Shapkin Yu.G., Seliverstov P.A.

Saratov State Medical University named after V.I. Razumovskiy, Saratov, Russia


Currently, the mortality after polytrauma is still high – 15-24 % even in the advanced clinics [1, 29]. The improvement in organizational and anti-shock procedures leads to decreasing mortality in the early phase of polytrauma, but the relative amount of deaths from late complications [1, 40]. In 10-53 % of patients with polytrauma, despite of timely prevention, venous thromboembolic complications (VTEC) appear, including deep venous thrombosis (DVT) and pulmonary embolism (PE) [11, 22, 27, 34, 43, 46]. Skeletal injuries in polytrauma appear in 70-93 % [4, 40]. Fractures of the lower extremities and the pelvis prevail in their incidence (60-78 %), significantly influencing on development of VTEC [4, 27]. The rate of DVT in polytrauma with fractures of the above-mentioned bones achieves 46-60 % [6, 34, 37]. Venous thrombosis in polytrauma increases the period of hospital stay and costs for treatment [17, 44], with increasing incidence of multiple organ dysfunction and mortality [13, 20, 24]. About 45 % of fatal outcomes of PE are associated with multiple injuries [48].
Insufficient exploration of multiple risk factors and of features of VTEC pathophysiology in associated injury hinders the development of prevention standards and improvement in polytrauma management.


Venous thrombosis develops in combination of three factors (Virchow's triad): bradyhemarrhea, endothelial vascular wall injury and disorders in hemostasis system (hypercoagulation and fibrinolysis depression).
Bradyhemarrhea in polytrauma is associated with local systemic hemodynamic disorders which are caused by hypodynamia, traumatic shock and acute massive blood loss. Systolic arterial pressure below 90 mm Hg [16, 38] and duration of immobilization and bed rest are the independent risk factors of VTEC in polytrauma [25, 42, 48].

The high energy mechanism of polytrauma determines the significant injury to the venous vascular wall. About 70-90 % of patients receive polytrauma in road traffic accidents or after falling from height [4, 11, 27]. As result, complex fragmented fractures of types B
  and C (AO/ASIF classification) are identified in 42-75 % of polytrauma with skeletal injuries, i.e. 2-3 times higher than in single injuries. 20-27 % of patients demonstrate opened fractures with extensive soft tissue injuries [4, 40].

Vascular endothelial injuries appear in polytrauma and are mediated by systemic pathological processes. A systemic inflammatory response appears after multiple tissue injuries, shock and acute blood loss. Tissue lesions and release of mitochondrial damage-associated molecular patterns (mtDAMPs) from injured cells cause the activation of neutrophil leukocytes, which produce proinflammatory cytokines and strong oxidants. Oxidative stress, tissue hypoperfusion and hypoxia cause death of endotheliocytes and exposure of the subendothelial layer, resulting in thrombosis [29]. Systemic disorders of cellular immunity, leukocytosis and lymphopenia with activation of B- and T-lymphocytes promote endothelial dysfunction and weakening of clot fixation to the vascular wall. Floating clots in polytrauma with fractures of the lower extremities and the pelvis are identified in 25-68 % of patients with DVT, resulting in possible fatal PE [6, 22, 37].

Shock and massive blood loss in polytrauma cause the significant disorders in blood-dotting sequence. Posttraumatic coagulopathy has a complex and non-investigated mechanism of development. The experimental studies with polytrauma model including the femoral bone fracture showed a relationship between coagulopathy values and systemic inflammatory response, and regularity in changes in phases of hyper- and hypocoagulation that are confirmed by results of clinical studies [10]. The signs of hypercoagulation (according to thromboelastography) are observed within a week after polytrauma [44]. The hypercoagulation phase is much more intense in polytrauma with severe skeletal injuries than in single skeletal injury [47].

Coagulopathy with INR > 1.5 is associated with increasing rate of VTEC and higher mortality after trauma [26]. The prediction criteria of VTEC in patients with polytrauma are lymphocytic adhesion, IL-2, D-dimer, activated partial thromboplastin time,
IL10-1082G>A and IL2-303Т>G gene polymorphism regulating the influence of IL-2 and IL-10 on clot formation [11, 49]. According to some studies, the thromboelastographic signs of hypercoagulation are not associated with incidence of VTEC in polytrauma [44]. Another study showed two-fold increase in incidence of DVT in the lower extremities in patients with hypercoagulation values in thromboelastography [5].
Metabolic acidosis (pH < 7.2) and hypothermia (< 35 °C) induce and intensify coagulopathy, consisting “the death triad”. Hyperlactataemia and hyperglycemia reflect the severe disorders of tissue metabolism and are determined by the risk factors of VTEC in polytrauma [37, 38]. Massive hemotransfusion in polytrauma favors the disorders in blood-dotting sequence. Transfusion of four and more dosages of erythrocytic media in the first day after injury is the predictor of VTEC [21].

Polytrauma causes the phenomenon of mutual burdening of injuries. This phenomenon causes progressive increase in the incidence of complications and lethal outcomes. The mechanisms of increasing rate of VTEC in presence of this phenomenon cause cumulative increase in shock potential of trauma, development of more intense systemic inflammatory response and coagulopathy [36, 40].

The phenomenon of mutual burdening of injuries explains the increasing rate of VTEC with higher ISS [20, 49] and TMPM
(Trauma Mortality Prediction Model) [25]. It testifies that combinations of the most severe injuries exert the dominating influence on formation of VTEC. In patients with two or more leading injuries, VTEC develop with higher frequency and are identified in uncommonly early periods – 7-10 days after polytrauma [40].
Fractures of long bones, of pelvic bones and of the spine with spinal cord injury [30], traumatic brain injury (TBI) [16, 49], abdominal and thoracic injuries with AIS (Abbreviated Injury Scale) > 2 have the highest significance for formation of phenomenon of mutual burdening of injuries and present the independent predictors of VTEC [17, 23, 38].

Pelvic, femoral, spinal and leg fractures significantly increase the incidence of VTEC in polytrauma by means of high increase in blood loss and shock potential of an injury, with limited mobility of the patient [16, 21, 37, 49]. The risk of VTEC is highest for multiple fractures of the pelvis of the lower extremities [6, 14, 42]. Multiple pelvic injuries with AIS ≥ 3 present the independent risk factor of DVT in polytrauma [7, 20, 24].

Complex high energy fractures of the long bones with massive soft tissue injuries after polytrauma are accompanied by release of high amount of inflammatory mediators and tissue factor which initiate the processes of blood clotting. The experimental studies show that systemic inflammatory response is much more intense in combination of a fracture with extensive soft tissue injury in comparison with single injuries [28]. Severe soft tissue injury in the lower extremities is the independent predictors of VTEC [25, 38].

TBI severity correlates with incidence of VTEC. So, GCS (Glasgow Coma Scale) < 8 during 4 hours is the independent predictor of VTEC [21]. The increasing risk of VTEC in TBI is explained by disorder of the hematoencephalic barrier and by delivery of tissue factor, which participates in thrombin formation, into systemic blood flow from cerebral injury foci [19]. However E.J. Vale et al. (2014) showed that traumatic brain injury did not increase the incidence of VTEC in polytrauma, despite presence of more intense signs of hypercoagulation in thromboelastography [43].

The spinal cord injury significantly increases the risk of DVT by means of immobility of the patient, disordered innervation of blood vessels and slow venous flow. The incidence of DVT in polytrauma with the spinal cord injury show the highest values (about 75 %) [34].

There are some attempts to identify and to combine the main factors of VTEC risk in polytrauma into the integral values and the prediction scores [21, 27, 46]. The identification includes the risk factors of VTEC, like in Military Field Surgery-Injury scale, which changes during treatment (severity of injuries, age, concurrent diseases) and the factors relating to condition severity, which changes during treatment [27]. It allows timely correcting the prevention of VTEC and estimating its efficiency.


For prevention of VTEC in polytrauma, first of all, it is necessary to remove the influence of the factors promoting phlebothrombosis: recovery of circulating blood volume, hemodynamics normalization, creation of conditions for fast activation of the patient.
Early (within two days) stable and functional osteosynthesis of the long bones, the pelvis and the spine with adherence to Early Total Care (ETC) prevents the progression of local and systemic responses, allows fast activation of patients and decrease the risk of VTEC in polytrauma [6, 12, 39].

However traumatic and long-lasting final internal osteosynthesis, which presents the surgical injury, can cause the second hit and increase the risk of systemic and thromboembolic complications, neutralizing the positive moments of early fixation. The duration of surgery more than two hours is the independent risk factor of VTEC in severe injury [21].

The second hit phenomenon in polytrauma develops as result of postsurgical worsening systemic inflammatory response, hypercoagulation, vascular endothelial damages and disordered venous flow in narcosis with myorelaxants. The most unfavorable time intervals for osteosynthesis are the days 3-5, when the intensity of systemic inflammatory response and hypercoagulation are maximal [39].

The staged surgical management for long bones and pelvic fractures (Damage Control Orthopedics – DCO) and for thoracic and lumbar vertebrae (Spine Damage Control – SDC) decreases the risk of the second hit, incidence of postsurgical complications and mortality in polytrauma [27, 29, 39, 40, 41, 50].
Other authors compared the mortality and the incidence of VTEC and did not find any advantages of temporary external fixation in concordance with DCO before early primary intramedullary fixation [31] or before skeletal traction during preparation for final fixation [35]. Moreover, recurrent osteosynthesis in staged treatment become the risk factors of VTEC [8, 20, 44].

According to ultrasonography data, the forced attitude of the lower extremity in skeletal traction caused the deformation of the femoral vein and development of “splint phlebothrombosis” in 46 % of patients with polytrauma [6].

Closed locking intramedullary osteosynthesis of the long bones is characterized by low traumatic potential of the intervention, low intrasurgical blood loss and appropriate fixation of fragments, resulting in early activation of the patient. However in case of polytrauma, early intramedullary fixation can initiate the progression of inflammatory responses and coagulation disorders. The experimental and clinical studies showed that intramedullary fixation of femoral and tibial bones, especially with the intramedullary canal drilling, cause the additional significant increase in IL-6 in the blood and increasing hypercoagulation within 10 days after surgery [3, 47]. The risk of VTEC and lethal outcome increases in single-stage intramedullary fixation, particularly in combination with the chest injury [18].

Objective estimation of the patient’s condition severity and choice of optimal time of surgical intervention for polytrauma give the maximal advantages of DCO and ETC and prevent the second hit phenomenon.

  R. Pfeifer и H.C. Pape (2016) developed the concept of safe definitive surgery for polytrauma on the basis of graduation of severity of patients’ condition with consideration of acidosis, coagulopathy, hypothermia, shock and severity of injuries. ETC is allowed for stable condition of the patient. For borderline or unstable condition, it is recommended to adhere to DCO staged management [29].
B.R. Childs et al. (2016) showed the lactate level < 4 mmol/l, pH ≥ 7.25 or base excess ≥ -5.5 mmol/l. VTEC and mortality showed the lowest values in patients who were operated in presence of the above-mentioned indices within 36 hours after polytrauma [8].

The Russian clinical recommendations [33], the manual from Eastern Association for the Surgery of
Trauma (EAST) [32] and the guidelines from American College of Chest Physicians (ACCP) [15] are considered as the main guidelines for pharmacological, mechanic and surgical prevention of VTEC after trauma. According to these guidelines, it is optimally to use preventive doses of low weight molecular heparins, preferably with intermittent pneumatic compression. Oral anticoagulants can be used in the postsurgical period.
However the mechanical methods of venous thrombosis prevention are sometimes impossible to use for patients with polytrauma, owing to frequent damages of the lower extremities. The time intervals for initiation of anticoagulation pharmacological therapy in TBI with intracranial hemorrhage and in spinal cord and parenchymal organ injuries are not clear and can be delayed for 24-72 hours after trauma, to the moment of hemostatis achievement [32, 33, 45]. Traumatic brain injury without intracranial bleeding, damage of parenchymal organs and retroperitoneal hematoma in pelvic fractures or full spinal cord injury without ongoing bleeding are not considered as contraindications for anticoagulants [33]. For ongoing bleeding it is offered to use only non-pharmacological preventive measures, with addition of anticoagulants after disappearance of possibility of bleeding. VTEC prevention is not recommended to delay or stop because of planned surgical interventions [15, 33].

The indications for implantation of temporary or constant cava-filters for prevention of fatal PE in polytrauma are not standardized, and they vary significantly. Each method is offered to use in patients with DVT in presence of contraindications to anticoagulant therapy because of high risk of bleedings or in extensive floating thrombosis of femoral or iliac veins and in recurrent PE [15, 32, 33]. EAST guidelines extend the indications for placement of cava-filters for patients without DVT who cannot receive the anticoagulants because of risk of bleeding or in presence of one of the following injuries: severe TBI with GCS < 8, partial spinal cord injury with para- or tetraplegia, a complex fracture of the pelvic bones in combination with a long bone fracture, multiple fractures of the long bones [32]. The adherence to EAST would result in implantation of the cava-filter in 25 % of polytrauma cases, but it is really installed not more than in 4 % of such patients, and without significant increase in incidence of PE [2, 9]. The prevention technique of PE with implantation of cava-filters is not without serious complications and to be used in substantiated indications.

The high incidence of symptomless DVT in polytrauma with skeletal injuries and formation of embologenic floating clots require for timely diagnosis for correction of management techniques. The gold standard of diagnosis of DVT in the lower extremities is compression ultrasonography. The time and periodicity of compression ultrasonography for polytrauma are disputable and are not clearly determined in the guidelines. Ultrasonic screening is the most essential for impossibility of anticoagulation therapy, for presence of spinal cord injuries, fractures of the lower extremities and the pelvis, and for severe TBI [15, 33]. Ultrasonography is recommended to conduct at least one time per week, beginning from the days 3-5 from polytrauma, the days 1-2 before surgery and 2-3 days after surgery [6, 22, 39]. The study is reasonably to repeat before recurrent surgical intervention and before increase in movement activity [27].

Prevention of VTEC in polytrauma with skeletal injuries is optimally to continue at least to the moment of restoration of movement activity – from 4 weeks to 3 months after trauma or surgery [6, 13, 33]. Some studies showed that 50-62 % of all cases of VTC and 54-96 % of deaths from PE were registered after hospital discharge [4, 25, 48]. It determines the need for development of clear recommendations for prevention of VTEC in the period of hospital treatment and in the outpatient phase of rehabilitation.


The patients with polytrauma are related to the group of high risk of VTEC. The factors, which increase the risk of VTEC in polytrauma, are traumatic shock and acute massive blood loss, multiple high-energy fractures of bones with extensive soft tissue injuries, systemic inflammatory response and coagulopathy, the phenomenon of mutual burdening of complications. The severity and multiplicity of injuries correlate with intensity of systemic inflammation, hypercoagulation and incidence of VTEC. Complex pelvic, femoral, leg and spinal fractures, TBI and spinal cord injuries significantly increase the risk of VTEC.
Polytrauma requires for complex prevention of VTEC. The important components are anti-shock procedures, maximally early stable functional osteosynthesis of the long bones, the pelvis and the spine with low traumatic techniques. Damage Control Orthopedics allows minimizing the risk of the second hit phenomenon in borderline or unstable patients. Low molecular weight heparins make the basis of pharmacological prevention, which should be initiated before hemostasis achievement. Implantation of cava-filters is indicated for DVT with high risk of fatal PE. The need for implantation of cava-filters in patients without DVT has the low degree of evidences.

Currently, the clear recommendations for prevention of VTEC in polytrauma have not been developed and standardized. It is mainly associated with absence of sufficient evidences, multiple variants of combinations of injuries and difficulties of pathophysiology of mutual interaction.

 Information on financing and conflict of interests

The study was conducted without sponsorship.
The authors declare the absence of clear or potential conflicts of interests relating to publishing this article.


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