Since ERAS was advocated by University of Copenhagen professor H. Kehlet, ERAS has been widely used in management during the perioperative period. Coagulopathy still is a primary cause of death in general and orthopedic trauma patients.(22) The recent versions of ACCP and AAOS guidelines do not distinguish between revision and primary THA.(7, 8) And there is no optimal coagulation management protocol for revision surgery. In patients undergoing revision surgery, the risk of bleeding complications and VTE is also higher than primary surgery. So, quite a few surgeons have chosen more aggressive chemoprophylaxis due to this characteristic of revision surgery, which could lead to poorer outcomes. Thus, rapid assessment and correction of coagulopathy are vital for the survival of these patients. In 2005, a study by Douglas et al.(15) was the first time evidence was reported that demonstrated the association between hypercoagulability state measured by TEG and postoperative thromboembolic complications in surgical patients. And TEG is a useful adjunctive test for assessment of thrombophilia, even if conventional thrombophilia screen methods were normal.(18) However, to our knowledge, only a handful of studies in the literature have reported coagulation monitoring by TEG following primary arthroplasty (9, 19, 20, 23, 24) but there is no data regarding TEG after revision arthroplasty on ERAS.
We found 32.86% (23) revision THA patients with a hypercoagulable state on postoperative day 7, which was a lot more than the preoperative percentum of hypercoagulable state. For 78.26% (18) of these patients, their hypercoagulable state was mixed hypercoagulability. Therefore, single use of antithrombotic (E.g. Aspirin) or antithrombin (E.g. Low molecular weight heparin) therapy may be inappropriate. How to establish an appropriate personalized anticoagulation program is an important direction for future research. In addition TEG may be an important test to guide individualized anticoagulation.
There are many reasons for hypercoagulability in patients after hip replacement. The concomitant diseases such as hypertension and infection may be the causes of hypercoagulable.(22, 25–27) Furthermore the trauma of subsequent revision surgery, intraoperative blood loss and transfusions may lead to a hypercoagulable state. The main risk factors of thrombosis following trauma of surgery include: physical disruption of the endothelium in trauma or surgery, blood flow is relatively static, stasis and local accumulation of tissue factor, the expression of tissue factors caused by stimulation of inflammatory mediators.(28) Furthermore, platelet-leukocyte aggregation under inflammatory stimuli following surgery can further promote thrombosis.(28, 29) In a study by Ng et al (30), the development of a hypercoagulable state is related to mild to moderate degree of intraoperative blood loss. In our study, intraoperative blood loss averaged 486.43 ml, which may play a role in inducing a hypercoagulable state. Red blood cell (RBC) transfusions may increase postoperative hypercoagulable state, and in some patients, surgery and perioperative RBC transfusions may have synergistic effects of increased related risk for VTE development.(31) Furthermore, the revision surgery itself may be the cause of postoperative hypercoagulable state, and further studies are needed to explore the correlation between the parameters of revision surgery and postoperative hypercoagulable state.
In our institution, we routinely use rivaroxaban to reduce the risk of thrombosis. Rivaroxaban does not require routine coagulation monitoring, but in certain clinical situations (overdose, impaired renal function, acute bleeding episodes, elderly patients) we should evaluate the anticoagulant effect.(32) The present study found rivaroxaban prolongs R and K (assessment of time to clot formation), while decreasing α angle and MA (assessment of clot strength).(32, 33) Therefore another explanation for hypercoagulable state may be that, the recommended dose of rivaroxaban was insufficient or some patients are not sensitive to rivaroxaban. In addition, we routinely use TXA to reduced postoperative blood loss and the transfusion rate. Previous study reported that they used TEG to monitor coagulation in patients who received TXA, which showed significant reduced R, K and increased MA, α angle, and they found a three-fold increased risk of vascular events in intravenous TXA group compared to placebo.(34) Therefore, in our study the postoperative hypercoagulable state of patients may be attributed to the use of tranexamic acid.
In our study, the proportion of patients with perioperative hypocoagulability is small. Perioperative management of ERAS may be the main reason for these results. Ecchymosis, a local bleeding complication, is mainly caused by vascular wall damage and coagulation dysfunction caused by local bleeding complications.(35) The revision THA inevitably damages the vessel walls and it is more severe than primary THA. Despite there are so many advantages of Rivaroxaban, there was research showing that its application was associated with a higher risk for bleeding complications.(36) In addition, the difference in sensitivity of patients to rivaroxaban may also be an important cause of perioperative hypocoagulability. Therefore, the damage of the blood vessel wall caused by surgery and the use of rivaroxaban may be the main cause of postoperative ecchymosis. On the other hand, according to the relationship between thromboelastography and ecchymosis of case 1 and case 2, Monitoring TEG daily may be a better way to guide individualized anticoagulation.
1 patient suffered melena at POD5. The TEG values of this patient showed hypercoagulable at POD5 and POD7. In a study by Henriksson AE et al. during an acute episode, the coagulation status of a patient with gastrointestinal bleeding was hypercoagulable state.(37) The development of a hypo-fibrinolytic state can promote a hypercoagulable state in patients with upper gastrointestinalbleeding.(38) In addition, hypertension, periprosthetic joint infection, pulmonary infection, intraoperative bleeding 700 ml, postoperative blood transfusion of 600 ml, and surgical trauma may all be the cause of postoperative hypercoagulability in this patient. The coagulation management of this special patient needs further research.
There are several limitations to this study. This is a retrospective study, which may be more susceptible to selection bias. Furthermore relatively small number of cases, short follow-up and no routine Color Duplex ultrasound might have concealed or diminished the recorded incidence rate of VTE or hypercoagulable state. The heterogeneity of operative procedures may also be limitations of this study. We did not research the potential patient-related risk factors for VTE. Despite these limitations, we believe that our study is worthy of consideration; because it is the first time patients undergoing hip arthroplasty revision,have been examind for changes in perioperative TEG parameters of patient undergoing hip arthroplasty revision; and it provides a reference for the use of TEG to guide individualized anticoagulation.