We evaluated 136 hips (104 patients) to determine the prevalence of and contributing factors in deep vein thrombosis (DVT) and pulmonary embolism (PE) in those who were not given thromboprophylaxis when undergoing primary cementless total hip arthroplasty (THA). We performed coagulation assays, a full blood count, blood typing, and serum chemical profile tests for all patients on three separate occasions. Molecular genetic testing was performed preoperatively to detect the genetic traits involving DVT. DVT was diagnosed by roentgenographic venography, and PE was diagnosed by perfusion lung scanning. Our patients had a low prevalence of DVT and no patient had PE. Patients with bilateral THA had similar rates (p = 0.158; CI, -0.134-0.125) of venographic DVT as patients with unilateral THA (16 of 65 or 25% versus 12 of 72 or 17% respectively). We observed a relationship between DVT and factor V Leiden mutation, antithrombin-III level, and prothrombin promoter G20210A mutation. We saw no relationship between DVT and coagulation or thrombophilic data. We conclude combinations of absent thrombophilic polymorphisms with low clinical prothrombotic risk factors led to low prevalence of DVT and virtually absent PE after THA in the current series of patients, who had not received any form of prophylactic or therapeutic treatment for DVT.
Copyright remains with the authors and publisher.
We evaluated 136 hips (104 patients) to determine the prevalence of and contributing factors in deep vein thrombosis (DVT) and pulmonary embolism (PE) in those who were not given thromboprophylaxis when undergoing primary cementless total hip arthroplasty (THA). We performed coagulation assays, a full blood count, blood typing, and serum chemical profile tests for all patients on three separate occasions. Molecular genetic testing was performed preoperatively to detect the genetic traits involving DVT. DVT was diagnosed by roentgenographic venography, and PE was diagnosed by perfusion lung scanning. Our patients had a low prevalence of DVT and no patient had PE. Patients with bilateral THA had similar rates (p = 0.158; CI, -0.134-0.125) of venographic DVT as patients with unilateral THA (16 of 65 or 25% versus 12 of 72 or 17% respectively). We observed a relationship between DVT and factor V Leiden mutation, antithrombin-III level, and prothrombin promoter G20210A mutation. We saw no relationship between DVT and coagulation or thrombophilic data. We conclude combinations of absent thrombophilic polymorphisms with low clinical prothrombotic risk factors led to low prevalence of DVT and virtually absent PE after THA in the current series of patients, who had not received any form of prophylactic or therapeutic treatment for DVT.
Copyright remains with the authors and publisher.