The main findings of the present study were that D-dimer level and Troponin levels were detected higher than normal in COVID-19 positive trauma patients, although no significant vascular pathology could be detected in these COVID-19 positive trauma patients, as reported in the literature(8, 23).
Three important factors for thrombus formation within the vein, blood flow, blood component and blood vessels have been recognized as the Virchow triad(19). Major trauma can lead to collapse of one or all of the Virchow triad of hypercoagulation, endothelial injury, and venous stasis(31). Long-term bed rest, immobilization, or thrombosis caused by direct damage to blood vessels can cause intimal damage, leading to hypoperfusion and paralysis, and all these factors support venous stasis. Hak stated that the Virchow triad is present in the majority of trauma patients and this causes a high risk of thromboembolism(17). Reduced antithrombin III levels (28, 33) and suppression of fibrinolysis (2, 11) can cause hypercoagulation of the trauma patient. Okamura et al. reported that the levels of d-dimer and soluble fibrin monomer complex were higher than normal in patients with hip fractures(27). Many studies have shown that after trauma, thromboplastin (Tissue factor; TF) and thrombin formation markers are increased and natural anticoagulant levels such as antithrombin (AT), protein C (PC) and protein S (PS) are decreased(9, 12, 24). In addition to the consumption of coagulation factors, acidosis and hypothermia and dilution of intravenous fluids that occurs as a result of decreased activity are among the causes of traumatic coagulopathy(5). Inactivity is also a known cause of VTE. The absence of the pumping effect of muscle contractions leads to a decrease in blood flow and accumulation of blood in the calf intramuscular sinuses, resulting in DVT(26). Increased hematocrit, high fibrinogen and von Willebrand factor macromolecular complex levels increase blood viscosity, which may further affect blood flow(25). Reduced blood flow can lead to endothelial damage, local accumulation of activation products, clotting products and local reduction in inhibitor levels, which increase blood coagulability(14).
COVID-19 is a severe acute respiratory syndrome disease caused by coronavirus 2 (SARS-CoV-2), and can also make patients prone to thrombotic disease in both venous and arterial circulation due to excessive inflammation, platelet activation, and endothelial dysfunction(4). Some recent studies have reported that the incidence of arterial and venous thrombosis is higher in COVID-19 patients(22, 23, 36). In the present study 6.7% of the patients had DVT. In a retrospective study by Cui et al., 25% of 81 severe COVID-19-positive patients followed up in intensive care were reported to have VTE(6). In a multicentre study of 184 patients with severe COVID-19 from the Netherlands, 28 (15.2%) VTE cases were reported and the cumulative incidence of VTE was estimated to be 27%(20). Rodriguez et al. stated that 23 of 156 patients had DVT in their retrospective study and as in other series, the probability of developing DVT was high in patients with COVID-19 positivity and a high D-dimer level(8). The low incidence of DVT in the patients in the current series can be considered to be due to the initiation of antithrombotic medication and wearing antiembolic socks from the time of hospitalization, and in-bed exercise was also started immediately on hospitalization. Moreover, none of the patients in the current study had severe COVID-19 disease.In the present study, all the patients operated on for lower limb fractures were discharged with routine COVID-19 therapy, and none developed severe COVID-19 disease.
The D-dimer levels were found to be above the normal level in all the patients screened, but this was predictable due to both trauma and COVID-19 positivity. However, DVT was detected radiologically in only two of these patients and thrombolytic therapy was started. Cardiovascular surgery consultation was requested for the patient with DVT and 0.6 ml of enoxoparin sodium was started twice a day with the recommendation of cardiovascular surgery and it was recommended to continue using antiembolic socks. Following the completion of the orthopedic treatment, the patient was followed up for the DVT treatment by the cardiovascular surgeon. The high D-dimer level in the other patients could have been secondary to trauma or due to COVID-19 disease alone.
The cardiac troponin level in the blood tends to increase in trauma patients without cardiac trauma, and also tends to increase in situations where the right ventricle of the heart is forced, such as in the occurrence of pulmonary embolism. In the current study, troponin levels were also investigated and levels above normal were determined in 22 patients.
There were several limitations to this study, primarily the low small sample size, the lack of long-term follow-up, and none of the patients followed up had severe COVID-19 disease. There is a clear need for further large series to be able to make comparisons with COVID-19 negative patients and similar traumas.
In conclusion, it can be recommended that extra attention should be given to vascular complications in COVID-19 positive trauma patients, as both the effect of trauma itself increases hypercoagulability and COVID-19 disease seems to have the potential to increase hypercoagulability.