238.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  94. 94.

    Ageno W, Haas S, Weitz JI, Goldhaber SZ, Turpie AGG, Goto S, et al. Characteristics and management of patients with venous thromboembolism: the GARFIELD-VTE registry. Thromb Haemost. 2019;119(2):319–27.

    Article  Google Scholar 

  95. 95.

    Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ, et al. Antithrombotic therapy for VTE disease: antithrombotic therapy and prevention of thrombosis, 9thed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e419S–96S.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  96. 96.

    Ma Q-B, Zheng Y-A, Zhu J-H, Chen Y-G, Dong S-J, Gao W-B, et al. Consensus on antithrombotic therapy for acute thrombotic diseases in China. Emer Med Chin. 2019;39(06):501–31.

    Google Scholar 

  97. 97.

    Lin A, Vazquez SR, Jones AE, Witt DM. Description of anti-Xa monitoring practices during low molecular weight heparin use. J Thromb Thrombolysis. 2019;48(4):623–8.

    CAS  Article  PubMed  Google Scholar 

  98. 98.

    Thrombus prevention and treatment Committee of cardiovascular physicians branch of Chinese Medical Association, editorial board of Chinese Medical Journal. Expert consensus on heparin induced thrombocytopenia in China (2017). Natl Med J China. 2018;98(6):408–17 [in Chinese].

    Google Scholar 

  99. 99.

    Tran HA, Gibbs H, Merriman E, Curnow JL, Young L, Bennett A, et al. New guidelines from the thrombosis and Haemostasis Society of Australia and new Zealand for the diagnosis and management of venous thromboembolism. Med J Aust. 2019;210(5):227–35.

    Article  PubMed  Google Scholar 

  100. 100.

    Alter SM, Mazer BA, Solano JJ, Shih RD, Hughes MJ, Clayton LM, et al. Antiplatelet therapy is associated with a high rate of intracranial hemorrhage in patients with head injuries. Trauma Surg Acute Care Open. 2020;5(1):e000520.

    Article  PubMed  PubMed Central  Google Scholar 

  101. 101.

    Ratnatunga CP, Edmondson SF, Rees GM, Kovacs IB. High-dose aspirin inhibits shear-induced platelet reaction involving thrombin generation. Circulation. 1992;85(3):1077–82.

    CAS  Article  PubMed  Google Scholar 

  102. 102.

    Bjornsson TD, Schneider DE, Berger H Jr. Aspirin acetylates fibrinogen and enhances fibrinolysis. Fibrinolytic effect is independent of changes in plasminogen activator levels. J Pharmacol Exp Ther. 1989;250(1):154–61.

    CAS  PubMed  Google Scholar 

  103. 103.

    Narouze S, Benzon HT, Provenzano D, Buvanendran A, De Andres J, Deer T, et al. Interventional spine and pain procedures in patients on antiplatelet and anticoagulant medications (second edition): guidelines from the American Society of Regional Anesthesia and Pain Medicine, the European Society of Regional Anaesthesia and Pain Therapy, the American Academy of Pain Medicine, the International Neuromodulation Society, the North American Neuromodulation Society, and the World Institute of Pain. Reg Anesth Pain Med. 2018;43(3):225–62.

    PubMed  Google Scholar 

  104. 104.

    Angiolillo DJ, Rollini F, Storey RF, Bhatt DL, James S, Schneider DJ, et al. International expert consensus on switching platelet P2Y12 receptor-inhibiting therapies. Circulation. 2017;136(20):1955–75.

    CAS  Article  PubMed  Google Scholar 

  105. 105.

    Specialty Committee on Prevention and Treatment of Thrombosis of Chinese College of Cardiovascular Physicians, Section of Interventional Cardiology of Chinese Society of Cardiology of Chinese Medical Association, Editorial Board of Chinese Journal of Cardiology. Chinese experts consensus on antiplatelet therapy for medically managed acute coronary syndromes (2018). Chin J Cardiol. 2019;47(6):430–42 [in Chinese].

    Google Scholar 

  106. 106.

    Dengler R, Diener HC, Schwartz A, Grond M, Schumacher H, Machnig T, et al. Early treatment with aspirin plus extended-release dipyridamole for transient ischaemic attack or ischaemic stroke within 24 h of symptom onset (EARLY trial): a randomised, open-label, blinded-endpoint trial. Lancet Neurol. 2010;9(2):159–66.

    CAS  Article  PubMed  Google Scholar 

  107. 107.

    Gresele P, Momi S, Falcinelli E. Anti-platelet therapy: phosphodiesterase inhibitors. Br J Clin Pharmacol. 2011;72(4):634–46.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  108. 108.

    Chinese Society of Cardiology of Chinese Medical Association, Editorial Board of Chinese Journal of Cardiology. 2019 Chinese Society of Cardiology (CSC) guidelines for the diagnosis and management of patients with ST-segment elevation myocardial infarction. Chin J Cardiol. 2019;47(10):766–83 [in Chinese].

    Google Scholar 

  109. 109.

    Stroke Prevention and Treatment Engineering Committee of National Health Commission, Neurointerventional group of Neurosurgery Branch of Chinese Medical Association, interventional group of Radiology branch of Chinese Medical Association. Chinese expert consensus on endovascular treatment of acute macrovascular occlusive ischemic stroke (2019). Chin J Neurosurg. 2019;35(9):868–79 [in Chinese].

    Google Scholar 

  110. 110.

    Chinese Society of Neurology, Chinese Stroke Society. Chinese guidelines for diagnosis and treatment of cerebral venous thrombosis 2019. Chin J Neurol. 2020;53(09):648–63 [in Chinese].

    Google Scholar 

  111. 111.

    Chinese College of Interverntionalists. Expert consensus on interventional therapy for deep venous thrombosis of lower extremity (2nd edition). Natl Med J China. 2018;98(23):1813–21 [in Chinese].

    Google Scholar 

  112. 112.

    Vedantham S. Interventional therapy for venous thromboembolism. J Thromb Haemost. 2015;13(Suppl 1):S245–51.

    CAS  Article  PubMed  Google Scholar 

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JCS, WQL as the main person in charge of the consensus, presided over the expert seminar and coordinated the expert groups. LKY, WZ, FZ, GW and YPC were the main participants in the consensus discussion, formulating the consensus framework and proposing to update the main points. JCS was the first writing author of the manuscript. Other experts participate in literature review, consensus discussion and suggestions. All authors read and approved the final manuscript.

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Zhao-Yue Wang (the First Affiliated Hospital of Soochow University); Qing Song (the First Medical Center of Chinese PLA General Hospital); Hong-Yuan Lin (the Fourth Medical Center of Chinese PLA General Hospital).

Members of the Editorial Board.

Yao-Peng Chen (the 923th Hospital of Joint Logistics Support Forces of Chinese PLA), Jing Dai (Ruijin Hospital Affiliated to Medical College of Shanghai Jiaotong University), Ren-Yu Ding (the First Affiliated Hospital of Chinese Medical University), Wei-Wei Ding (General Hospital of Eastern Theater Command of Chinese PLA), Pei-Gen Gui (First Affiliated Hospital of Nanhua University), Bao-Hui Jia (Zhengzhou Central Hospital Affiliated to Zhengzhou University), Chuan-Bao Li (Beijing Hospital), Wei-Qin Li (General Hospital of Eastern Theater Command of Chinese PLA), Ben Lv (the Third Xiangya Hospital of Central South University), Heng Mei (Union Hospital, Tongji Medical College, Huazhong University of Science and Technology), Jing-Chun Song (the 908th Hospital of Joint Logistics Support Forces of Chinese PLA), Ning Tang (Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology), Gang Wang (the Second Affiliated Hospital of Xi’an Jiaotong University), Qiu-Shi Wang (Shengjing Hospital Affiliated to China Medical University), Jun Wu (Beijing Jishuitan Hospital),Zhen-Ju Song (Zhongshan Hospital Affiliated to Fudan University), Li-Kun Yang (the 904th Hospital of Joint Logistics Support Forces of Chinese PLA), Gen-Sheng Zhang (the Second Affiliated Hospital of Medical College of Zhejiang University), Wei Zhang (the 900th Hospital of Joint Logistics Support Forces of Chinese PLA), Wei Zhao (Nanfang Hospital Affiliated to Southern Medical University),Jing Zhou (West China Hospital Affiliated to Sichuan University), Feng Zhu (Shanghai East Hospital Affiliated to Tongji University), Hong-quan Zhu (the First Affiliated Hospital of Gannan Medical University).

Corresponding authors

Correspondence to Jing-Chun Song or Wei-Qin Li.

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Song, JC., Yang, LK., Zhao, W. et al. Chinese expert consensus on diagnosis and treatment of trauma-induced hypercoagulopathy. Military Med Res 8, 25 (2021).

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  • Trauma
  • Coagulation dysfunction
  • Thrombosis
  • Diagnosis
  • Treatment