As a result of the longer surgical time, potential for greater femoral vessel occlusion, and insertion of cement, it is theorized that HRA may result in a greater risk for thrombogenesis when compared with THA. However, the patient population for HRA is typically younger than the population for THA, so it is difficult to compare the incidence of thromboembolism between the two groups. The use of biochemical markers of the clotting cascade has proven useful in prior studies to ascertain the risk of thromboembolism in THA [23, 24]. Therefore, we compared the degree of activation of thrombogenesis between HRA and noncemented traditional THA.
Our study is subject to several limitations. First, we did not determine either mortality or numbers of patients with PE or deep vein thrombosis (DVT). The ultimate studies assess a 3-month risk of symptomatic PE and all-cause mortality, but this requires large cohorts to define risk [26, 28]. Perioperative DVT can be detected with venography or ultrasonography, but larger numbers are needed (in the hundreds) and the cost is substantial. Intraoperative thrombogenesis has also been assessed using transesophageal echocardiography  and by quantifying the embolic load during surgery [4, 18]. This requires an intubated patient and cannot be used with epidural anesthesia. Second, thrombogenesis can be assessed by a number of markers of thrombin generation [8, 23, 24]. By using markers of thrombosis, fewer patients are required and an understanding of the timing of the onset of thrombogenesis can be defined. Third, although these markers of thrombosis have been useful in defining the timing and degree of activation of thrombosis, preoperative levels of these markers have not proven useful to predict DVT or PE . Furthermore, there have been no studies demonstrating any relationship between the increase in these markers and the ultimate development of DVT or PE. Thus, although these markers assess activation of thrombosis, they do not necessarily relate to a risk of DVT or PE after surgery.
Activation of thrombin generation during HRA is similar to THA, suggesting the thrombogenic risk is similar for both procedures. Therefore, HRA should be considered at risk for thromboembolism and treated using similar guidelines to other patients undergoing THA. Despite the reemergence of HRA, there are little objective data on the risk of DVT or PE after this procedure. The Birmingham Group reported on their experience by assessing bilateral Doppler ultrasound after surgery and followup with patients for evidence of PE or DVT. They found a low rate of DVT (10.2%) with HRA and a rate of 4.6% if pneumatic compression was also used . These rates are similar to another publication using multimodal thromboprophylaxis . There are no other large series assessing clinical outcome for PE, venography, or markers of thrombosis.
There are a number of ways to approach the thrombogenic risks of surgery. Prothrombin F1 + 2 is the cleavage product formed when prothrombin is converted to thrombin. Thrombin acts on fibrinogen to form fibrin that crosslinks to form clots. Thrombin is subsequently inactivated to form TAT III complexes. F1 + 2 and TAT both circulate in the bloodstream and can be measured with commercially available enzyme-linked immunosorbent assay kits (Dade Behring Enzygnost®; Siemens Healthcare Diagnostics, Inc, Deerfield, IL). Markers of thrombin generation (F1 + 2, TAT, and FpA) have been used to define the timing of thrombogenesis during surgery and quantify the degree of activation [1, 8, 23, 24]. During THA, thrombin generation peaks during surgery on the femur and declines after surgery [8, 23]. Insertion of a cemented femoral component results in greater thrombin generation than a noncemented femoral prosthesis . In TKA, thrombin generation increases during surgery [10, 25] and appears to be greater when surgery is performed using a tourniquet [13, 14], although others found no difference .
Blood levels of F1 + 2 and TAT have been used to assess the relative risk of developing DVT. Several studies report that patients who develop DVT (using ultrasound or venography) have elevated F1 + 2 or TAT [5, 6, 11]. However, these tests are not sufficiently specific to be clinically useful [5, 16]. Values of F1 + 2 and TAT have been used to assess the clinical response to anticoagulation [3, 17, 24]. Increases in F1 + 2 and TAT have been noted 4 to 6 weeks after surgery, which provides the rationale for extending anticoagulation therapy well into the postoperative period [2, 3]. It is interesting that clinically used doses of anticoagulants do not normalize levels of F1 + 2 and TAT after surgery [2, 3].
Although this is a preliminary study, it suggests the risk of developing thromboembolism after HRA is the same as other forms of THA. This information is useful because, when compared with THA, HRA involves a larger incision, longer surgical time, more potential occlusion of the femoral vessels, and insertion of cement. It is possible that the avoidance of femoral canal preparation with HRA might compensate for these risks, resulting in a thrombogenic potential comparable to THA. Until large outcome studies demonstrate that the risk of PE is lower, patients undergoing HRA should receive similar thromboprophylaxis to other forms of THA.
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