Changes in coagulation-fibrinolysis marker and neutrophil elastase following the use of tourniquet during total knee arthroplasty and the influence of neutrophil elastase on thromboembolism

To clarify in detail the mechanism underlying the development and exacerbation of deep venous thrombosis (DVT) and/or pulmonary thromboembolism (PTE), we focused on the following factors: the thrombin-antithrombin III complex (TAT), D-dimer and neutrophil elastase (NE). We basically investigated whether NE played an important role in the development of PTE I a mice model. Nineteen rheumatoid arthritis (RA) and six osteoarthritis (OA) patients underwent total knee arthroplasty (TKA) with tourniquet, and 13 RA and 12 OA patients underwent TKA without tourniquet in each group. The blood levels of TAT, D-dimer and NE were measured before surgery, immediately after and during the days following surgery. For the induction of experimental PTE due to coagulation of platelets, adenosine diphosphate (ADP) was administrated, and human NE with ADP was also administrated for the development of DVT and/or PTE. The rates of increase in the mean TAT, D-dimer and NE levels in the group with tourniquet were statistically higher than those in the group without tourniquet after surgery. The mortality of the mouse due to PTE increased from 43 to 67% following ADP and human NE administration compared to a single ADP administration. Histological changes of the lungs in the mice receiving NE and ADP injections were characterized by a diffuse and extensive accumulation of platelets and fibrin in alveolar capillaries and other microvessels. We suggest that during TKA, the use of tourniquet induces local release of a large amount of NE from neutrophils, inducing the development of DVT and/or PTE and their exacerbation.